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 hereditary disorder characterized by HYPOPHOSPHATEMIA; RICKETS; OSTEOMALACIA; renal defects in phosphate reabsorption and vitamin D metabolism; and growth retardation. Autosomal and X-linked dominant and recessive variants have been reported.
An inherited condition of abnormally low serum levels of PHOSPHATES (below 1 mg/liter) which can occur in a number of genetic diseases with defective reabsorption of inorganic phosphorus by the PROXIMAL RENAL TUBULES. This leads to phosphaturia, HYPOPHOSPHATEMIA, and disturbances of cellular and organ functions such as those in X-LINKED HYPOPHOSPHATEMIC RICKETS; OSTEOMALACIA; and FANCONI SYNDROME.
A membrane-bound metalloendopeptidase that may play a role in the degradation or activation of a variety of PEPTIDE HORMONES and INTERCELLULAR SIGNALING PEPTIDES AND PROTEINS. Genetic mutations that result in loss of function of this protein are a cause of HYPOPHOSPHATEMIC RICKETS, X-LINKED DOMINANT.
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 non-electrogenic sodium-dependent phosphate transporter. It is found primarily in apical membranes of PROXIMAL RENAL TUBULES.
A condition of an abnormally low level of PHOSPHATES in the blood.
Genetic diseases that are linked to gene mutations on the X CHROMOSOME in humans (X CHROMOSOME, HUMAN) or the X CHROMOSOME in other species. Included here are animal models of human X-linked diseases.
A disorder characterized by HYPOPHOSPHATEMIA; RICKETS; OSTEOMALACIA; resulting from lack of phosphate reabsorption by the kidneys and possible defects in vitamin D metabolism.
Excretion of abnormally high level of CALCIUM in the URINE, greater than 4 mg/kg/day.
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 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 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.
Hydroxy analogs of vitamin D 3; (CHOLECALCIFEROL); including CALCIFEDIOL; CALCITRIOL; and 24,25-DIHYDROXYVITAMIN D 3.
Inorganic salts of phosphoric acid.
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.
An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1.
9,10-Secoergosta-5,7,10(19),22-tetraene-3,25-diol. Biologically active metabolite of vitamin D2 which is more active in curing rickets than its parent. The compound is believed to attach to the same receptor as vitamin D2 and 25-hydroxyvitamin D3.
A condition characterized by calcification of the renal tissue itself. It is usually seen in distal RENAL TUBULAR ACIDOSIS with calcium deposition in the DISTAL KIDNEY TUBULES and the surrounding interstitium. Nephrocalcinosis causes RENAL INSUFFICIENCY.
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.
Derivatives of ERGOSTEROL formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. They differ from CHOLECALCIFEROL in having a double bond between C22 and C23 and a methyl group at C24.
A mitochondrial cytochrome P450 enzyme that catalyzes the 1-alpha-hydroxylation of 25-hydroxyvitamin D3 (also known as 25-hydroxycholecalciferol) in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP27B1 gene, converts 25-hydroxyvitamin D3 to 1-alpha,25-dihydroxyvitamin D3 which is the active form of VITAMIN D in regulating bone growth and calcium metabolism. This enzyme is also active on plant 25-hydroxyvitamin D2 (ergocalciferol).
Derivative of 7-dehydroxycholesterol formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. It differs from ERGOCALCIFEROL in having a single bond between C22 and C23 and lacking a methyl group at C24.
Proteins, usually found in the cytoplasm, that specifically bind calcitriol, migrate to the nucleus, and regulate transcription of specific segments of DNA with the participation of D receptor interacting proteins (called DRIP). Vitamin D is converted in the liver and kidney to calcitriol and ultimately acts through these receptors.
A hereditary or acquired form of generalized dysfunction of the PROXIMAL KIDNEY TUBULE without primary involvement of the KIDNEY GLOMERULUS. It is usually characterized by the tubular wasting of nutrients and salts (GLUCOSE; AMINO ACIDS; PHOSPHATES; and BICARBONATES) resulting in HYPOKALEMIA; ACIDOSIS; HYPERCALCIURIA; and PROTEINURIA.
Oil obtained from fresh livers of the cod family, Gadidae. It is a source of VITAMIN A and VITAMIN D.
Production of a radiographic image of a small or very thin object on fine-grained photographic film under conditions which permit subsequent microscopic examination or enlargement of the radiograph at linear magnifications of up to several hundred and with a resolution approaching the resolving power of the photographic emulsion (about 1000 lines per millimeter).
Disorders caused by nutritional imbalance, either overnutrition or undernutrition, occurring in infants ages 1 month to 24 months.
Large, chiefly nocturnal mammals of the cat family FELIDAE, species Panthera leo. They are found in Africa and southern Asia.
Process by which organic tissue becomes hardened by the physiologic deposit of calcium salts.
A family of small polypeptide growth factors that share several common features including a strong affinity for HEPARIN, and a central barrel-shaped core region of 140 amino acids that is highly homologous between family members. Although originally studied as proteins that stimulate the growth of fibroblasts this distinction is no longer a requirement for membership in the fibroblast growth factor family.
An inward slant of the thigh in which the knees are close together and the ankles far apart. Genu valgum can develop due to skeletal and joint dysplasias (e.g., OSTEOARTHRITIS; HURLER SYNDROME); and malnutrition (e.g., RICKETS; FLUORIDE POISONING).
Irradiation directly from the sun.
A metabolic disease characterized by the defective transport of CYSTINE across the lysosomal membrane due to mutation of a membrane protein cystinosin. This results in cystine accumulation and crystallization in the cells causing widespread tissue damage. In the KIDNEY, nephropathic cystinosis is a common cause of RENAL FANCONI SYNDROME.
Cholecalciferols substituted with two hydroxy groups in any position.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
The part of the face above the eyes.

Clinical and subclinical vitamin D deficiency in Bradford children. (1/316)

A survey of the vitamin D status of Bradford schoolchildren was carried out in April 1973, employing conventional biochemistry, radiology, and measurement of 25-hydroxycholecalciferol levels. Biochemical evidence of rickets was present in 45% of the Asians. When re-examined in September, several children showed spontaneous biochemical resolution; nevertheless, radiological abnormalities were present in 12% of the original sample. No evidence of rickets was detected in the smaller White sample. Minor biochemical abnormalities were present in 9 of the 40 West Indian children. A study of admissions of Bradford hospitals in the 4 years 1969-1972 inclusive confirmed that clinical vitamin D deficiency was confined to Asians except for a few cases of infantile rickets in White children. The probability that one Asian child in 40 may require admission during the period from birth to adolescence emphasizes the urgent need for the introduction of prophylactic measures.  (+info)

An inborn error of bile acid synthesis (3beta-hydroxy-delta5-C27-steroid dehydrogenase deficiency) presenting as malabsorption leading to rickets. (2/316)

Deficiency of 3beta-hydroxy-delta5-C27-steroid dehydrogenase (3beta-HSDH), the enzyme that catalyses the second reaction in the principal pathway for the synthesis of bile acids, has been reported to present with prolonged neonatal jaundice with the biopsy features of neonatal hepatitis. It has also been shown to present between the ages of 4 and 46 months with jaundice, hepatosplenomegaly, and steatorrhoea (a clinical picture resembling progressive familial intrahepatic cholestasis). This paper reports two children with 3beta-HSDH deficiency who developed rickets during infancy and did not develop clinically evident liver disease until the age of 3 years. Bile acid replacement resulted in considerable clinical and biochemical improvement. The importance of thorough investigation of fat soluble vitamin deficiencies in infancy is emphasised.  (+info)

Forgotten mysteries in the early history of vitamin D. (3/316)

In the early 1920s, workers in both England and the US had discovered that rats on a rachitic diet would remain healthy if irradiated with ultraviolet light. However, they also found, to their surprise, that "control" rats too would recover if either their jar was irradiated without the rat in it or if a cage-mate was removed for irradiation and then returned. The ideas that either air or material objects that had been irradiated continued themselves to convey healthful secondary radiations were investigated but not confirmed. There was then the commercially important finding that with irradiation, some rachitic diets would become anti-rachitic. However, this effect did not explain all the previous findings. Consumption of either small irradiated fecal particles or of feces from irradiated rats was the likely explanation for the recovery of nonirradiated rats, but this was not tested by direct experiment, and it now appears unlikely that feces from irradiated rats would show significant antirachitic activity. It is suggested that an alternative possibility--activity of grease from irradiated fur--deserves investigation.  (+info)

A comparison of calcium, vitamin D, or both for nutritional rickets in Nigerian children. (4/316)

BACKGROUND: Nutritional rickets remains prevalent in many tropical countries despite the fact that such countries have ample sunlight. Some postulate that a deficiency of dietary calcium, rather than vitamin D, is often responsible for rickets after infancy. METHODS: We enrolled 123 Nigerian children (median age, 46 months) with rickets in a randomized, double-blind, controlled trial of 24 weeks of treatment with vitamin D (600,000 U intramuscularly at enrollment and at 12 weeks), calcium (1000 mg daily), or a combination of vitamin D and calcium. We compared the calcium intake of the children at enrollment with that of control children without rickets who were matched for sex, age, and weight. We measured serum calcium and alkaline phosphatase and used a 10-point radiographic score to assess the response to treatment at 24 weeks. RESULTS: The daily dietary calcium intake was low in the children with rickets and the control children (median, 203 mg and 196 mg, respectively; P=0.64). Treatment produced a smaller increase in the mean (+/-SD) serum calcium concentration in the vitamin D group (from 7.8+/-0.8 mg per deciliter [2.0+/-0.2 mmol per liter] at base line to 8.3+/-0.7 mg per deciliter [2.1+/-0.2 mmol per liter] at 24 weeks) than in the calcium group (from 7.5+/-0.8 [1.9+/-0.2 mmol per liter] to 9.0+/-0.6 mg per deciliter [2.2+/-0.2 mmol per liter], P<0.001) or the combination-therapy group (from 7.7+/-1.0 [1.9+/-0.25 mmol per liter] to 9.1+/-0.6 mg per deciliter [2.3+/-0.2 mmol per liter], P<0.001). A greater proportion of children in the calcium and combination-therapy groups than in the vitamin D group reached the combined end point of a serum alkaline phosphatase concentration of 350 U per liter or less and radiographic evidence of nearly complete healing of rickets (61 percent, 58 percent, and 19 percent, respectively; P<0.001). CONCLUSIONS: Nigerian children with rickets have a low intake of calcium and have a better response to treatment with calcium alone or in combination with vitamin D than to treatment with vitamin D alone.  (+info)

Enzymatic properties of human 25-hydroxyvitamin D3 1alpha-hydroxylase coexpression with adrenodoxin and NADPH-adrenodoxin reductase in Escherichia coli. (5/316)

We have cloned human 25-hydroxyvitamin D3 1alpha-hydroxylase cDNAs from normal subjects and patients with pseudovitamin D-deficient rickets (PDDR), and expressed the cDNAs in Escherichia coli JM109 cells. Kinetic analysis of normal 1alpha-hydroxylase in the reconstituted system revealed that Km values for 25(OH)D3 and (24R), 25(OH)2D3 were 2.7 and 1.1 microM, respectively. The lower Km value and higher Vmax/Km value for (24R),25(OH)2D3 indicated that it is a better substrate than 25(OH)D3 for 1alpha-hydroxylase. These results are quite similar to those of mouse 1alpha-hydroxylase. To establish a highly sensitive in vivo system, 1alpha-hydroxylase, adrenodoxin and NADPH-adrenodoxin reductase were coexpressed in E. coli cells. The recombinant E. coli cells showed remarkably high 1alpha-hydroxylase activity, suggesting that the electrons were efficiently transferred from NADPH-adrenodoxin reductase through adrenodoxin to 1alpha-hydroxylase in E. coli cells. Using this system, the activities of four mutants of 1alpha-hydroxylase, R107H, G125E, R335P and P382S, derived from patients with PDDR were examined. Although no significant reduction in expression of these mutants was observed, none showed detectable activity. These results strongly suggest that the mutations found in the patients with PDDR completely abolished 1alpha-hydroxylase activity by replacement of one amino acid residue.  (+info)

Demonstration of the rapid action of pure crystalline 1 alpha-hydroxy vitamin D3 and 1 alpha,25-dihydroxy vitamin D3 on intestinal calcium uptake. (6/316)

The biological effects of crystalline 1alpha-hydroxyvitamin D3 and crystalline 1alpha,25-dihydroxyvitamin D3 have been compared on the intestinal uptake of calcium-45 by everted duodenal gut sacs from rachitic rats. Peak calcium-45 uptake was observed 1 hr after intravenous administration and both crystalline vitamin D2 analogs were of comparable potency. The rapid onset of calcium-45 uptake and the rapid attainment of maximal calcium-45 transport suggests a direct effect of these crystalline analogs on the mucosal membranes of the intestinal cell.  (+info)

Malnutrition in infants receiving cult diets: a form of child abuse. (7/316)

Severe nutritional disorders, including kwashiorkor, marasmus, and rickets, were seen in four children and were due to parental food faddism, which should perhaps be regarded as a form of child abuse. All disorders were corrected with more normal diets and vitamin supplements. In view of the potentially serious consequences of restricted diets being fed to children, families at risk should be identified and acceptable nutritional advice given. When children are found to be suffering from undernutrition due to parental food faddism a court order will normally be a necessary step in providing adequate treatment and supervision.  (+info)

The function of vitamin D receptor in vitamin D action. (8/316)

Vitamin D has roles in a variety of biological actions such as calcium homeostasis, cell proliferation and cell differentiation to many target tissues. Most of these biological actions of vitamin D are now considered to be exerted through the nuclear vitamin D receptor (VDR)-mediated control of target genes. VDR belongs to the nuclear hormone receptor superfamily and acts as a ligand-inducible transcription factor. For the ligand-induced transactivation of VDR, coactivator complexes have recently been shown to be essential. The function of VDR as a ligand-induced transcription factor is overviewed, and the phenotype of VDR gene knock-out mice and the VDR-mediated transcriptional and negative regulation of the key enzyme in vitamin D biosynthesis are also described, based mainly on our recent findings, to gain a better understanding of the function of VDR in the transcriptional control of vitamin D target genes.  (+info)

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.

Familial Hypophosphatemic Rickets (FHR) is a genetic disorder characterized by impaired reabsorption of phosphate in the kidneys, leading to low levels of phosphate in the blood (hypophosphatemia). This condition results in defective mineralization of bones and teeth, causing rickets in children and osteomalacia in adults.

FHR is typically caused by mutations in the PHEX gene, which encodes a protein that helps regulate phosphate levels in the body. In FHR, the mutation leads to an overproduction of a hormone called fibroblast growth factor 23 (FGF23), which increases phosphate excretion in the urine and decreases the activation of vitamin D, further contributing to hypophosphatemia.

Symptoms of FHR may include bowing of the legs, bone pain, muscle weakness, short stature, dental abnormalities, and skeletal deformities. Treatment typically involves oral phosphate supplements and active forms of vitamin D to correct the hypophosphatemia and improve bone mineralization. Regular monitoring of blood phosphate levels, kidney function, and bone health is essential for effective management of this condition.

Familial Hypophosphatemia is a genetic disorder characterized by low levels of phosphate in the blood (hypophosphatemia) due to impaired absorption of phosphates in the gut. This condition results from mutations in the SLC34A3 gene, which provides instructions for making a protein called NaPi-IIc, responsible for reabsorbing phosphates from the filtrate in the kidney tubules back into the bloodstream.

In familial hypophosphatemia, the impaired function of NaPi-IIc leads to excessive loss of phosphate through urine, resulting in hypophosphatemia. This condition can cause rickets (a softening and weakening of bones) in children and osteomalacia (softening of bones) in adults. Symptoms may include bowed legs, bone pain, muscle weakness, and short stature.

Familial Hypophosphatemia is inherited as an autosomal recessive trait, meaning that an individual must inherit two copies of the mutated gene (one from each parent) to develop the condition.

PHEX (Phosphate Regulating Endopeptidase Homolog, X-Linked) is a gene that encodes for an enzyme called phosphate regulating neutral endopeptidase. This enzyme is primarily expressed in osteoblasts, which are cells responsible for bone formation.

The main function of the PHEX protein is to regulate the levels of a hormone called fibroblast growth factor 23 (FGF23) by breaking it down. FGF23 plays an essential role in maintaining phosphate homeostasis by regulating its reabsorption in the kidneys and its absorption from the gut.

Inactivating mutations in the PHEX gene can lead to X-linked hypophosphatemia (XLH), a genetic disorder characterized by low levels of phosphate in the blood, impaired bone mineralization, and rickets. In XLH, the production of FGF23 is increased due to the lack of regulation by PHEX, leading to excessive excretion of phosphate in the urine and decreased absorption from the gut. This results in hypophosphatemia, impaired bone mineralization, and other skeletal abnormalities.

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.

Sodium-phosphate cotransporter proteins, type IIc (NPTIIc), are a subtype of sodium-dependent phosphate transporters that play a crucial role in the regulation of phosphate homeostasis within the body. They are located primarily in the kidney's proximal tubule cells and intestinal epithelial cells.

NPTIIc proteins facilitate the active transport of inorganic phosphate (Pi) ions across the cell membrane, in conjunction with sodium ions (Na+). This symport mechanism allows for the movement of Pi against its concentration gradient, from areas of low concentration to high concentration. The energy required for this process is derived from the electrochemical gradient of sodium ions.

These transporters are essential for maintaining normal phosphate levels in the body, as they help reabsorb a significant portion of filtered phosphate in the kidneys and absorb dietary phosphate in the intestines. Dysregulation of NPTIIc proteins can lead to various disorders related to phosphate homeostasis, such as hypophosphatemia (low serum phosphate levels) or hyperphosphatemia (high serum phosphate levels), which can have detrimental effects on bone health, mineral metabolism, and overall body function.

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.

X-linked genetic diseases refer to a group of disorders caused by mutations in genes located on the X chromosome. These conditions primarily affect males since they have only one X chromosome and therefore don't have a second normal copy of the gene to compensate for the mutated one. Females, who have two X chromosomes, are typically less affected because they usually have one normal copy of the gene on their other X chromosome.

Examples of X-linked genetic diseases include Duchenne and Becker muscular dystrophy, hemophilia A and B, color blindness, and fragile X syndrome. Symptoms and severity can vary widely depending on the specific condition and the nature of the genetic mutation involved. Treatment options depend on the particular disease but may include physical therapy, medication, or in some cases, gene therapy.

Hypophosphatemic Rickets is a genetic disorder characterized by impaired reabsorption of phosphate in the kidneys, leading to low levels of phosphate in the blood (hypophosphatemia). This condition results in defective mineralization of bones and teeth, causing rickets in children and osteomalacia in adults.

The disorder is usually caused by mutations in the gene responsible for producing a protein called PHEX (Phosphate-Regulating Endopeptidase Homolog X-Linked). This protein plays a crucial role in regulating phosphate levels in the body, and its deficiency leads to excessive excretion of phosphate in the urine (familial hypophosphatemic rickets) and subsequent development of rickets.

The symptoms of Hypophosphatemic Rickets include bowing of the legs, bone pain, muscle weakness, short stature, dental abnormalities, and increased risk of fractures. Treatment typically involves supplementation with phosphate and active vitamin D metabolites to correct the mineral imbalance and improve bone health. Regular monitoring of blood phosphate levels, renal function, and growth is necessary to adjust treatment and prevent complications.

Hypercalciuria is a medical condition characterized by an excessive amount of calcium in the urine. It can occur when the body absorbs too much calcium from food, or when the bones release more calcium than usual. In some cases, it may be caused by certain medications, kidney disorders, or genetic factors.

Hypercalciuria can increase the risk of developing kidney stones and other kidney problems. It is often diagnosed through a 24-hour urine collection test that measures the amount of calcium in the urine. Treatment may include changes in diet, increased fluid intake, and medications to help reduce the amount of calcium in the urine.

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.

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.

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.

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.

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.

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.

Alkaline phosphatase (ALP) is an enzyme found in various body tissues, including the liver, bile ducts, digestive system, bones, and kidneys. It plays a role in breaking down proteins and minerals, such as phosphate, in the body.

The medical definition of alkaline phosphatase refers to its function as a hydrolase enzyme that removes phosphate groups from molecules at an alkaline pH level. In clinical settings, ALP is often measured through blood tests as a biomarker for various health conditions.

Elevated levels of ALP in the blood may indicate liver or bone diseases, such as hepatitis, cirrhosis, bone fractures, or cancer. Therefore, physicians may order an alkaline phosphatase test to help diagnose and monitor these conditions. However, it is essential to interpret ALP results in conjunction with other diagnostic tests and clinical findings for accurate diagnosis and treatment.

25-Hydroxyvitamin D 2 (25(OH)D2) is a form of vitamin D that is produced in the body as a result of the metabolism of ergocalciferol, also known as vitamin D2. Vitamin D2 is found in some plant-based foods and is sometimes used as a dietary supplement.

When vitamin D2 is ingested or absorbed through the skin after exposure to sunlight, it is converted in the liver to 25(OH)D2. This form of vitamin D is then further metabolized in the kidneys to the active form of vitamin D, calcitriol (1,25-dihydroxyvitamin D).

Like other forms of vitamin D, 25(OH)D2 is important for maintaining healthy bones and muscles by regulating the absorption of calcium and phosphorus from the diet. It may also have other health benefits, such as reducing the risk of certain cancers and autoimmune disorders.

It's worth noting that 25-Hydroxyvitamin D2 is not usually measured in clinical settings, as it is converted to 25-Hydroxyvitamin D3 (25(OH)D3) in the body, and total 25(OH)D (which includes both 25(OH)D2 and 25(OH)D3) is typically measured to assess vitamin D status.

Nephrocalcinosis is a medical condition characterized by the deposition of calcium salts in the renal parenchyma, specifically within the tubular epithelial cells and interstitium of the kidneys. This process can lead to chronic inflammation, tissue damage, and ultimately impaired renal function if left untreated.

The condition is often associated with metabolic disorders such as hyperparathyroidism, distal renal tubular acidosis, or hyperoxaluria; medications like loop diuretics, corticosteroids, or calcineurin inhibitors; and chronic kidney diseases. The diagnosis of nephrocalcinosis is typically made through imaging studies such as ultrasound, CT scan, or X-ray. Treatment usually involves addressing the underlying cause, modifying dietary habits, and administering medications to control calcium levels in the body.

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.

Ergocalciferols are a form of vitamin D, specifically vitamin D2, that is found in some plants. They are not produced by the human body and must be obtained through diet or supplementation. Ergocalciferols can be converted into an active form of vitamin D in the body, which is important for maintaining healthy bones and calcium levels. However, vitamin D3 (cholecalciferol), which is produced by the body in response to sunlight exposure, is generally considered to be more effective at raising and maintaining vitamin D levels in the body than ergocalciferols.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase is an enzyme that is responsible for converting 25-hydroxyvitamin D3 (a precursor form of vitamin D) to its active form, 1,25-dihydroxyvitamin D3. This activation process occurs primarily in the kidneys and is tightly regulated by various factors such as calcium levels, parathyroid hormone, and vitamin D status.

The activated form of vitamin D, 1,25-dihydroxyvitamin D3, plays a crucial role in maintaining calcium homeostasis by increasing the absorption of calcium from the gut and promoting bone health. It also has various other functions, including modulation of immune function, cell growth regulation, and protection against cancer.

Deficiencies in 25-Hydroxyvitamin D3 1-alpha-Hydroxylase can lead to vitamin D deficiency and its associated symptoms, such as osteomalacia (softening of the bones) and osteoporosis (brittle bones). Conversely, overactivity of this enzyme can result in hypercalcemia (elevated levels of calcium in the blood), which can cause a range of symptoms including kidney stones, abdominal pain, nausea, and vomiting.

Cholecalciferol is the chemical name for Vitamin D3. It is a fat-soluble vitamin that is essential for the regulation of calcium and phosphate levels in the body, which helps to maintain healthy bones and teeth. Cholecalciferol can be synthesized by the skin upon exposure to sunlight or obtained through dietary sources such as fatty fish, liver, and fortified foods. It is also available as a dietary supplement.

Calcitriol receptors, also known as Vitamin D receptors (VDR), are nuclear receptor proteins that bind to calcitriol (1,25-dihydroxyvitamin D3), the active form of vitamin D. These receptors are found in various tissues and cells throughout the body, including the small intestine, bone, kidney, and parathyroid gland.

When calcitriol binds to its receptor, it forms a complex that regulates the expression of genes involved in calcium and phosphate homeostasis, cell growth, differentiation, and immune function. Calcitriol receptors play a critical role in maintaining normal levels of calcium and phosphate in the blood by increasing the absorption of these minerals from the gut, promoting bone mineralization, and regulating the production of parathyroid hormone (PTH).

Calcitriol receptors have also been implicated in various disease processes, including cancer, autoimmune disorders, and infectious diseases. Modulation of calcitriol receptor activity has emerged as a potential therapeutic strategy for the treatment of these conditions.

Fanconi syndrome is a medical condition that affects the proximal tubules of the kidneys. These tubules are responsible for reabsorbing various substances, such as glucose, amino acids, and electrolytes, back into the bloodstream after they have been filtered through the kidneys.

In Fanconi syndrome, there is a defect in the reabsorption process, causing these substances to be lost in the urine instead. This can lead to a variety of symptoms, including:

* Polyuria (excessive urination)
* Polydipsia (excessive thirst)
* Dehydration
* Metabolic acidosis (an imbalance of acid and base in the body)
* Hypokalemia (low potassium levels)
* Hypophosphatemia (low phosphate levels)
* Vitamin D deficiency
* Rickets (softening and weakening of bones in children) or osteomalacia (softening of bones in adults)

Fanconi syndrome can be caused by a variety of underlying conditions, including genetic disorders, kidney diseases, drug toxicity, and heavy metal poisoning. Treatment typically involves addressing the underlying cause, as well as managing symptoms such as electrolyte imbalances and acid-base disturbances.

Cod liver oil is a dietary supplement derived from the livers of Atlantic cod (Gadus morhua) or other related species of fish. It is a rich source of omega-3 fatty acids, specifically eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which have been shown to support heart health, brain function, and eye health.

Additionally, cod liver oil contains high levels of vitamin A and vitamin D. Vitamin A is important for maintaining healthy vision, immune function, and cell growth, while vitamin D plays a crucial role in bone health, calcium metabolism, and immune function. However, it's worth noting that excessive intake of vitamin A can lead to toxicity, so it's essential to follow recommended dosage guidelines when consuming cod liver oil.

The oil is typically obtained by cooking and pressing the livers or through a solvent extraction process. It is available in liquid and capsule forms and is often used as a dietary supplement to support overall health and well-being.

Microradiography is a radiographic technique that uses X-rays to produce detailed images of small specimens, such as microscopic slides or individual cells. In this process, the specimen is placed in close contact with a high-resolution photographic emulsion, and then exposed to X-rays. The resulting image shows the distribution of radiopaque materials within the specimen, providing information about its internal structure and composition at a microscopic level.

Microradiography can be used for various applications in medical research and diagnosis, including the study of bone and tooth microstructure, the analysis of tissue pathology, and the examination of mineralized tissues such as calcifications or osteogenic lesions. The technique offers high resolution and contrast, making it a valuable tool for researchers and clinicians seeking to understand the complex structures and processes that occur at the microscopic level in living organisms.

Infant nutrition disorders refer to a group of conditions that occur when an infant's diet does not provide adequate nutrients for growth, development, and health. These disorders can result from various factors such as inadequate feeding practices, poor nutrient quality or composition of the diet, food intolerances or allergies, and medical conditions affecting nutrient absorption or metabolism.

Examples of infant nutrition disorders include:

1. Failure to thrive (FTT): A condition characterized by an infant's failure to gain weight or height at the expected rate due to inadequate nutrition.
2. Malnutrition: A condition resulting from a deficiency, excess, or imbalance of nutrients in an infant's diet.
3. Obesity: A condition characterized by excessive body fat accumulation in an infant due to poor dietary habits and lack of physical activity.
4. Food intolerances or allergies: Adverse reactions to specific foods or food components that can cause digestive, skin, or respiratory symptoms in infants.
5. Vitamin and mineral deficiencies: A condition resulting from an insufficient intake or absorption of essential vitamins and minerals required for normal growth and development.
6. Metabolic disorders: Inborn errors of metabolism that affect the body's ability to process specific nutrients, leading to a buildup of toxic substances in the body.

Infant nutrition disorders can have serious consequences on an infant's health and development, and it is essential to identify and address them promptly through appropriate medical interventions and feeding practices.

I'm sorry for any confusion, but "Lions" is not a term typically used in medical definitions. Lions are large, carnivorous mammals that are part of the Felidae family, specifically Panthera leo. If you have any questions about lions or if there's another term you meant to ask about, please provide more context so I can give you a more accurate response.

Physiologic calcification is the normal deposit of calcium salts in body tissues and organs. It is a natural process that occurs as part of the growth and development of the human body, as well as during the repair and remodeling of tissues.

Calcium is an essential mineral that plays a critical role in many bodily functions, including bone formation, muscle contraction, nerve impulse transmission, and blood clotting. In order to maintain proper levels of calcium in the body, excess calcium that is not needed for these functions may be deposited in various tissues as a normal part of the aging process.

Physiologic calcification typically occurs in areas such as the walls of blood vessels, the lungs, and the heart valves. While these calcifications are generally harmless, they can sometimes lead to complications, particularly if they occur in large amounts or in sensitive areas. For example, calcification of the coronary arteries can increase the risk of heart disease, while calcification of the lung tissue can cause respiratory symptoms.

It is important to note that pathologic calcification, on the other hand, refers to the abnormal deposit of calcium salts in tissues and organs, which can be caused by various medical conditions such as chronic kidney disease, hyperparathyroidism, and certain infections. Pathologic calcification is not a normal process and can lead to serious health complications if left untreated.

Fibroblast Growth Factors (FGFs) are a family of growth factors that play crucial roles in various biological processes, including cell survival, proliferation, migration, and differentiation. They bind to specific tyrosine kinase receptors (FGFRs) on the cell surface, leading to intracellular signaling cascades that regulate gene expression and downstream cellular responses. FGFs are involved in embryonic development, tissue repair, and angiogenesis (the formation of new blood vessels). There are at least 22 distinct FGFs identified in humans, each with unique functions and patterns of expression. Some FGFs, like FGF1 and FGF2, have mitogenic effects on fibroblasts and other cell types, while others, such as FGF7 and FGF10, are essential for epithelial-mesenchymal interactions during organ development. Dysregulation of FGF signaling has been implicated in various pathological conditions, including cancer, fibrosis, and developmental disorders.

"Genu valgum," also known as "knock-knee," is a condition where there is an excessive angle between the thighbone (femur) and the shinbone (tibia), causing the knees to touch or come close together while the ankles remain separated when standing with the feet and knees together. This abnormal alignment can lead to difficulty walking, running, and participating in certain activities, as well as potential long-term complications such as joint pain and osteoarthritis if not properly addressed. Genu valgum is typically diagnosed through physical examination and imaging studies such as X-rays, and treatment may include observation, physical therapy, bracing, or surgery depending on the severity of the condition and the individual's age and overall health.

I'm sorry for any confusion, but "sunlight" is not a term with a specific medical definition. However, sunlight does have various implications in the field of medicine. It is the light that comes from the sun, which is a star at the center of our solar system. Sunlight is essential for the production of vitamin D in humans, and it can also have effects on mood and sleep patterns due to its influence on circadian rhythms.

In a medical context, sunlight is often discussed in relation to its potential health benefits and risks. For instance, moderate sun exposure can help increase vitamin D levels, which are important for bone health, immune function, and other bodily processes. However, excessive sun exposure can lead to harmful effects, such as sunburn, premature skin aging, and an increased risk of skin cancer.

It's essential to balance the benefits and risks of sunlight exposure by practicing safe sun habits, such as wearing protective clothing, using a broad-spectrum sunscreen with an SPF of at least 30, seeking shade during peak sunlight hours, and avoiding intentional tanning.

Cystinosis is a rare, inherited metabolic disorder that affects primarily the eyes, kidneys, and liver. It is characterized by an abnormal accumulation of the amino acid cystine within lysosomes (cellular organelles responsible for breaking down and recycling waste products) due to a defect in the gene CTNS that encodes for a protein called cystinosin. This leads to the formation of crystals, which can cause cell damage and multi-organ dysfunction.

There are three main types of cystinosis:

1. Nephropathic or infantile cystinosis: This is the most severe form, with symptoms appearing within the first year of life. It primarily affects the kidneys, leading to Fanconi syndrome (a condition characterized by excessive loss of nutrients in urine), growth failure, and kidney dysfunction. If left untreated, it can progress to end-stage renal disease (ESRD) around the age of 10.
2. Intermediate cystinosis: This form presents during childhood with milder kidney involvement but can still lead to ESRD in adolescence or early adulthood. Eye and central nervous system abnormalities may also be present.
3. Non-nephropathic or ocular cystinosis: This is the mildest form, primarily affecting the eyes. Symptoms include photophobia (sensitivity to light), corneal opacities, and decreased vision. Kidney function remains normal in this type.

Treatment for cystinosis typically involves a combination of medications to manage symptoms and slow disease progression. Cysteamine therapy, which helps remove excess cystine from cells, is the primary treatment for all types of cystinosis. Regular monitoring and management of complications are essential to maintain quality of life and prolong survival.

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.

An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.

A forehead, in medical terms, refers to the portion of the human skull that lies immediately above the eyes and serves as an attachment site for the frontal bone. It is a common area for the examination of various clinical signs, such as assessing the level of consciousness (by checking if the patient's eyebrows or eyelids twitch in response to a light touch) or looking for signs of increased intracranial pressure (such as bulging fontanelles in infants). Additionally, the forehead is often used as a site for non-invasive procedures like Botox injections.

Hypophosphatemia-related rickets Congenital Vitamin D-resistant rickets Autosomal dominant hypophosphatemic rickets (ADHR) ... By 1945, rickets had all but been eliminated in the United States.[citation needed] The word rickets may be from the Old ... In developed countries, rickets is a rare disease (incidence of less than 1 in 200,000). Recently, cases of rickets have been ... Vitamin D-related rickets Vitamin D deficiency Vitamin D-dependent rickets (VDDR) Type 1: insufficiency in activation VDDR1A: ...
... (ADHR) is a rare hereditary disease in which excessive loss of phosphate in the ... "Hypophosphatemic Rickets". The Merck Manual Home Health Handbook. Merck Sharp & Dohme Corp. December 2006. Archived from the ... Hypophosphatemic rickets are associated with at least nine other genetic mutations. Clinical management of hypophosphatemic ... "Hereditary hypophosphatemic rickets". Genetics Home Reference. September 2010. Archived from the original on 17 September 2012 ...
"Rickets". The Alkaloidal Clinic. Clinic Publishing Company. 7 (1). The earliest bone lesion that we find in incipient rickets ... The prominent knobs of bone at the costochondral joints of rickets patients are known as a rachitic rosary or beading of the ... Palpation ( Beads formation) , on chest X-ray Will be present throughout the life (rickets should be treated first) John Little ... Causes include: Rickets : Nodularity at costochondral junction (rachitic rosary). Scurvy : More angular costochondral junction ...
Osteomalacia/rickets in adolescents. Osteopetrosis. Osteosarcoma. Rickets. Septic arthritis, a severe infection of the joint ... Hazzazi MA, Alzeer I, Tamimi W, Al Atawi M, Al Alwan I (2013). "Clinical presentation and etiology of osteomalacia/rickets in ...
Rickets was formerly a major public health problem among the US population. In Denver, almost two-thirds of 500 children had ... Rickets, a childhood disease, is characterized by impeded growth and soft, weak, deformed long bones that bend and bow under ... Rickets typically appears between 3 and 18 months of age. Cases continue to be reported in North American and other Western ... Nutritional rickets exists in countries with intense year-round sunlight such as Nigeria and can occur without vitamin D ...
Price, Norman Lloyd; Davie, Thomas Benjamin (January 1937). "Renal Rickets". British Journal of Surgery. Bristol: John Wright ... that exhibited the typical features of renal rickets. The new drawings have been made by Miss D. Pillers, and I am greatly ... ", "florist", and "chemist". Pillers' colleague, Norman Lloyd Price (she had illustrated his 1937 paper Renal Rickets), the ...
Kaneshiro, Neil K. "Rickets Osteomalacia in children; Vitamin D Deficiency; Renal Rickets; Hepatic Rickets". Vorvick, Linda J ... Additional studies done on South African children show that this deficiency can lead to Rickets. Rickets causes weakness and ... Pettifor, JM; Ross P; Wang J; Moodley G; Couper-Smith J (1978). "Rickets in Children of Rural Origin in South Africa: is Low ...
with J. Preston Maxwell & Cheng Hsiang Hu (程胡襄): Maxwell, J. Preston; Hu, C. H.; Turnbull, H. M. (1932). "Foetal rickets". The ...
SLC34A3 Hypophosphatemic rickets; 300554; CLCN5 Hypophosphatemic rickets, AR; 241520; DMP1 Hypophosphatemic rickets, autosomal ... RPIA Rickets due to defect in vitamin D 25-hydroxylation; 600081; CYP2R1 Rickets, vitamin D-resistant, type IIA; 277440; VDR ... UBA1 Vitamin D-dependent rickets, type I; 264700; CYP27B1 Vitamin K-dependent clotting factors, combined deficiency of, 2; ... dominant; 193100; FGF23 Hypophosphatemic rickets, autosomal recessive, 2; 613312; ENPP1 Hypoplastic left heart syndrome; 241550 ...
"Osteomalacia and Rickets". The Lecturio Medical Concept Library. Retrieved 27 August 2021. "Osteomyelitis". The Lecturio ...
"Osteomalacia and Rickets". The Lecturio Medical Concept Library. Retrieved 26 August 2021. "Osteogenesis Imperfecta". The ...
"Olympedia - Dave Rickets". olympedia.org. Retrieved November 16, 2021. Neil Strauss (August 14, 1996). "Mel Taylor, 62, Who ...
... in children is known as rickets, and because of this, use of the term "osteomalacia" is often restricted to the ... "Osteomalacia and Rickets". The Lecturio Medical Concept Library. Retrieved 23 August 2021. Holick, Michael F. (19 July 2007). " ... "Osteomalacia and Rickets". The Lecturio Medical Concept Library. Retrieved 23 August 2021. Eisman, John A. (1988). "6 ... "Osteomalacia and Rickets". The Lecturio Medical Concept Library. Retrieved 23 August 2021. Chakravorty, N. K. (1980). " ...
Scholia has a profile for Signe Normand (Q21663404). Normand, S; Rickets, R.E.; Skov F- (2011). "Postglacial migration ...
Hutchison, Florence (1992). "Osteomalacia and rickets". Seminars in Nephrology. 12 (2): 127-45. PMID 1561493. Callis, Gyle ( ...
Big Rock (in Chamcook Lake) Odell Island (in Chamcook Lake) Rickets Island (in Waweig River) Canada census - Saint Croix ... including Rickets Island. Saint Croix originally included five grants in Oak Bay that are now in Saint David Parish, parts of ...
Lucas RC (1833). "Form of late rickets associated with albuminuria, rickets of adolescents". The Lancet. 1 (3119): 993-994. doi ... "Osteomalacia and Rickets". The Lecturio Medical Concept Library. Retrieved 27 August 2021. Nassar, George M.; Ayus, Juan Carlos ...
Rickets, Palmer C. (1934). History of Rensselaer Polytechnic Institute 1824-1934 (PDF) (3rd ed.). New York: John Wiley & Sons, ...
Rickets 2000, p. 388. Garnett 2015, p. 24. "Bateman's". www.nationaltrustcollections.org.uk. National Trust Collections. ...
"56 cases of Rickets". Department of Health. NHS Choices: Blackburn With Darwen PCT Archived 11 February 2008 at the Wayback ... in particular there have been reports of an increase in cases of rickets in the area. In response to this the Living Better, ...
"Rams to Play in 2022 Legends Classic; Rickets on Sale Now!". Virginia Commonwealth University. Retrieved June 30, 2022. "2022- ...
The Rickets and Brooks Building. The Verchamp Building. The Telephone/Exchange Building. The Aubineau-Andreates Building. Old ... The Coconino Chop House - built in 1898 and located at 10 East Route 66 The Rickets and Brooks Building - built 1911 in and ...
The working group on rickets was closely knit in experience and interests. It seems to have been inspired by the inaugural ... An English translation appearing the following year, under the title A Treatise of the Rickets: Being a Diseas common to ... Hochberg, Ze'ev (2003). "Rickets - Past and Present" (PDF). Karger. Karger Medical and Scientific Publishers. Retrieved 5 ... Glisson, Francis (1651). "A Treatise of the Rickets, being a disease common to children". Early English Books Text Creation ...
Calcium and Vitamin D levels should be obtained to rule out rickets, and in mothers who have prenatal labs concerning for T. ... It is the first sign in children and infants with rickets.[citation needed] Other conditions which can cause craniotabes ... Elidrissy, Abdelwahab T. H. (31 May 2016). "The Return of Congenital Rickets, Are We Missing Occult Cases?". Calcified Tissue ... Paterson, Colin R.; Ayoub, David (October 2015). "Congenital rickets due to vitamin D deficiency in the mothers". Clinical ...
It was later discovered that the actual cause of rickets is lack of vitamin D due to lack of sunlight which can be prevented or ... He discovered that feeding caged dogs on a diet of porridge induced rickets, which could then be cured with cod liver oil and ... Experimental Rickets (1925) The Fat-Soluble Vitamins (1933) A Story of Nutritional Research (1950) The Chemical Manipulation of ... Harrison, DC; Mellanby, E (October 1939). "Phytic acid and the rickets-producing action of cereals". Biochem. J. 33 (10): 1660- ...
Soon after, a generation of children grew up on cod-liver oil, and rickets was virtually wiped out. Harry Day, a colleague and ... His group tested more than 300 diets on rats, finally finding that cod-liver oil could prevent rickets. Building on the work of ... The oil could no longer cure night blindness but did cure rickets. After his rats recovered, he named the substance for the ... McCollum's research during the early 1920s found that rats could develop rickets when fed a plain cereal diet. ...
Rickets, David (3 October 2018). "An audience with Andreas Utermann: the CEO who listens to his mum". Financial News. Retrieved ... Rickets, David (11 November 2019). "Allianz Global Investors boss to retire in January". Baron's. Retrieved 18 January 2019. " ...
Rickets, Chris (20 April 2019). "John Boyne flying flag for trans people even if he is holding it upside down". The Irish Times ...
deKroo, Karl; Rickets, Steve (3 May 2010). "Cooper Cronk replaces injured Thurston for Test". Courier-Mail. Retrieved 7 May ...
Rickets, Peter (16 September 2020). "Kim Darroch and the art of the diplomat". New Statesman. Retrieved 2 November 2020. ...
Hypophosphatemia-related rickets Congenital Vitamin D-resistant rickets Autosomal dominant hypophosphatemic rickets (ADHR) ... By 1945, rickets had all but been eliminated in the United States.[citation needed] The word rickets may be from the Old ... In developed countries, rickets is a rare disease (incidence of less than 1 in 200,000). Recently, cases of rickets have been ... Vitamin D-related rickets Vitamin D deficiency Vitamin D-dependent rickets (VDDR) Type 1: insufficiency in activation VDDR1A: ...
Rickets causes soft, weak bones in children. It usually occurs when they do not get enough vitamin D. Read about symptoms and ... ClinicalTrials.gov: Rickets (National Institutes of Health) * ClinicalTrials.gov: Rickets, Hypophosphatemic (National ... Hereditary hypophosphatemic rickets: MedlinePlus Genetics (National Library of Medicine) * Vitamin D-dependent rickets: ... Rickets (Mayo Foundation for Medical Education and Research) Also in Spanish * Vitamin D (National Institutes of Health, Office ...
Rickets is a disease of growing bone that is unique to children and adolescents. It is caused by a failure of osteoid to ... The incidence of rickets in Europe is similar to that in the United States. In sunny areas, such as in the Middle East, rickets ... Rickets may lead to skeletal deformity and short stature. In females, pelvic distortion from rickets may cause problems with ... encoded search term (Rickets) and Rickets What to Read Next on Medscape ...
... results in skeletal abnormalities caused by low blood calcium levels. ... Vitamin D-Dependent Rickets. Vitamin D-Dependent Rickets results in skeletal abnormalities caused by low blood calcium levels. ... Vitamin D-Dependent Rickets is a disorder characterized by abnormal conversion of dietary vitamin D into its biologically ... A novel CYP27B1 mutation causes a feline vitamin D-dependent rickets type IA. Journal of Feline Medicine and Surgery, 14(8), ...
Tagged .uk deformity exercise games gaming health Increase Mario NHS PC prevention ps3 rickets Rise Social sunshine super ... Video games blamed for rise in rickets. 22 January 2010. Gerald Lynch Gaming, Health, Tech Digest news ... Nope, its being attributed to a sharp rise in RICKETS in UK children, a condition not widely seen since the Victorian age. ...
Rickets, the bone disease that causes bowed legs and stunted growth in children and is associated with Victorian England, is ... Vitamin D, made by the action of sunlight on the skin, is essential to prevent rickets and people who spend a lot of time ... By your third or fourth child, that child is born already without enough vitamin D. So theyll be presenting with rickets at ... 0Rise in rickets linked to ethnic groups that shun the sun. ... Rise in rickets linked to ethnic groups that shun the sun. ...
Find all Natural Cures for Rickets only on NaturalCures.com - the worlds #1 resource of natural health cures and remedies, ... Rickets in adults is known as osteomalacia or soft bones.. The most common cause of rickets comes as a result of a lack of ... The main cause of rickets is a lack of vitamin D; not having enough calcium in ones diet may also be a cause of rickets, as ... Heres a list of the main symptoms of rickets:. *Pain - The bones affected by rickets are often sore and painful, which may ...
Rickets has been identified in a Neolithic skeleton from the Scottish island of Tiree, making it the earliest case of the ... Neolithic skeleton reveals early history of rickets. Neolithic skeleton reveals early history of rickets. Published: Thursday ... Rickets has been identified in a Neolithic skeleton from the Scottish island of Tiree, making it the earliest case of the ... The bones show a number of deformities that are caused by rickets - particularly in the breastbone, ribs, and the arms and legs ...
Tommy Rickets and other kinds of academic papers in our essays database at Many Essays. ...
... a causative factor of tumor-induced osteomalacia and also as a responsible gene for autosomal dominant hypophosphatemic rickets ... FGF-23 transgenic mice demonstrate hypophosphatemic rickets with reduced expression of sodium phosphate cotransporter type IIa ... the notion that the excessive action of FGF-23 plays a causative role in the development of several hypophosphatemic rickets/ ... a causative factor of tumor-induced osteomalacia and also as a responsible gene for autosomal dominant hypophosphatemic rickets ...
Rickets - the bone disease caused by Vitamin D deficiency - is on the rise in England. Even children getting ... So Rickets has always been on my personal radar… I make sure that my kids get plenty of sun (without sunscreen as much as ... Rickets - the bone disease caused by Vitamin D deficiency - is on the rise in England. Even children getting "plenty" of sun ... Sun Exposure Not Enough To Prevent Rickets. January 25, 2011. by Kristen Michaelis CNC 63 Comments , Affiliate Disclosure ...
Rickets is an entity in which mineralization is decreased at the level of the growth plates, resulting in growth retardation ... encoded search term (Rickets Imaging) and Rickets Imaging What to Read Next on Medscape ... Any child with rickets also has osteomalacia, but the reverse is not necessarily true. [1, 2, 3, 4] Children with ... By definition, rickets is found only in children before closure of the growth plates, while osteomalacia occurs in persons of ...
... JEFFERSON COUNTY Anita Rickets killed in Birmingham crash on ... Anita Lovoy Rickets, a 74-year-old resident of Birmingham, was fatally injured in the crash that happened around 1:13 p.m. in ... Rickets was pronounced dead at UAB Hospital.. Details about what happened leading up to the accident are still unclear, as the ... Anita Lovoy Rickets, a 74-year-old resident of Birmingham, lost her life following a head-on accident Monday afternoon along ...
It doesnt stick out like the pictures of spraddle leg that Ive seen so Im thinking it might be rickets. Has anyone had this ...
Multiple Fractures in a Child with Rickets - Pediatric Oncall ... Multiple Fractures in a Child with Rickets. Rahul Sinha, ... Rickets is an entity in which mineralization is decreased at the level of the growth plates, resulting in growth retardation ... Vitamin D: Rickets in children and osteomalacia in pregnant women. In The Prescriber: Guidelines on the Rational Use of Drugs ... Multiple Fractures in a Child with Rickets 01/09/2014 00:00:00 Rahul Sinha, Kirandeep Sodhi, Y K Kiran 04/01/2011 00:00:00 ...
Giving diseases a national identity, an inanely xenophobic practice at best, is now regarded as politically incorrect. Referring to rubella as German measles might still be considered merely naïve, but any mention of mongolism (once a widely used synonym for Downs Syndrome) is likely to be met with severe censure. The term French letters has [...]. ...
Calcium deficiency has been found to play a major role in Nigerian children with rickets, with only one third of rickets ... hereditary vitamin D dependent rickets, and hereditary hypophosphataemic rickets. All patients included responded to vitamin D ... Children affected by rickets are smaller, both in height and weight, than the normal population.7 In this cohort, males had a ... The increasing frequency of rickets in the UK has recently been highlighted4,31 with Ladhani et al reporting data on 65 cases. ...
Bowing of legs is it always rickets? A case report.. Objective: Familial Blount disease is a rare developmental disorder that ...
Rickets (osteomalacia) is a softening of the bones that leads to fractures and deformity. The majority of cases of rickets ... Rickets (osteomalacia). Rickets (osteomalacia) is a softening of the bones that leads to fractures and deformity. The majority ... But the history of rickets shows that a typical rickets case often had a history of smallpox, measles, or whooping cough.12) ... The study compared 123 Nigerian children who had rickets with matched control subjects. Of the 134 subjects with rickets, only ...
The incidence of rickets in children attending hospitals in Bristol from September 1938 to May 1941 ... The incidence of rickets in children attending hospitals in Bristol from September 1938 to May 1941 ...
Bowed legs is not the primary indication of rickets (3 other indications of rickets are seen more often) Some Rickets is due to ... Vitamin D and Rickets consensus took 80 years Rickets category has 126. items items in BOTH of categories: Infant-Child and ... Overview of Rickets and vitamin D contains the following summary Rate of rickets is usually < 0.1% of births, unless dark skin ... Sometimes rickets is also associated with a poor vitamin D receptor Giving enough Vitamin D to the mother PREVENTS Rickets Rate ...
Rickets in Sheep [16]. / Dunlop, George. In: Nature, Vol. 173, No. 4401, 01.12.1954.. Research output: Contribution to journal ... Dunlop G. Rickets in Sheep [16]. Nature. 1954 Dec 1;173(4401). doi: 10.1038/173453a0 ... Dunlop, G 1954, Rickets in Sheep [16], Nature, vol. 173, no. 4401. https://doi.org/10.1038/173453a0 ... Dunlop, G. (1954). Rickets in Sheep [16]. Nature, 173(4401). https://doi.org/10.1038/173453a0 ...
Bowed legs is not the primary indication of rickets (3 other indications of rickets are seen more often) Some Rickets is due to ... Vitamin D and Rickets consensus took 80 years Rickets category has 126. items Loading Dose of Vitamin D category has the ... Overview of Rickets and vitamin D contains the following summary. Rate of rickets is usually < 0.1% of births, unless dark skin ... Sometimes rickets is also associated with a poor vitamin D receptor Giving enough Vitamin D to the mother PREVENTS Rickets Rate ...
Therefore, we report here a case of hypophosphatemic rickets.. AIM AND OBJECTIVE: To report a case of hypophosphatemic rickets ... CONCLUSION: Hypophosphatemic rickets or osteomalacia, possibly hereditary, is a rare cause of recurrent pathological fractures. ... Hypophosphatemic rickets: A case of recurrent pathological fractures.. Arjun Baidya, Subhankar Chowdhury, Satinath Mukhopadhyay ... INTRODUCTION: Renal phosphate-wasting disorders are the most common form of hereditary rickets and osteomalacia in western ...
Retrieved from "https://www.wikidoc.org/index.php?title=Rickets&oldid=1243611" ...
... including rickets, renal diseases (renal osteodystrophy, Fanconi syndrome), tumor-induced osteomalacia, hypophosphatasia, ... Receptor defect rickets (type II vitamin D-dependent rickets). Receptor defect rickets (hereditary 1,25-dihydroxyvitamin D- ... Rickets. Nutritional rickets. A recommended daily allowance (RDA) for vitamin D has not been defined. [3] Because no strong ... Osteodystrophy (ie, renal rickets) is the only type of rickets with a high serum phosphate level. It can be adynamic (a ...
Rickets is a disease of growing bone that is unique to children and adolescents. It is caused by a failure of osteoid to ... encoded search term (Rickets) and Rickets What to Read Next on Medscape ... Rickets Differential Diagnoses. Updated: Apr 17, 2014 * Author: Steven M Schwarz, MD, FAAP, FACN, AGAF; Chief Editor: Jatinder ... Lowdon J. Rickets: concerns over the worldwide increase. J Fam Health Care. 2011 Mar-Apr. 21(2):25-9. [QxMD MEDLINE Link]. ...
... is defined as failure of mineralisation of growing bone or osteoid tissue. Rickets is a metabolic disturbance of home ...
Rickets is a disease of growing bone that is unique to children and adolescents. It is caused by a failure of osteoid to ... The incidence of rickets in Europe is similar to that in the United States. In sunny areas, such as in the Middle East, rickets ... Rickets may lead to skeletal deformity and short stature. In females, pelvic distortion from rickets may cause problems with ... encoded search term (Rickets) and Rickets What to Read Next on Medscape ...
Malnutrition is the excess or inadequacy of basic nutrients in the body, this lack or excess of nutrients can cause several diseases. Some of these diseases are so severe that they can lead to death. In underdeveloped countries malnutrition is the biggest reason behind childhood mortality, in developed countries malnutrition is present in children in the form of obesity. The …. Read More » ...
  • Hereditary forms of hypophosphatemic rickets include X-linked, autosomal dominant, and autosomal recessive disease, as well as hypophosphatemic rickets with hypercalciuria. (boneandspine.com)
  • A form of hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is known to occur due to mutations in the proximal tubule type 2c sodium-phosphate cotransporter (NaPi2c). (msdmanuals.com)
  • What are the causes of hereditary hypophosphatemic rickets with hypercalciuria (HHRH)? (bengalurukidsortho.in)
  • Vitamin D, made by the action of sunlight on the skin, is essential to prevent rickets and people who spend a lot of time indoors and cover up when they go out may become deficient. (independent.co.uk)
  • Foods Rich in Vitamin D - Getting enough vitamin D supports strong bones and can help prevent rickets. (naturalcures.com)
  • We've been told that 15 minutes of exposure to the sun, twice per week would be enough for us to produce enough Vitamin D to prevent Rickets. (foodrenegade.com)
  • We've been told that fortifying our milk and other dairy with synthetic Vitamin D would prevent Rickets. (foodrenegade.com)
  • conducted a study to determine whether vitamin D supplementation should be required to prevent rickets in breast-fed infants. (mpkb.org)
  • Findings in patients with rickets. (medscape.com)
  • Calcitriol levels may be normal in patients with rickets, suggesting that it is not the only active form of the vitamin. (medscape.com)
  • Signs and symptoms of rickets include swollen wrists and ankles, muscle weakness, bone and joint pain, and growth problems. (lybrate.com)
  • In rare cases, a parathyroid adenoma can mimic the signs and symptoms of rickets or contribute to ricket-like changes in the body. (panafrican-med-journal.com)
  • The incidence of nutritional rickets (NR) is rising globally, and hospitalization is increasing even in high-income countries. (medscape.com)
  • The diagnosis of nutritional rickets is made on the basis of history, physical examination, and biochemical testing and is confirmed by radiographs. (medscape.com)
  • To define the demographics and clinical characteristics of cases presenting with nutritional rickets to paediatric centres in Sydney, Australia. (bmj.com)
  • Despite a clearer understanding of predisposing factors and attempts at preventative strategies, nutritional rickets has made a surprising resurgence in many parts of the world. (bmj.com)
  • The belief that nutritional rickets has been eliminated from developed societies is widespread and can inhibit recognition, appropriate management, and institution of preventative strategies. (bmj.com)
  • Objective: To compare the efficacy of daily versus low dose depot oral vitamin D3 for treating nutritional rickets. (vitamindwiki.com)
  • Conclusion: Low dose oral depot vitamin D3 is an effective alternative to daily oral vitamin D3 for nutritional rickets. (vitamindwiki.com)
  • Intestinal malabsorption of fat and diseases of the liver or kidney may produce the clinical and secondary biochemical picture of nutritional rickets. (medscape.com)
  • Most cases of rickets (especially nutritional rickets) can be treated and cured when doctors or healthcare professionals are able to catch them early.In most cases, changes to the diet, added vitamin supplements, and more sunlight exposure are enough to cure this disease. (lybrate.com)
  • ABSTRACT Nutritional rickets is the failure of normal bone formation in children , caused by vitamin D deficiency , low calcium intake, or a combination of both. (bvsalud.org)
  • The majority of cases of rickets occur among children in developing countries who suffer from severe malnutrition. (mpkb.org)
  • In many cases of rickets the patient is someone with a deficiency of vitamin D so you should test the level of vitamin D and calcium in the blood of the child. (babyinfo.com.au)
  • A condition which affects bone development in children, rickets can cause the bones to become soft and malformed, even leading to bone deformities. (naturalcures.com)
  • The bones show a number of deformities that are caused by rickets - particularly in the breastbone, ribs, and the arms and legs. (bradford.ac.uk)
  • A rare autosomal recessive renal phosphate-wasting disorder characterized by childhood-onset hypophosphatemia that clinically manifests with rickets and/or osteomalacia slow growth/short stature bone pain and skeletal deformities. (globalgenes.org)
  • It's also important to note that some skeletal deformities caused by rickets may require corrective surgeries. (lybrate.com)
  • Rickets can be traced back to Ancient Rome where bone deformities in infants were attributed to the failure of mothers to nurture and clean their children. (baby-magazine.co.uk)
  • The disease is cited as a primary reason for consuming vitamin D regularly even though research has demonstrated that rickets is not caused by vitamin D deficiency but by hypophosphatemia. (mpkb.org)
  • The team concluded that rickets is not caused by a deficiency of vitamin D but instead results from hypophosphatemia, a condition where the level of phosphorous in the blood is too low. (mpkb.org)
  • Hypophosphatemic rickets is a genetic disorder characterized by hypophosphatemia, defective intestinal absorption of calcium, and rickets or osteomalacia unresponsive to vitamin D . It is usually hereditary. (msdmanuals.com)
  • The disease manifests as a spectrum of abnormalities, from hypophosphatemia alone to growth retardation and short stature to severe rickets or osteomalacia. (msdmanuals.com)
  • XLHR is the most common type of genetic hypophosphatemia and causes rickets and osteomalacia in children due to elevated secretion of fibroblast growth factor 23 and renal phosphate wasting. (endocrinologyadvisor.com)
  • The pathophysiology of rickets is not completely understood, nor is the role of the many vitamin D metabolites. (medscape.com)
  • X-linked hypophosphatemic rickets and autosomal recessive hypophosphatemic rickets are the result of mutations in PHEX (a phosphate-regulating gene with homologies to endopeptidases on the X chromosome) and dentin matrix protein 1 ( DMP1 ), respectively. (medscape.com)
  • Autosomal recessive hypophosphatemic rickets. (boneandspine.com)
  • Newly diagnosed with Autosomal recessive hypophosphatemic rickets? (globalgenes.org)
  • Hypophosphatemic rickets can be classified into three further categories: X-linked dominant hypophosphatemic rickets (the most common type), autosomal dominant hypophosphatemic rickets, and autosomal recessive hypophosphatemic rickets. (lybrate.com)
  • The most common cause of rickets is a vitamin D deficiency, although hereditary genetic forms also exist. (wikipedia.org)
  • The most common cause of rickets comes as a result of a lack of vitamin D and calcium. (naturalcures.com)
  • Rickets is a condition that results in weak or soft bones in children, and is caused by either dietary deficiency or genetic causes. (wikipedia.org)
  • In rare cases, children can be born with a genetic form of rickets. (naturalcures.com)
  • Being a genetic disorder, hypophosphatemic rickets is present from conception. (boneandspine.com)
  • The primary cause of congenital rickets is vitamin D deficiency in the mother's blood, which the baby shares. (wikipedia.org)
  • Congenital rickets may also be caused by other maternal diseases, including severe osteomalacia, untreated celiac disease, malabsorption, pre-eclampsia, and premature birth. (wikipedia.org)
  • Rickets may lead to skeletal deformity and short stature. (medscape.com)
  • An outstanding feature of familial hypophosphatemic rickets is disproportionate short stature. (boneandspine.com)
  • Less commonly, a dietary deficiency of calcium or phosphorus may also produce rickets. (medscape.com)
  • Premature infants who are breast fed and do not receive mineral supplements may develop severe phosphorus deficiency that presents as rickets. (medscape.com)
  • Rickets arises due to decreased availability of phosphorus and calcium to mineralize the skeletal matrix, leading to growth plate disorganization and accumulation of undermineralized osteoid. (unboundmedicine.com)
  • Not getting enough vitamin D can lead to conditions like rickets, which is when the bones of your child don't have enough calcium and phosphorus. (lybrate.com)
  • At higher exposure levels, especially under conditions of inadequate calcium, phosphorus, and vitamin D, stable strontium will interfere with normal bone development, causing `strontium rickets' of variable severity. (cdc.gov)
  • The underlying calcium deprivation manifests not only as reduced bone mineralization (rickets and osteomalacia) but also as hypocalcaemic seizures, tetany, and dilated cardiomyopathy, including cardiac failure and death. (medscape.com)
  • Rickets is an entity in which mineralization is decreased at the level of the growth plates, resulting in growth retardation and delayed skeletal development [1]. (pediatriconcall.com)
  • Degradation of matrix extracellular phosphoglycoprotein (MEPE) and DMP-1 and release of acidic serine-rich and aspartate-rich MEPE-associated motif (ASARM) peptides are chiefly responsible for the hypophosphatemic rickets mineralization defect and changes in osteoblast-osteoclast differentiation. (medscape.com)
  • Deficiency impairs bone mineralization, causing rickets in children and osteomalacia in adults and possibly contributing. (msdmanuals.com)
  • Professor Ian Armit from the University of Bradford explains: "The earliest case of rickets in Britain until now dated from the Roman period, but this discovery takes it back more than 3,000 years. (bradford.ac.uk)
  • ntil recently, when I heard of a case of rickets, there were generally two images that would spring to mind. (baby-magazine.co.uk)
  • Bowed legs are a sign of rickets. (mpkb.org)
  • This causes the level of phosphate in the body to drop, leading to the altered bone formation seen in rickets. (mpkb.org)
  • Any child with rickets also has osteomalacia, but the reverse is not necessarily true. (medscape.com)
  • Sinha R, Sodhi K, Kiran Y K. Multiple Fractures in a Child with Rickets. (pediatriconcall.com)
  • A much wider range of ultraviolet rays than that commonly thought effective helps in the prevention or treatment of rickets, Prof. John W.M. Bunker of the Massachusetts Institute of Technology and Robert S. Harris, research associate at the Institute, reported to the American Public Health Association at its meeting in Ft. Worth, Texas, this week. (sciencenews.org)
  • Rickets can be treated with an extra dose of oral vitamin D. During the treatment of rickets, a doctor monitors the levels of 25-OH-D in the plasma to raise it to a normal value. (organicfacts.net)
  • An X-ray or radiograph of an advanced patient with rickets tends to present in a classic way: the bowed legs (outward curve of long bone of the legs) and a deformed chest. (wikipedia.org)
  • The image below illustrates findings in a patient with rickets. (medscape.com)
  • 7 Various nutritional, ethnic, cultural, and societal factors are likely to account for either an increase in the prevalence of rickets or increasing recognition, 7 with different factors likely to predominate in different regions. (bmj.com)
  • Retrospective descriptive study of 126 cases seen from 1993 to 2003 with a diagnosis of vitamin D deficiency and/or confirmed rickets defined by long bone x ray changes. (bmj.com)
  • The diagnosis itself came remarkably quickly, where the consultant spotted swollen wrists and strongly suspected that rickets was the underlying issue. (baby-magazine.co.uk)
  • Sagittal suture fusion and Chiari type 1 malformation are commonly observed complications of X-linked hypophosphatemic rickets (XLHR), and because the presence of craniovertebral anomalies can be underestimated, radiologic imaging should be considered in this population to ensure an accurate diagnosis, according to study findings published in the Journal of Bone and Mineral Research . (endocrinologyadvisor.com)
  • Rickets in children is similar to osteoporosis in the elderly, with brittle bones. (wikipedia.org)
  • Rickets causes soft, weak bones in children. (medlineplus.gov)
  • In addition to dietary rickets, children can get an inherited form of the disease. (medlineplus.gov)
  • Rickets is a disease of growing bone that is unique to children and adolescents. (medscape.com)
  • Severe rickets has been associated with respiratory failure in children. (medscape.com)
  • Nope, its being attributed to a sharp rise in RICKETS in UK children, a condition not widely seen since the Victorian age. (techdigest.tv)
  • Rickets, the bone disease that causes bowed legs and stunted growth in children and is associated with Victorian England, is making a comeback. (independent.co.uk)
  • Common during Victorian times, but mostly disappeared in the Western world during the 1940s thanks to the fortification with vitamin D of foods such as margarine and cereal, rickets still affects thousands of children each year. (naturalcures.com)
  • When ultraviolet rays from the sun hit the skin, the result is synthesis of vitamin D, but it is worth noting that children with very dark skin or those who do not get enough sun exposure are susceptible to a vitamin D deficiency and therefore rickets. (naturalcures.com)
  • For these children, it is important that their rickets diet contain several of the other foods rich in vitamin D, calcium and/or phosphorous. (naturalcures.com)
  • Vitamin D deficiency results in rickets in children with growing bones and causes osteomalacia in adults with completed growth and closed growth plates. (medscape.com)
  • By definition, rickets is found only in children before closure of the growth plates, while osteomalacia occurs in persons of any age. (medscape.com)
  • Although this problem was largely corrected though health measures that provides children with adequate Vitamin D, rickets remains a major problem in developing countries with a prevalence rate of 10% [3]. (pediatriconcall.com)
  • UNICEF has estimated that up to 25% of children in China have some evidence of rickets [4]. (pediatriconcall.com)
  • One team assessed the absorption of calcium in 15 Nigerian children with active rickets. (mpkb.org)
  • They found that all 15 children had resolution or improvement of rickets after six months of treatment with calcium supplements. (mpkb.org)
  • We measured how much calcium was absorbed in a group of children with rickets and compared that with how much was absorbed by children that did not have rickets. (mpkb.org)
  • We found that children with rickets were able to absorb calcium normally. (mpkb.org)
  • This means that it is probably another factor in the diet or an overall lack of calcium that causes the rickets rather than an inability of some children to absorb the calcium that is in their diet. (mpkb.org)
  • Nutritional or classical rickets (here labeled as "rickets") is a worldwide disease involving mostly infants and young children having inadequate sunlight exposure, often associated with a low dietary intake of Vitamin D. Rickets targets all layers of society independently of economic status with historical information spanning more than two millennia. (vitamindwiki.com)
  • Vitamin D is critical for the absorption of calcium and prevention of rickets in children as well as osteomalacia in adults. (vitamindwiki.com)
  • These conditions may result in failure of osteoid calcification (rickets) in children because of a disruption in the pathway of either vitamin D or phosphate metabolism. (medscape.com)
  • Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. (medscape.com)
  • In children, osteomalacia can lead to growth plate abnormalities, termed rickets. (unboundmedicine.com)
  • Rickets is mostly diagnosed in children under the age of 5 years. (babyinfo.com.au)
  • Children who have an insufficient intake of calcium in their diet tend to eventually develop symptoms of rickets. (babyinfo.com.au)
  • Rickets is a rare disease (or medical condition) that mainly affects children, making their bones soft and malleable. (lybrate.com)
  • Rickets is common in children who don't get the amount of sunlight that's usually required by their bodies. (lybrate.com)
  • In fact, children who have parents of Asian, Middle Eastern, or African-Caribbean descent are more likely to get rickets because their darker skin requires more sunlight to absorb adequate amounts of vitamin D. (lybrate.com)
  • This is especially important for young children because they are more susceptible to developing a vitamin D deficiency or medical conditions like rickets. (lybrate.com)
  • Rickets is a condition that affects bone development in children. (baby-magazine.co.uk)
  • However, its deficiency can cause rickets in children and osteomalacia in adults. (organicfacts.net)
  • Rickets is a disease of the bones found in children. (organicfacts.net)
  • Increasing awareness of the rationale for and importance of vitamin D supplements for all breastfed infants and children should reduce the incidence of vitamin D deficiency rickets and prevent bone deformity . (bvsalud.org)
  • Renal phosphate-wasting disorders are the most common form of hereditary rickets and osteomalacia in western countries, but are rarely reported in India. (qxmd.com)
  • The defect is in the cells of the proximal renal tubule leading to solute-wasting, hypercalciuria,, kidney stones, renal failure, and in some cases rickets. (boneandspine.com)
  • Phosphopenic or hypophosphatemic rickets usually result from increased renal excretion of phosphate, while calcipenic rickets happen primarily because of a lack of calcium in a person's body. (lybrate.com)
  • An increase in serum phosphatase activity is associated with primary hyperparathyroidism, secondary hyperparathyroidism owing to chronic renal disease, rickets, and osteitis deformans juvenilia due to vitamin D deficiency and malabsorption or renal tubular dystrophies. (cdc.gov)
  • Vitamin D deficiency rickets is easily treated once it has been recognised, however it has significant potential for morbidity and mortality including hypocalcaemic seizures, failure to thrive, increased susceptibility to serious infections, and potential for chronic problems with growth and skeletal deformity. (bmj.com)
  • Rickets (osteomalacia) is a softening of the bones that leads to fractures and deformity. (mpkb.org)
  • The researchers found that if the mice were given a diet high in calcium and phosphorous they did not develop rickets and their bones were just as strong as normal mice with active Vitamin D Receptors. (mpkb.org)
  • What's the difference between rickets and scurvy? (lybrate.com)
  • Vitamin D-Dependent Rickets results in skeletal abnormalities caused by low blood calcium levels. (wisdompanel.com)
  • Exclusively breast-fed infants may require rickets prevention by vitamin D supplementation or an increased exposure to sunlight. (wikipedia.org)
  • Despite abundant sunlight, rickets and osteomalacia are prevalent in South Asian countries. (mpkb.org)
  • Rickets is a metabolic disturbance of home growth and results from dietary lack of vitamin D or ultraviolet rays of sunlight. (namat.net)
  • People who mostly stay indoors tend to be the ones to show up with symptoms of rickets due to lack of exposure to sunlight. (babyinfo.com.au)
  • Rickets is more common in developing countries, where people do not get adequate sunlight exposure. (lybrate.com)
  • The World Health Organization (WHO) has confirmed that rickets is making a comeback and is now a more common (or widespread) problem in parts of the world where there is less sunlight. (lybrate.com)
  • Originality/value - Since malnutrition (e.g. iron-deficiency anemia, rickets, zinc deficiency, protein-calorie malnutrition) is common in sub-Saharan Africa, the information which is provided should increase awareness among agricultur al and public health officials of the nutritional value of seven underappreciated and underutilized ILVs that are indigenous to Ghana and many other parts of Africa. (cdc.gov)
  • Rickets in adults is known as osteomalacia or soft bones. (naturalcures.com)
  • Rickets causes the bones to become painful, soft and weak. (naturalcures.com)
  • Pain - The bones affected by rickets are often sore and painful, which may mean the child is reluctant to walk, or may tire easily. (naturalcures.com)
  • Foods Rich in Phosphorous - Phosphorous is necessary for strong bones, so a rickets diet should also contain foods that provide essential mineral. (naturalcures.com)
  • Vegetarian Diets - A vegetarian diet may lack the essential nutrients necessary to support strong bones and may lead to rickets, so fortified foods or vitamin supplements may help in the prevention of nutrient deficiencies to which vegetarians are susceptible. (naturalcures.com)
  • In literature most of the cases reported with rickets present with green stick fractures which are commonly seen in weight bearing bones [6]. (pediatriconcall.com)
  • In other words, rickets is a condition that causes the weakening and softening of bones in kids, usually as a result of insufficient vitamin D levels in their bodies. (lybrate.com)
  • Rickets is a disease that interferes with the body's ability to use vitamin D and calcium, leading to softening of the bones. (lybrate.com)
  • Her ankles and wrists bones were visibly enlarged, the latter I now know is a common symptom of rickets. (baby-magazine.co.uk)
  • Findings in rickets are illustrated in the image below. (medscape.com)
  • Similar findings were noted in the study where 17.5% fractures were present in mobile infant and toddlers with rickets [7]. (pediatriconcall.com)
  • Vitamin D deficiency rickets occurs when the metabolites of vitamin D are deficient. (medscape.com)
  • 2019. https://peds.unboundmedicine.com/pedscentral/view/5-Minute-Pediatric-Consult/617030/all/Rickets_Osteomalacia. (unboundmedicine.com)
  • As rickets is caused by a deficiency in at least one of three essential nutrients: vitamin D, calcium or phosphorous, your child's diet needs to include foods rich in at least one of these nutrients. (naturalcures.com)
  • other micronutrient deficiencies of concern are subclinical vitamin A deficiency, rickets and iodine deficiency. (who.int)
  • Signs and symptoms of dietary deficiency rickets can include bone tenderness, and a susceptibility for bone fractures, particularly greenstick fractures. (wikipedia.org)
  • Our case report highlights an unusual presentation of rickets with multiple fractures. (pediatriconcall.com)
  • Hypophosphatemic rickets: A case of recurrent pathological fractures. (qxmd.com)
  • To report a case of hypophosphatemic rickets presenting with recurrent pathological fractures. (qxmd.com)
  • Hypophosphatemic rickets or osteomalacia, possibly hereditary, is a rare cause of recurrent pathological fractures. (qxmd.com)
  • The health benefits of vitamin D, also known as calciferol, include curing rickets, the treatment of osteomalacia, protection against peripheral arterial disease (PAD), slowing the progression of cancer, preventing bone fractures, and treating rachitic rosary. (organicfacts.net)
  • Vitamin D-Dependent Rickets is a disorder characterized by abnormal conversion of dietary vitamin D into its biologically active form calcitriol (D3). (wisdompanel.com)
  • 4) Interestingly, the paper goes on to say that subjects who are at risk for rickets had low dietary calcium consumption and significantly low calcium consumption. (mpkb.org)
  • Rickets is a skeletal disorder caused by the deficiency of vitamin D, phosphate, and calcium. (organicfacts.net)
  • Rare metabolic bone diseases, including hypophosphatasia , have been confused with rickets in infancy. (medscape.com)
  • Low levels are associated with hyperthyroidism, and with the rare condition of idiopathic hypophosphatasia associated with rickets and the excretion of excess phosphatidyl ethanolamine in the urine. (cdc.gov)
  • Some childhood kidney and liver diseases can also cause rickets, as can digestive disorder complications that affect calcium and phosphorous absorption. (naturalcures.com)
  • Milk - Fortified milk is a beneficial addition to a rickets diet because it contains vitamin D, calcium and phosphorous. (naturalcures.com)
  • Rickets occurs relatively commonly in the Middle East, Africa, and Asia. (wikipedia.org)
  • During the Industrial Revolution, rickets appeared in epidemic form in temperate zones where the pollution from factories blocked the sun's ultraviolet rays. (medscape.com)
  • In the United States, dairy milk is fortified with vitamin D (400 IU/L). Human milk contains little vitamin D, generally less than 20-40 IU/L. Therefore, infants who are breastfed are at risk for rickets, especially those who receive no oral supplementation and those who have darkly pigmented skin, which blocks penetration of ultraviolet light. (medscape.com)
  • Hypophosphatemic rickets is a hereditary form of rickets characterized by low serum phosphate levels and resistance to treatment with ultraviolet radiation or vitamin D ingestion. (boneandspine.com)
  • The hereditary form of vitamin D-dependent rickets type II causes that calcium cannot be absorbed. (labogen.com)
  • The hereditary form of vitamin D-dependent rickets type II is caused by a defect in the vitamin D receptor gene VDR, which makes the active hormone calcitriol unable to bind. (labogen.com)
  • Rickets in toddlers is a large problem in parts of Africa, especially Nigeria. (mpkb.org)