Disorders in the processing of calcium in the body: its absorption, transport, storage, and utilization.
Pathological conditions resulting from abnormal anabolism or catabolism of lipids in the body.
Disorders in the processing of phosphorus in the body: its absorption, transport, storage, and utilization.
Generic term for diseases caused by an abnormal metabolic process. It can be congenital due to inherited enzyme abnormality (METABOLISM, INBORN ERRORS) or acquired due to disease of an endocrine organ or failure of a metabolically important organ such as the liver. (Stedman, 26th ed)
Disorders in the processing of iron in the body: its absorption, transport, storage, and utilization. (From Mosby's Medical, Nursing, & Allied Health Dictionary, 4th ed)
Pathological conditions in which the BLOOD GLUCOSE cannot be maintained within the normal range, such as in HYPOGLYCEMIA and HYPERGLYCEMIA. Etiology of these disorders varies. Plasma glucose concentration is critical to survival for it is the predominant fuel for the CENTRAL NERVOUS SYSTEM.
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 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.
Stable calcium atoms that have the same atomic number as the element calcium, but differ in atomic weight. Ca-42-44, 46, and 48 are stable calcium isotopes.
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 specialized CONNECTIVE TISSUE that is the main constituent of the SKELETON. The principle cellular component of bone is comprised of OSTEOBLASTS; OSTEOCYTES; and OSTEOCLASTS, while FIBRILLAR COLLAGENS and hydroxyapatite crystals form the BONE MATRIX.
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.
Abnormally high level of calcium in the blood.
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.
Signal transduction mechanisms whereby calcium mobilization (from outside the cell or from intracellular storage pools) to the cytoplasm is triggered by external stimuli. Calcium signals are often seen to propagate as waves, oscillations, spikes, sparks, or puffs. The calcium acts as an intracellular messenger by activating calcium-responsive proteins.
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 disease of pregnant and lactating cows and ewes leading to generalized paresis and death. The disease, which is characterized by hypocalcemia, occurs at or shortly after parturition in cows and within weeks before or after parturition in ewes.
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.
Native, inorganic or fossilized organic substances having a definite chemical composition and formed by inorganic reactions. They may occur as individual crystals or may be disseminated in some other mineral or rock. (Grant & Hackh's Chemical Dictionary, 5th ed; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Unstable isotopes of calcium that decay or disintegrate emitting radiation. Ca atoms with atomic weights 39, 41, 45, 47, 49, and 50 are radioactive calcium isotopes.
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 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.
Uptake of substances through the lining of the INTESTINES.
Hydroxy analogs of vitamin D 3; (CHOLECALCIFEROL); including CALCIFEDIOL; CALCITRIOL; and 24,25-DIHYDROXYVITAMIN D 3.
Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue.
An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands.
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.
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.
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.
Cholecalciferols substituted with two hydroxy groups in any position.

I alpha-hydroxycholecalciferol: a treatment of renal bone disease. (1/44)

Three patients with chronic renal failure on maintenance haemodialysis have been treated with 1 alpha-hydroxycholecalciferol (1 alpha-OHCC), a synthetic vitamin D analogue. A daily dose of 2 mug by mouth produced a significant increase in both calcium absorption from the gastrointestinal tract and calcium content of bone. Treatment with 1 alpha-OHCC appears to be effective in cases of metabolic bone disease associated with chronic renal failure.  (+info)

Idiopathic external root resorption associated to hypercalciuria. (2/44)

Although external root resorption (ERR) is a physiological process in deciduous dentition, it is very infrequent in permanent dentition - where the phenomenon is related to the existence of inadequate occlusal forces, periodontal pathology and microtraumatisms, etc. However, in many cases root resorption cannot be attributed to any concrete cause; such cases are defined as idiopathic external root resorption (IERR). Epidemiological studies have found that the underlying cause can only be established in 5% of all ERR. The present study describes three cases of IERR with different degrees of involvement and associated to mild calciuria and a history of nephrolithiasis. Hypercalciuria with normal blood calcium levels is usually idiopathic and exhibits a familial trait, with a prevalence of 20-40 cases per 1,000 individuals in adults. A form of hypercalciuria associated to nephrolithiasis with a mutation of the CLCN5 gene has been identified, involving low molecular weight proteinuria - though this mutation has not been uniformly demonstrated in most cases of idiopathic hypercalciuria. The peculiarity of the cases described in the present study is attributable to the coexistence of IERR with normocalcemic hypercalciuria and nephrolithiasis - thus pointing to the need for in-depth evaluation of the possible association of these three clinical situations.  (+info)

Reduced bone mass in children with idiopathic hypercalciuria and in their asymptomatic mothers. (3/44)

BACKGROUND: Patients with nephrolithiasis and idiopathic hypercalciuria (IH) may exhibit reduced bone mineral density (BMD). Most studies measuring BMD in IH patients employing dual-energy X-ray absorptiometry (DEXA) have been performed in adults, and no study has been conducted in North-American children. Optimal bone mineral accretion during childhood and adolescence is critical to the attainment of a healthy adult skeleton. Bone mineral accretion and eventual adult peak bone mass are largely dependent on genetic factors. Hypercalciuria is also frequently linked to genetic determinants. Therefore, we carried out a cross-sectional evaluation of bone mineral metabolism in children with IH, and in their asymptomatic premenopausal mothers. METHODS: Quantitative BMD using DEXA was performed in 21 children with IH and in their asymptomatic mothers. Bone resorption was assessed by measuring the urinary concentrations of pyridinoline and deoxypiridinoline. Simultaneous calcium-modulating hormonal determinations, including serum intact immunoreactive parathyroid hormone and 1,25(OH)(2)D(3), were performed. The expression of interleukin-1alpha (IL-1alpha) by peripheral blood mononuclear cells (PBMCs) was determined by polymerase chain reaction. RESULTS: Reduced BMD values were observed in eight children (38%) and in seven mothers (33%). The children of osteopenic mothers exhibited significantly reduced BMD Z-score values of lumbar spine (P<0.05) when compared with children of mothers with normal BMD. Bone resorption markers were normal in most children with IH. Hypercalciuria was detected in five out of 20 (25%) asymptomatic mothers and it correlated (r=-0.81) to femoral BMD in mothers with osteopenia. The expression of IL-1alpha mRNA by PBMCs from IH children did not differ from controls. CONCLUSIONS: Reduced BMD was detected in a large proportion of children with IH. Hypercalciuria and reduced BMD were uncovered in a substantial number of their otherwise healthy asymptomatic mothers. The diminished BMD in adults with IH may start early in life, could be influenced by genetic factors, and may represent a risk factor for osteoporosis later in life.  (+info)

Epithelial Ca(2+) channel (ECAC1) in autosomal dominant idiopathic hypercalciuria. (4/44)

BACKGROUND: The epithelial Ca(2+) channel (ECaC) exhibits the defining properties for being the gatekeeper in 1,25-dihydroxyvitamin D(3)-regulated Ca(2+) (re)absorption. Its recently cloned human orthologue (ECaC1) could, therefore, represent a crucial molecule in human disorders related to Ca(2+)-wasting such as idiopathic hypercalciuria (IH). METHODS: Fifty-seven members of nine families with IH were investigated. Phenotyping was performed by measurements of urinary Ca(2+) excretion, while other underlying disorders were appropriately excluded. Initially, the recently suggested locus for kidney stone-associated hypercalciuria on chromosome 1q23.3-q24 was investigated. Next, direct mutation analysis of all 15 exons of the ECAC1 gene and 2.9 kb upstream from the start codon was performed. hECaC1, heterologously expressed in human embryonic kidney 293 cells, was characterized by patch-clamp analysis. RESULTS: The mode of inheritance in the studied pedigrees is consistent with an autosomal dominant trait. Haplotype analysis did not implicate a role of the locus on chromosome 1. The coding sequence of the ECAC1 gene was not different between the affected and the non-affected family members. In the 5'-flanking region, three single nucleotide polymorphisms were encountered, but these polymorphisms were observed regardless of the affection status of the screened family members. Patch-clamp analysis of hECaC1 was performed as the putative pore region contains four non-conserved amino acid substitutions compared with the other species. This analysis revealed the distinctive properties of ECaC, including a high Ca(2+) selectivity, inward rectification, and Ca(2+)-dependent inactivation. CONCLUSION: These results do not support a primary role for hECaC1 in IH in nine affected families. Because of the heterogeneity of the disease, however, the involvement of ECaC1 in other subtypes of IH cannot be excluded and needs further investigation. The electrophysiological properties of hECaC1 further substantiate its prime role in Ca(2+) (re)absorption.  (+info)

Urinary calcium excretion in children with vesicoureteral reflux. (5/44)

BACKGROUND: Renal malformations including vesico-ureteral reflux (VUR) are associated with urolithiasis. However, studies on urinary calcium excretion in children with VUR have not been reported. This study was conducted to find out whether children with VUR have a higher prevalence of hypercalciuria and whether their family members are affected by hypercalciuria and/or urolithiasis. METHODS: We studied the prevalence of hypercalciuria and urolithiasis in 46 children (12 males and 34 females) with VUR and in their parents. RESULTS: Three out of 46 children had renal colic and nine out of 46 exhibited calyceal microlithiasis in the renal sonography. According to Stapleton's criteria, we found that 27 out of 46 children (58.6%) had hypercalciuria. These children were significantly shorter than children with normal calciuria and showed lower values of maximal urinary osmolality. We found no differences in urinary calcium excretion values related to the VUR grading, or to the presence or absence of renal scars, or to whether VUR was still unresolved or already resolved at the time of study. Seventeen out of 27 children with hypercalciuria (63%) had one or both parents affected by hypercalciuria, and there was a history of urolithiasis in six first-degree relatives and in four second-degree relatives (37%). Besides, 10 out of 19 children without hypercalciuria (52.6%) had one or both parents affected by hypercalciuria and there was a history of urolithiasis in three first-degree relatives and in three second-degree relatives (31.6%). Among the 27 children whose parents had hypercalciuria, four had both parents affected, 19 had only the mother affected and in four patients only the father was affected. CONCLUSION: Our results showed that the prevalence of hypercalciuria was greater in paediatric patients with VUR than in the general population. Urolithiasis in patients with VUR had a metabolic origin. Hypercalciuria was inherited as an autosomal dominant trait although with a higher probability to be inherited from the mother.  (+info)

Disruption of the caveolin-1 gene impairs renal calcium reabsorption and leads to hypercalciuria and urolithiasis. (6/44)

Using LoxP/Cre technology, we generated a knockout mouse homozygous for a null mutation in exon 2 of Cav1. In male Cav1-/- animals, we observed a dramatic increase in the incidence of urinary calcium stone formation. In 5-month-old male mice, the incidence of early urinary calculi was 67% in Cav1-/- mice compared to 19% in Cav1+/+ animals. Frank stone formation was observed in 13% of Cav1-/- males but was not seen in Cav1+/+ mice. Urine calcium concentration was significantly higher in Cav1-/- male mice compared to Cav1+/+ mice. In Cav1-/- mice, distal convoluted tubule cells were completely devoid of Cav1 and the localization of plasma membrane calcium ATPase was disrupted. Functional studies confirmed that active calcium absorption was significantly reduced in Cav1-/- compared to Cav1+/+ male mice. These results demonstrate that disruption of the Cav1 gene promotes the progressive steps required for urinary calcium stone formation and establish a new mouse model for urinary stone disease.  (+info)

Quantitative trait loci for hypercalciuria in a rat model of kidney stone disease. (7/44)

Hypercalciuria is the most common risk factor for kidney stones and has a recognized familial component. The genetic hypercalciuric stone-forming (GHS) rat is an animal model that closely resembles human idiopathic hypercalciuria, with excessive intestinal calcium absorption, increased bone resorption, and impaired renal calcium reabsorption; overexpression of the vitamin D receptor (VDR) in target tissues; and calcium nephrolithiasis. For identifying genetic loci that contribute to hypercalciuria in the GHS rat, an F2 generation of 156 rats bred from GHS female rats and normocalciuric WKY male rats was studied. The calcium excretion was six- to eightfold higher in the GHS female than in the WKY male progenitors. Selective genotyping of those F2 rats with the highest 30% and lowest 30% rates of calcium excretion was performed, scoring 98 markers with a mean interval of 23 cM across all 20 autosomes and the X chromosome. With the use of strict criteria for significance, significant linkage was found between hypercalciuria and a region of chromosome 1 at D1Rat169 (LOD, 2.91). Suggestive linkage to regions of chromosomes 4, 7, 10, and 14 was found. The proportion of phenotypic variance contributed by the region on chromosome 1, with appropriate adjustments, was estimated to be 7%. Candidate genes encoding the VDR and the calcium-sensing receptor were localized to regions on rat chromosomes 7 and 11, respectively, but the suggestive quantitative trait locus on chromosome 7 was not in the region of the VDR gene locus. Identification of genes that contribute to hypercalciuria in this animal model should prove valuable in understanding idiopathic hypercalciuria and kidney stone disease in humans.  (+info)

Hypercalciuria is a common and important finding in postmenopausal women with osteoporosis. (8/44)

OBJECTIVE AND DESIGN: The prevalence and the effects of hypercalciuria on bone in patients with primary osteoporosis are poorly defined. We therefore retrospectively analyzed the data of 241 otherwise healthy women. They were 45-88 years of age and had been referred for their first visit to our Unit for Metabolic Bone Diseases over a 2-year period because of primary osteoporosis (bone density T-score < -2.5). METHODS: The main parameters of calcium and skeletal metabolism had been analyzed in all subjects. This population was then divided into two groups, according to the presence (HC+) or absence (HC-) of hypercalciuria. RESULTS: Elevated urinary calcium was present in 19% of the subjects. Due to the selection criteria, spinal and femoral bone loss was similar in the two groups. Urinary calcium, phosphate and fractional calcium excretion were higher in hypercalciuric patients. In a logistic regression model, the higher the Tm of phosphate, the lower the risk of hypercalciuria (odds ratio 0.33, confidence interval 0.18-0.62). On the contrary, hypercalciuria was the most important predictor of low bone mass in HC+ (accounting for more than 50% of the variance in spinal bone density). CONCLUSIONS: Hypercalciuria is a common feature in postmenopausal bone loss. Since increased urinary calcium excretion and low bone mass appear to be linked, hypercalciuria seems to be an important determinant of reduced bone density in this setting as well.  (+info)

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.

Lipid metabolism disorders are a group of conditions that result from abnormalities in the breakdown, transport, or storage of lipids (fats) in the body. These disorders can lead to an accumulation of lipids in various tissues and organs, causing them to function improperly.

There are several types of lipid metabolism disorders, including:

1. Hyperlipidemias: These are conditions characterized by high levels of cholesterol or triglycerides in the blood. They can increase the risk of cardiovascular disease and pancreatitis.
2. Hypercholesterolemia: This is a condition characterized by high levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood. It can increase the risk of cardiovascular disease.
3. Hypocholesterolemias: These are conditions characterized by low levels of cholesterol in the blood. Some of these disorders may be associated with an increased risk of cancer and neurological disorders.
4. Hypertriglyceridemias: These are conditions characterized by high levels of triglycerides in the blood. They can increase the risk of pancreatitis and cardiovascular disease.
5. Lipodystrophies: These are conditions characterized by abnormalities in the distribution of body fat, which can lead to metabolic abnormalities such as insulin resistance, diabetes, and high levels of triglycerides.
6. Disorders of fatty acid oxidation: These are conditions that affect the body's ability to break down fatty acids for energy, leading to muscle weakness, liver dysfunction, and in some cases, life-threatening neurological complications.

Lipid metabolism disorders can be inherited or acquired, and their symptoms and severity can vary widely depending on the specific disorder and the individual's overall health status. Treatment may include lifestyle changes, medications, and dietary modifications to help manage lipid levels and prevent complications.

Phosphorus metabolism disorders refer to a group of conditions that affect the body's ability to properly regulate the levels and utilization of phosphorus. Phosphorus is an essential mineral that plays a critical role in many biological processes, including energy production, bone formation, and nerve function.

Disorders of phosphorus metabolism can result from genetic defects, kidney dysfunction, vitamin D deficiency, or other medical conditions. These disorders can lead to abnormal levels of phosphorus in the blood, which can cause a range of symptoms, including muscle weakness, bone pain, seizures, and respiratory failure.

Examples of phosphorus metabolism disorders include:

1. Hypophosphatemia: This is a condition characterized by low levels of phosphorus in the blood. It can be caused by various factors, such as malnutrition, vitamin D deficiency, and kidney dysfunction.
2. Hyperphosphatemia: This is a condition characterized by high levels of phosphorus in the blood. It can be caused by kidney failure, tumor lysis syndrome, and certain medications.
3. Hereditary hypophosphatemic rickets: This is a genetic disorder that affects the body's ability to regulate vitamin D and phosphorus metabolism. It can lead to weakened bones and skeletal deformities.
4. Oncogenic osteomalacia: This is a rare condition that occurs when tumors produce substances that interfere with phosphorus metabolism, leading to bone pain and weakness.

Treatment for phosphorus metabolism disorders depends on the underlying cause of the disorder and may include dietary changes, supplements, medications, or surgery.

Metabolic diseases are a group of disorders caused by abnormal chemical reactions in your body's cells. These reactions are part of a complex process called metabolism, where your body converts the food you eat into energy.

There are several types of metabolic diseases, but they most commonly result from:

1. Your body not producing enough of certain enzymes that are needed to convert food into energy.
2. Your body producing too much of certain substances or toxins, often due to a genetic disorder.

Examples of metabolic diseases include phenylketonuria (PKU), diabetes, and gout. PKU is a rare condition where the body cannot break down an amino acid called phenylalanine, which can lead to serious health problems if left untreated. Diabetes is a common disorder that occurs when your body doesn't produce enough insulin or can't properly use the insulin it produces, leading to high blood sugar levels. Gout is a type of arthritis that results from too much uric acid in the body, which can form crystals in the joints and cause pain and inflammation.

Metabolic diseases can be inherited or acquired through environmental factors such as diet or lifestyle choices. Many metabolic diseases can be managed with proper medical care, including medication, dietary changes, and lifestyle modifications.

Iron metabolism disorders are a group of medical conditions that affect the body's ability to absorb, transport, store, or utilize iron properly. Iron is an essential nutrient that plays a crucial role in various bodily functions, including oxygen transportation and energy production. However, imbalances in iron levels can lead to several health issues.

There are two main types of iron metabolism disorders:

1. Iron deficiency anemia (IDA): This condition occurs when the body lacks adequate iron to produce sufficient amounts of hemoglobin, a protein in red blood cells responsible for carrying oxygen throughout the body. Causes of IDA may include inadequate dietary iron intake, blood loss, or impaired iron absorption due to conditions like celiac disease or inflammatory bowel disease.
2. Hemochromatosis: This is a genetic disorder characterized by excessive absorption and accumulation of iron in various organs, including the liver, heart, and pancreas. Over time, this excess iron can lead to organ damage and diseases such as cirrhosis, heart failure, diabetes, and arthritis. Hemochromatosis is typically caused by mutations in the HFE gene, which regulates iron absorption in the intestines.

Other iron metabolism disorders include:

* Anemia of chronic disease (ACD): A type of anemia that occurs in individuals with chronic inflammation or infection, where iron is not efficiently used for hemoglobin production due to altered regulation.
* Sideroblastic anemias: These are rare disorders characterized by the abnormal formation of ringed sideroblasts (immature red blood cells containing iron-laden mitochondria) in the bone marrow, leading to anemia and other symptoms.
* Iron-refractory iron deficiency anemia (IRIDA): A rare inherited disorder caused by mutations in the TMPRSS6 gene, resulting in impaired regulation of hepcidin, a hormone that controls iron absorption and distribution in the body. This leads to both iron deficiency and iron overload.

Proper diagnosis and management of iron metabolism disorders are essential to prevent complications and maintain overall health. Treatment options may include dietary modifications, iron supplementation, phlebotomy (bloodletting), or chelation therapy, depending on the specific disorder and its severity.

Glucose metabolism disorders are a group of conditions that result from abnormalities in the body's ability to produce, store, or use glucose, which is a simple sugar that serves as the primary source of energy for the body's cells. These disorders can be categorized into two main types: those caused by insufficient insulin production (such as type 1 diabetes) and those caused by impaired insulin action (such as type 2 diabetes).

In healthy individuals, glucose is absorbed from food during digestion and enters the bloodstream. The pancreas responds to this increase in blood glucose levels by releasing insulin, a hormone that signals cells throughout the body to take up glucose from the bloodstream and use it for energy production or storage.

Glucose metabolism disorders can disrupt this process at various stages, leading to high blood glucose levels (hyperglycemia) or low blood glucose levels (hypoglycemia). Some common examples of these disorders include:

1. Diabetes Mellitus: A group of metabolic disorders characterized by high blood glucose levels due to insufficient insulin production, impaired insulin action, or both. Type 1 diabetes results from the autoimmune destruction of pancreatic beta-cells that produce insulin, while type 2 diabetes is caused by a combination of insulin resistance and inadequate insulin secretion.
2. Gestational Diabetes: A form of high blood glucose that develops during pregnancy due to hormonal changes that impair insulin action.
3. Prediabetes: A condition where blood glucose levels are higher than normal but not yet high enough to be classified as diabetes.
4. Hypoglycemia: Abnormally low blood glucose levels, which can result from certain medications, hormonal deficiencies, or other medical conditions.
5. Glycogen Storage Diseases: A group of rare inherited metabolic disorders that affect the body's ability to store and break down glycogen, a complex carbohydrate that serves as an energy reserve in muscles and the liver.
6. Maturity-Onset Diabetes of the Young (MODY): A group of monogenic forms of diabetes caused by mutations in specific genes involved in insulin secretion or action.
7. Glucose Galactose Malabsorption: An inherited disorder that impairs the absorption of glucose and galactose, leading to severe diarrhea, dehydration, and high blood glucose levels.
8. Fructose Intolerance: A condition where the body cannot metabolize fructose properly due to a deficiency in the enzyme aldolase B, resulting in abdominal pain, diarrhea, and high blood glucose levels.

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.

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.

Calcium isotopes refer to variants of the chemical element calcium (ca) that have different numbers of neutrons in their atomic nuclei, and therefore differ in their atomic masses while having the same number of protons. The most common and stable calcium isotope is Calcium-40, which contains 20 protons and 20 neutrons. However, calcium has several other isotopes, including Calcium-42, Calcium-43, Calcium-44, and Calcium-46 to -52, each with different numbers of neutrons. Some of these isotopes are radioactive and decay over time. The relative abundances of calcium isotopes can vary in different environments and can provide information about geological and biological processes.

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.

"Bone" is the hard, dense connective tissue that makes up the skeleton of vertebrate animals. It provides support and protection for the body's internal organs, and serves as a attachment site for muscles, tendons, and ligaments. Bone is composed of cells called osteoblasts and osteoclasts, which are responsible for bone formation and resorption, respectively, and an extracellular matrix made up of collagen fibers and mineral crystals.

Bones can be classified into two main types: compact bone and spongy bone. Compact bone is dense and hard, and makes up the outer layer of all bones and the shafts of long bones. Spongy bone is less dense and contains large spaces, and makes up the ends of long bones and the interior of flat and irregular bones.

The human body has 206 bones in total. They can be further classified into five categories based on their shape: long bones, short bones, flat bones, irregular bones, and sesamoid bones.

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.

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.

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.

Calcium signaling is the process by which cells regulate various functions through changes in intracellular calcium ion concentrations. Calcium ions (Ca^2+^) are crucial second messengers that play a critical role in many cellular processes, including muscle contraction, neurotransmitter release, gene expression, and programmed cell death (apoptosis).

Intracellular calcium levels are tightly regulated by a complex network of channels, pumps, and exchangers located on the plasma membrane and intracellular organelles such as the endoplasmic reticulum (ER) and mitochondria. These proteins control the influx, efflux, and storage of calcium ions within the cell.

Calcium signaling is initiated when an external signal, such as a hormone or neurotransmitter, binds to a specific receptor on the plasma membrane. This interaction triggers the opening of ion channels, allowing extracellular Ca^2+^ to flow into the cytoplasm. In some cases, this influx of calcium ions is sufficient to activate downstream targets directly. However, in most instances, the increase in intracellular Ca^2+^ serves as a trigger for the release of additional calcium from internal stores, such as the ER.

The release of calcium from the ER is mediated by ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP3Rs), which are activated by specific second messengers generated in response to the initial external signal. The activation of these channels leads to a rapid increase in cytoplasmic Ca^2+^, creating a transient intracellular calcium signal known as a "calcium spark" or "calcium puff."

These localized increases in calcium concentration can then propagate throughout the cell as waves of elevated calcium, allowing for the spatial and temporal coordination of various cellular responses. The duration and amplitude of these calcium signals are finely tuned by the interplay between calcium-binding proteins, pumps, and exchangers, ensuring that appropriate responses are elicited in a controlled manner.

Dysregulation of intracellular calcium signaling has been implicated in numerous pathological conditions, including neurodegenerative diseases, cardiovascular disorders, and cancer. Therefore, understanding the molecular mechanisms governing calcium homeostasis and signaling is crucial for the development of novel therapeutic strategies targeting these diseases.

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.

Parturient paresis, also known as Eclampsia or Puerperal eclampsia, is a serious condition that can occur during pregnancy or after childbirth. It is characterized by the onset of seizures (convulsions) and coma in a woman who has previously developed high blood pressure and proteinuria (protein in the urine) – a condition known as preeclampsia.

Eclampsia is considered a medical emergency, and it can lead to severe complications for both the mother and the baby if not promptly treated. The exact cause of eclampsia is not fully understood, but it is thought to be related to problems with the blood vessels that supply the placenta.

Symptoms of eclampsia include high blood pressure, severe headaches, visual disturbances, nausea and vomiting, and sudden weight gain. If left untreated, eclampsia can lead to serious complications such as brain damage, stroke, kidney failure, and even death for the mother and the baby.

Treatment typically involves close monitoring of the mother and the baby, medication to control seizures and lower blood pressure, and delivery of the baby if necessary. In some cases, eclampsia may occur after the baby has been delivered, in which case it is known as postpartum eclampsia.

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.

In the context of nutrition and health, minerals are inorganic elements that are essential for various bodily functions, such as nerve impulse transmission, muscle contraction, maintaining fluid and electrolyte balance, and bone structure. They are required in small amounts compared to macronutrients (carbohydrates, proteins, and fats) and are obtained from food and water.

Some of the major minerals include calcium, phosphorus, magnesium, sodium, potassium, and chloride, while trace minerals or microminerals are required in even smaller amounts and include iron, zinc, copper, manganese, iodine, selenium, and fluoride.

It's worth noting that the term "minerals" can also refer to geological substances found in the earth, but in medical terminology, it specifically refers to the essential inorganic elements required for human health.

Calcium radioisotopes are radioactive isotopes of the element calcium. An isotope is a variant of an element that has the same number of protons in its atoms but a different number of neutrons, resulting in different mass numbers. Calcium has several radioisotopes, including calcium-41, calcium-45, calcium-47, and calcium-49.

These radioisotopes are used in various medical applications, such as in diagnostic imaging and research. For example, calcium-45 is commonly used in bone scans to help diagnose conditions like fractures, tumors, or infections. When administered to the patient, the calcium-45 is taken up by the bones, and a special camera can detect the gamma rays emitted by the radioisotope, providing images of the skeleton.

Similarly, calcium-47 is used in research to study calcium metabolism and bone physiology. The short half-life and low energy of the radiation emitted by these radioisotopes make them relatively safe for medical use, with minimal risk of harm to patients. However, as with any medical procedure involving radiation, appropriate precautions must be taken to ensure safety and minimize exposure.

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.

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.

Intestinal absorption refers to the process by which the small intestine absorbs water, nutrients, and electrolytes from food into the bloodstream. This is a critical part of the digestive process, allowing the body to utilize the nutrients it needs and eliminate waste products. The inner wall of the small intestine contains tiny finger-like projections called villi, which increase the surface area for absorption. Nutrients are absorbed into the bloodstream through the walls of the capillaries in these villi, and then transported to other parts of the body for use or storage.

Hydroxycholecalciferols are metabolites of vitamin D that are formed in the liver and kidneys. They are important for maintaining calcium homeostasis in the body by promoting the absorption of calcium from the gut and reabsorption of calcium from the kidneys.

The two main forms of hydroxycholecalciferols are 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D (1,25(OH)2D). 25-hydroxyvitamin D is the major circulating form of vitamin D in the body and is used as a clinical measure of vitamin D status. It is converted to 1,25-dihydroxyvitamin D in the kidneys by the enzyme 1α-hydroxylase, which is activated in response to low serum calcium or high phosphate levels.

1,25-dihydroxyvitamin D is the biologically active form of vitamin D and plays a critical role in regulating calcium homeostasis by increasing intestinal calcium absorption and promoting bone health. Deficiency in hydroxycholecalciferols can lead to rickets in children and osteomalacia or osteoporosis in adults, characterized by weakened bones and increased risk of fractures.

Calcium channels are specialized proteins that span the membrane of cells and allow calcium ions (Ca²+) to flow in and out of the cell. They are crucial for many physiological processes, including muscle contraction, neurotransmitter release, hormone secretion, and gene expression.

There are several types of calcium channels, classified based on their biophysical and pharmacological properties. The most well-known are:

1. Voltage-gated calcium channels (VGCCs): These channels are activated by changes in the membrane potential. They are further divided into several subtypes, including L-type, P/Q-type, N-type, R-type, and T-type. VGCCs play a critical role in excitation-contraction coupling in muscle cells and neurotransmitter release in neurons.
2. Receptor-operated calcium channels (ROCCs): These channels are activated by the binding of an extracellular ligand, such as a hormone or neurotransmitter, to a specific receptor on the cell surface. ROCCs are involved in various physiological processes, including smooth muscle contraction and platelet activation.
3. Store-operated calcium channels (SOCCs): These channels are activated by the depletion of intracellular calcium stores, such as those found in the endoplasmic reticulum. SOCCs play a critical role in maintaining calcium homeostasis and signaling within cells.

Dysregulation of calcium channel function has been implicated in various diseases, including hypertension, arrhythmias, migraine, epilepsy, and neurodegenerative disorders. Therefore, calcium channels are an important target for drug development and therapy.

Sarcoidosis is a multi-system disorder characterized by the formation of granulomas (small clumps of inflammatory cells) in various organs, most commonly the lungs and lymphatic system. These granulomas can impair the function of the affected organ(s), leading to a variety of symptoms. The exact cause of sarcoidosis is unknown, but it's thought to be an overactive immune response to an unknown antigen, possibly triggered by an infection, chemical exposure, or another environmental factor.

The diagnosis of sarcoidosis typically involves a combination of clinical evaluation, imaging studies (such as chest X-rays and CT scans), and laboratory tests (including blood tests and biopsies). While there is no cure for sarcoidosis, treatment may be necessary to manage symptoms and prevent complications. Corticosteroids are often used to suppress the immune system and reduce inflammation, while other medications may be prescribed to treat specific organ involvement or symptoms. In some cases, sarcoidosis may resolve on its own without any treatment.

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.

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.

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.

Dihydroxycholecalciferols are a form of calcifediol, which is a type of secosteroid hormone that is produced in the body as a result of the exposure to sunlight and the dietary intake of vitamin D. The term "dihydroxycholecalciferols" specifically refers to the compounds 1,25-dihydroxycholecalciferol (calcitriol) and 24,25-dihydroxycholecalciferol. These compounds are produced in the body through a series of chemical reactions involving enzymes that convert vitamin D into its active forms.

Calcitriol is the biologically active form of vitamin D and plays an important role in regulating the levels of calcium and phosphorus in the blood, as well as promoting the absorption of these minerals from the gut. It also has other functions, such as modulating cell growth and immune function.

24,25-dihydroxycholecalciferol is a less active form of vitamin D that is produced in larger quantities than calcitriol. Its exact role in the body is not well understood, but it is thought to have some effects on calcium metabolism and may play a role in regulating the levels of other hormones in the body.

Dihydroxycholecalciferols are typically measured in the blood as part of an evaluation for vitamin D deficiency or to monitor treatment with vitamin D supplements. Low levels of these compounds can indicate a deficiency, while high levels may indicate excessive intake or impaired metabolism.

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