Reduction of the blood calcium below normal. Manifestations include hyperactive deep tendon reflexes, Chvostek's sign, muscle and abdominal cramps, and carpopedal spasm. (Dorland, 27th ed)
A condition caused by a deficiency of PARATHYROID HORMONE (or PTH). It is characterized by HYPOCALCEMIA and hyperphosphatemia. Hypocalcemia leads to TETANY. The acquired form is due to removal or injuries to the PARATHYROID GLANDS. The congenital form is due to mutations of genes, such as TBX1; (see DIGEORGE SYNDROME); CASR encoding CALCIUM-SENSING RECEPTOR; or PTH encoding parathyroid hormone.
A polypeptide hormone (84 amino acid residues) secreted by the PARATHYROID GLANDS which performs the essential role of maintaining intracellular CALCIUM levels in the body. Parathyroid hormone increases intracellular calcium by promoting the release of CALCIUM from BONE, increases the intestinal absorption of calcium, increases the renal tubular reabsorption of calcium, and increases the renal excretion of phosphates.
A nutritional condition produced by a deficiency of magnesium in the diet, characterized by anorexia, nausea, vomiting, lethargy, and weakness. Symptoms are paresthesias, muscle cramps, irritability, decreased attention span, and mental confusion, possibly requiring months to appear. Deficiency of body magnesium can exist even when serum values are normal. In addition, magnesium deficiency may be organ-selective, since certain tissues become deficient before others. (Harrison's Principles of Internal Medicine, 12th ed, p1936)
The calcium salt of gluconic acid. The compound has a variety of uses, including its use as a calcium replenisher in hypocalcemic states.
Surgical removal of the thyroid gland. (Dorland, 28th ed)
Two pairs of small oval-shaped glands located in the front and the base of the NECK and adjacent to the two lobes of THYROID GLAND. They secrete PARATHYROID HORMONE that regulates the balance of CALCIUM; PHOSPHORUS; and MAGNESIUM in the body.
A hereditary syndrome clinically similar to HYPOPARATHYROIDISM. It is characterized by HYPOCALCEMIA; HYPERPHOSPHATEMIA; and associated skeletal development impairment and caused by failure of response to PARATHYROID HORMONE rather than deficiencies. A severe form with resistance to multiple hormones is referred to as Type 1a and is associated with maternal mutant allele of the ALPHA CHAIN OF STIMULATORY G PROTEIN.
Abnormally high level of calcium in the blood.
A class of G-protein-coupled receptors that react to varying extracellular CALCIUM levels. Calcium-sensing receptors in the PARATHYROID GLANDS play an important role in the maintenance of calcium HOMEOSTASIS by regulating the release of PARATHYROID HORMONE. They differ from INTRACELLULAR CALCIUM-SENSING PROTEINS which sense intracellular calcium levels.
Excision of one or more of the parathyroid glands.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Condition with a variable constellation of phenotypes due to deletion polymorphisms at chromosome location 22q11. It encompasses several syndromes with overlapping abnormalities including the DIGEORGE SYNDROME, VELOCARDIOFACIAL SYNDROME, and CONOTRUNCAL AMOMALY FACE SYNDROME. In addition, variable developmental problems and schizoid features are also associated with this syndrome. (From BMC Med Genet. 2009 Feb 25;10:16) Not all deletions at 22q11 result in the 22q11deletion syndrome.
Abnormally elevated PARATHYROID HORMONE secretion as a response to HYPOCALCEMIA. It is caused by chronic KIDNEY FAILURE or other abnormalities in the controls of bone and mineral metabolism, leading to various BONE DISEASES, such as RENAL OSTEODYSTROPHY.
A non-metal element that has the atomic symbol P, atomic number 15, and atomic weight 31. It is an essential element that takes part in a broad variety of biochemical reactions.
Disorders caused by interruption of BONE MINERALIZATION manifesting as OSTEOMALACIA in adults and characteristic deformities in infancy and childhood due to disturbances in normal BONE FORMATION. The mineralization process may be interrupted by disruption of VITAMIN D; PHOSPHORUS; or CALCIUM homeostasis, resulting from dietary deficiencies, or acquired, or inherited metabolic, or hormonal disturbances.
A condition of abnormally elevated output of PARATHYROID HORMONE (or PTH) triggering responses that increase blood CALCIUM. It is characterized by HYPERCALCEMIA and BONE RESORPTION, eventually leading to bone diseases. PRIMARY HYPERPARATHYROIDISM is caused by parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. SECONDARY HYPERPARATHYROIDISM is increased PTH secretion in response to HYPOCALCEMIA, usually caused by chronic KIDNEY DISEASES.
A metallic element that has the atomic symbol Mg, atomic number 12, and atomic weight 24.31. It is important for the activity of many enzymes, especially those involved in OXIDATIVE PHOSPHORYLATION.
The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.
A vitamin that includes both CHOLECALCIFEROLS and ERGOCALCIFEROLS, which have the common effect of preventing or curing RICKETS in animals. It can also be viewed as a hormone since it can be formed in SKIN by action of ULTRAVIOLET RAYS upon the precursors, 7-dehydrocholesterol and ERGOSTEROL, and acts on VITAMIN D RECEPTORS to regulate CALCIUM in opposition to PARATHYROID HORMONE.
Congenital syndrome characterized by a wide spectrum of characteristics including the absence of the THYMUS and PARATHYROID GLANDS resulting in T-cell immunodeficiency, HYPOCALCEMIA, defects in the outflow tract of the heart, and craniofacial anomalies.
A condition of abnormally elevated output of PARATHYROID HORMONE due to parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. It is characterized by the combination of HYPERCALCEMIA, phosphaturia, elevated renal 1,25-DIHYDROXYVITAMIN D3 synthesis, and increased BONE RESORPTION.
Inorganic salts of phosphoric acid.
Disorders in the processing of calcium in the body: its absorption, transport, storage, and utilization.
Pathological processes of the PARATHYROID GLANDS. They usually manifest as hypersecretion or hyposecretion of PARATHYROID HORMONE that regulates the balance of CALCIUM; PHOSPHORUS; and MAGNESIUM in the body.
A disorder characterized by muscle twitches, cramps, and carpopedal spasm, and when severe, laryngospasm and seizures. This condition is associated with unstable depolarization of axonal membranes, primarily in the peripheral nervous system. Tetany usually results from HYPOCALCEMIA or reduced serum levels of MAGNESIUM that may be associated with HYPERVENTILATION; HYPOPARATHYROIDISM; RICKETS; UREMIA; or other conditions. (From Adams et al., Principles of Neurology, 6th ed, p1490)
A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)
A peptide hormone that lowers calcium concentration in the blood. In humans, it is released by thyroid cells and acts to decrease the formation and absorptive activity of osteoclasts. Its role in regulating plasma calcium is much greater in children and in certain diseases than in normal adults.
Pathological processes involving the THYROID GLAND.
Calcium compounds used as food supplements or in food to supply the body with calcium. Dietary calcium is needed during growth for bone development and for maintenance of skeletal integrity later in life to prevent osteoporosis.
A common form of hyperthyroidism with a diffuse hyperplastic GOITER. It is an autoimmune disorder that produces antibodies against the THYROID STIMULATING HORMONE RECEPTOR. These autoantibodies activate the TSH receptor, thereby stimulating the THYROID GLAND and hypersecretion of THYROID HORMONES. These autoantibodies can also affect the eyes (GRAVES OPHTHALMOPATHY) and the skin (Graves dermopathy).
Organic compounds which contain P-C-P bonds, where P stands for phosphonates or phosphonic acids. These compounds affect calcium metabolism. They inhibit ectopic calcification and slow down bone resorption and bone turnover. Technetium complexes of diphosphonates have been used successfully as bone scanning agents.
A condition of an abnormally low level of PHOSPHATES in the blood.
A small colorless crystal used as an anticonvulsant, a cathartic, and an electrolyte replenisher in the treatment of pre-eclampsia and eclampsia. It causes direct inhibition of action potentials in myometrial muscle cells. Excitation and contraction are uncoupled, which decreases the frequency and force of contractions. (From AMA Drug Evaluations Annual, 1992, p1083)
Decalcification of bone or abnormal bone development due to chronic KIDNEY DISEASES, in which 1,25-DIHYDROXYVITAMIN D3 synthesis by the kidneys is impaired, leading to reduced negative feedback on PARATHYROID HORMONE. The resulting SECONDARY HYPERPARATHYROIDISM eventually leads to bone disorders.
Disorder caused by an interruption of the mineralization of organic bone matrix leading to bone softening, bone pain, and weakness. It is the adult form of rickets resulting from disruption of VITAMIN D; PHOSPHORUS; or CALCIUM homeostasis.
Tumors or cancer of the PARATHYROID GLANDS.
Agents that inhibit BONE RESORPTION and/or favor BONE MINERALIZATION and BONE REGENERATION. They are used to heal BONE FRACTURES and to treat METABOLIC BONE DISEASES such as OSTEOPOROSIS.
A condition of abnormally high level of PHOSPHATES in the blood, usually significantly above the normal range of 0.84-1.58 mmol per liter of serum.
A salt used to replenish calcium levels, as an acid-producing diuretic, and as an antidote for magnesium poisoning.
A ubiquitously expressed member of the syntaxin subfamily of SNARE proteins that localizes to the GOLGI APPARATUS.
Therapy of heavy metal poisoning using agents which sequester the metal from organs or tissues and bind it firmly within the ring structure of a new compound which can be eliminated from the body.

Microdeletion 22q11 and oesophageal atresia. (1/502)

Oesophageal atresia (OA) is a congenital defect associated with additional malformations in 30-70% of the cases. In particular, OA is a component of the VACTERL association. Since some major features of the VACTERL association, including conotruncal heart defect, radial aplasia, and anal atresia, have been found in patients with microdeletion 22q11.2 (del(22q11.2)), we have screened for del(22q11.2) by fluorescent in situ hybridisation (FISH) in 15 syndromic patients with OA. Del(22q11.2) was detected in one of them, presenting with OA, tetralogy of Fallot, anal atresia, neonatal hypocalcaemia, and subtle facial anomalies resembling those of velocardiofacial syndrome. The occurrence of del(22q11.2) in our series of patients with OA is low (1/15), but this chromosomal anomaly should be included among causative factors of malformation complexes with OA. In addition, clinical variability of del(22q11.2) syndrome is further corroborated with inclusion of OA in the list of the findings associated with the deletion.  (+info)

Recurrent hyperparathyroidism. (2/502)

Recurrent hyperparathyroidism occurred in 11 of 295 patients from 10 months to 34 years after an initially successful operation. Seven patients with recurrent hyperparathyroidism had either multiple endocrine adenomatosis type I (MEA) or familial hyperparathyroidism (FHP), one patient had parathyroid cancer, and two patients had renal failure at the time of recurrence. Four of these patients ahd their initial operations elsewhere. Recurrence developed in 33% of patients with MEA or FHP but in only 0.4% of 242 patients without MEA or FHP. The presence of MEA or FHP was known before parathyroid exploration in 18 (86%) of the 21 patients. In patients with MEA or FHP, subtotal parathyroidectomy should be performed if there is more than one gland involved. Other patients should be treated by selective removal of an adenoma because recurrence is rare. Subtotal parathyroidectomy should be reserved for patients with diffuse hyperplasia.  (+info)

Effect of rate of calcium reduction and a hypocalcemic clamp on parathyroid hormone secretion: a study in dogs. (3/502)

BACKGROUND: The parathyroid hormone (PTH) calcium curve is used to evaluate parathyroid function in clinical studies. However, unanswered questions remain about whether PTH secretion is affected by the rate of calcium reduction and how the maximal PTH response to hypocalcemia is best determined. We performed studies in normal dogs to determine whether (a) the rate of calcium reduction affected the PTH response to hypocalcemia and (b) the reduction in PTH values during a hypocalcemic clamp from the peak PTH value observed during the nadir of hypocalcemia was due to a depletion of stored PTH. METHODS: Fast (30 min) and slow (120 min) ethylenediamine-tetraacetic acid (EDTA) infusions were used to induce similar reductions in ionized calcium. In the fast EDTA infusion group, serum calcium was maintained at the hypocalcemic 30-minute value for an additional 90 minutes (hypocalcemic clamp). To determine whether the reduction in PTH values during the hypocalcemic clamp represented depletion of PTH stores, three subgroups were studied. Serum calcium was rapidly reduced from established hypocalcemic levels in the fast-infusion group at 30 and 60 minutes (after 30 min of a hypocalcemic clamp) and in the slow-infusion group at 120 minutes. RESULTS: At the end of the fast and slow EDTA infusions, serum ionized calcium values were not different (0.84 +/- 0.02 vs. 0.82 +/- 0.03 mM), but PTH values were greater in the fast-infusion group (246 +/- 19 vs. 194 +/- 13 pg/ml, P < 0.05). During the hypocalcemic clamp, PTH rapidly decreased (P < 0.05) to value of approximately 60% of the peak PTH value obtained at 30 minutes. A rapid reduction in serum calcium from established hypocalcemic levels at 30 minutes did not stimulate PTH further, but also PTH values did not decrease as they did when a hypocalcemic clamp was started at 30 minutes. At 60 minutes, the reduction in serum calcium increased (P < 0.05) PTH to peak values similar to those before the hypocalcemic clamp. The reduction in serum calcium at 120 minutes in the slow EDTA infusion group increased PTH values from 224 +/- 11 to 302 +/- 30 pg/ml (P < 0.05). CONCLUSIONS: These results suggest that (a) the reduction in PTH values during the hypocalcemic clamp may not represent a depletion of PTH stores. (b) The use of PTH values from the hypocalcemic clamp as the maximal PTH may underestimate the maximal secretory capacity of the parathyroid glands and also would change the analysis of the PTH-calcium curve, and (c) the PTH response to similar reductions in serum calcium may be less for slow than fast reductions in serum calcium.  (+info)

Evidence for the promotion of bone mineralization by 1alpha,25-dihydroxycholecalciferol in the rat unrelated to the correction of deficiencies in serum calcium and phosphorus. (4/502)

Concurrent administration of 1alpha,25-dihydroxycholecalciferol [1alpha,25-(OH)2-CC] to intact and thyroparathyroidectomized rats treated with ethane-1-hydroxy-1,1-diphosphonate (EHDP) prevented or reversed the EHDP-induced inhibition of bone mineralization as measured by changes in epiphyseal plate width and ash content of bone. An analog, 1alpha-droxycholecalciferol, was also effective. Recovery of bone after EHDP treatment was also significantly improved by administration of 1alpha,25-(OH)2-CC as evidenced by enhanced uptake of 45Ca by epiphyseal plates and decreased plate widths. Cholecalciferol (CC), ergocalciferol, dihydrotachysterol2, 5,6-trans-CC, 25-OH-CC, 5,6-Trans-25-OH-CC, and 1alpha24R,25-(OH)3-CC also blocked EHDP-induced epiphyseal plate widening, but required high, pharmacological dose levels. 24R,25- (OH)2-CC was inactive at doses up to 10 microgram/day. Since EHDP-treated rats are not deficient in calcium or phosphate, these data suggest that 1alpha,25-dihydroxycholecalciferol promoted bone mineralization independently of effects upon the intestinal absorption of calcium and phosphate.  (+info)

Calcitonin is a major regulator for the expression of renal 25-hydroxyvitamin D3-1alpha-hydroxylase gene in normocalcemic rats. (5/502)

Regulation of vitamin D metabolism has long been examined by using vitamin D-deficient hypocalcemic animals. We previously reported that, in a rat model of chronic hyperparathyroidism, expression of 25-hydroxyvitamin D3-1alpha-hydroxylase (CYP27B1) mRNA was markedly increased in renal proximal convoluted tubules. It is believed that the major regulator for the expression of renal CYP27B1 is parathyroid hormone (PTH). However, in the normocalcemic state, the mechanism to regulate the renal CYP27B1 gene could be different, since plasma levels of PTH are very low. In the present study, the effect of PTH and calcitonin (CT) on the expression of renal CYP27B1 mRNA was investigated in normocalcemic sham-operated rats and normocalcemic thyroparathyroidectomized (TPTX) rats generated by either PTH or CaCl2 infusion. A single injection of CT dose-dependently decreased the expression of vitamin D receptor mRNA in the kidney of normocalcemic sham-TPTX rats. Concomitantly, CT greatly increased the expression of CYP27B1 mRNA in the kidney of normocalcemic sham-TPTX rats. CT also increased the expression of CYP27B1 mRNA in the kidney of normocalcemic TPTX rats. Conversion of serum [3H]1alpha,25(OH)2D3 from 25-hydroxy[3H]vitamin D3 in vivo was also greatly increased by the injection of CT into sham-TPTX rats and normocalcemic TPTX rats, but not into hypocalcemic TPTX rats. In contrast, administration of PTH did not induce the expression of CYP27B1 mRNA in the kidney of vitamin D-replete sham-TPTX rats and hypocalcemic TPTX rats. PTH increased the expression of renal CYP27B1 mRNA only in vitamin D-deficient hypocalcemic TPTX rats. These results suggest that CT plays an important role in the maintenance of serum 1alpha,25(OH)2D3 under normocalcemic physiological conditions, at least in rats.  (+info)

Calcimimetic compound NPS R-568 stimulates calcitonin secretion but selectively targets parathyroid gland Ca(2+) receptor in rats. (6/502)

N-(3-[2-Chlorophenyl]propyl)-(R)-alpha-methyl-3-methoxybenzylamine (NPS R-568) is an orally active compound that activates Ca(2+) receptors on parathyroid cells and rapidly suppresses plasma levels of parathyroid hormone (PTH) and Ca(2+) (ED(50), 1 and 10 mg/kg, respectively). We now show that increased calcitonin secretion contributes to NPS R-568-induced hypocalcemia. In parathyroidectomized thyroid-intact rats in which normocalcemia was restored by PTH infusion, NPS R-568 rapidly reduced plasma Ca(2+) levels, indicating that decreased PTH secretion was not solely responsible for the hypocalcemia seen in normal animals. NPS R-568 decreased plasma Ca(2+) levels in thyroidectomized parathyroid-intact rats, but the rate of onset of hypocalcemia was slower than in controls. In contrast, NPS R-568 had no effect on plasma Ca(2+) levels in PTH-infused, thyroparathyroidectomized rats, providing evidence that increased calcitonin secretion caused the hypocalcemia in PTH-infused parathyroidectomized rats. NPS R-568 rapidly increased plasma calcitonin levels to a peak at 10 to 20 min after oral dosing (ED(50) 40 mg/kg). NPS R-568 did not affect the rate of disappearance of (45)Ca from blood, indicating that hypocalcemia resulted from decreased influx of Ca(2+) into the circulation and not from increased efflux. This suggests that NPS R-568-induced hypocalcemia resulted solely from reduced efflux of Ca(2+) from bone after increased calcitonin and reduced PTH secretion. Thus, NPS R-568 causes hypocalcemia by activating Ca(2+) receptors on C cells and parathyroid cells; however, NPS R-568 is about 40 times more potent in reducing PTH levels than in increasing calcitonin levels.  (+info)

Calciotrophic hormones during experimental hypocalcaemia and hypercalcaemia in spontaneously diabetic rats. (7/502)

1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) concentrations have been found to be decreased in diabetic humans and rats. To investigate further the regulation of plasma Ca in diabetes, first we measured Ca(2+), P, Mg, parathyroid hormone(1-34) (PTH), and total and free 1,25(OH)(2)D(3) in male spontaneously diabetic rats 7 and 28 days after the onset of glycosuria. Secondly, we studied changes in the levels of PTH and 1,25(OH)(2)D(3) in response to hypocalcaemia induced by an i.v. infusion of EGTA (2.5%, wt/vol.) for 24 h, and changes in the levels of 1,25(OH)(2)D(3) in response to an i.v. infusion of rat PTH (10 microgram over 24 h) without or with concomitant EGTA infusion (producing hypercalcaemia or normo/hypocalcaemia respectively), in diabetic and control rats. Ca(2+), P, Mg and PTH concentrations remained within the control ranges after 7 and 28 days of glycosuria; 1,25(OH)(2)D(3) concentrations were decreased after 7, but not after 28, days of glycosuria. PTH concentrations showed a similar rise during EGTA-induced hypocalcaemia in control and diabetic rats compared with saline-infused rats, whereas 1,25(OH)(2)D(3) concentrations were unchanged in both groups. Total and free 1,25(OH)(2)D(3) levels were comparably (about 3-fold) increased during PTH, but not during combined PTH and EGTA infusion in control and diabetic rats. Total 1, 25(OH)(2)D(3) concentrations were lower in the diabetic groups infused with saline or PTH than in their respective controls, and there was a similar trend in the PTH+EGTA-infused group; free 1, 25(OH)(2)D(3) levels, however, were normal or increased in the diabetic groups, confirming our previous data. The novel finding of this study is that, despite severe insulin deficiency and altered 1, 25(OH)(2)D(3) levels, the in vivo response of PTH levels to hypocalcaemia and the in vivo response of 1,25(OH)(2)D(3) levels to PTH in diabetic rats are comparable with those found in nondiabetic rats.  (+info)

Hormonal control of calcium homeostasis. (8/502)

Calcium homeostasis in the extracellular fluid is tightly controlled and defended physiologically. Hypercalcemia always represents considerable underlying pathology and occurs when the hormonal control of calcium homeostasis is overwhelmed. The major hormones that are responsible for normal calcium homeostasis are parathyroid hormone and 1,25-dihydroxyvitamin D; these hormones control extracellular fluid calcium on a chronic basis. Over- or underproduction of these hormones or the tumor peptide, parathyroid hormone-related peptide, are the major causes of aberrant extracellular fluid calcium concentrations. These hormonal defense mechanisms are reviewed here.  (+info)

Hypocalcemia is a medical condition characterized by an abnormally low level of calcium in the blood. Calcium is a vital mineral that plays a crucial role in various bodily functions, including muscle contraction, nerve impulse transmission, and bone formation. Normal calcium levels in the blood usually range from 8.5 to 10.2 milligrams per deciliter (mg/dL). Hypocalcemia is typically defined as a serum calcium level below 8.5 mg/dL or, when adjusted for albumin (a protein that binds to calcium), below 8.4 mg/dL (ionized calcium).

Hypocalcemia can result from several factors, such as vitamin D deficiency, hypoparathyroidism (underactive parathyroid glands), kidney dysfunction, certain medications, and severe magnesium deficiency. Symptoms of hypocalcemia may include numbness or tingling in the fingers, toes, or lips; muscle cramps or spasms; seizures; and, in severe cases, cognitive impairment or cardiac arrhythmias. Treatment typically involves correcting the underlying cause and administering calcium and vitamin D supplements to restore normal calcium levels in the blood.

Hypoparathyroidism is a medical condition characterized by decreased levels or insufficient function of parathyroid hormone (PTH), which is produced and released by the parathyroid glands. These glands are located in the neck, near the thyroid gland, and play a crucial role in regulating calcium and phosphorus levels in the body.

In hypoparathyroidism, low PTH levels result in decreased absorption of calcium from the gut, increased excretion of calcium through the kidneys, and impaired regulation of bone metabolism. This leads to low serum calcium levels (hypocalcemia) and high serum phosphorus levels (hyperphosphatemia).

Symptoms of hypoparathyroidism can include muscle cramps, spasms, or tetany (involuntary muscle contractions), numbness or tingling sensations in the fingers, toes, and around the mouth, fatigue, weakness, anxiety, cognitive impairment, and in severe cases, seizures. Hypoparathyroidism can be caused by various factors, including surgical removal or damage to the parathyroid glands, autoimmune disorders, radiation therapy, genetic defects, or low magnesium levels. Treatment typically involves calcium and vitamin D supplementation to maintain normal serum calcium levels and alleviate symptoms. In some cases, recombinant PTH (Natpara) may be prescribed as well.

Parathyroid hormone (PTH) is a polypeptide hormone that plays a crucial role in the regulation of calcium and phosphate levels in the body. It is produced and secreted by the parathyroid glands, which are four small endocrine glands located on the back surface of the thyroid gland.

The primary function of PTH is to maintain normal calcium levels in the blood by increasing calcium absorption from the gut, mobilizing calcium from bones, and decreasing calcium excretion by the kidneys. PTH also increases phosphate excretion by the kidneys, which helps to lower serum phosphate levels.

In addition to its role in calcium and phosphate homeostasis, PTH has been shown to have anabolic effects on bone tissue, stimulating bone formation and preventing bone loss. However, chronic elevations in PTH levels can lead to excessive bone resorption and osteoporosis.

Overall, Parathyroid Hormone is a critical hormone that helps maintain mineral homeostasis and supports healthy bone metabolism.

Magnesium deficiency, also known as hypomagnesemia, is a condition characterized by low levels of magnesium in the blood. Magnesium is an essential mineral that plays a crucial role in many bodily functions, including muscle and nerve function, heart rhythm, bone strength, and immune system regulation.

Hypomagnesemia can occur due to various factors, such as poor dietary intake, malabsorption syndromes, chronic alcoholism, diabetes, certain medications (such as diuretics), and excessive sweating or urination. Symptoms of magnesium deficiency may include muscle cramps, tremors, weakness, heart rhythm abnormalities, seizures, and mental status changes.

It is important to note that mild magnesium deficiency may not cause any symptoms, and the diagnosis typically requires blood tests to measure magnesium levels. Treatment for hypomagnesemia usually involves oral or intravenous magnesium supplementation, along with addressing the underlying causes of the deficiency.

Calcium gluconate is a medical compound that is used primarily as a medication to treat conditions related to low calcium levels in the body (hypocalcemia) or to prevent calcium deficiency. It is also used as an antidote for treating poisoning from certain chemicals, such as beta-blockers and fluoride.

Calcium gluconate is a form of calcium salt, which is combined with gluconic acid, a natural organic acid found in various fruits and honey. This compound has a high concentration of calcium, making it an effective supplement for increasing calcium levels in the body.

In medical settings, calcium gluconate can be administered orally as a tablet or liquid solution, or it can be given intravenously (directly into a vein) by a healthcare professional. The intravenous route is typically used in emergency situations to quickly raise calcium levels and treat symptoms of hypocalcemia, such as muscle cramps, spasms, or seizures.

It's important to note that while calcium gluconate can be beneficial for treating low calcium levels, it should only be used under the guidance of a healthcare provider, as improper use or overdose can lead to serious side effects, including kidney damage and heart problems.

Thyroidectomy is a surgical procedure where all or part of the thyroid gland is removed. The thyroid gland is a butterfly-shaped endocrine gland located in the neck, responsible for producing hormones that regulate metabolism, growth, and development.

There are different types of thyroidectomy procedures, including:

1. Total thyroidectomy: Removal of the entire thyroid gland.
2. Partial (or subtotal) thyroidectomy: Removal of a portion of the thyroid gland.
3. Hemithyroidectomy: Removal of one lobe of the thyroid gland, often performed to treat benign solitary nodules or differentiated thyroid cancer.

Thyroidectomy may be recommended for various reasons, such as treating thyroid nodules, goiter, hyperthyroidism (overactive thyroid), or thyroid cancer. Potential risks and complications of the procedure include bleeding, infection, damage to nearby structures like the parathyroid glands and recurrent laryngeal nerve, and hypoparathyroidism or hypothyroidism due to removal of or damage to the parathyroid glands or thyroid gland, respectively. Close postoperative monitoring and management are essential to minimize these risks and ensure optimal patient outcomes.

The parathyroid glands are four small endocrine glands located in the neck, usually near or behind the thyroid gland. They secrete parathyroid hormone (PTH), which plays a critical role in regulating calcium and phosphate levels in the blood and bones. PTH helps maintain the balance of these minerals by increasing the absorption of calcium from food in the intestines, promoting reabsorption of calcium in the kidneys, and stimulating the release of calcium from bones when needed. Additionally, PTH decreases the excretion of calcium through urine and reduces phosphate reabsorption in the kidneys, leading to increased phosphate excretion. Disorders of the parathyroid glands can result in conditions such as hyperparathyroidism (overactive glands) or hypoparathyroidism (underactive glands), which can have significant impacts on calcium and phosphate homeostasis and overall health.

Pseudohypoparathyroidism (PHP) is a rare genetic disorder characterized by the body's resistance to the action of parathyroid hormone (PTH), leading to hypocalcemia (low serum calcium levels) and hyperphosphatemia (high serum phosphate levels). Despite normal or elevated PTH levels, target organs such as the kidneys and bones do not respond appropriately to its actions.

There are several types of PHP, with the most common being type Ia, which is caused by mutations in the GNAS gene. This gene provides instructions for making a protein called the alpha-subunit of the stimulatory G protein (Gs-alpha), which plays a crucial role in transmitting signals within cells. In PHP type Ia, there is a reduced amount or functionally impaired Gs-alpha protein, leading to resistance to PTH and other hormones that use this signaling pathway, such as thyroid-stimulating hormone (TSH) and gonadotropins.

PHP type Ia patients often exhibit physical features known as Albright's hereditary osteodystrophy (AHO), including short stature, round face, obesity, brachydactyly (shortened fingers and toes), and ectopic ossifications (formation of bone in abnormal places). However, it is important to note that not all individuals with AHO have PHP, and not all PHP patients display AHO features.

PHP type Ib is another common form of the disorder, characterized by PTH resistance without the physical manifestations of AHO. This type is caused by mutations in the STX16 gene or other genes involved in the intracellular trafficking of Gs-alpha protein.

Pseudohypoparathyroidism should be differentiated from hypoparathyroidism, a condition where there is an insufficient production or secretion of PTH by the parathyroid glands, leading to similar biochemical abnormalities but without resistance to PTH action.

Hypercalcemia is a medical condition characterized by an excess of calcium ( Ca2+ ) in the blood. While the normal range for serum calcium levels is typically between 8.5 to 10.2 mg/dL (milligrams per deciliter) or 2.14 to 2.55 mmol/L (millimoles per liter), hypercalcemia is generally defined as a serum calcium level greater than 10.5 mg/dL or 2.6 mmol/L.

Hypercalcemia can result from various underlying medical disorders, including primary hyperparathyroidism, malignancy (cancer), certain medications, granulomatous diseases, and excessive vitamin D intake or production. Symptoms of hypercalcemia may include fatigue, weakness, confusion, memory loss, depression, constipation, nausea, vomiting, increased thirst, frequent urination, bone pain, and kidney stones. Severe or prolonged hypercalcemia can lead to serious complications such as kidney failure, cardiac arrhythmias, and calcification of soft tissues. Treatment depends on the underlying cause and severity of the condition.

Calcium-sensing receptors (CaSR) are a type of G protein-coupled receptor that play a crucial role in the regulation of extracellular calcium homeostasis. They are widely expressed in various tissues, including the parathyroid gland, kidney, and bone.

The primary function of CaSR is to detect changes in extracellular calcium concentrations and transmit signals to regulate the release of parathyroid hormone (PTH) from the parathyroid gland. When the concentration of extracellular calcium increases, CaSR is activated, which leads to a decrease in PTH secretion, thereby preventing further elevation of calcium levels. Conversely, when calcium levels decrease, CaSR is inhibited, leading to an increase in PTH release and restoration of normal calcium levels.

In addition to regulating calcium homeostasis, CaSR also plays a role in other physiological processes, including cell proliferation, differentiation, and apoptosis. Dysregulation of CaSR has been implicated in various diseases, such as hyperparathyroidism, hypoparathyroidism, and cancer. Therefore, understanding the function and regulation of CaSR is essential for developing new therapeutic strategies to treat these conditions.

Parathyroidectomy is a surgical procedure for the removal of one or more of the parathyroid glands. These glands are located in the neck and are responsible for producing parathyroid hormone (PTH), which helps regulate the levels of calcium and phosphorus in the body.

Parathyroidectomy is typically performed to treat conditions such as hyperparathyroidism, where one or more of the parathyroid glands become overactive and produce too much PTH. This can lead to high levels of calcium in the blood, which can cause symptoms such as weakness, fatigue, bone pain, kidney stones, and mental confusion.

There are different types of parathyroidectomy procedures, including:

* Partial parathyroidectomy: removal of one or more, but not all, of the parathyroid glands.
* Total parathyroidectomy: removal of all four parathyroid glands.
* Subtotal parathyroidectomy: removal of three and a half of the four parathyroid glands, leaving a small portion of one gland to prevent hypoparathyroidism (a condition where the body produces too little PTH).

The choice of procedure depends on the underlying condition and its severity. After the surgery, patients may need to have their calcium levels monitored and may require calcium and vitamin D supplements to maintain normal calcium levels in the blood.

Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:

Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.

Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.

Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.

22q11 Deletion Syndrome, also known as DiGeorge Syndrome or Velocardiofacial Syndrome, is a genetic disorder caused by the deletion of a small piece of chromosome 22 at a specific location (q11.2). This deletion results in the poor development of several body systems, including the following:

* The third and fourth pharyngeal pouches, which give rise to various structures in the neck, such as the parathyroid glands and thymus. As a result, affected individuals often have hypocalcemia (low levels of calcium in the blood) due to decreased parathyroid hormone production, and may have immune deficiencies due to abnormal or missing thymus tissue.
* The fourth pharyngeal arch, which forms parts of the aortic arch, the cranial base, and the neck. This can lead to congenital heart defects, such as tetralogy of Fallot or interrupted aortic arch.
* The branchial arches, which contribute to the formation of the face and neck. This can result in distinctive facial features, such as a prominent nasal bridge, hooded eyelids, a small jaw, and low-set ears.

The severity of 22q11 Deletion Syndrome can vary widely, even among members of the same family. Common symptoms include heart defects, palate abnormalities, immune deficiencies, developmental delays, learning disabilities, behavioral problems, and hearing loss. Some individuals with this syndrome may also have psychiatric disorders, such as schizophrenia or anxiety disorders.

Treatment for 22q11 Deletion Syndrome typically involves a multidisciplinary approach, addressing each of the affected body systems. For example, heart defects may require surgical repair, while immune deficiencies may be managed with medications or thymus transplantation. Calcium supplements and vitamin D may be prescribed to treat hypocalcemia. Speech therapy, occupational therapy, and special education services can help address developmental delays and learning disabilities.

Secondary hyperparathyroidism is a condition characterized by an overproduction of parathyroid hormone (PTH) from the parathyroid glands due to hypocalcemia (low levels of calcium in the blood). This condition is usually a result of chronic kidney disease, where the kidneys fail to convert vitamin D into its active form, leading to decreased absorption of calcium in the intestines. The body responds by increasing PTH production to maintain normal calcium levels, but over time, this results in high PTH levels and associated complications such as bone disease, kidney stones, and cardiovascular calcification.

Phosphorus is an essential mineral that is required by every cell in the body for normal functioning. It is a key component of several important biomolecules, including adenosine triphosphate (ATP), which is the primary source of energy for cells, and deoxyribonucleic acid (DNA) and ribonucleic acid (RNA), which are the genetic materials in cells.

Phosphorus is also a major constituent of bones and teeth, where it combines with calcium to provide strength and structure. In addition, phosphorus plays a critical role in various metabolic processes, including energy production, nerve impulse transmission, and pH regulation.

The medical definition of phosphorus refers to the chemical element with the atomic number 15 and the symbol P. It is a highly reactive non-metal that exists in several forms, including white phosphorus, red phosphorus, and black phosphorus. In the body, phosphorus is primarily found in the form of organic compounds, such as phospholipids, phosphoproteins, and nucleic acids.

Abnormal levels of phosphorus in the body can lead to various health problems. For example, high levels of phosphorus (hyperphosphatemia) can occur in patients with kidney disease or those who consume large amounts of phosphorus-rich foods, and can contribute to the development of calcification of soft tissues and cardiovascular disease. On the other hand, low levels of phosphorus (hypophosphatemia) can occur in patients with malnutrition, vitamin D deficiency, or alcoholism, and can lead to muscle weakness, bone pain, and an increased risk of infection.

Rickets is a medical condition characterized by the softening and weakening of bones in children, primarily caused by deficiency of vitamin D, calcium, or phosphate. It leads to skeletal deformities, bone pain, and growth retardation. Prolonged lack of sunlight exposure, inadequate intake of vitamin D-rich foods, or impaired absorption or utilization of vitamin D can contribute to the development of rickets.

Hyperparathyroidism is a condition in which the parathyroid glands produce excessive amounts of parathyroid hormone (PTH). There are four small parathyroid glands located in the neck, near or within the thyroid gland. They release PTH into the bloodstream to help regulate the levels of calcium and phosphorus in the body.

In hyperparathyroidism, overproduction of PTH can lead to an imbalance in these minerals, causing high blood calcium levels (hypercalcemia) and low phosphate levels (hypophosphatemia). This can result in various symptoms such as fatigue, weakness, bone pain, kidney stones, and cognitive issues.

There are two types of hyperparathyroidism: primary and secondary. Primary hyperparathyroidism occurs when there is a problem with one or more of the parathyroid glands, causing them to become overactive and produce too much PTH. Secondary hyperparathyroidism develops as a response to low calcium levels in the body due to conditions like vitamin D deficiency, chronic kidney disease, or malabsorption syndromes.

Treatment for hyperparathyroidism depends on the underlying cause and severity of symptoms. In primary hyperparathyroidism, surgery to remove the overactive parathyroid gland(s) is often recommended. For secondary hyperparathyroidism, treating the underlying condition and managing calcium levels with medications or dietary changes may be sufficient.

Magnesium is an essential mineral that plays a crucial role in various biological processes in the human body. It is the fourth most abundant cation in the body and is involved in over 300 enzymatic reactions, including protein synthesis, muscle and nerve function, blood glucose control, and blood pressure regulation. Magnesium also contributes to the structural development of bones and teeth.

In medical terms, magnesium deficiency can lead to several health issues, such as muscle cramps, weakness, heart arrhythmias, and seizures. On the other hand, excessive magnesium levels can cause symptoms like diarrhea, nausea, and muscle weakness. Magnesium supplements or magnesium-rich foods are often recommended to maintain optimal magnesium levels in the body.

Some common dietary sources of magnesium include leafy green vegetables, nuts, seeds, legumes, whole grains, and dairy products. Magnesium is also available in various forms as a dietary supplement, including magnesium oxide, magnesium citrate, magnesium chloride, and magnesium glycinate.

Calcitriol is the active form of vitamin D, also known as 1,25-dihydroxyvitamin D. It is a steroid hormone that plays a crucial role in regulating calcium and phosphate levels in the body to maintain healthy bones. Calcitriol is produced in the kidneys from its precursor, calcidiol (25-hydroxyvitamin D), which is derived from dietary sources or synthesized in the skin upon exposure to sunlight.

Calcitriol promotes calcium absorption in the intestines, helps regulate calcium and phosphate levels in the kidneys, and stimulates bone cells (osteoblasts) to form new bone tissue while inhibiting the activity of osteoclasts, which resorb bone. This hormone is essential for normal bone mineralization and growth, as well as for preventing hypocalcemia (low calcium levels).

In addition to its role in bone health, calcitriol has various other physiological functions, including modulating immune responses, cell proliferation, differentiation, and apoptosis. Calcitriol deficiency or resistance can lead to conditions such as rickets in children and osteomalacia or osteoporosis in adults.

Vitamin D is a fat-soluble secosteroid that is crucial for the regulation of calcium and phosphate levels in the body, which are essential for maintaining healthy bones and teeth. It can be synthesized by the human body when skin is exposed to ultraviolet-B (UVB) rays from sunlight, or it can be obtained through dietary sources such as fatty fish, fortified dairy products, and supplements. There are two major forms of vitamin D: vitamin D2 (ergocalciferol), which is found in some plants and fungi, and vitamin D3 (cholecalciferol), which is produced in the skin or obtained from animal-derived foods. Both forms need to undergo two hydroxylations in the body to become biologically active as calcitriol (1,25-dihydroxyvitamin D3), the hormonally active form of vitamin D. This activated form exerts its effects by binding to the vitamin D receptor (VDR) found in various tissues, including the small intestine, bone, kidney, and immune cells, thereby influencing numerous physiological processes such as calcium homeostasis, bone metabolism, cell growth, and immune function.

DiGeorge syndrome is a genetic disorder caused by the deletion of a small piece of chromosome 22. It is also known as 22q11.2 deletion syndrome. The symptoms and severity can vary widely among affected individuals, but often include birth defects such as congenital heart disease, poor immune system function, and palatal abnormalities. Characteristic facial features, learning disabilities, and behavioral problems are also common. Some people with DiGeorge syndrome may have mild symptoms while others may be more severely affected. The condition is typically diagnosed through genetic testing. Treatment is focused on managing the specific symptoms and may include surgery, medications, and therapy.

Primary hyperparathyroidism is a medical condition characterized by excessive secretion of parathyroid hormone (PTH) from one or more of the parathyroid glands in the neck. These glands are normally responsible for regulating calcium levels in the body by releasing PTH, which helps to maintain an appropriate balance of calcium and phosphate in the bloodstream.

In primary hyperparathyroidism, the parathyroid gland(s) become overactive and produce too much PTH, leading to elevated calcium levels (hypercalcemia) in the blood. This can result in a variety of symptoms, such as fatigue, weakness, bone pain, kidney stones, and cognitive impairment, although some individuals may not experience any symptoms at all.

The most common cause of primary hyperparathyroidism is a benign tumor called an adenoma that develops in one or more of the parathyroid glands. In rare cases, primary hyperparathyroidism can be caused by cancer of the parathyroid gland(s) or by enlargement of all four glands (four-gland hyperplasia). Treatment typically involves surgical removal of the affected parathyroid gland(s), which is usually curative.

Phosphates, in a medical context, refer to the salts or esters of phosphoric acid. Phosphates play crucial roles in various biological processes within the human body. They are essential components of bones and teeth, where they combine with calcium to form hydroxyapatite crystals. Phosphates also participate in energy transfer reactions as phosphate groups attached to adenosine diphosphate (ADP) and adenosine triphosphate (ATP). Additionally, they contribute to buffer systems that help maintain normal pH levels in the body.

Abnormal levels of phosphates in the blood can indicate certain medical conditions. High phosphate levels (hyperphosphatemia) may be associated with kidney dysfunction, hyperparathyroidism, or excessive intake of phosphate-containing products. Low phosphate levels (hypophosphatemia) might result from malnutrition, vitamin D deficiency, or certain diseases affecting the small intestine or kidneys. Both hypophosphatemia and hyperphosphatemia can have significant impacts on various organ systems and may require medical intervention.

Calcium metabolism disorders refer to a group of medical conditions that affect the body's ability to properly regulate the levels of calcium in the blood and tissues. Calcium is an essential mineral that plays a critical role in many bodily functions, including bone health, muscle contraction, nerve function, and blood clotting.

There are several types of calcium metabolism disorders, including:

1. Hypocalcemia: This is a condition characterized by low levels of calcium in the blood. It can be caused by various factors such as vitamin D deficiency, hypoparathyroidism, and certain medications. Symptoms may include muscle cramps, spasms, and tingling sensations in the fingers and toes.
2. Hypercalcemia: This is a condition characterized by high levels of calcium in the blood. It can be caused by various factors such as hyperparathyroidism, cancer, and certain medications. Symptoms may include fatigue, weakness, confusion, and kidney stones.
3. Osteoporosis: This is a condition characterized by weak and brittle bones due to low calcium levels in the bones. It can be caused by various factors such as aging, menopause, vitamin D deficiency, and certain medications. Symptoms may include bone fractures and loss of height.
4. Paget's disease: This is a condition characterized by abnormal bone growth and deformities due to disordered calcium metabolism. It can be caused by various factors such as genetics, age, and certain medications. Symptoms may include bone pain, fractures, and deformities.

Treatment for calcium metabolism disorders depends on the underlying cause of the condition. It may involve supplements, medication, dietary changes, or surgery. Proper diagnosis and management are essential to prevent complications such as kidney stones, bone fractures, and neurological damage.

Parathyroid diseases refer to conditions that affect the parathyroid glands, which are small endocrine glands located in the neck, near or attached to the back surface of the thyroid gland. The primary function of the parathyroid glands is to produce and secrete parathyroid hormone (PTH), a crucial hormone that helps regulate calcium and phosphorus levels in the blood and bones.

There are four parathyroid glands, and they can develop various diseases, including:

1. Hyperparathyroidism: A condition where one or more parathyroid glands produce excessive amounts of PTH. This can lead to an imbalance in calcium and phosphorus levels, resulting in symptoms such as fatigue, weakness, bone pain, kidney stones, and increased risk of osteoporosis. Hyperparathyroidism can be primary (caused by a benign or malignant tumor in the parathyroid gland), secondary (due to chronic kidney disease or vitamin D deficiency), or tertiary (when secondary hyperparathyroidism becomes autonomous and continues even after correcting the underlying cause).
2. Hypoparathyroidism: A condition where the parathyroid glands do not produce enough PTH, leading to low calcium levels in the blood (hypocalcemia) and high phosphorus levels (hyperphosphatemia). Symptoms of hypoparathyroidism may include muscle spasms, tingling sensations in the fingers, toes, or lips, anxiety, cataracts, and seizures. Hypoparathyroidism can be caused by surgical removal of the parathyroid glands, autoimmune disorders, radiation therapy, or genetic conditions.
3. Parathyroid tumors: Abnormal growths in the parathyroid glands can lead to hyperparathyroidism. Benign tumors (adenomas) are the most common cause of primary hyperparathyroidism. Malignant tumors (carcinomas) are rare but can also occur, leading to more severe symptoms and a worse prognosis.
4. Parathyroid dysfunction in genetic disorders: Some genetic syndromes, such as multiple endocrine neoplasia type 1 (MEN1), multiple endocrine neoplasia type 2A (MEN2A), and hyperparathyroidism-jaw tumor syndrome (HPT-JT), can involve parathyroid gland abnormalities, leading to hyperparathyroidism or other related conditions.

Proper diagnosis and management of parathyroid disorders are crucial for maintaining optimal calcium homeostasis and preventing complications associated with hypocalcemia or hypercalcemia. Treatment options may include surgery, medication, dietary modifications, and monitoring hormone levels.

Tetany is a medical condition characterized by involuntary muscle spasms and cramps, often starting in the hands and feet and can spread to other parts of the body. It is typically caused by an imbalance of minerals such as calcium and magnesium in the blood, which can be due to various underlying medical conditions such as hypoparathyroidism, hypocalcemia, or alkalosis. Tetany can also occur after surgical removal of the parathyroid glands (a procedure called parathyroidectomy). In some cases, tetany can be a symptom of other neuromuscular disorders.

The muscle spasms associated with tetany can be painful and can interfere with normal functioning. They are often triggered by sensory stimuli such as touch, sound, or temperature changes. Tetany can also cause numbness, tingling, or a crawling sensation in the skin (paresthesia). In severe cases, it can lead to seizures, difficulty breathing, and cardiac arrhythmias.

Treatment of tetany typically involves addressing the underlying medical condition causing the imbalance of minerals in the blood. This may involve supplementation with calcium or magnesium, medication to regulate parathyroid hormone levels, or other treatments depending on the specific cause.

Vitamin D deficiency is a condition characterized by insufficient levels of vitamin D in the body, typically defined as a serum 25-hydroxyvitamin D level below 20 nanograms per milliliter (ng/mL) or 50 nanomoles per liter (nmol/L). Vitamin D is an essential fat-soluble vitamin that plays a crucial role in maintaining healthy bones and teeth by regulating the absorption of calcium and phosphorus. It also has various other functions in the body, including modulation of cell growth, immune function, and neuromuscular activity.

Vitamin D can be obtained through dietary sources such as fatty fish, fortified dairy products, and supplements, but the majority of vitamin D is produced in the skin upon exposure to sunlight. Deficiency can occur due to inadequate dietary intake, insufficient sun exposure, or impaired absorption or metabolism of vitamin D.

Risk factors for vitamin D deficiency include older age, darker skin tone, obesity, malabsorption syndromes, liver or kidney disease, and certain medications. Symptoms of vitamin D deficiency can be subtle and nonspecific, such as fatigue, bone pain, muscle weakness, and mood changes. However, prolonged deficiency can lead to more severe health consequences, including osteoporosis, osteomalacia, and increased risk of fractures.

Calcitonin is a hormone that is produced and released by the parafollicular cells (also known as C cells) of the thyroid gland. It plays a crucial role in regulating calcium homeostasis in the body. Specifically, it helps to lower elevated levels of calcium in the blood by inhibiting the activity of osteoclasts, which are bone cells that break down bone tissue and release calcium into the bloodstream. Calcitonin also promotes the uptake of calcium in the bones and increases the excretion of calcium in the urine.

Calcitonin is typically released in response to high levels of calcium in the blood, and its effects help to bring calcium levels back into balance. In addition to its role in calcium regulation, calcitonin may also have other functions in the body, such as modulating immune function and reducing inflammation.

Clinically, synthetic forms of calcitonin are sometimes used as a medication to treat conditions related to abnormal calcium levels, such as hypercalcemia (high blood calcium) or osteoporosis. Calcitonin can be administered as an injection, nasal spray, or oral tablet, depending on the specific formulation and intended use.

Thyroid diseases are a group of conditions that affect the function and structure of the thyroid gland, a small butterfly-shaped endocrine gland located in the base of the neck. The thyroid gland produces hormones that regulate many vital functions in the body, including metabolism, growth, and development.

Thyroid diseases can be classified into two main categories: hypothyroidism and hyperthyroidism. Hypothyroidism occurs when the thyroid gland does not produce enough hormones, leading to symptoms such as fatigue, weight gain, cold intolerance, constipation, and depression. Hyperthyroidism, on the other hand, occurs when the thyroid gland produces too much hormone, resulting in symptoms such as weight loss, heat intolerance, rapid heart rate, tremors, and anxiety.

Other common thyroid diseases include:

1. Goiter: an enlargement of the thyroid gland that can be caused by iodine deficiency or autoimmune disorders.
2. Thyroid nodules: abnormal growths on the thyroid gland that can be benign or malignant.
3. Thyroid cancer: a malignant tumor of the thyroid gland that requires medical treatment.
4. Hashimoto's disease: an autoimmune disorder that causes chronic inflammation of the thyroid gland, leading to hypothyroidism.
5. Graves' disease: an autoimmune disorder that causes hyperthyroidism and can also lead to eye problems and skin changes.

Thyroid diseases are diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as ultrasound or CT scan. Treatment options depend on the specific type and severity of the disease and may include medication, surgery, or radioactive iodine therapy.

Dietary calcium is a type of calcium that is obtained through food sources. Calcium is an essential mineral that is necessary for many bodily functions, including bone formation and maintenance, muscle contraction, nerve impulse transmission, and blood clotting.

The recommended daily intake of dietary calcium varies depending on age, sex, and other factors. For example, the recommended daily intake for adults aged 19-50 is 1000 mg, while women over 50 and men over 70 require 1200 mg per day.

Good dietary sources of calcium include dairy products such as milk, cheese, and yogurt; leafy green vegetables like broccoli and kale; fortified cereals and juices; and certain types of fish, such as salmon and sardines. It is important to note that some foods can inhibit the absorption of calcium, including oxalates found in spinach and rhubarb, and phytates found in whole grains and legumes.

If a person is unable to get enough calcium through their diet, they may need to take calcium supplements. However, it is important to talk to a healthcare provider before starting any new supplement regimen, as excessive intake of calcium can lead to negative health effects.

Graves' disease is defined as an autoimmune disorder that leads to overactivity of the thyroid gland (hyperthyroidism). It results when the immune system produces antibodies that stimulate the thyroid gland, causing it to produce too much thyroid hormone. This can result in a variety of symptoms such as rapid heartbeat, weight loss, heat intolerance, and bulging eyes (Graves' ophthalmopathy). The exact cause of Graves' disease is unknown, but it is more common in women and people with a family history of the disorder. Treatment may include medications to control hyperthyroidism, radioactive iodine therapy to destroy thyroid tissue, or surgery to remove the thyroid gland.

Diphosphonates are a class of medications that are used to treat bone diseases, such as osteoporosis and Paget's disease. They work by binding to the surface of bones and inhibiting the activity of bone-resorbing cells called osteoclasts. This helps to slow down the breakdown and loss of bone tissue, which can help to reduce the risk of fractures.

Diphosphonates are typically taken orally in the form of tablets, but some forms may be given by injection. Commonly prescribed diphosphonates include alendronate (Fosamax), risedronate (Actonel), and ibandronate (Boniva). Side effects of diphosphonates can include gastrointestinal symptoms such as nausea, heartburn, and abdominal pain. In rare cases, they may also cause esophageal ulcers or osteonecrosis of the jaw.

It is important to follow the instructions for taking diphosphonates carefully, as they must be taken on an empty stomach with a full glass of water and the patient must remain upright for at least 30 minutes after taking the medication to reduce the risk of esophageal irritation. Regular monitoring of bone density and kidney function is also recommended while taking these medications.

Hypophosphatemia is a medical condition characterized by abnormally low levels of phosphate (phosphorus) in the blood, specifically below 2.5 mg/dL. Phosphate is an essential electrolyte that plays a crucial role in various bodily functions such as energy production, bone formation, and maintaining acid-base balance.

Hypophosphatemia can result from several factors, including malnutrition, vitamin D deficiency, alcoholism, hormonal imbalances, and certain medications. Symptoms of hypophosphatemia may include muscle weakness, fatigue, bone pain, confusion, and respiratory failure in severe cases. Treatment typically involves correcting the underlying cause and administering phosphate supplements to restore normal levels.

Magnesium Sulfate is an inorganic salt with the chemical formula MgSO4. It is often encountered as the heptahydrate sulfate mineral epsomite (MgSO4·7H2O), commonly called Epsom salts. Magnesium sulfate is used medically as a vasodilator, to treat constipation, and as an antidote for magnesium overdose or poisoning. It is also used in the preparation of skin for esthetic procedures and in the treatment of eclampsia, a serious complication of pregnancy characterized by seizures.

Renal osteodystrophy is a bone disease that occurs in individuals with chronic kidney disease (CKD). It is characterized by abnormalities in the bones' structure and mineral composition due to disturbances in the metabolism of calcium, phosphorus, and vitamin D. These metabolic disturbances result from the kidneys' decreased ability to maintain balance in the levels of these minerals and hormones.

Renal osteodystrophy can manifest as several bone disorders, including:

1. Osteitis fibrosa cystica: Increased bone turnover due to excessive parathyroid hormone (PTH) production, leading to high levels of alkaline phosphatase and increased resorption of bones.
2. Adynamic bone disease: Decreased bone turnover due to reduced PTH levels, resulting in low bone formation rates and increased fracture risk.
3. Mixed uremic osteodystrophy: A combination of high and low bone turnover, with varying degrees of mineralization defects.
4. Osteomalacia: Defective mineralization of bones due to vitamin D deficiency or resistance, leading to soft and weak bones.

Symptoms of renal osteodystrophy may include bone pain, muscle weakness, fractures, deformities, and growth retardation in children. Diagnosis typically involves laboratory tests, imaging studies, and sometimes bone biopsies. Treatment focuses on correcting the metabolic imbalances through dietary modifications, medications (such as phosphate binders, vitamin D analogs, and calcimimetics), and addressing any secondary hyperparathyroidism if present.

Osteomalacia is a medical condition characterized by the softening of bones due to defective bone mineralization, resulting from inadequate vitamin D, phosphate, or calcium. It mainly affects adults and is different from rickets, which occurs in children. The primary symptom is bone pain, but muscle weakness can also occur. Prolonged osteomalacia may lead to skeletal deformities and an increased risk of fractures. Treatment typically involves supplementation with vitamin D, calcium, and sometimes phosphate.

Parathyroid neoplasms refer to abnormal growths in the parathyroid glands, which are small endocrine glands located in the neck, near or within the thyroid gland. These neoplasms can be benign (non-cancerous) or malignant (cancerous).

Benign parathyroid neoplasms are typically called parathyroid adenomas and are the most common type of parathyroid disorder. They result in overproduction of parathyroid hormone (PTH), leading to a condition known as primary hyperparathyroidism. Symptoms may include kidney stones, osteoporosis, fatigue, depression, and abdominal pain.

Malignant parathyroid neoplasms are called parathyroid carcinomas. They are rare but more aggressive than adenomas, with a higher risk of recurrence and metastasis. Symptoms are similar to those of benign neoplasms but may also include hoarseness, difficulty swallowing, and enlarged lymph nodes in the neck.

It is important to note that parathyroid neoplasms can only be definitively diagnosed through biopsy or surgical removal and subsequent histopathological examination.

Bone density conservation agents, also known as anti-resorptive agents or bone-sparing drugs, are a class of medications that help to prevent the loss of bone mass and reduce the risk of fractures. They work by inhibiting the activity of osteoclasts, the cells responsible for breaking down and reabsorbing bone tissue during the natural remodeling process.

Examples of bone density conservation agents include:

1. Bisphosphonates (e.g., alendronate, risedronate, ibandronate, zoledronic acid) - These are the most commonly prescribed class of bone density conservation agents. They bind to hydroxyapatite crystals in bone tissue and inhibit osteoclast activity, thereby reducing bone resorption.
2. Denosumab (Prolia) - This is a monoclonal antibody that targets RANKL (Receptor Activator of Nuclear Factor-κB Ligand), a key signaling molecule involved in osteoclast differentiation and activation. By inhibiting RANKL, denosumab reduces osteoclast activity and bone resorption.
3. Selective estrogen receptor modulators (SERMs) (e.g., raloxifene) - These medications act as estrogen agonists or antagonists in different tissues. In bone tissue, SERMs mimic the bone-preserving effects of estrogen by inhibiting osteoclast activity and reducing bone resorption.
4. Hormone replacement therapy (HRT) - Estrogen hormone replacement therapy has been shown to preserve bone density in postmenopausal women; however, its use is limited due to increased risks of breast cancer, cardiovascular disease, and thromboembolic events.
5. Calcitonin - This hormone, secreted by the thyroid gland, inhibits osteoclast activity and reduces bone resorption. However, it has largely been replaced by other more effective bone density conservation agents.

These medications are often prescribed for individuals at high risk of fractures due to conditions such as osteoporosis or metabolic disorders that affect bone health. It is essential to follow the recommended dosage and administration guidelines to maximize their benefits while minimizing potential side effects. Regular monitoring of bone density, blood calcium levels, and other relevant parameters is also necessary during treatment with these medications.

Hyperphosphatemia is a medical condition characterized by an excessively high level of phosphate (a form of the chemical element phosphorus) in the blood. Phosphate is an important component of various biological molecules, such as DNA, RNA, and ATP, and it plays a crucial role in many cellular processes, including energy metabolism and signal transduction.

In healthy individuals, the concentration of phosphate in the blood is tightly regulated within a narrow range to maintain normal physiological functions. However, when the phosphate level rises above this range (typically defined as a serum phosphate level greater than 4.5 mg/dL or 1.46 mmol/L), it can lead to hyperphosphatemia.

Hyperphosphatemia can result from various underlying medical conditions, including:

* Kidney dysfunction: The kidneys are responsible for filtering excess phosphate out of the blood and excreting it in the urine. When the kidneys fail to function properly, they may be unable to remove enough phosphate, leading to its accumulation in the blood.
* Hypoparathyroidism: The parathyroid glands produce a hormone called parathyroid hormone (PTH), which helps regulate calcium and phosphate levels in the body. In hypoparathyroidism, the production of PTH is insufficient, leading to an increase in phosphate levels.
* Hyperparathyroidism: In contrast, excessive production of PTH can also lead to hyperphosphatemia by increasing the release of phosphate from bones and decreasing its reabsorption in the kidneys.
* Excessive intake of phosphate-rich foods or supplements: Consuming large amounts of phosphate-rich foods, such as dairy products, nuts, and legumes, or taking phosphate supplements can raise blood phosphate levels.
* Tumor lysis syndrome: This is a complication that can occur after the treatment of certain types of cancer, particularly hematological malignancies. The rapid destruction of cancer cells releases large amounts of intracellular contents, including phosphate, into the bloodstream, leading to hyperphosphatemia.
* Rhabdomyolysis: This is a condition in which muscle tissue breaks down, releasing its contents, including phosphate, into the bloodstream. It can be caused by various factors, such as trauma, infection, or drug toxicity.

Hyperphosphatemia can have several adverse effects on the body, including calcification of soft tissues, kidney damage, and metabolic disturbances. Therefore, it is essential to diagnose and manage hyperphosphatemia promptly to prevent complications. Treatment options may include dietary modifications, medications that bind phosphate in the gastrointestinal tract, and dialysis in severe cases.

Calcium chloride is an inorganic compound with the chemical formula CaCl2. It is a white, odorless, and tasteless solid that is highly soluble in water. Calcium chloride is commonly used as a de-icing agent, a desiccant (drying agent), and a food additive to enhance texture and flavor.

In medical terms, calcium chloride can be used as a medication to treat hypocalcemia (low levels of calcium in the blood) or hyperkalemia (high levels of potassium in the blood). It is administered intravenously and works by increasing the concentration of calcium ions in the blood, which helps to regulate various physiological processes such as muscle contraction, nerve impulse transmission, and blood clotting.

However, it is important to note that calcium chloride can have adverse effects if not used properly or in excessive amounts. It can cause tissue irritation, cardiac arrhythmias, and other serious complications. Therefore, its use should be monitored carefully by healthcare professionals.

Syntaxin 16 is a type of SNARE (Soluble N-ethylmaleimide sensitive factor attachment protein receptor) protein that is primarily involved in the intracellular transport of vesicles and fusion of membranes within the cell. It is particularly found in the Golgi apparatus and endosomes, where it plays a crucial role in mediating the docking and fusion of transport vesicles with target membranes during the process of vesicle trafficking.

Syntaxin 16 forms a complex with other SNARE proteins such as Vti1a, SNAP-23/25, and VAMP4 to facilitate the formation of a stable four-helix bundle, which brings the vesicle and target membranes into close proximity and promotes their fusion. This process is essential for the proper sorting and transport of proteins and lipids between different intracellular compartments, as well as for the regulation of various cellular processes such as receptor internalization, neurotransmitter release, and hormone secretion.

Mutations in syntaxin 16 have been associated with certain human diseases, including forms of cancer and neurological disorders. Therefore, understanding the structure and function of syntaxin 16 is important for gaining insights into the molecular mechanisms underlying these conditions and for developing potential therapeutic strategies.

Chelation therapy is a medical treatment that involves the use of chelating agents to remove heavy metals and minerals from the body. A chelating agent is a molecule that bonds with the metal ions, forming a stable, water-soluble complex that can be excreted through urine or stool.

The most common chelating agent used in medical settings is ethylene diamine tetraacetic acid (EDTA), which is administered intravenously. EDTA binds with metals such as lead, mercury, iron, and calcium, and helps to eliminate them from the body.

Chelation therapy is primarily used to treat heavy metal poisoning, such as lead or mercury toxicity. It may also be used in some cases to treat cardiovascular disease, although its effectiveness for this use is still a matter of debate and controversy.

It's important to note that chelation therapy should only be administered under the supervision of a qualified healthcare professional, as improper use can lead to serious side effects and complications.

About 18% of people who are being treated in hospital have hypocalcemia. The neuromuscular symptoms of hypocalcemia are caused ... "Hypocalcemia as a predictor of mortality and transfusion. A scoping review of hypocalcemia in trauma and hemostatic ... hypocalcemia in animals) Calcium deficiency (plant disorder) Hypomagnesemia with secondary hypocalcemia Soar, J; Perkins, GD; ... But if the hypocalcemia has been severe and chronic, then this regimen can be fatal, because there is a degree of ...
Both early onset hypocalcemia (presents within 72h of birth) and late onset hypocalcemia (presents in 3-7 days after birth) ... Neonatal hypocalcemia is an abnormal clinical and laboratory hypocalcemia condition that is frequently observed in infants. It ... Hypocalcemia is a low blood calcium level. A total serum calcium of less than 8 mg/dL (2mmol/L) or ionized calcium less than ... Neonatal hypocalcemia can cause seizures in infants requiring a calcium infusion until homeostasis is achieved; allowing for ...
... (HSH) is an autosomal recessive genetic disorder that affects the absorption of ... Consequently, there is a decrease in both PTH and serum calcium levels, resulting in secondary hypocalcemia. One of the main ... Laboratory testing reveals hypomagnesemia (decreased serum magnesium levels), hypocalcemia (decreased serum calcium levels), ... "Hypomagnesemia with secondary hypocalcemia is caused by mutations in TRPM6, a new member of the TRPM gene family". Nat Genet. ...
Murphy, E; Williams (2009). "Hypocalcemia". Medicine. 37 (9): 465-468. doi:10.1016/j.mpmed.2009.06.003. Freund, Herbert; ...
Goyal A, Anastasopoulou C, Ngu M, Singh S (8 May 2022). "Hypocalcemia". StatPearls. StatPearls Publishing LLC. PMID 28613662. ...
Hypocalcemia: Hyperphosphatemia is a common finding in TLS, and high phosphorus levels can in turn contribute to hypocalcemia. ... Hypocalcemia. Because of the hyperphosphatemia, calcium is precipitated to form calcium phosphate, leading to hypocalcemia. ... Symptoms of hypocalcemia include (but are not limited to): tetany paresthesias muscle cramps muscle weakness sudden changes in ... Moreover, any symptomatic hypocalcemia should constitute clinical TLS. It is important to prevent life-threatening ...
Hypocalcemia can be parathyroid related or vitamin D related. Parathyroid related hypocalcemia includes post-surgical ... Vitamin D related hypocalcemia may be associated with a lack of vitamin D in the diet, a lack of sufficient UV exposure, or ... Hypocalcemia is common and can occur unnoticed with no symptoms or, in severe cases, can have dramatic symptoms and be life- ... Like hypocalcemia, hypercalcemia can be non-severe and present with no symptoms, or it may be severe, with life-threatening ...
APOA1 Hypocalcemia, autosomal dominant; 146200; CASR Hypocalciuric hypercalcemia, type I; 145980; CASR Hypochondroplasia; ... EGF Hypomagnesemia with secondary hypocalcemia; 602014; TRPM6 Hypomagnesemia, primary; 248250; CLDN16 Hypomagnesemia, renal, ...
leading to marked hypocalcemia. However, this is a minor effect with no physiological significance in humans. It is also a ...
See Hypocalcaemia.) Zn2+ - zinc ions are found in very small concentrations in the body, and their main purpose is that of an ...
In rare cases, Cushing's can cause hypocalcemia. The excess cortisol may also affect other endocrine systems and cause, for ...
It is contraindicated in people with hypocalcemia; sufficient calcium and vitamin D levels must be reached before starting on ... "FDA investigating risk of severe hypocalcemia in patients on dialysis". U.S. Food and Drug Administration (FDA). 22 November ... There is an increased risk of infections such as cellulitis, hypocalcemia (low blood calcium), hypersensitivity allergy ...
Hypocalcemia did not occur in either group. Hoy SM (September 2021). "Upacicalcet: First Approval". Drugs. 81 (13): 1593-1596. ...
Hypocalcemia (low levels of calcium in the blood) is also common, usually occurring within two to three months after birth. ... Transient hypocalcemia in a mother and son. Am. J. Dis. Child. 111, 201-207 Caffey, J. (1967). Congenital stenosis of medullary ... Blood tests can detect episodes of low levels of calcium in the blood (hypocalcemia). Treatment may be required to control ... Common methods of controlling hypocalcemia include the taking of oral calcium and vitamin D supplements. Other than this there ...
... , postparturient hypocalcemia, or parturient paresis is a disease, primarily in dairy cattle but also seen in beef ... Due to this large increase in demand for calcium, most cows will experience some degree of hypocalcemia for a short period ... It is believed that hypocalcemia causing milk fever is due to a lower level of responsiveness of the cow's tissues to ... When the mammary drain of plasma calcium causes hypocalcemia severe enough to compromise neuromuscular function, the cow is ...
Hypocalcaemia may also occur. Calcium channel blockers, also known as calcium channel antagonists, are widely used for a number ...
Hypocalcaemia: lack of 25-hydroxycholecalciferol (the way that vitamin D is stored in the body). As vitamin D regulates the ... Hypocalcaemia may be relative; calcium levels should be adjusted based on the albumin level and ionized calcium levels should ... vitamin D and calcium are also taken orally in case the alteration of vitamin D causes severe hypocalcaemia, this treatment has ...
Hypocalcemia should, therefore, be corrected before starting therapy. Etidronate has the same disadvantage as pyrophosphate in ... by a creatinine clearance below 30ml/min Hypersensitivity to alendronate or another ingredient in the product Hypocalcemia ...
In some cases, exposures can lead to hypocalcemia. Breathing in the HF fumes can result in fevers, pulmonary edema (fluid ...
"Disruption of TRPM6/TRPM7 complex formation by a mutation in the TRPM6 gene causes hypomagnesemia with secondary hypocalcemia ... "Primary hypomagnesemia with secondary hypocalcemia in an infant". Pediatrics. 41 (2): 385-402. PMID 5637791. Weber S, Hoffmann ...
Hyperkalemia Hyperventilation Hypocalcemia, and in turn: Hypermagnesemia, a condition in which hypocalcemia itself is typically ... It can also be a sign of hypocalcemia. Dental paresthesia is loss of sensation caused by maxillary or mandibular anesthetic ... Symptoms of hypocalcemia usually occur when ionized levels fall to ...
Following parathyroidectomy, hypocalcaemia is common. This results from a combination of suppressed parathyroid glands due to ...
Chrystal's hypocalcemia results in her bones rupturing, killing her. Prisca returns and slashes Charles with a rusted knife, ...
Sutters M, Gaboury CL, Bennett WM (1996). "Severe hyperphosphatemia and hypocalcemia: a dilemma in patient management". Journal ... such as hypocalcemia). Calcitriol Increase in serum phosphate. Fibroblast growth factor-23 (FGF23) is produced in osteoblasts ( ... hypocalcemia, and hypercalcemia. hPTH-(1-84) crystallizes as a slightly bent, long, helical dimer. The extended helical ... while secondary hyperparathyroidism is an appropriately high PTH level seen as a physiological response to hypocalcemia. A low ...
This leads to hypocalcemia and a subsequent increase in parathyroid hormone secretion in an attempt to increase the serum ... If the underlying cause of the hypocalcemia can be addressed, the hyperparathyroidism will resolve. In people with chronic ... Both processes lead to hypocalcemia and hence secondary hyperparathyroidism. Secondary hyperparathyroidism can also result from ... by the parathyroid glands in response to hypocalcemia (low blood calcium levels), with resultant hyperplasia of these glands. ...
Hypocalcemia (decreased calcium levels) is a contraindication of cinacalcet. Those who have serum calcium levels less than 7.5 ... Cinacalcet should not be administered until serum calcium levels are above 8.0 mg/dL and/or hypocalcemia symptoms are resolved ... Hypocalcemia symptoms include parethesias, myalgias, muscle cramping, tetany, and convulsions. ...
Hypocalcemia is not a term for tetany but is rather a cause of tetany. French Professor Armand Trousseau (1801-1867) devised ... Oct 1996). "Severe hyperphosphatemia and hypocalcemia: a dilemma in patient management". J Am Soc Nephrol. 7 (10): 2056-61. doi ... Hypocalcemia is the primary cause of tetany. Low ionized calcium levels in the extracellular fluid increase the permeability of ... calcium ions interact with the exterior surface of sodium channels in the plasma membrane of nerve cells and hypocalcemia ...
"Mutation of TRPM6 causes familial hypomagnesemia with secondary hypocalcemia". Nature Genetics. 31 (2): 171-174. doi:10.1038/ ...
"Neonatal Hypocalcemia in the Infant of a Diabetic Mother". Neonatal Network. 39 (4): 200-204. doi:10.1891/0730-0832.39.4.200. ...
"Disruption of TRPM6/TRPM7 complex formation by a mutation in the TRPM6 gene causes hypomagnesemia with secondary hypocalcemia ... "Mutation of TRPM6 causes familial hypomagnesemia with secondary hypocalcemia". Nature Genetics. 31 (2): 171-4. doi:10.1038/ ...
About 18% of people who are being treated in hospital have hypocalcemia. The neuromuscular symptoms of hypocalcemia are caused ... "Hypocalcemia as a predictor of mortality and transfusion. A scoping review of hypocalcemia in trauma and hemostatic ... hypocalcemia in animals) Calcium deficiency (plant disorder) Hypomagnesemia with secondary hypocalcemia Soar, J; Perkins, GD; ... But if the hypocalcemia has been severe and chronic, then this regimen can be fatal, because there is a degree of ...
... hypocalcemia). Explore symptoms, inheritance, genetics of this condition. ... Autosomal dominant hypocalcemia is characterized by low levels of calcium in the blood ( ... Autosomal dominant hypocalcemia is characterized by low levels of calcium in the blood (hypocalcemia). Affected individuals can ... Autosomal dominant hypocalcemia is primarily caused by mutations in the CASR gene; these cases are known as type 1. A small ...
"Our takeaway message is the 1-hour level PTH is very reliable in predicting hypocalcemia," he added. This measure can serve as ... Post-thyroidectomy hypocalcemia remains a major complication in patients who have undergone total thyroidectomy, and early ... The sensitivity of the early PTH assay, defined as "measured below 14 pg/ml," was 100% to detect hypocalcemia, with an area ... However, the results suggest that early measurement of PTH at 1 hour after surgery is an accurate predictor of hypocalcemia in ...
Hypocalcemia is frequently encountered in patients who are hospitalized. ... The presentations of patients with hypocalcemia vary widely, from asymptomatic to life-threatening situations. ... The treatment of hypocalcemia depends on the cause, the severity, the presence of symptoms, and how rapidly the hypocalcemia ... The following surgical procedures may result in hypocalcemia:. * Parathyroidectomy causes a transient hypocalcemia due to end- ...
Laboratory hypocalcemia is often asymptomatic, and its treatment in neonates is controversial. ... Hypocalcemia is a laboratory and clinical abnormality that is observed with relative frequency, especially in neonatal ... Early onset neonatal hypocalcemia. Early neonatal hypocalcemia, which occurs within 48-72 hours of birth, is most commonly seen ... Overall, one of the most common causes of hypocalcemia in children is renal failure, which results in hypocalcemia because of ...
Case reports of cardiac arrest or symptoms of hypocalcemia during chelation therapy should be reported to the CDC Lead ... Deaths Associated with Hypocalcemia from Chelation Therapy --- Texas, Pennsylvania, and Oregon, 2003--2005. ... The medical examiner determined the cause of death to be cardiac arrhythmia resulting from hypocalcemia associated with EDTA ... The myocardial necrosis resulted from hypocalcemia associated with administration of Na2EDTA. The case is under investigation ...
FDA is investigating the risk of severe hypocalcemia with serious outcomes, including hospitalization and death, in patients ... Prolia (denosumab) by Amgen: Drug Safety Communication - FDA Investigating Risk of Severe Hypocalcemia in Patients on Dialysis ... ISSUE: The FDA is investigating the risk of severe hypocalcemia with serious outcomes, including hospitalization and death, in ... Prolia (denosumab) by Amgen: Drug Safety Communication - FDA Investigating Risk of Severe Hypocalcemia in Patients on Dialysis ...
talk contribs‎ 4,435 bytes +4‎ →‎ CONFIRM HYPOCALCEMIA Tag: Visual edit. *curprev. 22:1222:12, 28 June 2018‎ Gunnam. talk ... talk contribs‎ 5,247 bytes +295‎ →‎ CONFIRM HYPOCALCEMIA Tag: Visual edit. *curprev. 17:1117:11, 28 June 2018‎ Gunnam. talk ... talk contribs‎ m 4,560 bytes +207‎ →‎Laboratory Differential Diagnosis of Hypocalcemia. *curprev. 16:4116:41, 30 March 2015‎ ... talk contribs‎ m 4,353 bytes −38‎ →‎Laboratory Differential Diagnosis of Hypocalcemia. *curprev. 16:4016:40, 30 March 2015‎ ...
CND significantly increases the rate of postoperative hypocalcemia, which can be prevented by routine postoperative ... hypocalcemia than the group without CND. The incidences of symptomatic and laboratory hypocalcemia were significantly decreased ... Prevention of postoperative hypocalcemia with routine oral calcium and vitamin D supplements in patients with differentiated ... Conclusions: Compared with total thyroidectomy alone, CND significantly increases the rate of postoperative hypocalcemia, which ...
During hypocalcemia, the total calcium level and the ionized calcium level fall below the laboratory reference range. ... Hypocalcemia may occur subsequent to failure of any of the mechanisms by whic... ... Hypocalcemia is a state of electrolyte imbalance in which the circulating serum calcium level is low. ... Hypocalcemia is a state of electrolyte imbalance in which the circulating serum calcium level is low. During hypocalcemia, the ...
This webinar will review calcium metabolism with a focus on early and late onset of neonatal hypocalcemia, utilizing an actual ... Monet Sayegh reviews calcium metabolism with a focus on early and late onset of neonatal hypocalcemia, utilizing an actual case ... Those interested in hypocalcemia, particularly in the neonatal and young children population ... Those interested in treatment options for early or late onset of neonatal hypocalcemia ...
If you have any problems, or just want to say hi, you can find us right here ...
The prevalence of ionised hypocalcaemia was very low (2.89 [2.04-4.07]%) compared with the prevalence of total hypocalcaemia (p ... The prevalence of total crude and total albumin-corrected hypocalcaemia in this study was 61.64 [58.69-64.50]% and 56.70 [53.72 ... This study compares the prevalence of hypocalcaemia in apparently healthy pregnant women from the ionised, and total calcaemia ... Only 2.89% of all apparently healthy pregnant women have ionised hypocalcaemia in late pregnancy, while 56.70% have total ...
Hypocalcemia Risk with Prolia Use in Dialysis Patients: The FDA explained it issued the alert because of the frequency and ... hypocalcemia side effect issue first came to our attention late last year with the release of this November 22, 2022 document ... hypocalcemia side effect safety signal according to this recent FDA information, October - December 2022 , Potential Signals ... FDA Drug Safety Communication: FDA investigating risk of severe hypocalcemia in patients on dialysis receiving osteoporosis ...
Are you sure you want to trigger topic in your Anconeus AI algorithm? ...
Preoperative vitamin D levels do not relate with the risk of hypocalcemia following total thyroidectomy. A cohort study - ... BACKGROUND: Hypocalcemia is the most common complication following total thyroidectomy. Few factors may relate with increased ... Preoperative vitamin D levels do not relate with the risk of hypocalcemia following total thyroidectomy. A cohort study. Alexis ... CONCLUSIONS: In our cohort of patients, preoperative vitamin D levels were not associated with a higher risk of hypocalcemia ...
A case of hypocalcaemia was also reported after high dose intravenous fusidic acid and hypocalcaemia was thought to be due to ... Discussion Two cases of hypocalcaemia related to fusidic acid were reported by Biswas et al. [1] In both cases, hypocalcaemia ... An unusual case of hypocalcaemia. Ye Kyaw 1 , Jennifer Tringham 1 , Tim Wang 2 & Emma Bingham 1 ... They postulated that hypocalcaemia secondary to fusidic acid was likely to be due to impaired vitamin D synthesis in liver and ...
Is there any real connection with feline hypocalcemia and the minerals calcium and phosphorus, or is this just another myth? ... Calcium is critical with Feline Hypocalcemia. THE SIGNS AND SYMPTOMS. The initial signs of Feline Hypocalcemia will be ... Feline Hypocalcemia In almost every case is the result of low calcium levels. ... However they are a must in most dogs and cats to maintain the proper nutritional mix, and to fight against Feline Hypocalcemia ...
Differentiating Hypocalcemia from other Diseases. Epidemiology and Demographics. Risk Factors. Screening. Natural History, ... Electrolyte Disturbances • Hyperkalemia • Hypokalemia • Hypercalcemia • Hypocalcemia • Nonspecific Changes Other Heart Diseases ... Retrieved from "https://www.wikidoc.org/index.php?title=Hypocalcemia&oldid=1489830" ...
Differentiating Hypocalcemia from other Diseases. Epidemiology and Demographics. Risk Factors. Screening. Natural History, ... Electrolyte Disturbances • Hyperkalemia • Hypokalemia • Hypercalcemia • Hypocalcemia • Nonspecific Changes Other Heart Diseases ... Retrieved from "https://www.wikidoc.org/index.php?title=Hypocalcemia&oldid=1489830" ...
CT scan damage control resuscitation damage control surgery diagnosis gallbladder hemostasis hemothorax hypocalcemia ...
Definition of Hypocalcemia - Glossary of Physiology Terms, Phrases, and Abbreviations ... Home , Glossary , H , Hypocalcemia. Note: Some functions of this site require your browser to support JavaScript. JavaScript is ...
Hypocalcemia And Mineral Metabolism. Hypocalcemia may be exacerbated by the use of Prolia. Pre-existing hypocalcemia must be ... Hypocalcemia. Pre-existing hypocalcemia must be corrected prior to initiating therapy with Prolia [see WARNINGS AND PRECAUTIONS ... Hypocalcemia. Decreases in serum calcium levels to less than 8.5 mg/dL at any visit were reported in 0.4% women in the placebo ... Low calcium levels in your blood (hypocalcemia). Prolia may lower the calcium levels in your blood. If you have low blood ...
In this article we will discuss the Signs and Symptoms of Hypocalcemia ...
Hypocalcemia is a condition where the levels in ones blood of calcium are below normal. A long-term calcium deficiency can ... Doctors define hypocalcemia, or a calcium deficiency, as a calcium concentration of less than 8.8 milligrams per deciliter. ... Calcium Deficiency (Hypocalcemia). October 10, 2022 , by Yashaswi Pathakamuri , Posted in Deficiency, Minerals ...
Hypocalcemia is frequently encountered in patients who are hospitalized. ... The presentations of patients with hypocalcemia vary widely, from asymptomatic to life-threatening situations. ... The treatment of hypocalcemia depends on the cause, the severity, the presence of symptoms, and how rapidly the hypocalcemia ... Complications of chronic hypocalcemia predominantly are those of bone disease. In addition, severe hypocalcemia may result in ...
How are hypoparathyroidism and hypocalcaemia treated?. Generally hypocalcaemia is treated with oral calcium and vitamin D ...
5.2 Hypocalcemia. Hypocalcemia associated with tetany (i.e., muscle cramps, twitching) and seizure activity has been reported ... Hypocalcemia: Hypocalcemia with tetany (i.e. muscle cramps, twitching) and seizure activity have been reported. ... Hypocalcemia [see Warnings and Precautions (5.2)] •. Malignancy [see Warnings and Precautions (5.3)] 6.1 Clinical Trials ... Hypocalcemia has been reported. Ensure adequate intake of calcium and vitamin D (5.2). •. Malignancy: A meta-analysis of 21 ...
Patients with sepsis demonstrate hypocalcemia usually associated with hypoalbuminemia.. Table 1: Causes of Hypocalcemia. ... Chronic moderate hypocalcemia may be completely asymptomatic. Acute hypocalcemia causes increased neuromuscular irritability, ... Acute pancreatitis precipitates calcium as a soap in the abdomen, causing hypocalcemia. Hungry bone syndrome is hypocalcemia ... Hypocalcemia after surgery can be mediated by the citrate content of transfused blood or by a large volume of fluid ...
Hypocalcemia: Management & boost your knowledge! Study for your classes, USMLE, MCAT or MBBS. Learn online with high-yield ... Hypocalcemia (Clinical) Hypocalcemia, a serum calcium < 8.5 mg/dL, can result from various conditions. The causes may ... Hypocalcemia Hypocalcemia, a serum calcium , 8.5 mg/dL, can result from various conditions. The causes may include ... Correction of calcium is dictated by the degree of severity of hypocalcemia. In severe cases, IV calcium administration is ...
  • The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect (i.e. increased responsiveness) due to the decreased interaction of calcium with sodium channels. (wikipedia.org)
  • Intravenous calcium infusion is essential to raise calcium levels and resolve or minimize symptoms in the setting of acute hypocalcemia. (springer.com)
  • This measure can serve as a guide for discharging patients the same day, with instructions to return if they develop any symptoms of hypocalcemia. (medscape.com)
  • The treatment of hypocalcemia depends on the cause, the severity, the presence of symptoms, and how rapidly the hypocalcemia developed. (medscape.com)
  • Advise patients on dialysis to immediately seek help if they experience symptoms of hypocalcemia. (fda.gov)
  • Quantitatively severe hypocalcemia can sometimes present with few symptoms, if onset has been protracted and chronic. (bmj.com)
  • Sodium 146 mmol/LL, potassium 4.9 mmol/L, urea 26.7 mmol/L, and creatinine 236 µmol/L, eGFR 23 ml/minute, adjusted calcium 1.6 mmol/L and phosphate 1.34 mmol/L). He did not have any signs and symptoms of hypocalcaemia. (endocrine-abstracts.org)
  • The symptoms of hypocalcemia can vary from person to person and from time to time. (nutritionfact.in)
  • Generally hypocalcaemia is treated with oral calcium and vitamin D keeping the blood calcium levels within the normal range and preventing the development of symptoms.Calcium carbonate is the cheapest form of oral calcium. (endocrinesurgeon.co.uk)
  • Acute hypocalcemia causes increased neuromuscular irritability, underlying the most prominent symptoms. (teachmemedicine.org)
  • Symptoms and signs of neonatal hypocalcemia rarely occur unless total serum calcium is 7 mg/dL ( 1.75 mmol/L) or the ionized calcium is 3.0 mg/dL ( 0.75 mmol/L). Signs include hypotonia, tachycardia, tachypnea, apnea, poor feeding, jitteriness, tetany, and seizures. (msdmanuals.com)
  • Systemic signs and symptoms include hypocalcemia and hyperkalemia, which leads to dysrhythmias, seizures, and possibly death. (cdc.gov)
  • The utility of postoperative PTH for predicting symptomatic hypocalcemia is beneficial for guiding postoperative management of patients following total thyroidectomy," said Larissa Sweeny, MD, of the University of Miami, Florida, who served as a moderator for the session in which the study was presented. (medscape.com)
  • In addition, adverse event reports submitted to the FDA suggested in a separate, internal study that patients on dialysis treated with Prolia are at 'substantial risk for severe and symptomatic hypocalcemia, including hospitalization and death. (drug-injury.com)
  • Postoperative PTH appears to be the most sensible item to predict the risk of postoperative symptomatic hypocalcemia. (minervamedica.it)
  • Parathyroid hormone deficiency or resistance is an important cause of symptomatic hypocalcemia in children. (ispae-jped.com)
  • In addition, adverse event reports submitted to FDA showed severe and symptomatic hypocalcemia, including hospitalization and death, is occurring in patients with advanced kidney disease treated with Prolia. (medlineplus.gov)
  • Preliminary results from a separate internal FDA study investigating the risk of hypocalcemia suggest that patients on dialysis treated with Prolia are at substantial risk for severe and symptomatic hypocalcemia, including hospitalization and death. (medlineplus.gov)
  • The most common cause for hypocalcemia is iatrogenic hypoparathyroidism. (wikipedia.org)
  • Hypoparathyroidism is a common cause of hypocalcemia. (wikipedia.org)
  • Some people with autosomal dominant hypocalcemia also have low levels of a hormone called parathyroid hormone (hypoparathyroidism). (medlineplus.gov)
  • The most frequent cause of hypocalcemia is postsurgical hypoparathyroidism, while a more comprehensive search for other causes is needed for appropriate treatment in the non PTH-mediated forms. (springer.com)
  • How are hypoparathyroidism and hypocalcaemia treated? (endocrinesurgeon.co.uk)
  • Hypoparathyroidism is the most common cause of hypocalcemia and often develops because of surgery in the central neck requiring radical resection of head and neck cancers. (teachmemedicine.org)
  • Mutations affecting intracellular processing of the pre-pro-PTH molecule are also described and lead to hypoparathyroidism, hypocalcemia, or both. (teachmemedicine.org)
  • Our study showed no evidence for concerns about the safety of D2 use in hypoparathyroidism, as we saw no more toxicity from D2 than from calcitriol and actually saw more hypocalcemia requiring medical attention in the calcitriol group," she observed. (medscape.com)
  • Dr. Streeten concluded, "We recommend that clinicians consider using D2 in treating hypoparathyroidism, particularly in patients who experience recurrent hypocalcemia. (medscape.com)
  • Activating genetic mutations have been identified which cause a hypocalcaemic syndrome of varying severity, termed 'autosomal dominant hypocalcaemia or hypoparathyroidism' as well as Bartter's syndrome type V [ 2 , 3 ] . (patient.info)
  • On occasion, severe hypocalcemia may result in seizures, tetany, refractory hypotension, or arrhythmias that require a more aggressive approach, including intravenous infusions of calcium. (medscape.com)
  • According to FDA and CDC, the safety and effectiveness of Na 2 EDTA in pediatric patients has not been established, and its use is not recommended because it induces hypocalcemia and possibly fatal tetany ( 1 ). (cdc.gov)
  • Acute hypocalcemia can lead to paresthesia, tetany, and seizures (characteristic physical signs may be observed, including Chvostek sign, which is poorly sensitive and specific of hypocalcemia, and Trousseau sign). (bmj.com)
  • Tetany is seen in severe hypocalcemia (ionized Ca level lower than 1.1 mmol/L). Milder forms of neuromuscular irritability are paresthesias and numbness of the fingertips and perioral area. (teachmemedicine.org)
  • In children, hypocalcemia is defined as a total serum calcium concentration less than 2.1 mmol/L (8.5 mg/dL). (medscape.com)
  • In term infants, hypocalcemia is defined as total serum calcium concentration less than 2 mmol/L (8 mg/dL) or ionized fraction of less than 1.1 mmol/L (4.4 mg/dL). (medscape.com)
  • In preterm infants, hypocalcemia is defined as total serum calcium concentration less than 1.75 mmol/L (7 mg/dL) is defined as hypocalcemia in infants weighing less than 1500 g birthweight. (medscape.com)
  • Hypocalcemia is a total serum calcium concentration 8 mg/dL ( 2 mmol/L) in term infants or 7 mg/dL ( 1.75 mmol/L) in preterm infants. (msdmanuals.com)
  • Hypocalcemia is a state of electrolyte imbalance in which the circulating serum calcium level is low. (bmj.com)
  • Congenital causes of hypocalcemia include activating mutations of calcium-sensing receptor, which has reset the calcium-parathyroid hormone (PTH) relation to a lower serum calcium level. (teachmemedicine.org)
  • Vitamin D deficiency leads to hypocalcemia when associated with decreased dietary calcium intake. (teachmemedicine.org)
  • the elevated phosphate level leads to hypocalcemia. (msdmanuals.com)
  • The aim of this clinical narrative review is to summarize and critically appraise the literature on the differential diagnosis of hypocalcemia and to provide its correct management. (springer.com)
  • Diagnosis and management of hypocalcaemia. (bmj.com)
  • Both calcium and ionized calcium are discussed, in detail, in conjunction with the role of magnesium, serum albumin, phosphate, blood pH, and Vitamin D play in the proper diagnosis of hypocalcemia. (siemens-healthineers.com)
  • Appreciate the complexity involved in the diagnosis of hypocalcemia in patients. (siemens-healthineers.com)
  • The purpose of this investigation was to determine the prevalence of hypocalcaemia on admission to critical care, to assess the current diagnosis and treatment regime and to attempt to identify any correlation between severity of illness and the prevalence of hypocalcaemia. (biomedcentral.com)
  • Similarly, a diagnosis of sepsis, severe sepsis and septic shock was not associated with hypocalcaemia. (biomedcentral.com)
  • P71.1 is a billable diagnosis code used to specify a medical diagnosis of other neonatal hypocalcemia. (icdlist.com)
  • The response to treatment determines diagnosis, but since hypocalcemia can lead to ketosis, treating for both is a good idea anyway. (5acresandadream.com)
  • In this webinar, Dr. Monet Sayegh reviews calcium metabolism with a focus on early and late onset of neonatal hypocalcemia, utilizing an actual case report. (siemens-healthineers.com)
  • Gain an understanding of the types, causes, and treatment of neonatal hypocalcemia. (siemens-healthineers.com)
  • [ 1 ] Symptomatic patients with classic clinical findings of acute hypocalcemia require immediate resuscitation and evaluation. (medscape.com)
  • SOCIETY FOR ENDOCRINOLOGY ENDOCRINE EMERGENCY GUIDANCE: Emergency management of acute hypocalcaemia in adult patients. (bmj.com)
  • Acute pancreatitis precipitates calcium as a soap in the abdomen, causing hypocalcemia. (teachmemedicine.org)
  • Parturient Paresis in Cows Parturient paresis (milk fever, hypocalcemia, paresis puerperalis, parturient apoplexy) is a disease of adult dairy cows in which acute hypocalcemia causes acute to peracute, afebrile, flaccid. (merckvetmanual.com)
  • However, most cases of hypocalcemia are discovered by clinical suspicion and appropriate laboratory testing. (medscape.com)
  • Most cases of hypocalcemia are clinically mild and require only supportive treatment and further laboratory evaluation. (medscape.com)
  • Hypocalcemia is a laboratory and clinical abnormality that is observed with relative frequency, especially in neonatal pediatric patients. (medscape.com)
  • Laboratory hypocalcemia is often asymptomatic, and its treatment in neonates is controversial. (medscape.com)
  • During hypocalcemia, the total calcium level and the ionized calcium level fall below the laboratory reference range. (bmj.com)
  • Specific laboratory tests obtained during a period of hypocalcemia will provide important diagnostic information regarding the underlying etiology. (mhmedical.com)
  • Returning to the November 2022 FDA Drug Safety Communication about the Prolia - hypocalcemia side effect safety signal, we point out this FDA statement: 'We will communicate our final conclusions and recommendations when we have completed our review or have more information to share. (drug-injury.com)
  • The authors therefore prospectively evaluated the clinical usefulness of routine oral calcium and vitamin D supplementation for prevention of hypocalcemia after total thyroidectomy and CND. (nih.gov)
  • The clinical features of hypocalcemia largely manifest through neuromuscular excitability. (bmj.com)
  • 70 confirmed cases of malaria were included in the present study to determine the clinical and prognostic implications of hypocalcemia and correlated QT interval (QTc) prolongation in malaria. (thepharmajournal.com)
  • In dogs, supplementation with oral calcium during pregnancy may predispose the animal to eclampsia during peak lactation, because excessive calcium intake during pregnancy causes downregulation of the calcium regulatory system and subsequent clinical hypocalcemia when calcium demand is high. (merckvetmanual.com)
  • That there was no apparent increase in the prevalence of denosumab-induced hypocalcaemia, suggests that the regulatory action had an impact in the clinical setting studied. (elsevierpure.com)
  • Disorders causing hypocalcemia can be divided into parathyroid hormone (PTH) and non-PTH mediated. (springer.com)
  • Postoperative parathyroid hormone (PTH) showed 100% sensitivity in predicting post-thyroidectomy hypocalcemia, according to the results of a prospective study of 60 patients. (medscape.com)
  • In a presentation at the annual meeting of the American Academy of Otolaryngology-Head and Neck Surgery, Youssef presented results of the study which looked at early post-operative parathyroid hormone as a predictor of post-thyroidectomy hypocalcemia. (medscape.com)
  • with agenesis or dysgenesis of the parathyroid glands have both early and late (prolonged) hypocalcemia. (msdmanuals.com)
  • Compared with total thyroidectomy alone, CND significantly increases the rate of postoperative hypocalcemia, which can be prevented by routine postoperative supplementation with oral calcium and vitamin D. (nih.gov)
  • Few factors may relate with increased risk of postoperative hypocalcemia. (minervamedica.it)
  • To evaluate the association of preoperative vitamin D levels with postoperative hypocalcaemia after total thyroidectomy. (biomedcentral.com)
  • 10 ng/mL), is an independent predictive factor of postoperative hypocalcaemia after total thyroidectomy. (biomedcentral.com)
  • Postoperative hypocalcaemia is the most common complication. (biomedcentral.com)
  • Despite an increasing number of studies investigating predictors of postoperative hypocalcaemia, there have been conflicting results regarding the impact of preoperative vitamin D deficiency. (biomedcentral.com)
  • The present study aims to evaluate the potential for using preoperative serum vitamin D concentrations to predict postoperative hypocalcaemia after total thyroidectomy in a homogenous group of patients. (biomedcentral.com)
  • 6 mg/dL) can lead to hypocalcemia by inhibiting PTH secretion. (teachmemedicine.org)
  • Abnormalities in this physiological response can lead to hypocalcemia in the neonate. (mhmedical.com)
  • Hospital pharmacies should evaluate whether continued stocking of Na 2 EDTA is necessary, given the established risk for hypocalcemia, the availability of less toxic alternatives, and an ongoing safety review by the Food and Drug Administration (FDA). (cdc.gov)
  • The FDA explained it issued the alert because of 'the frequency and seriousness' of the risk for hypocalcemia and resulting complications. (drug-injury.com)
  • The etiology and treatment of hypocalcemia is often determined by the age of onset. (mhmedical.com)
  • Impairment of the processes that increase calcium can also disrupt the normal regulation of other molecules, such as phosphate and magnesium, leading to other signs of autosomal dominant hypocalcemia. (medlineplus.gov)
  • The initial signs of Feline Hypocalcemia will be restlessness, rapid breathing, an uncoordinated gait, and then a very high and very dangerous fever. (petvitaminhealth.com)
  • It is said to occur before the other signs of hypocalcaemia and is both specific and sensitive. (patient.info)
  • Extensive osteoblastic skeletal metastases (prostate and breast cancers) may also cause hypocalcemia. (teachmemedicine.org)
  • Blood tests on admission showed severe hypocalcaemia with renal failure. (endocrine-abstracts.org)
  • We present a patient who developed severe hypocalcaemia after administration of denosumab in the context of severe vitamin D deficiency and a normal kidney function. (bmj.com)
  • For more information on hypocalcemia in children, see Pediatric Hypocalcemia . (medscape.com)
  • For more information on hypocalcemia, see the Medscape Reference articles Hypocalcemia in Emergency Medicine and Pediatric Hypocalcemia . (medscape.com)
  • The FDA is investigating the risk of severe hypocalcemia with serious outcomes, including hospitalization and death, in patients with advanced kidney disease on dialysis treated with the osteoporosis medicine Prolia (denosumab). (fda.gov)
  • Preliminary results from a separate internal FDA study further investigating hypocalcemia in dialysis patients treated with Prolia show a substantial risk with serious outcomes, including hospitalization and death. (fda.gov)
  • The most common features of autosomal dominant hypocalcemia include muscle spasms in the hands and feet (carpopedal spasms) and muscle cramping, prickling or tingling sensations (paresthesias), or twitching of the nerves and muscles (neuromuscular irritability) in various parts of the body. (medlineplus.gov)
  • As soon as the cuff is deflated, the patient is asked to take deep breaths at a rate of 40 per minute and carpopedal spasm is induced in hypocalcaemia. (patient.info)
  • A case of hypocalcaemia was also reported after high dose intravenous fusidic acid and hypocalcaemia was thought to be due to high phosphate contents in the intravenous antibiotics. (endocrine-abstracts.org)
  • The prevalence of autosomal dominant hypocalcemia is unknown. (medlineplus.gov)
  • We assessed four indicators: (a) the proportion of patients with calcium supplementation at the initial denosumab treatment, (b) the proportion of patients who underwent a serum calcium test, (c) the average number of serum calcium tests performed and (d) the prevalence of hypocalcaemia. (elsevierpure.com)
  • There was a significant difference in the prevalence of hypocalcaemia in data set two. (elsevierpure.com)
  • Hypocalcemia manifests as central nervous system (CNS) irritability and poor muscular contractility. (medscape.com)
  • Hypocalcemia varies from an asymptomatic biochemical abnormality to a life-threatening disorder, depending on the duration, severity, and rapidity of development. (teachmemedicine.org)
  • Correction of calcium is dictated by the degree of severity of hypocalcemia. (lecturio.com)
  • There was no correlation between the severity of disease and the occurrence of hypocalcaemia. (biomedcentral.com)
  • Hypocalcemia is a medical condition characterized by low calcium levels in the blood serum. (wikipedia.org)
  • As a result, calcium levels in the blood remain low, causing hypocalcemia. (medlineplus.gov)
  • However, children with hypocalcemia in pediatric intensive care units (PICUs) have mortality rates higher than those of children with normal calcium levels. (medscape.com)
  • FDA's review of interim results from an ongoing safety study of Prolia suggests an increased risk of hypocalcemia, or low calcium levels in the blood, in patients with advanced kidney disease. (fda.gov)
  • Circulating calcium levels are impaired by several factors, but hypocalcemia is mainly secondary to the imbalance of calcium absorption, excretion, and distribution. (bmj.com)
  • Serum and ionized calcium levels were reviewed for the presence of hypocalcaemia on admission and evidence of improvement over time. (biomedcentral.com)
  • Supplementation of calcium gluconate based on daily serum calcium levels was found to be an effective treatment for hypocalcaemia and led to a significant increase in both ionized and serum calcium concentrations on day 3 ( P = 0.001 and 0.020). (biomedcentral.com)
  • Serum calcium levels tend to underestimate hypocalcaemia compared with ionized calcium. (biomedcentral.com)
  • Although the existing treatment strategy was found to be effective in general, the use of ionized calcium levels for detection and treatment of hypocalcaemia might be more effective [ 2 ]. (biomedcentral.com)
  • Oral calcium and/or vitamin D supplementation is the most frequently used as treatment of chronic hypocalcemia. (springer.com)
  • Hypocalcemia occurs when the doe's diet contains an improper calcium/phosphorous ratio. (5acresandadream.com)
  • Neonatal hypocalcaemia occurs within the first two days of life and is most often caused by prematurity, being small for gestational age, maternal diabetes or hyperparathyroidism, and perinatal asphyxia. (pediatricsconferences.org)
  • The definition of hypocalcemia is based on both gestational and postnatal age in neonates and is different for children. (medscape.com)
  • However they are a must in most dogs and cats to maintain the proper nutritional mix, and to fight against Feline Hypocalcemia and Milk Fever. (petvitaminhealth.com)
  • Pregnancy toxemia (also called ketosis or twin lamb disease) and hypocalcemia (milk fever), are life threatening conditions which must be addressed immediately or the doe (or ewe) will die. (5acresandadream.com)
  • 1] In both cases, hypocalcaemia was associated with renal failure and hepatic impairment. (endocrine-abstracts.org)
  • They postulated that hypocalcaemia secondary to fusidic acid was likely to be due to impaired vitamin D synthesis in liver and renal failure. (endocrine-abstracts.org)
  • It seems that renal failure is more likely precipitant for hypocalcaemia in fusidic acid antibiotic therapy. (endocrine-abstracts.org)
  • Hungry bone syndrome is hypocalcemia after surgery for hyperparathyroidism (HPT) in patients with severe prolonged disease (secondary or tertiary HPT in renal failure). (teachmemedicine.org)
  • There were 54 cases of cerebral malaria, of which 23 had hypocalcemia as well as QTc prolongation, 15 of them developed renal failure and 14 had high parasitaemia. (thepharmajournal.com)
  • 1 The hypocalcemia may be transient, permanent, or intermittent, as with vitamin D deficiency during the winter. (teachmemedicine.org)
  • while the odds of symptomatic hypocalcaemia for patients with severe vitamin D deficiency was 10.18 times (95% CI: 1.14-90.86, P = 0.04) greater than for those with vitamin D sufficiency. (biomedcentral.com)
  • A meta-analysis of risk factors for hypocalcaemia after total thyroidectomy pooling the results of eight studies indicated that the incidence of hypocalcaemia was significantly increased in patients with vitamin D deficiency [ 4 ]. (biomedcentral.com)
  • Hypocalcaemia is a known side-effect of denosumab treatment. (bmj.com)
  • This case report emphasises the importance of screening and ongoing monitoring of risk factors for iatrogenic hypocalcaemia with denosumab treatment. (bmj.com)
  • What is known and Objective: Since its introduction in April 2012, denosumab has been administered to approximately 7,300 patients as of August 2012, and 32 cases of serious hypocalcaemia after denosumab administration, including two deaths, have been reported in Japan. (elsevierpure.com)
  • A Dear Healthcare Professional Letter of Rapid Safety Communication ('Blue letter') was released to warn about the risks of hypocalcaemia associated with denosumab. (elsevierpure.com)
  • The goal of this study therefore was to measure the impact of regulatory action on denosumab-induced hypocalcaemia in Japan by using an electronic medical information database (MID). (elsevierpure.com)
  • a hereditary condition caused by calcium sensing receptor gene mutations, resulting in calcium-hypersensitivity, and compensatory hypocalcemia and hypercalciuria. (icdlist.com)
  • Post-thyroidectomy hypocalcemia remains a major complication in patients who have undergone total thyroidectomy, and early identification can reduce disease burden and improve outcomes, according to Ahmed Sobhy Youssef, MD, of the University of Oklahoma Health Sciences Center, Oklahoma City, and colleagues. (medscape.com)
  • BACKGROUND: Hypocalcemia is the most common complication following total thyroidectomy. (minervamedica.it)
  • Autosomal dominant hypocalcemia is characterized by low levels of calcium in the blood (hypocalcemia). (medlineplus.gov)
  • Some people with autosomal dominant hypocalcemia have high levels of calcium in their urine (hypercalciuria), which can lead to deposits of calcium in the kidneys (nephrocalcinosis) or the formation of kidney stones (nephrolithiasis). (medlineplus.gov)
  • The combination of features of these two conditions is sometimes referred to as autosomal dominant hypocalcemia with Bartter syndrome or Bartter syndrome type V. (medlineplus.gov)
  • There are two types of autosomal dominant hypocalcemia distinguished by their genetic cause. (medlineplus.gov)
  • Derangements above (hypercalcaemia) and below (hypocalcaemia) this level interfere with the normal function of most body cells but nerve and muscle cells in particular. (patient.info)
  • Health care professionals should consider the risks of hypocalcemia with the use of Prolia in patients on dialysis. (fda.gov)
  • The FDA said its review of these interim results suggested an increased risk of hypocalcemia with Prolia in patients with advanced kidney disease. (drug-injury.com)
  • Of course, we will watch for the FDA's determination on possible regulatory action as regards this Prolia - hypocalcemia side effect -- for example, stronger drug safety warnings in a revised Prolia drug label -- and report on any such developments here on Drug Injury Watch. (drug-injury.com)
  • Our review of the interim results from this ongoing safety study suggests an increased risk of hypocalcemia with Prolia in patients with advanced kidney disease. (medlineplus.gov)
  • 19:56 19:56, 30 August 2012 ‎ Charmaine Patel talk contribs ‎ 643 bytes +643 ‎ Created page with '__NOTOC__ {{Hypocalcemia}} {{CMG}} Please help WikiDoc by adding more content here. (wikidoc.org)