A condition of an abnormally low level of PHOSPHATES in the blood.
Neoplasms composed of connective tissue, including elastic, mucous, reticular, osseous, and cartilaginous tissue. The concept does not refer to neoplasms located in connective tissue.
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.
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 mixed mesenchymal tumor composed of two or more mesodermal cellular elements not commonly associated, not counting fibrous tissue as one of the elements. Mesenchymomas are widely distributed in the body and about 75% are malignant. (Dorland, 27th ed; Holland et al., Cancer Medicine, 3d ed, p1866)
Hydroxy analogs of vitamin D 3; (CHOLECALCIFEROL); including CALCIFEDIOL; CALCITRIOL; and 24,25-DIHYDROXYVITAMIN D 3.
A tumor composed of spindle cells with a rich vascular network, which apparently arises from pericytes, cells of smooth muscle origin that lie around small vessels. Benign and malignant hemangiopericytomas exist, and the rarity of these lesions has led to considerable confusion in distinguishing between benign and malignant variants. (From Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1364)
In patients with neoplastic diseases a wide variety of clinical pictures which are indirect and usually remote effects produced by tumor cell metabolites or other products.
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.
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.
A specialized CONNECTIVE TISSUE that is the main constituent of the SKELETON. The principle cellular component of bone is comprised of OSTEOBLASTS; OSTEOCYTES; and OSTEOCLASTS, while FIBRILLAR COLLAGENS and hydroxyapatite crystals form the BONE MATRIX.
A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98.
Inorganic salts of phosphoric acid.
Decalcification of bone or abnormal bone development due to chronic KIDNEY DISEASES, in which 1,25-DIHYDROXYVITAMIN D3 synthesis by the kidneys is impaired, leading to reduced negative feedback on PARATHYROID HORMONE. The resulting SECONDARY HYPERPARATHYROIDISM eventually leads to bone disorders.
A fibrous degeneration, cyst formation, and the presence of fibrous nodules in bone, usually due to HYPERPARATHYROIDISM.
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.
A genetic metabolic disorder resulting from serum and bone alkaline phosphatase deficiency leading to hypercalcemia, ethanolamine phosphatemia, and ethanolamine phosphaturia. Clinical manifestations include severe skeletal defects resembling vitamin D-resistant rickets, failure of the calvarium to calcify, dyspnea, cyanosis, vomiting, constipation, renal calcinosis, failure to thrive, disorders of movement, beading of the costochondral junction, and rachitic bone changes. (From Dorland, 27th ed)
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
The largest of three bones that make up each half of the pelvic girdle.
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 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.
Cholecalciferols substituted with two hydroxy groups in any position.
An antiepileptic agent related to the barbiturates; it is partly metabolized to PHENOBARBITAL in the body and owes some of its actions to this metabolite. Adverse effects are reported to be more frequent than with PHENOBARBITAL. (From Martindale, The Extra Pharmacopoeia, 30th ed, p309)
Process by which organic tissue becomes hardened by the physiologic deposit of calcium salts.
A sugar acid derived from D-glucose in which both the aldehydic carbon atom and the carbon atom bearing the primary hydroxyl group are oxidized to carboxylic acid groups.
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.
Diseases of BONES.
A condition of abnormally elevated output of PARATHYROID HORMONE (or PTH) triggering responses that increase blood CALCIUM. It is characterized by HYPERCALCEMIA and BONE RESORPTION, eventually leading to bone diseases. PRIMARY HYPERPARATHYROIDISM is caused by parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. SECONDARY HYPERPARATHYROIDISM is increased PTH secretion in response to HYPOCALCEMIA, usually caused by chronic KIDNEY DISEASES.
A 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.
A disease of bone marked by thinning of the cortex by fibrous tissue containing bony spicules, producing pain, disability, and gradually increasing deformity. Only one bone may be involved (FIBROUS DYSPLASIA, MONOSTOTIC) or several (FIBROUS DYSPLASIA, POLYOSTOTIC).
The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.
A group of genetic disorders of the KIDNEY TUBULES characterized by the accumulation of metabolically produced acids with elevated plasma chloride, hyperchloremic metabolic ACIDOSIS. Defective renal acidification of URINE (proximal tubules) or low renal acid excretion (distal tubules) can lead to complications such as HYPOKALEMIA, hypercalcinuria with NEPHROLITHIASIS and NEPHROCALCINOSIS, and RICKETS.
Fractures of the short, constricted portion of the thigh bone between the femur head and the trochanters. It excludes intertrochanteric fractures which are HIP FRACTURES.
An anticonvulsant that is used to treat a wide variety of seizures. It is also an anti-arrhythmic and a muscle relaxant. The mechanism of therapeutic action is not clear, although several cellular actions have been described including effects on ion channels, active transport, and general membrane stabilization. The mechanism of its muscle relaxant effect appears to involve a reduction in the sensitivity of muscle spindles to stretch. Phenytoin has been proposed for several other therapeutic uses, but its use has been limited by its many adverse effects and interactions with other drugs.
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 polypeptide hormone (84 amino acid residues) secreted by the PARATHYROID GLANDS which performs the essential role of maintaining intracellular CALCIUM levels in the body. Parathyroid hormone increases intracellular calcium by promoting the release of CALCIUM from BONE, increases the intestinal absorption of calcium, increases the renal tubular reabsorption of calcium, and increases the renal excretion of phosphates.
An element of the alkaline earth family of metals. It has the atomic symbol Sr, atomic number 38, and atomic weight 87.62.
Dilatation of the intestinal lymphatic system usually caused by an obstruction in the intestinal wall. It may be congenital or acquired and is characterized by DIARRHEA; HYPOPROTEINEMIA; peripheral and/or abdominal EDEMA; and PROTEIN-LOSING ENTEROPATHIES.
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)
Fractures occurring as a result of disease of a bone or from some undiscoverable cause, and not due to trauma. (Dorland, 27th ed)
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.
Irradiation directly from the sun.
The major circulating metabolite of VITAMIN D3. It is produced in the LIVER and is the best indicator of the body's vitamin D stores. It is effective in the treatment of RICKETS and OSTEOMALACIA, both in azotemic and non-azotemic patients. Calcifediol also has mineralizing properties.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
A benign neoplasm derived from mesodermal cells that form cartilage. It may remain within the substance of a cartilage or bone (true chondroma or enchondroma) or may develop on the surface of a cartilage (ecchondroma or ecchondrosis). (Dorland, 27th ed; Stedman, 25th ed)
Abnormally elevated PARATHYROID HORMONE secretion as a response to HYPOCALCEMIA. It is caused by chronic KIDNEY FAILURE or other abnormalities in the controls of bone and mineral metabolism, leading to various BONE DISEASES, such as RENAL OSTEODYSTROPHY.
Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis (OSTEOPOROSIS, POSTMENOPAUSAL) and age-related or senile osteoporosis.
A non-electrogenic sodium-dependent phosphate transporter. It is found primarily in apical membranes of PROXIMAL RENAL TUBULES.
Excision of the whole (total gastrectomy) or part (subtotal gastrectomy, partial gastrectomy, gastric resection) of the stomach. (Dorland, 28th ed)
Fractures of the lower jaw.
A hypnotic and sedative. Its use has been largely superseded by other drugs.
Extracellular substance of bone tissue consisting of COLLAGEN fibers, ground substance, and inorganic crystalline minerals and salts.
Tumors or cancer of the MANDIBLE.
A severe sometimes chronic anemia, usually macrocytic in type, that does not respond to ordinary antianemic therapy.
Necrotic jaws or other maxillofacial skeleton necrosis associated with bisphosphonate use (see BISPHOSPHONATES). Injury, dental procedures, and trauma can trigger the necrotic process.
Disorders in the processing of calcium in the body: its absorption, transport, storage, and utilization.
The creation of a visual display of the inside of the entire body of a human or animal for the purposes of diagnostic evaluation. This is most commonly achieved by using MAGNETIC RESONANCE IMAGING; or POSITRON EMISSION TOMOGRAPHY.
Native, inorganic or fossilized organic substances having a definite chemical composition and formed by inorganic reactions. They may occur as individual crystals or may be disseminated in some other mineral or rock. (Grant & Hackh's Chemical Dictionary, 5th ed; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
General term for a group of MALNUTRITION syndromes caused by failure of normal INTESTINAL ABSORPTION of nutrients.
Purplish or brownish red discoloration of the skin associated with increase in circulating polyclonal globulins, usually GAMMA-GLOBULINS. This syndrome often occurs on the legs of women aged 20 to 40 years.
Mature osteoblasts that have become embedded in the BONE MATRIX. They occupy a small cavity, called lacuna, in the matrix and are connected to adjacent osteocytes via protoplasmic projections called canaliculi.
Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.
Any adverse condition in a patient occurring as the result of treatment by a physician, surgeon, or other health professional, especially infections acquired by a patient during the course of treatment.
The amount of mineral per square centimeter of BONE. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by X-RAY ABSORPTIOMETRY or TOMOGRAPHY, X RAY COMPUTED. Bone density is an important predictor for OSTEOPOROSIS.
Therapy for the insufficient cleansing of the BLOOD by the kidneys based on dialysis and including hemodialysis, PERITONEAL DIALYSIS, and HEMODIAFILTRATION.
Tumors or cancer located in bone tissue or specific BONES.
Two pairs of small oval-shaped glands located in the front and the base of the NECK and adjacent to the two lobes of THYROID GLAND. They secrete PARATHYROID HORMONE that regulates the balance of CALCIUM; PHOSPHORUS; and MAGNESIUM in the body.
The continuous turnover of BONE MATRIX and mineral that involves first an increase in BONE RESORPTION (osteoclastic activity) and later, reactive BONE FORMATION (osteoblastic activity). The process of bone remodeling takes place in the adult skeleton at discrete foci. The process ensures the mechanical integrity of the skeleton throughout life and plays an important role in calcium HOMEOSTASIS. An imbalance in the regulation of bone remodeling's two contrasting events, bone resorption and bone formation, results in many of the metabolic bone diseases, such as OSTEOPOROSIS.
A clinical syndrome associated with the retention of renal waste products or uremic toxins in the blood. It is usually the result of RENAL INSUFFICIENCY. Most uremic toxins are end products of protein or nitrogen CATABOLISM, such as UREA or CREATININE. Severe uremia can lead to multiple organ dysfunctions with a constellation of symptoms.
A malabsorption syndrome that is precipitated by the ingestion of foods containing GLUTEN, such as wheat, rye, and barley. It is characterized by INFLAMMATION of the SMALL INTESTINE, loss of MICROVILLI structure, failed INTESTINAL ABSORPTION, and MALNUTRITION.
Drugs used to prevent SEIZURES or reduce their severity.
Tumors or cancer of the PARATHYROID GLANDS.
FIBROSIS of the hepatic parenchyma due to obstruction of BILE flow (CHOLESTASIS) in the intrahepatic or extrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC; BILE DUCTS, EXTRAHEPATIC). Primary biliary cirrhosis involves the destruction of small intra-hepatic bile ducts and bile secretion. Secondary biliary cirrhosis is produced by prolonged obstruction of large intrahepatic or extrahepatic bile ducts from a variety of causes.
Bone-forming cells which secrete an EXTRACELLULAR MATRIX. HYDROXYAPATITE crystals are then deposited into the matrix to form bone.
Neoplasms of whatever cell type or origin, occurring in the extraskeletal connective tissue framework of the body including the organs of locomotion and their various component structures, such as nerves, blood vessels, lymphatics, etc.
Uptake of substances through the lining of the INTESTINES.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Calcium compounds used as food supplements or in food to supply the body with calcium. Dietary calcium is needed during growth for bone development and for maintenance of skeletal integrity later in life to prevent osteoporosis.
A barbituric acid derivative that acts as a nonselective central nervous system depressant. It potentiates GAMMA-AMINOBUTYRIC ACID action on GABA-A RECEPTORS, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations.
The second longest bone of the skeleton. It is located on the medial side of the lower leg, articulating with the FIBULA laterally, the TALUS distally, and the FEMUR proximally.
Inorganic or organic compounds containing trivalent iron.
A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)
The longest and largest bone of the skeleton, it is situated between the hip and the knee.
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.
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.
Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., COLLAGEN; ELASTIN; FIBRONECTINS; and LAMININ).
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
Pathological processes of the KIDNEY or its component tissues.
Regular course of eating and drinking adopted by a person or animal.
Elements of limited time intervals, contributing to particular results or situations.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.

Biochemical indices of osteomalacia in pregnant Asian immigrants in Britain. (1/293)

Serum calcium, phosphate and alkaline phosphatase, and urinary calcium excretion were examined during the second trimester of uncomplicated normal pregnancy in Asian immigrants to Britain and in local Caucasians. The mean serum calcium was significantly lower in Asians than in Caucasians, and the mean serum alkaline phosphatase was significantly higher in Asians. The geometric mean of the urinary calcium excretion was highly significantly lower in Asians than in Caucasians. The variances of the serum calcium, serum alkaline phosphatase, and urine calcium excretion did not differ significantly in the two populations. This indicates that there is a shift in values of immigrant Asians as a group compared with Caucasians. A comparison with figures obtained on normal nonpregnant persons of both suggests that the shift is not an inherent feature of the Asian population.  (+info)

Use of ultrasonography in the diagnosis of osteomalacia: preliminary results on experimental osteomalacia in the rat. (2/293)

This study was performed to investigate the ability of ultrasonographic technique to distinguish osteomalacia from normal bone with the same mineral content. Ten rats with experimentally induced osteomalacia (group A) and 12 control rats having similar body size and weight (group B) were studied. Histomorphometric analysis confirmed the presence of osteomalacia in two rats from group A and showed normally mineralized bone in two rats from group B. Whole body bone mineral density, measured by dual-energy x-ray absorptiometry, was similar in the two groups (86 +/- 6 mg/cm2 in group A and 89 +/- 4 mg/cm2 in group B). The velocity of the ultrasound beam in bone was measured by densitometer at the first caudal vertebra of each rat. The velocity was measured when the first peak of the waveform reached a predetermined minimum amplitude value (amplitude-dependent speed of sound) as well as at the lowest point of this curve before it reaches the predetermined minimum amplitude (first minimum speed of sound). Although the amplitude-dependent speed of sound was similar in the two groups (1381.9 +/- 11.8 m/s in group A and 1390.9 +/- 17.8 m/s in group B), the first minimum speed of sound was clearly different (1446.1 +/- 8.9 m/s in group A and 1503.3 +/- 10.9 m/s in group B; P < 0.001). This study shows that ultrasonography could be used to identify alterations in bone quality, such as osteomalacia, but further studies need to be carried out before this method can be introduced into clinical practice.  (+info)

Bone histology in patients with nephrotic syndrome and normal renal function. (3/293)

BACKGROUND: The prevalence of metabolic bone disease in patients with nephrotic syndrome (NS) at normal level of renal function remains uncertain. METHODS: To address this issue, we studied 30 patients (20 men and 10 women, mean age 27.3 +/- 11.7 years) with NS who had normal renal function (mean creatinine clearance 103 +/- 4 ml/min). We evaluated their serum calcium, phosphorus, alkaline phosphatase, immunoreactive parathyroid hormone (iPTH), vitamin D metabolites, urinary calcium, and skeletal survey. The extent of bone mineralization was analyzed by histomorphometric analysis of iliac crest bone biopsy specimens in all patients. The findings on bone histology were correlated with biochemical parameters. RESULTS: The mean duration of NS was 35.5 +/- 26.9 months, with a protein excretion of 7.3 +/- 3.2 g/24 hr and a serum albumin of 2.2 +/- 0.8 g/dl. Total serum calcium was 7.8 +/- 0.8 mg/dl, whereas ionized calcium was 5.7 +/- 0.7 mg/dl, phosphorus 3.2 +/- 1.2 mg/dl, and alkaline phosphatase 149 +/- 48.6 U/liter. Serum iPTH levels were normal in all except two patients. The mean serum 25-hydroxyvitamin D [25(OH)D] level was 3.9 +/- 1.2 ng/ml (normal 15 to 30 ng/ml), whereas 1,25-dihydroxyvitamin D was 24 +/- 4.7 pg/ml (normal 16 to 65). There was an inverse correlation between serum levels of 25(OH)D and the magnitude of proteinuria (r = -0.42, P < 0.05). The mean 24-hour urinary calcium excretion was 82 +/- 21 mg/day. The skeletal survey was normal in all patients. Bone histology was normal in 33.3% of the patients, whereas 56.7% had isolated osteomalacia (OSM), and 10% had an increased bone resorption in association with defective mineralization. The severity of OSM measured by mineralization lag time correlated linearly with the duration (r = 0.94, P < 0.0001) and the amount (r = 0.97, P < 0.0001) of proteinuria. All patients with NS for more than three years had histological changes. Patients with OSM had lower 25(OH)D and serum albumin as compared with those with normal histology (P < 0.005). Bone mineralization had no significant correlation with serum iPTH, divalent ions, or vitamin D levels. CONCLUSIONS: OSM is a frequent finding in adult patients with NS, even at a normal level of renal function. Its severity correlates with the amount and duration of proteinuria.  (+info)

Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. (4/293)

For adults, the 5-microg (200 IU) vitamin D recommended dietary allowance may prevent osteomalacia in the absence of sunlight, but more is needed to help prevent osteoporosis and secondary hyperparathyroidism. Other benefits of vitamin D supplementation are implicated epidemiologically: prevention of some cancers, osteoarthritis progression, multiple sclerosis, and hypertension. Total-body sun exposure easily provides the equivalent of 250 microg (10000 IU) vitamin D/d, suggesting that this is a physiologic limit. Sailors in US submarines are deprived of environmentally acquired vitamin D equivalent to 20-50 microg (800-2000 IU)/d. The assembled data from many vitamin D supplementation studies reveal a curve for vitamin D dose versus serum 25-hydroxyvitamin D [25(OH)D] response that is surprisingly flat up to 250 microg (10000 IU) vitamin D/d. To ensure that serum 25(OH)D concentrations exceed 100 nmol/L, a total vitamin D supply of 100 microg (4000 IU)/d is required. Except in those with conditions causing hypersensitivity, there is no evidence of adverse effects with serum 25(OH)D concentrations <140 nmol/L, which require a total vitamin D supply of 250 microg (10000 IU)/d to attain. Published cases of vitamin D toxicity with hypercalcemia, for which the 25(OH)D concentration and vitamin D dose are known, all involve intake of > or = 1000 microg (40000 IU)/d. Because vitamin D is potentially toxic, intake of >25 microg (1000 IU)/d has been avoided even though the weight of evidence shows that the currently accepted, no observed adverse effect limit of 50 microg (2000 IU)/d is too low by at least 5-fold.  (+info)

Is low plasma 25-(OH)vitamin D a major risk factor for hyperparathyroidism and Looser's zones independent of calcitriol? (5/293)

BACKGROUND: Recent reports suggest that calcitriol might not be the sole active metabolite of vitamin D and that plasma concentrations of 25-(OH)vitamin D (25OHD) are often abnormally low in hemodialysis patients. We have therefore evaluated plasma 25OHD as a risk factor for parathyroid hormone (PTH) hypersecretion and radiological bone disease. We carried out a cross-sectional study during the month of September in an Algerian dialysis center of 113 patients who were not taking supplements of alphacalcidol or calcitriol. METHODS: Plasma 25OHD, calcitriol, PTH, calcium, phosphate, bicarbonate, and aluminum were measured, and x-rays of the hands and pelvis were obtained for evaluation of subperiosteal resorption and Looser's zones. RESULTS: The median plasma 25OHD was 47.5 nmol/liter (range 2.5 to 170.0). Univariate analysis showed that plasma PTH was correlated positively with months on maintenance dialysis and negatively with plasma 25OHD, calcitriol, calcium, bicarbonate and aluminum, but not with that of phosphate. plasma 25OHD was positively correlated with calcium and calcitriol. Using multiple regression analysis, only plasma 25OHD (negative) and the duration on maintenance dialysis (positive) were independently linked to plasma PTH. The prevalence of isolated subperiosteal resorption (ISR) was 34%, and that of the combination of resorption with Looser's zones (CRLZ) was 9%; thus, only 57% of the patients had a normal x-ray appearance. These groups were comparable with regards to age, gender, and duration on dialysis. When the biochemical measurements of the patients with CRLZ were compared with those from patients without radiological lesions, plasma 25OHD was the only parameter to show a statistically significant difference, being significantly lower in the CRLZ group (26 +/- 18 vs. 57 nmol/liter, ANOVA, P < 0.004). Plasma 25OHD was also significantly lower in the ISR group (44, P < 0.05) than in the normal x-ray group, and plasma Ca (P < 0.003) and bicarbonate (P < 0.02) were lower. Logistical analysis showed that the presence of resorption was independently linked only with plasma PTH. Looser's zones and subperiosteal resorption were not seen in patients with plasma 25OHD of more than 40 (Looser's zones) and more than 100 nmol/liter (subperiosteal resorption). The optimal range for intact PTH in hemodialysis patients with mild aluminum overload is 10 to 25 pmol/liter. We found that plasma PTH was inappropriately high only when plasma 25OHD was less than 100 nmol/liter. With a plasma 25OHD of between 100 and 170 nmol/liter, hypercalcemia was present with a plasma PTH of less than 10 pmol/liter in only one case. CONCLUSIONS: This cross sectional study shows that low plasma 25OHD is a major risk factor for hyperparathyroidism and Looser's zones. In dialysis patients, we suggest that the plasma levels of 25OHD are maintained around the upper limit of the reference range of sunny countries.  (+info)

Bone scintigraphy in renal osteodystrophy. (6/293)

Bone scintigraphy with Tc-99m HEDP was performed in 30 patients on maintenance hemodialysis, and the results of quantitative analysis were compared with those of a normal group. To permit this comparison, elevated background activity due to the absence of renal radiotracer excretion was reduced by hemodialysis to levels found in the normals. Histologic proof of renal osteodystrophy had been obtained in all patients. The incidence of radiographic abnormalities was 46%, whereas abnormal scans were found in 25 patients (83%); skeletal lesions were also more pronounced and detected earlier. However, even when the scans appeared normal, the quantitative analysis showed increased skeletal activity in all patients. The total skeletal activity proved to be a good index of the severity of renal osteodystrophy and appeared dependent on both osteomalacia and hyperparathyroidism. These findings show that bone scintigraphy is a sensitive method to detect skeletal involvement in renal osteodystrophy.  (+info)

Increased bone strontium levels in hemodialysis patients with osteomalacia. (7/293)

BACKGROUND: In this study, we report on the association between increased bone strontium levels and the presence of osteomalacia in end-stage renal failure patients treated by hemodialysis. METHODS: We performed a histologic examination and determined the strontium content and strontium/calcium ratios in bone biopsies of 100 hemodialysis patients recruited from various centers all over the world. Aside from the bone strontium concentration, the bone aluminum content was assessed. The bone zinc concentration, a nonrelevant element for bone toxicity, was also measured. RESULTS: Bone strontium levels and bone strontium/calcium ratios were increased in subjects with osteomalacia when compared with those with the other types of renal osteodystrophy. Bone strontium and bone calcium levels correlated with each other. The slope of the linear regression curve correlating these parameters was much steeper in the osteomalacic group (Y = 2.22X - 120) as compared with the other types of renal osteodystrophy (Y = 0.52X - 5.7). Within the group of patients with osteomalacia, bone strontium levels also significantly correlated with the bone aluminum content (r = 0.72, P = 0.018). No such correlation was found for the other types of renal osteodystrophy. The bone zinc concentration of subjects with normal renal function did not differ significantly from the values noted for the various types of renal osteodystrophy taken as separate groups, nor could increased bone zinc concentrations be associated with a particular bone lesion. CONCLUSIONS: Our data demonstrate an association between osteomalacia and increased bone strontium concentrations in dialysis patients. Further studies are warranted to establish whether strontium plays either a primary, secondary, or contributive role in the development of the latter type of renal osteodystrophy.  (+info)

Use of quantitative ultrasonography in differentiating osteomalacia from osteoporosis: preliminary study. (8/293)

The aim of this work was to use ultrasonographic technology to differentiate osteoporosis from osteomalacia on the basis of different patterns of the graphic trace. Three patients with osteomalacia and three with osteoporosis, all with the same lumbar spine bone mineral density, were studied. The velocity of the ultrasound beam in bone was measured by a DBM Sonic 1,200/I densitometer at the proximal phalanges of the hands in all the patients. The ultrasound beam velocity was measured when the first peak of the waveform reached a predetermined minimum amplitude value (amplitude-dependent speed of sound) as well as at the lowest point prior to the first and second peaks, before they reached the predetermined minimum amplitude value (first and second minimum speeds of sound). The graphic traces were further analyzed by Fourier analysis, and both the main frequency (f0) and the width of the peak centered in the f0 (full width at half maximum) were measured. The first and second minimum speeds of sound were significantly lower in the patients with osteomalacia than in the osteoporosis group. The first minimum speed of sound was 2,169 +/- 73 m/s in osteoporosis and 1,983 +/- 61 m/s in osteomalacia (P < 0.0001); the second minimum peak speed of sound was 1,895 +/-59 m/s in osteoporosis and 1,748 +/- 38 m/s in osteomalacia (P < 0.0001). The f0 was similar in the two groups (osteoporosis, 0.85 +/- 0.14 MHz; osteomalacia, 0.9 +/- 0.22 MHz; P = 0.72), and the full width at half maximum was significantly higher in the osteomalacia patients (0.52 +/- 0.14 MHz) than in the osteoporosis patients (0.37 +/- 0.15 MHz) (P = 0.022). This study confirms that ultrasonography is a promising, noninvasive method that could be used to differentiate osteoporosis from osteomalacia, but further studies should be carried out before this method can be introduced into clinical practice.  (+info)

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A rare case of Oncogenic Osteomalacia treated at Apollo Hospitals Chennai. Oncogenic Osteomalacia is a rare condition causing debilitating illness.
Crippa BL, Leon E, Calhoun A, Lowichik A, Pasquali M, Longo N. Biochemical abnormalities in Pearson syndrome. Am J Med Genet A. 2015 Mar;167(3):621-8.. ...
Clinical trial for Familial Hypophosphatemic Rickets , Study of Longitudinal Observation for Patient With X-linked Hypophosphatemic Rickets/Osteomalacia in Collaboration With Asian Partners
Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome characterized by severe hypophosphatemia and osteomalacia. Nonspecific symptoms make the diagnosis elusive. In addition, locating the responsible tumor(s) is challenging. The aim of this study was to investigate the clinical management and outcomes of TIO. The clinical features, diagnostic procedures, treatment, and outcomes of 12 patients were reviewed retrospectively. The cohort comprised six men and six women (mean age 45.5 ± 9.9 years, range 23-61 years). The mean duration of disease was 3.7 ± 2.6 years. All patients manifested progressive bone pain, muscle weakness, and/or difficulty walking. Serum phosphorus concentrations were low in all patients (mean 0.42 ± 0.12 mmol/L). Technetium-99m octreotide scintigraphy was performed in 11 patients and showed lesions in the right distal femur, left femoral head, and right tibial plateau, respectively, in three patients. Magnetic resonance imaging (MRI) was negative for lesions in one
1. A patient with familial adult-onset hypophosphataemia, whose myopathy was closely related to the plasma phosphate concentration, was investigated by phosphorus nuclear magnetic resonance spectroscopy (31P n.m.r.) in vivo of the right flexor digitorum superficialis muscle.. 2. During hypophosphataemia induced by stopping oral phosphate a significant reduction in measured muscle strength occurred, but the ratios of the intramyocellular levels of phosphocreatine (PCr), adenosine triphosphate (ATP) and inorganic phosphate (Pi) remained unchanged at rest. During exercise these levels changed, as did the intramyocellular pH, but they did not differ from the pattern previously recorded in normal subjects.. 3. In four adults with inherited infantile-onset hypophosphataemia (vitamin D-resistant rickets, VDRR) without myopathy, the n.m.r. measurements were normal at rest and during exercise.. 4. In one patient with inherited hyperphosphataemia (tumoral calcinosis) the resting PCr: Pi ratio was ...
Severe osteomalacia (confirmed by the examination of thin undecalcified bone biopsy sections) associated with hypophosphataemia developed in a 60 year old woman. A skeletal x-ray survey showed a lytic lesion in the right proximal femur, and this was curetted, showing a vascular tumour. The patients symptoms improved almost immediately and serum phosphate concentrations returned to normal. Some time later the syndrome and the tumour recurred. The tumour was excised, and again the patient improved. Morphological examination of the tumour showed a lesion which closely resembled haemangiopericytoma. Review of published reports confirmed that most reported cases have been associated with vascular mesenchymal tumours both in intraosseous and extraosseous sites.. ...
The FDA has recently approved CRYSVITA for the treatment of tumor-induced osteomalacia (TIO). Read all about it here at PatientWorthy!
The syndrome of tumor-induced osteomalacia has been previously thought to occur only in association with mesenchymal tumors, although one report has linked prostatic carcinoma with the syndrome. We report the case of a patient who presented first with the clinical and biochemical features of the syndrome of inappropriate antidiuretic hormone secretion, and then oncogenic osteomalacia. The first syndrome was characterized by headaches, nausea, and vomiting; serum sodium determinations ranged between 107 and 118 meq/L with simultaneous urine spot sodium concentrations of 100 to 116 meq/L. The circulating antidiuretic hormone level was markedly elevated to 261.5 µU/mL. The osteomalacia was discovered incidentally when depressed serum phosphorus levels of 1.2 to 1.7 mg/dL were noted in association with 24-hour urine phosphorus excretion exceeding 1000 mg/24 h. Undecalcified tetracycline-labeled bone biopsy samples confirmed oncogenic osteomalacia. Only afterward was a small-cell carcinoma of the ...
Oncogenic hypophostphatemic osteomalacia is rare form of osteomalacia with few cases reported in the literature. It is characterized by later onset in adulthood, renal phosphate loss with hypophosphatemia and poor bone mineralization. The syndrome is associated with mesenchymal tumours or prostatic CA. We report a case of oncogenic hypophosphatemic ostoemalacia associated with neurofibromatosis.. Key words: Oncogenic hypophoosphatemic osteomalacia, neurofibromatosis, mesenchymal tumors ...
Dive into the research topics of Malignant transformation of phosphaturic mesenchymal tumor: A case report and literature review. Together they form a unique fingerprint. ...
DIAGNOSIS Phosphaturic Mesenchymal Tumor, Mixed Connective Tissue Variant (PMT-MCT). DISCUSSION. Osteomalacia is a bone disease characterized by gradual softening and bending of the bones due to inadequate mineralization of osteoid. The most common etiologies of osteomalacia include vitamin D deficiency and renal tubular dysfunction; however, in rare instances, osteomalacia can be associated with bone and soft tissue tumors as a paraneoplastic syndrome (i.e. oncogenic osteomalacia) (1, 4, 8). Though the mechanism behind the inadequate mineralization of osteoid in this setting is not entirely understood, it is hypothesized that tumor over-expression of FGF-23 may play a role. This protein appears to inhibit trans-epithelial phosphate transport in renal tubules, resulting in renal phosphate wasting and subsequent osteomalacia (2-4, 11). While a heterogeneous group of tumors may cause oncogenic osteomalacia, PMT-MCT is the most common (1, 6). Tumors associated with oncogenic osteomalacia are ...
en] We report the case of a patient with severe muscular and articular tenderness that caused almost complete immobility. This subject had severe hypophosphatemia due to hyperphosphaturia. Fibroblast growth factor 23 (FGF-23) was abnormally high and the diagnostic of tumor-induced osteomalacia was made. Despite multiple tests, the tumor was not localized. In this report, we discuss different possible investigations to localize the tumor. Lastly, we review the potential therapy available when tumor is not found and can thus not ...
For many years, the existence of phosphatonins-substances secreted by certain tumors which result in profound renal phosphorus wasting and resultant osteomalacia-has been postulated.. Evidence has recently been accumulating that fibroblast growth factor 23 (FGF-23) is the phosphatonin we have been searching for:. High circulating levels of FGF23 are associated with hypophosphatemia, decreased 1,25 (OH) vitamin D levels, and rickets/bone disease.. The disease autosomal dominant hypophosphatemic rickets is caused by gain-of-function mutations in FGF23caused by splice site mutations. Conversely, the genetic disease inherited tumoral calcinosis, characterized by hyperphosphatemia, increased 1,25 (OH) vitamin D levels, and metastatic calcifications.. In ESRD, FGF23 levels are appropriately elevated in response to hyperphosphatemia, but due to a reduced GFR is unable to induce adequate phosphaturia.. How it works at a molecular level: FGF23 interacts with FGF receptors at the proximal tubule, ...
Composition: Sillicea 30x, Hekla Lava 12x, Calc. Phos 12x, Calc. Hypophos 6x, Chamomilla. 6x, Calc, Fluor 12x, Mercur Prace. Ruber 12x, Mezereum. 6x. Indications: Helpful in the growth of bones where fragility develops in conditions like rickets osteomalacia, arthritis and in nucleus pulposus. ...
In recent years there has been an increase in the diagnosis of Metabolic Bone disease in hedgehogs and it is a life-threatening syndrome. While the
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TY - JOUR. T1 - A 61-year-old woman with osteomalacia and a thoracic spine lesion. AU - Marshall, Ann E.. AU - Martin, Sarah E.. AU - Agaram, Narasimhan P.. AU - Chen, Jey Hsin. AU - Horn, Eric. AU - Douglas-Akinwande, Annette C.. AU - Hattab, Eyas M.. PY - 2010/3. Y1 - 2010/3. N2 - Phosphaturic mesenchymal tumor, mixed connective tissue variant (PMT-MCT) is a rare, largely benign, mesenchymal neoplasm almost invariably associated with oncogenic osteomalacia. It is generally found in the soft tissue and bone of the extremities. We report a case of a 61-year-old female with long-standing osteomalacia who was found to have PMT-MCT of the thoracic spine. There have been very few previously reported cases of PMT involving the spinal vertebrae and neuropathologists should be aware of this lesion. Recognition of PMT-MCT is critical for optimal patient care since complete surgical resection without additional therapy is curative.. AB - Phosphaturic mesenchymal tumor, mixed connective tissue variant ...
RTRP2 : Assessing renal reabsorption of phosphorus in a variety of pathological conditions associated with hypophosphatemia including hypophosphatemic rickets, tumor-induced osteomalacia, and tumoral calcinosis   Adjusting phosphate replacement therapy in severe deficiency states monitoring the renal tubular recovery from acquired Fanconi syndrome
Alkaline phosphatase levels in children - Medicine for high alkaline phosphatase levels? Wrong approach. Alkaline phosphatase is a lab value to tell a physician what is happening, not a medical problem to treat. It can be high just because you
Bone disease - Metabolic bone disease: The normal function of bone requires an adequate supply of amino acids (the building blocks for proteins) for the synthesis of collagen, the chief component of the organic matrix; of calcium and phosphate for mineralization of the organic matrix; and of other organic compounds and mineral elements. Also, growth, repair, and remodeling of the bone tissue require a precisely regulated supply of hormones, vitamins, and enzymes. Skeletal disease, when it is due to inadequacies in the supply or action of the above essentials, associated with abnormalities outside the skeleton, is termed metabolic; in such cases the entire skeleton is affected.
The Metabolic Bone Diseases Clinic at Tufts Medical Center in Boston provides care to manage increased risk for fragility fractures due to bone diseases, like osteoporosis.
ASBMR (2008) Chapter 9. Animal Models: Allelic Determinants for BMD, in Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, John Wiley & Sons, Inc., Hoboken, NJ, USA. doi: 10.1002/9780470623992.ch9 ...
In November 2015, Jumana, a teenage patient, arrived at the NIH seeking a cure for a rare disease that made her bones so fragile and muscles so weak that she was confined to her bed, barely able to lift her legs. Earlier this year, after a medical collaboration by NIH researchers and others around the world, Jumana was cured and is able to walk again.. The patient, who traveled nearly 6,000 miles from her home in the Palestinian territories to the Clinical Center, had a disease called tumor-induced osteomalacia (TIO). TIO is caused by a rare endocrine tumor that secretes FGF23, a hormone that regulates phosphate absorption and active vitamin D production. In high levels, as is seen in TIO, it causes low blood phosphate levels that leads to muscle weakness, bone pain and fractures.. There are only a few places in the world with expertise in diagnosing and treating TIO. When clinicians in Israel diagnosed the condition in this patient, but couldnt find the tumor, they called Dr. Michael Collins, ...
A 48-year-old man who had recently immigrated to France and had not yet established routine medical care presented to the emergency department with shortness
Oncogenic osteomalacia, or tumour-induced osteomalacia (TIO), is a rare paraneoplastic syndrome characterised by hypophosphataemia, phosphaturia, inappropriately low serum levels of 1,25-dihydroxyvitamin D for hypophosphataemia. TIO is caused by mesenchymal tumours that secrete phosphaturic substances, leading to increased renal wasting of phosphates. These tumours are very small in size and grow slowly. Localisation of these tumours has always been difficult with the available biochemical and imaging techniques. At times, despite all efforts, the tumour could not be localised. We report our experience with a 42-year-old woman with TIO where whole-body magnetic resonance imaging could not localise the tumour, a scapular haemangiopericytoma. PET/CT was helpful in the localisation of the tumour which, when surgically removed, resulted in the normalisation of biochemical parameters with clinical improvement.. Keywords: mesenchymal tumours, oncogenic osteomalacia, paraneoplastic syndrome, scapular ...
This case report describes an otherwise healthy woman in her 30s who presented with left-ear hearing loss, tinnitus, distorted hearing, and occasional otalgia o
Expertise, Disease and Conditions: Bone Disorders, Calcium disorders, Endocrinology, Glucocorticoid Induced Osteoporosis, Hypercalcemia, Hyperparathyroidism, Male Osteoporosis, Metabolic Bone Disease, Osteomalacia, Osteoporosis, Pagets Disease, Pseudohypoparathyroidism, Rickets, Right Heart Catheterization, Tumor-Induced Osteomalacia, X Linked Hypophosphatemic Rickets (XLH ...
Expertise, Disease and Conditions: Bone Disorders, Calcium disorders, Endocrinology, Glucocorticoid Induced Osteoporosis, Hypercalcemia, Hyperparathyroidism, Male Osteoporosis, Metabolic Bone Disease, Osteomalacia, Osteoporosis, Pagets Disease, Pseudohypoparathyroidism, Rickets, Right Heart Catheterization, Tumor-Induced Osteomalacia, X Linked Hypophosphatemic Rickets (XLH ...
Product Human 25 Hydroxy Vitamin D ELISA kit From B-Gene - A sandwich ELISA for quantitative measurement of Human 25 Hydroxy Vitamin D in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species. Kit contents: 1. MICROTITER PLATE * 1 2. ENZYME CONJUGATE*1 vial 3. STANDARD A*1 vial 4. STANDARD B*1 vial 5. STANDARD C*1 vial 6. STANDARD D*1 vial 7. STANDARD E*1 vial 8. STANDARD F*1 vial 9. SUBSTRATE A*1 vial 10. SUBSTRATE B*1 vial 11. STOP SOLUTION*1 vial 12. WASH SOLUTION (100 x)*1 vial 13. BALANCE SOLUTION*1 vial 14. INSTRUCTION*1
Phosphaturic mesenchymal tumor (PMT) represents a rare cause of osteomalacia. The clinical signs and symptoms are vague and these lead to diagnosis delay. In the presence of hypophosphatemia and relatively high urine phosphate excretion, this entity should be taken into consideration in the deferential diagnosis of osteomalacia. In the present article, we report 81-year-old man presented to our clinic for evaluation due to osteopenia. His laboratory results disclosed hypophosphatemia, relatively increased urine phosphate excretion and increased level of intact fibroblast growth factor 23 (FGF23). A 68Gallium DOTATATE PET/CT revealed pathological uptake in the upper aspect of the left shoulder adjacent to the coracoid process. For suspected PMT a wide resection of the tumor was performed and pathological findings were consistent for PMT. Laboratory tests were normalized postoperatively. Reviewing the literature, we had identified 33 reported cases of PMTs among elderly patients age ≥70 years. ...
This new report from VPGMarketResearch.com provides analysis of 25-Hydroxy Vitamin D2 and D3 testing, including clinical significance, current and emerging diagnostic ...
Bone disease. People with renal failure develop weaken bones from abnormal mineralization of the bone. Renal osteodystrophy is the name of this process where calcium and phosphorus do not deposit into the bone correctly and therefore the persons bones are prone to fractures ...
I am a 60-year-old female with osteoporosis. I took Fosamax 70 mg once weekly for seven months until I could no longer endure the side effects. For the following month, I took no medication. Since January 21, 2008, I have been on 680 mg strontium citrate once daily. I intend to relate my progress. My first DEXA scan was done May 8, 2007. My T-score at the lumbar spine was -3.0 (-2.0 at L1, -2.7 at L2, -3.4 at L3 and -3.8 at L4). My T-score at the left hip was -2.2 (-2.8 at neck, -2.0 at troch, -1.9 at inter). My BMD results in g/cm2 were 0.712 at the spine (L1-L4), 0.53 at the left hip (neck), and 0.670 at the left hip (total). A followup scan is planned for July 6, 2009. For these results, see: http://strontiumforbones.blogspot.com/2009/07/improved-t-scores-after-treatment. ...
On biochemical analysis, DHAP-AT activity, a membrane bound peroxisomal enzyme involved in the first step of biogenesis of plasmalogen, was severely diminished in fibroblasts from patients F-01 and F-04 with ZS (6.5% and 10.6% of control fibroblasts), determined as described previously.6 On the other hand, fibroblasts from F-05 with IRD had residual DHAP-AT activity (26.1% of the control) (table 1). Concerning β oxidation activity of lignoceric acid relative to that of palmitic acid (C24:0/C16:0), IRD fibroblasts also had residual activity (19.2% of the control), as compared to findings in fibroblasts from patients F-01 and F-04 with ZS (4.4% and 5.9% of the control), determined as described previously7 (table 1).. Next, we investigated the relationship between gene mutation, protein import machinery, and the residual activities using gene transfection. The PEX2-wild,PEX2-R125X, andPEX2-E55K gene sequences subcloned into the expression vector pUcD2SRαMCS8 were transfected toPEX2 deficient CHO ...
Results Demographic and clinical characteristics of both groups are shown in Table 1. Of the 108 patients evaluated, the genetic test results of 39 patients are available at this moment (the rest of the results are currently pending). 59% (23/39) tested positive for the genetic mutation.Despite data are still partial and although the results did not achieve statistical significance, we observed with a greater relevance a higher proportion of patients with HPP presenting with chronic bone pain (48,7% vs 25,6%,p=0,157), muscle weakness (15,4% vs 2,6%, p=0,112) and more necessity of analgesic medication (p=0,107) in patients with HPP in comparison with the control group. Furthermore, there was a non-significant trend in the HPP-group to present dental abnormalities and premature dental loss (7,6%), absent manifestations in the control group (p=0,123). In addition, orthopedic surgery was more common in the HPP group (12,8%) compared with the other group (0%), p=0,04. The prevalence of stress ...
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Ελληνική Γαστροεντερολογική Εταιρία. Annals of Gastroenterology.Τμήμα περιοδικού.Επιστημονικό άρθρο.Άρθρο.2007 . Creators: Konstantellou, Helen, Argyros, N., Sambani, Constantina, Kottaras, G., Hereti, Irini, Choremi, Helen, Cheracakis, P., Christodoulou, Martha.A,â-lipoproteinemia is an extremely rare genetic disorder of lipoprotein metabolism, associated with various biochemical abnormalities combined with clinical malabsorption. The aim of this study was to provide information concerning the cytogenetic and HLA patterns of three patients with A,â-lipoproteinemia, as well as to see if there is any correlation between specific HLA type and clinical course of the disease.The study included seven persons. There were 3 patients (a girl and two boys aged 32, 30 and 22 years respectively) and their 4 healthy, first-degree relatives (two parents, a brother and a sister). Cytogenetic studies wereperformed on PHA stimulated peripheral
One of these days, Im going to remember to switch to plain text when sending to the DML... :-) One could imagine this technique being used to distinguish other dwarf species... http://www.pnas.org/content/early/2010/04/29/1000781107 Guy Leahy ...
Low blood sugar, also known as hypoglycemia, is a relatively common biochemical abnormality documented in sick dogs and cats presented to the emergency room, as well as those hospitalized in Intensive Care Units for various illnesses. This week I spend some time discussing hypoglycemia so pet parents can be aware of this potential health issue. … [Read more…] ...
Chapter 15 The locomotor and nervous systems Introduction It is convenient to consider these systems in the same chapter. Although the diseases that affect them may show little or no overlap, there are obvious functional links. This chapter is mainly devoted to the clinical biochemistry of metabolic bone disease, articular disease and muscle disease. Numerous…
A turtle shell is made of two parts: the plastron and carapace. Both are covered with scutes. Retained scutes (dysecdysis), metabolic bone disease, and trauma are common diseases of the shell.
En condiciones normales la fosfaturia 24 h es de unos mg. Lo que debe asegurarse siempre es el tratamiento de la causa subyacente. Causes of hypophosphatemia. En: Up to Date. Rose BD, ed. Wellesley, MA, Agus ZS. Diagnosis and treatment of hypophosphatemia. Molecular pathogenesis of hypophosphatemic rickets. J Clin Endocrinol Metab ; Kronenberg HM. NPT2a-the key to phosphate homeostasis.. N Engl J Med ; Prolonged high-dose phosphate treatment: a risk factor for tertiary hyperparathyroidism in X-linked hypophosphatemic rickets. Clin Endocrinol Oxf ; Barcelona: Masson; Dipyridamole decreases renal phosphate leak and augments serum phosphorus in patients with low renal phosphate threshold. J Am Soc Nephrol ; Nephrolithiasis and osteoporosis associated with hypophosphatemia caused by mutations in the type 2a sodium-phosphate cotransporter.. Pathophysiology of X-linked hypophosphatemia, tumor-induced osteomalacia, and autosomal dominant hypophosphatemia: a perPHEXing problem. Genetic disorders of ...
Renal osteodystrophy is currently defined as an alteration of bone morphology in patients with chronic kidney disease (CKD). It is one measure of the skeletal component of the systemic disorder of chronic kidney disease-mineral and bone disorder (CKD-MBD). The term renal osteodystrophy was coined in 1943, 60 years after an association was identified between bone disease and renal failure. The traditional types of renal osteodystrophy have been defined on the basis of turnover and mineralization as follows: mild, slight increase in turnover and normal mineralization; osteitis fibrosa, increased turnover and normal mineralization; osteomalacia, decreased turnover and abnormal mineralization; adynamic, decreased turnover and acellularity; mixed, increased turnover with abnormal mineralization. A Kidney Disease: Improving Global Outcomes report has suggested that bone biopsies in patients with CKD should be characterized by determining bone turnover, mineralization, and volume (TMV system). On the ...
In July, 2012, four researchers at Ryerson University in Toronto, Canada, published a study in Bone entitled: Monitoring bone strontium levels of an osteoporotic subject due to self-administration of strontium citrate with a novel diagnostic tool, in vivo XRF: a case study. This study is significant because it used a non-invasive method (not an invasive method, such as bone biopsy) to analyze the strontium levels of bones in an osteoporotic patient who began taking strontium citrate for the study. Therefore, it was possible to obtain her baseline bone strontium levels prior to initiation of therapy with strontium citrate. The researchers wrote: By 120 hours, the increase (in bone strontium level) was statistically significant at 0.68 ± 0.07 and 0.93 ± 0.05 (for the finger and ankle), respectively. Further increases occurred within an interval of 90-180 days, with the most recent, after 800 days, at the finger and ankle being 7 and 15 times higher than the initial baseline reading. The ...
In this prospective longitudinal cohort study we studied the efficacy and safety of burosumab in real-clinical practice for ,13- and ,13-years old children affected with X-linked hypophosphatemia.. 57 children with XLH were switched from conventional treatment to burosumab. After 12 months we assessed the efficacy and safety of treatment with burosumab on the whole cohort and separately on the cohort of ,13-years old adolescents. ...
ASBMR (2008) Chapter 42. Genetics of Osteoporosis, in Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, John Wiley & Sons, Inc., Hoboken, NJ, USA. doi: 10.1002/9780470623992.ch42 ...
This clinic treats patients who have metabolic bone diseases - thin bones, thick bones, soft bones, brittle bones and irregular bones. These diseases are caused by problems with mineral metabolism, nutrition, and some genetic diseases. In addition to the above list, we see patients with many kinds of diseases, including:
Investigation of serum 25 hydroxy vitamin D level in critically ill children and its relation with demographic and clinical risk factors, Bahare Yaghmaie, Fatemeh Sayarifard, Moham
Im trying to culture rat BMMCs (from Brown Norway rats) using similar culture conditions to those weve used successfully with mouse BMMCs, but with no luck. My current media is pretty standard - RPMI, b-ME, 10% FBS, P/S/glut, sodium pyruvate. rrIl-3 added fresh, tested with and without rSCF. also tested ConA stimulated spleen conditioned media, as a source of IL-3, but my cells seemed to stick to the plate and die faster than previous cultures. I only change out half the media with each feeding, as with mouse BMMCs or the viability decreases. Very few problems with viability - routinely ,90% even after 35 days in culture. My main problem is that all of my cells keep adhering to the plastic - ive looked at the adherent cells by flow and spun some out onto slides and they appear to be monocytes / macs, which i dont want. All the suspension cells dwindle away quite quickly ...
Synonyms for electrolyte management: hypophosphatemia in Free Thesaurus. Antonyms for electrolyte management: hypophosphatemia. 38 synonyms for management: administration, control, rule, government, running, charge, care, operation, handling, direction, conduct, command, guidance.... What are synonyms for electrolyte management: hypophosphatemia?
JM Land, DJ Taylor, GJ Kemp, GK Radda, B Rajagopalan; Idiopathic Renal Hypophosphataemia: Oral Phosphate Reverses Abnormalities in Muscle. Clin Sci (Lond) 1 March 1992; 82 (s26): 26P. doi: https://doi.org/10.1042/cs082026Pa. Download citation file:. ...
Evolution of metabolic rates in amniotes (empirical evidence for extant species and inferences using bone histology for extinct ones ...
Bone Histology von Christian Crowder und Buchbewertungen gibt es auf ReadRate.com. Bücher können hier direkt online erworben werden.
ABSTRACT. The term metabolic bone disease encompasses an unrelated group of systemic conditions that impact on skeletal collagen and mineral metabolism. Their asymptomatic progression leads to advanced skeletal debilitation and late clinical manifestation. This article provides a brief overview of advances in the understanding of the pathogenesis of rickets, osteomalacia and age-related osteoporosis.. ...
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies. ...
From the author of the popular Clinical Chemistry medical student textbook. Although there are many competing texts on clinical chemistry, the vast majority concentrate on the technology; this book concentrates on the clinical. Ideally suited for preparat.
CONCLUSION: Hospitalization or death was not influenced by the type of RO, Al accumulation, or TMV classification. An elevated prevalence of osteoporosis and Al accumulation was detected. PMID: 32756862 [PubMed - in process]...
A gang of us used to play Loosers Softball every Memorial Day. We neede two ringers - guys who could actually get the ball over the plate. the rest of the teams were made up of people who couldnt run, pitch, hit, catch, or throw. You got as many swings as it took to hit the ball. Or if you got tired of swinging, you could take the base. If you could actually get under a ball and catch it, even if it bounced out of your glove, it counted. But the runner still got to stay on base. The only way you could actually be put out is if you knocked over someones beer. And if you tried keeping score, you were sent back to the house to get more beer, and no one would tell you what happened while you were gone. Then the Emericks started bringing the toxic waste margaritas and other people wanted to actually USE the diamond and the game sorta fizzled.. ReplyDelete ...
Round-Shaped Iliac Bones Symptom Checker: Possible causes include Skeletal Dysplasia. Check the full list of possible causes and conditions now! Talk to our Chatbot to narrow down your search.
Expect high-quality attention and the newest technology for bone biopsy with this certified specialist in Nuevo Laredo at low-prices
CRYSVITA is the only FDA-approved therapy indicated for the treatment of X-linked hypophosphatemia (XLH) in adult and pediatric patients 6 months of age and older.

No data available that match "osteomalacia"

No data available that match "osteomalacia"

  • Osteomalacia is the softening of the bones caused by impaired bone metabolism primarily due to inadequate levels of available phosphate , calcium , and vitamin D , or because of resorption of calcium. (wikipedia.org)
  • [7] Less common causes of osteomalacia can include hereditary deficiencies of vitamin D or phosphate (which would typically be identified in childhood) or malignancy. (wikipedia.org)
  • Oncogenic osteomalacia also known as oncogenic hypophosphatemic osteomalacia, is an uncommon disorder resulting in increased renal phosphate excretion, hypophosphatemia and osteomalacia. (wikipedia.org)
  • This tumor may cause tumor-induced osteomalacia, a paraneoplastic syndrome, by the secretion of FGF23, which has phosphaturic activity (by inhibition of renal tubular reabsorption of phosphate and renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D). The paraneoplastic effects can be debilitating and are only reversed on discovery and surgical resection of the tumor. (wikipedia.org)
  • If there is inappropriately high urine phosphate (phosphaturia) in the setting of low serum phosphate (hypophosphatemia), there should be a high suspicion for tumor-induced osteomalacia. (wikipedia.org)
  • Osteomalacia affects both children and adults and is a disease in which the bones don't contain enough bone mineral (mostly calcium and phosphate ). (massgeneral.org)
  • The term vitamin D-resistant rickets (VDRR) originally was used to describe a syndrome of hypophosphatemia and rickets (and/or osteomalacia) that resembled vitamin D deficiency but did not respond to vitamin D replacement or pharmacologic doses of vitamin D. Most of these cases were caused by renal phosphate wasting, leading to the alternate name of 'phosphate diabetes. (uptodate.com)
  • Several laboratory tests, such as serum electrolytes, calcium, phosphate, parathyroid hormone, and 25-hydoxy-Vitamin D, may support the specific cause of osteomalacia, and bone biopsy may be unnecessary if a common and treatable cause is identified. (psychiatryadvisor.com)
  • The serum electrolytes and PTH are important to make other findings interpretable and to avoid pitfalls, such as osteomalacia with abnormal phosphate management. (psychiatryadvisor.com)
  • If phosphate and creatinine are increased, phosphate retention with early renal failure should be considered rather than a primary metabolic osteomalacia. (psychiatryadvisor.com)
  • Hypophosphatemia, typically genetic and with several specific etiologies, will cause osteomalacia due to insufficiency of phosphate to allow mineralization, whereas elevated PTH allows calcium to remain normal. (psychiatryadvisor.com)
  • Research Papers on Osteomalacia look into the disease characterized by the softening of the bones due to inadequate levels of certain minerals, specifically calcium and phosphate. (papermasters.com)
  • Calcium and/or phosphate tolerance tests were performed on patients with familial hypophosphataemia, normal control subjects, and patients with vitamin D deficient osteomalacia. (bmj.com)
  • The phosphate tolerance test, which is known to be `flat' in patients with familial hypophosphataemia, was normal in patients with vitamin D deficient osteomalacia. (bmj.com)
  • Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome of abnormal phosphate metabolism caused by a small mesenchymal tumor that secrete fibroblast growth factor 23 (FGF23). (endocrine-abstracts.org)
  • Tumor-induced osteomalacia, also known as oncogenic osteomalacia, is a rare, acquired paraneoplastic disease characterized by hypophosphatemia and renal phosphate wasting. (cureus.com)
  • Treating conditions that affect vitamin D metabolism, such as kidney and liver disease or low phosphate levels, often helps improve the signs and symptoms of osteomalacia. (jpeeiclinic.com)
  • She did not fit into vitamin D related causes or phosphate deficiency conditions and what was left was a potential diagnosis of oncogenic osteomalacia. (radiologystories.com)
  • A diet that doesn't include phosphate can also lead to osteomalacia. (facty.com)
  • If osteomalacia is detected early enough, oral supplements of vitamin D, calcium, or phosphate may reverse the condition. (facty.com)
  • Individuals who are vitamin D- or phosphate-deficient are at an increased risk of developing osteomalacia, as are people who get very little exposure to sunshine. (facty.com)
  • Osteomalacia is the softening of the bones caused by defective bone mineralization secondary to inadequate levels of available phosphate and calcium, or because of overactive resorption of calcium from the bone which can be caused by hyperparathyroidism (which causes hypercalcemia). (icd.codes)
  • Osteomalacia develops due to deficiency of vitamin D or due to insufficient absorption of calcium and phosphate. (healthmd.net)
  • Owing to the role of FGF23 in renal phosphate handling and vitamin D synthesis, TIO is characterized by decreased renal tubular reabsorption of phosphate, by hypophosphataemia and by low levels of active vitamin D. Chronic hypophosphataemia ultimately results in osteomalacia (that is, inadequate bone mineralization). (elsevier.com)
  • Vitamin D and calcium supplements are measures that can be used to prevent and treat osteomalacia. (wikipedia.org)
  • Eating a diet rich in vitamin D and calcium and getting sufficient exposure to sunlight can help prevent osteomalacia due to vitamin D deficiency. (medlineplus.gov)
  • There are two main causes of osteomalacia: insufficient calcium absorption from the intestine because of lack of dietary calcium or a deficiency of, or resistance to, the action of vitamin D, or due to undiagnosed celiac disease. (wikipedia.org)
  • Treatment for osteomalacia involves providing enough vitamin D and calcium, both required to harden and strengthen bones, and treating disorders that might cause the condition. (mayoclinic.org)
  • The cause of osteomalacia is not getting enough calcium or vitamin D (vitamin D deficiency). (peacehealth.org)
  • When the disorder presents with fractures, bone pain, and reduced bone mineral density (BMD), it may masquerade as osteoporosis but in striking contrast to osteoporosis, osteomalacia usually has abnormal levels of serum calcium, inorganic phosphorus, or alkaline phosphatase activity. (renalandurologynews.com)
  • puerperal osteomalacia a type resulting from exhaustion of skeletal stores of calcium and phosphorus by repeated pregnancies and lactation. (thefreedictionary.com)
  • To allow bone mineralisation to take place the body needs enough minerals (calcium and phosphorus) and vitamin D. If the body doesn't have enough of any one of these, osteomalacia will develop. (arthritisresearchuk.org)
  • However, not having enough calcium is very unusual as a cause of osteomalacia in Western countries. (arthritisresearchuk.org)
  • Bone mineralization requires adequate minerals (calcium, phosphorus and vitamin D). Inadequate amounts of any one of these will develop into osteomalacia. (algaecal.com)
  • Osteomalacia is weak bones due to calcium and vitamin-D deficiency It is easy to control it with above medicines. (healthtap.com)
  • These findings suggest that rickets and osteomalacia in familial and some cases of non-familial hypophosphataemia are unrelated to abnormal metabolism of vitamin D. This hypothesis is supported by the fact that intestinal calcium absorption as measured by calcium tolerance test is normal in familial hypophosphataemia. (bmj.com)
  • Osteomalacia is a disease characterized by decreased bone mineral density caused by inadequate supply of vitamin D, calcium or phosphorus resulting from deficits in nutrition, renal failure or interference of certain drugs with calcium and vitamin D metabolism [ 1 ]. (pubmedcentralcanada.ca)
  • The first diagnosis was osteomalacia, treated with calcium and vitamin D, without any benefit. (cureus.com)
  • Medical Definition of Osteomalacia Medical Author: William C. Shiel Jr., MD, FACP, FACR Osteomalacia: Softening of bone, particularly in the sense of bone weakened by demineralization (the loss of mineral) and most notably by the depletion of calcium from bone. (raacked.com)
  • Osteomalacia is a condition in which the bones lose calcium and become softer. (raacked.com)
  • Rickets is vitamin D or calcium osteomalacia medical term the most common cause of osteomalacia. (raacked.com)
  • In adults, vitamin D deficiency disease is called osteomalacia and is usually related to your body's inability to absorb phosphorus and calcium properly. (taylortransformation.com)
  • Doctors will diagnose osteomalacia by conducting tests for low doses of vitamin D, phosphorus and calcium. (lybrate.com)
  • In most cases, treatment of osteomalacia through increased intake of vitamin D, calcium, and other bone-building nutrients proves effective. (facty.com)
  • Apart from these, due to the presence of a very low amount of calcium minerals in the blood, arrhythmia in the heart, numbness in the mouth and arms and legs, spasms (cramps) in the hands and feet can be seen in patients with osteomalacia. (healthmedic24.com)
  • With celiac disease, which develops in the form of an autoimmune response of the body against the protein called gluten found in barley, wheat and rye, and the metabolism of calcium, phosphorus and vitamin D is impaired in kidney and liver diseases, the possibility of developing osteomalacia greatly increases. (healthmedic24.com)
  • I have been claiming that the negative symptoms of schizophrenia are due to brains being compressed due to hidden osteomalacia arising from dysregulation of calcium homeostasis due to deficiencies in taurine. (schizepigenetics.com)
  • The causes of adult osteomalacia are varied, but ultimately result in a vitamin D deficiency: Insufficient nutritional quantities or faulty metabolism of vitamin D or phosphorus Renal tubular acidosis Malnutrition during pregnancy Malabsorption syndrome Hypophosphatemia Chronic kidney failure Tumor-induced osteomalacia (Oncogenic osteomalacia) Long-term anticonvulsant therapy Celiac disease Cadmium poisoning, itai-itai disease Biochemical features are similar to those of rickets. (wikipedia.org)
  • An acquired disorder, tumor-induced (or oncogenic) osteomalacia, has similar clinical manifestations to the familial syndromes. (uptodate.com)
  • oncogenic osteomalacia a type seen in association with usually benign mesenchymal neoplasms. (thefreedictionary.com)
  • This led on to further investigations which showed a normal vitamin-D and a very low 1.2 5 hydroxy vitamin D levels pointing to a rare condition called Oncogenic Osteomalacia. (apollohospitals.com)
  • Oncogenic Osteomalacia is a rare condition causing debilitating illness (so far about 200 reported cases). (apollohospitals.com)
  • Using recently developed immunometric assays, intact and C-terminal FGF23 levels are elevated in patients with oncogenic osteomalacia (OOM) and the tumors that cause this disease overexpress FGF23 mRNA. (endocrine-abstracts.org)
  • Following organizations serve the condition "Oncogenic osteomalacia" for support, advocacy or research. (diseaseinfosearch.org)
  • Finding the right clinical trial for Oncogenic osteomalacia can be challenging. (diseaseinfosearch.org)
  • The terms "Oncogenic osteomalacia" returned 34 free, full-text research articles on human participants. (diseaseinfosearch.org)
  • Localization of Oncogenic Osteomalacia by Systemic Venous Sampling of Fibroblast Growth Factor 23. (diseaseinfosearch.org)
  • Oncogenic osteomalacia: role of Ga-68 DOTANOC PET/CT scan in identifying the culprit lesion and its management. (diseaseinfosearch.org)
  • Oncogenic osteomalacia is a rare disease. (diseaseinfosearch.org)
  • Oncogenic osteomalacia and its symptoms: hypophosphatemia, bone pain and pathological fractures]. (diseaseinfosearch.org)
  • Oncogenic osteomalacia (OOM) is a rare paraneoplastic syndrome induced by tumor produced phosphaturic factors, i.e. phosphatonins. (diseaseinfosearch.org)
  • This is a rare case of oncogenic osteomalacia due to a paranasal sinus tumor. (cureus.com)
  • This combination is called oncogenic osteomalacia or tumor-induced osteomalacia (TIO) . (radiologystories.com)
  • We report on a patient with bilateral stress fractures of the tibia who subsequently showed classic biochemical features of oncogenic osteomalacia . (lookfordiagnosis.com)
  • Background: Oncogenic osteomalacia is a rare paraneoplastic syndrome, with only about 100 reported cases in the literature. (ke-i.org)
  • The majority of oncogenic osteomalacia is usually caused by phosphaturic mesenchymal tumors of mixed connective tissue. (ke-i.org)
  • Case Description: In this case report, the authors present a case of oncogenic osteomalacia in a patient who initially presented with hip pain for bilateral femoral head osteonecrosis and was noted to have multiple insufficiency fractures of unknown cause. (ke-i.org)
  • Literature Review: There have been only three case reports of a similar lesion in the proximal femur causing oncogenic osteomalacia in the literature, and each was treated differently with varying outcomes. (ke-i.org)
  • Clinical Relevance: Although an extremely rare disease, clinicians and pathologists should be aware of oncogenic osteomalacia and phosphaturic mesenchymal tumors as a cause of unexplained insufficiency fractures in patients with hypophosphatemia. (ke-i.org)
  • Oncogenic Osteomalacia of the Cervical Spine: A Rare Case of Curative Resection and Reconstruction. (ke-i.org)
  • A Haemangiopericytoma of the Ethmoid Sinus Causing Oncogenic Osteomalacia: A Case Report and Review of the Literature. (ke-i.org)
  • 3. Carpenter, T. O. "Oncogenic Osteomalacia--a Complex Dance of Factors. (ke-i.org)
  • Oncogenic Osteomalacia Associated with an Occult Phosphaturic Mesenchymal Tumour: Clinico-Radiologico-Pathological Correlation and Ultrastructural Studies. (ke-i.org)
  • Bone and in-111 Octreotide Imaging in Oncogenic Osteomalacia: A Case Report. (ke-i.org)
  • Oncogenic Osteomalacia Due to Phosphaturic Mesenchymal Tumor of the Craniofacial Sinuses. (ke-i.org)
  • Oncogenic Osteomalacia: Exact Tumor Localization by Co-Registration of Positron Emission and Computed Tomography. (ke-i.org)
  • Tumour-induced osteomalacia (TIO), also known as oncogenic osteomalacia, is a rare paraneoplastic disorder caused by tumours that secrete fibroblast growth factor 23 (FGF23). (elsevier.com)
  • In addition to low systemic levels of circulating mineral ions necessary for bone and tooth mineralization, accumulation of mineralization-inhibiting proteins and peptides (such as osteopontin and ASARM peptides) occurs in the extracellular matrix of bones and teeth, likely contributing locally to cause matrix hypomineralization (osteomalacia). (wikipedia.org)
  • Osteomalacia is a disease in which insufficient mineralization leads to a softening of the bones. (encyclopedia.com)
  • osteomalacia (osti-oh-mă- lay -shiă) n. softening of the bones due to inadequate mineralization: the adult counterpart of rickets. (encyclopedia.com)
  • Osteomalacia is softening of the bones. (medlineplus.gov)
  • More importantly, osteomalacia can look like weakening of the bones from osteoporosis on bone density testing. (medlineplus.gov)
  • Symptoms: Diffuse joint and bone pain (especially of spine, pelvis, and legs) Muscle weakness Difficulty walking, often with waddling gait Hypocalcemia (positive Chvostek sign) Compressed vertebrae and diminished stature Pelvic flattening Weak, soft bones Easy fracturing Bending of bones Osteomalacia in adults starts insidiously as aches and pains in the lumbar (lower back) region and thighs before spreading to the arms and ribs. (wikipedia.org)
  • Osteomalacia refers to a marked softening of your bones, most often caused by severe vitamin D deficiency. (mayoclinic.org)
  • The softened bones of children and young adults with osteomalacia can lead to bowing during growth, especially in weight-bearing bones of the legs. (mayoclinic.org)
  • If you have osteomalacia, you're more likely to break bones, particularly those in your ribs, spine and legs. (mayoclinic.org)
  • In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia , a bone-softening disease that leads to weak bones and often excruciating bone pain. (fluoridealert.org)
  • Osteomalacia is a condition in which the bones become soft. (peacehealth.org)
  • Symptoms of osteomalacia include bone pain and bones that fracture easily. (peacehealth.org)
  • Osteomalacia means softening of the bones and refers to defective or delayed mineralization of the organic matrix (osteoid) of cancellous and cortical bone. (renalandurologynews.com)
  • senile osteomalacia softening of bones in old age due to vitamin D deficiency. (thefreedictionary.com)
  • At its most basic level, osteomalacia is the inadequate mineralization of the human bones . (papermasters.com)
  • Osteomalacia or " soft bones " is a condition that affects your bones and is most often due to a lack of vitamin D and sometimes due to a mineral deficiency. (algaecal.com)
  • A related condition called osteomalacia can occur in adults with the same sort of vitamin D deficiency, but osteomalacia occurs only in adulthood after the growth plates of the bones have closed. (thefreedictionary.com)
  • Osteomalacia is abnormal bone formation leading to softening of the bones. (healthtap.com)
  • Structural changes and slight cracks in your bones that are visible on X-rays are characteristic of osteomalacia. (jpeeiclinic.com)
  • Adults can experience a similar condition, which is known as osteomalacia or soft bones. (raacked.com)
  • J. Bhan a, Rao DS, detect, treat or manage this disease in which the bones osteomalacia your. (raacked.com)
  • Osteomalacia is a condition that causes softening of bones, majorly due to deficiency of Vitamin D. In Osteomalacia, a person faces problems with bone formation or bone building process. (jghdelhi.net)
  • Osteomalacia is the softening of the bones due to defective bone mineralization. (blogspot.com)
  • Osteomalacia is one such condition that affects bones in the body in an undesirable way. (docprime.com)
  • Osteomalacia is a bone condition characterized by defective mineralization of newly formed bones and softening of bones, which leads to bone weakening. (ecosh.com)
  • Weakening of the bones is referred to as Osteomalacia. (lybrate.com)
  • Osteomalacia is a condition describes a condition of soft, weak bones that break easily. (facty.com)
  • Osteomalacia is characterized as weak bones. (facty.com)
  • The body can build, repair, and replace old bones, but bodies with osteomalacia have a limited ability to carry out this vital process. (facty.com)
  • The most common sign of osteomalacia are bones that fracture easily. (facty.com)
  • these can clearly show small cracks in the bones, indicators of osteomalacia. (facty.com)
  • If left untreated, osteomalacia leads to broken bones and severe deformity. (facty.com)
  • If osteomalacia is left untreated, it may result in lower bone density, which can subsequently cause osteoporosis, a bone condition similar to osteomalacia, except that the bones become brittle and fragile from loss of tissue. (facty.com)
  • Osteomalacia is a bone disorder caused due to softening of bones. (healthmd.net)
  • Osteomalacia is a softening of the bones, usually due to a vitamin D deficiency, MayoClinic.com reports. (livestrong.com)
  • In osteomalacia patients, the bones soften due to the unmineralised collagen fibers in the bones, and accordingly, they can bend, crack, and cause severe pain. (healthmedic24.com)
  • In the case of osteomalacia during growth in children and young adults, the problem of bending and distortion may occur, especially in the leg bones exposed to weight. (healthmedic24.com)
  • Osteomalacia disease can develop due to any disorder in the maturation process of the bones. (healthmedic24.com)
  • Osteomalacia, on the other hand, is a completely different condition that also affects the bones. (newlifeoutlook.com)
  • In older people, the softening bones of osteomalacia can result in bone breaks, just like in people with osteoporosis. (newlifeoutlook.com)
  • In season 2 of the USA Network series Royal Pains, Reshma Shetty (as Divya Katdare) diagnoses a storm chaser (Jamie Ray Newman) with recurring fractures to have tumor-induced osteomalacia. (wikipedia.org)
  • Osteomalacia in older adults can lead to fractures. (mayoclinic.org)
  • Osteomalacia is not the same as osteoporosis, another bone disorder that can also lead to bone fractures. (healthcentral.com)
  • hepatic osteomalacia osteomalacia as a complication of cholestatic liver disease, which may lead to severe bone pain and multiple fractures. (thefreedictionary.com)
  • osteomalacia y osteoporosis diferencia 5 : Johnell O. The socioeconomic burden of fractures today and in the 21st century. (rumblingpall.icu)
  • Osteomalacia can cause bone fractures, muscle weakness , and bone pain in various parts of the body. (lybrate.com)
  • Fractures tend to happen in people with osteomalacia even with small injuries. (lybrate.com)
  • Tumor-induced osteomalacia (TIO) is a rare paraneoplastic condition commonly characterized by bone pain, muscle weakness and fractures. (checkrare.com)
  • Osteomalacia in adults starts insidiously as aches and pains in the lumbar (lower back) region and thighs before spreading to the arms and ribs. (wikipedia.org)
  • The risk of developing osteomalacia is highest in people who don't get enough dietary vitamin D and have little sun exposure, such as older adults and those who are housebound or hospitalized. (mayoclinic.org)
  • Since we've been covering vitamin D lately, I thought we'd discuss some of the metabolic bone diseases caused by D deficiency in children and adults, like osteomalacia, aka rickets in children. (healthcentral.com)
  • Since we have a large number of individuals with this disorder (osteomalacia) in the U.S. and also in other countries, it's important that children/babies and adults get the required amounts of these nutrients to help to prevent some of these disorders. (healthcentral.com)
  • Because of this, osteomalacia is often associated with adults . (biology-online.org)
  • This chapter discusses primary metabolic osteomalacia presenting in adults. (psychiatryadvisor.com)
  • In adults, osteomalacia begins as aches and pains in the lumbar (lower spine) region, followed by the thighs and then the arms and ribs. (papermasters.com)
  • Nowadays it is rare to see rickets, but osteomalacia is still a threat to adults. (algaecal.com)
  • The enthesopathic changes of hypophosphatemic osteomalacia in adults: radiologic findings. (radiopaedia.org)
  • Definition Osteomalacia is a metabolic bone disease characterised by incomplete mineralisation of the underlying mature organic bone matrix (osteoid) following growth plate closure in adults. (raacked.com)
  • rickets is a disorder of impaired mineralization of cartilaginous growth plates.Adults have fused growth plates so they are only affected by osteomalacia.In children, whose growth plates are open, the disorders can occur simultaneously. (raacked.com)
  • Osteomalacia is a softening of the bone in adults, and it often occurs on a cellular level with the loss of minerals necessary for bone growth. (iahealth.net)
  • Osteomalacia is, therefore, the terminology that is typically designated for adults only and is typically a milder form of the same disease. (iahealth.net)
  • In adults, the condition is named as Osteomalacia. (docprime.com)
  • In adults, the equivalent disease is called osteomalacia. (nih.gov)
  • In contrast, serum 1,25-dihydroxyvitamin D levels are usually elevated owing to the concomitant hyperparathyroidism and do not contribute to the diagnosis of osteomalacia except in the rare abnormalities of vitamin D resistance [when 1,25-dihydroxyvitamin D levels are extraordinarily high] or when 1-alpha hydroxylation is defective [and 1,25-dihydroxyvitamin D levels are low or undetectable]. (renalandurologynews.com)
  • Absolute diagnosis of osteomalacia requires a bone biopsy with analysis of undecalcified sections (different from a regular bone marrow, which is decalcified so that undecalcified bone cannot be determined). (psychiatryadvisor.com)
  • A diagnosis of Osteomalacia was made and was commenced on treatment for this. (apollohospitals.com)
  • A diagnosis of osteomalacia related to vitamin D deficiency was given. (lymphedemapeople.com)
  • Finally she received a diagnosis of osteomalacia and was worked up. (radiologystories.com)
  • Like rickets, osteomalacia can cause bone pain and increase the risk of fracture. (massgeneral.org)
  • Osteomalacia causes bone pain and can increase the risk of fracture. (massgeneral.org)
  • Patients can be asymptomatic even with striking biochemical and densitometric findings of osteomalacia (eg: 29 year old women with severe vitamin D deficiency at 4 ng/ml, PTH at 100 pg/ml (range: 12-88) and low bone mineral density was evaluated for pathologic fracture. (renalandurologynews.com)
  • Johns Hopkins Medicine: "Osteoporosis and Osteomalacia. (webmd.com)
  • If there is an imbalance between the resorption and formation stage, it can lead to bone loss and diseases such as osteoporosis and osteomalacia. (algaecal.com)
  • The debate between osteoporosis and osteomalacia is a great example of this struggle to identify the correct condition. (newlifeoutlook.com)
  • Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome characterized by severe hypophosphatemia and osteomalacia. (biomedcentral.com)
  • Thus started the search for an FGF-secreting tumor that produces phosphaturia, hypophosphatemia and osteomalacia. (radiologystories.com)
  • Osteomalacia can occur because of reduced exposure to sunlight (which, after touching the skin, causes the body to make vitamin D), insufficient intake of vitamin D - enriched foods (like vitamin D - fortified milk), or improper digestion and absorption of food with vitamin D (as in bowel disorders such as lactose intolerance or celiac disease). (encyclopedia.com)
  • Main cause of osteomalacia is due to the low absorption of Vitamin D. Vitamin D is the essential for building the bone structure. (lybrate.com)
  • Supplements are generally the first line of treatment if osteomalacia stems from absorption problems. (facty.com)
  • Osteomalacia, on the other hand, has more to do with your body's absorption of essential vitamins and minerals, or your body's ability to use them effectively. (newlifeoutlook.com)
  • Osteomalacia can be diagnosed by blood and urine tests and confirmed by bone biopsy and X-rays. (encyclopedia.com)
  • In this photomicrograph of a bone biopsy specimen taken from a patient with osteomalacia, normally mineralized bone is blue and unmineralized bone matrix or osteoid is red. (renalandurologynews.com)
  • Severe osteomalacia (confirmed by the examination of thin undecalcified bone biopsy sections) associated with hypophosphataemia developed in a 60 year old woman. (bmj.com)
  • Although a bone biopsy is accurate in detecting osteomalacia, it's rarely needed to make the diagnosis. (jpeeiclinic.com)
  • OBJECTIVE: This study was undertaken to describe the musculoskeletal manifestations in a selected population of 26 patients with biopsy -proven osteomalacia (OM) and provide a literature update. (lookfordiagnosis.com)
  • Bone biopsy is conducted to understand osteomalacia the bone strength of the patients. (lybrate.com)
  • Bone biopsy is another method of diagnosing osteomalacia in which a long thin needle is sent through the skin in the affected portion to withdraw a small tissue. (healthmd.net)
  • Certain rare disorders can cause normal kidneys to lose phosphorus, which causes osteomalacia, but the most common cause of the condition is a lack of vitamin D. (arthritisresearchuk.org)
  • Tumor-induced osteomalacia is usually referred to as a paraneoplastic phenomenon, however, the tumors are usually benign and the symptomatology is due to osteomalacia or rickets. (wikipedia.org)
  • Serum chemistries are identical in tumor-induced osteomalacia, X-linked hypophosphatemic rickets (XHR) and autosomal dominant hypophosphatemic rickets (ADHR). (wikipedia.org)
  • A negative family history can be useful in distinguishing tumor induced osteomalacia from XHR and ADHR. (wikipedia.org)
  • The etiology and treatment of hereditary hypophosphatemic rickets and tumor-induced osteomalacia will be reviewed here. (uptodate.com)
  • Called also tumor-induced osteomalacia . (thefreedictionary.com)
  • Tumor-induced osteomalacia caused by an FGF23-secreting myopericytoma : Case report and literature review]. (annals.org)
  • We report the case of a 66-year-old woman with tumor-induced osteomalacia (TIO) caused by fibroblast growth factor 23 (FGF-23) secreting mesenchymal tumor localized in a lumbar vertebra and review other cases localized to the axial skeleton. (hindawi.com)
  • Tumor-induced osteomalacia: The tumor may stay hidden! (ac.be)
  • Fibroblast growth factor 23 (FGF-23) was abnormally high and the diagnostic of tumor-induced osteomalacia was made. (ac.be)
  • Tumor-induced osteomalacia (TIO) is characterized by hypophosphatemia caused by a phosphaturic mesenchymal tumor. (diseaseinfosearch.org)
  • Locating tumors responsible for tumor-induced osteomalacia is often challenging. (biomedcentral.com)
  • Tumor induced osteomalacia (TIO) is a rare paraneoplastic syndrome caused by overproduction of fibroblast growth factor 23 (FGF23) secreted by benign mesenchymal neoplasm. (elsevier.com)
  • Nguyen, Ba D. / Molecular Imaging in Diagnosis of Tumor-induced Osteomalacia . (elsevier.com)
  • A phosphaturic mesenchymal tumor is a rare condition and typically secretes FGF-23 (fibroblastic growth factor) that produces osteomalacia. (radiologystories.com)
  • Tumor-Induced Osteomalacia--Unveiling a New Hormone. (ke-i.org)
  • No systematic data are available regarding long-term bone mineral density (BMD) changes after surgical cure of patients with tumor-induced osteomalacia. (schizepigenetics.com)
  • 5 males and 5 females) with tumor-induced osteomalacia. (schizepigenetics.com)
  • The target audience for this course is neurologists, rheumatologists, general practitioners, orthopedic specialists, and oncologists, and other related specialties involved in the diagnosis and management of tumor-induced osteomalacia (TIO). (checkrare.com)
  • However, it is unusual for toxins to accumulate enough to cause osteomalacia unless there is also renal impairment. (psychiatryadvisor.com)
  • Certain surgeries done on the stomach can cause osteomalacia. (healthmd.net)
  • This can cause osteomalacia. (healthmd.net)
  • There's no consensus among experts about what amount of sun exposure is safe and enough to prevent or treat osteomalacia. (mayoclinic.org)
  • What are foods that contain vitamin D to help treat osteomalacia? (webmd.com)
  • [12] Vitamin D supplements are given to treat or to prevent osteomalacia and rickets. (wikipedia.org)
  • The most common cause of osteomalacia is a deficiency of vitamin D , which is normally derived from sunlight exposure and, to a lesser extent, from the diet. (wikipedia.org)
  • People who live in areas where sunlight is limited, get little exposure to sunlight or eat a diet low in vitamin D can develop osteomalacia. (mayoclinic.org)
  • Possible causes of osteomalacia include insufficient exposure to sunlight, certain drugs and surgeries, celiac disease, kidney or liver disorders and insufficient intake of vitamin D. The most common cause of osteomalacia around the world is a diet lacking in vitamin D. Osteomalacia is less common among Americans, because many foods are fortified with vitamin D. (livestrong.com)
  • The most common cause of osteomalacia in the world is insufficient dietary vitamin D intake or living indoors or in areas with little sunlight. (healthmedic24.com)
  • Osteomalacia is a generalized bone condition in which there is inadequate mineralization of the bone. (wikipedia.org)
  • Osteomalacia caused by inadequate sun exposure or a diet low in vitamin D often can be prevented by getting enough vitamin D. (mayoclinic.org)
  • Rickets and osteomalacia are the classical deficiency diseases caused by inadequate vitamin D. (news-medical.net)
  • Bone metabolism does not develop properly in individuals with osteomalacia due to an inadequate amount of vitamins and minerals. (facty.com)
  • See 'Overview of rickets in children' and 'Epidemiology and etiology of osteomalacia' . (uptodate.com)
  • Osteomalacia is like rickets in children. (docprime.com)
  • Some drugs used to treat seizures, including phenytoin (Dilantin, Phenytek) and phenobarbital, can cause severe vitamin D deficiency and osteomalacia. (mayoclinic.org)
  • A 25-hydroxy-Vitamin D less than 10 ng/mL suggests osteomalacia secondary to severe Vitamin D deficiency. (psychiatryadvisor.com)
  • Osteomalacia with bone marrow fibrosis due to severe vitamin D deficiency after a gastrointestinal bypass operation for severe obesity has been reported. (greenmedinfo.com)
  • What are the symptoms of rickets and osteomalacia? (massgeneral.org)
  • Read more about the signs and symptoms of rickets and osteomalacia. (raacked.com)
  • We compared the characteristics of patients with osteomalacia who visited the neurology department with (1) those who did not visit the neurology department and (2) patients with idiopathic inflammatory myopathy. (springer.com)
  • However, pain was more common in osteomalacia than in myopathy ( p = 0.008), and patients with osteomalacia showed brisk deep tendon reflex more often ( p = 0.017). (springer.com)
  • 0.001) levels were lower in osteomalacia than in myopathy. (springer.com)
  • Benhamou J, Fontanges E, Streichenberger N, Petiot P (2015) Severe osteomalacia mimicking progressive myopathy. (springer.com)
  • Myopathy in hypophosphataemic osteomalacia presenting in adult life. (bmj.com)
  • Osteomalacia associated severe proximal myopathy may be due to vitamin D deficiency. (greenmedinfo.com)
  • Patients with proximal myopathy should be screened for osteomalacia symptoms secondary to celiac disease. (greenmedinfo.com)
  • Osteomalacia, as an acquired metabolic disease, can be divided into disorders preventing bone mineralization (mainly vitamin D deficiency) and disorders with excessive mineral loss and metabolic acidosis (mainly renal tubular acidosis). (psychiatryadvisor.com)
  • There are many subtypes of renal tubular acidosis, including a variety of transporter defects and metabolic challenges that may lead to odd presentations of osteomalacia. (psychiatryadvisor.com)
  • There are also other rare causes of primary metabolic osteomalacia that do not fall into the categories above. (psychiatryadvisor.com)
  • Specifically, metabolic acidosis indicates work-up for renal tubular acidosis, whereas low vitamin D suggests work-up of vitamin D deficiency induced osteomalacia (outlined in Table 1 ). (psychiatryadvisor.com)
  • Metabolic bone disease of liver cirrhosis: Is it parallel osteomalacia y osteoporosis diferencia the clinical severity of cirrhosis? (rumblingpall.icu)
  • Vitamin D deficiency is the most common cause of osteomalacia worldwide. (mayoclinic.org)
  • I hope this information helps to educate the reader on this medical disorder of osteomalacia and you're able to prevent or treat this nutrient deficiency. (healthcentral.com)
  • Although osteomalacia may be caused by a lack of vitamin D in the diet, the cause may be more complex - relating not to dietary deficiency of the vitamin but rather a failure to absorb or activate the vitamin. (medbroadcast.com)
  • A vitamin D deficiency leading to osteomalacia may be caused by a poor diet (malnutrition) or by a problem with the intestine (such as celiac disease) that prevents it from absorbing nutrients. (peacehealth.org)
  • Bhan A, Rao AD, Rao DS (2010) Osteomalacia as a result of vitamin D deficiency. (springer.com)
  • This chapter focuses on osteomalacia secondary to Vitamin D deficiency and renal tubular acidosis (RTA). (psychiatryadvisor.com)
  • Osteomalacia is now rarely observed in hemodialyzed patients since the prevention of aluminum intoxication and vitamin D deficiency. (fluoridealert.org)
  • Osteomalacia as a Result of Vitamin D Deficiency. (raacked.com)
  • The most common cause of both osteomalacia and rickets is vitamin D deficiency â ¦ Clinical trials. (raacked.com)
  • Osteomalacia is a disorder caused by vitamin D deficiency. (taylortransformation.com)
  • Vitamin D deficiency in the body can lead to Osteomalacia. (docprime.com)
  • Persistent, nonspecific musculoskeletal pain caused by conditions like osteomalacia may be due in part to vitamin D deficiency. (greenmedinfo.com)
  • Certain diseases of kidney and liver problems can cause deficiency of vitamin D. People who are consuming antiepileptic medications like phenytoin or Phenobarbital are prone to osteomalacia. (healthmd.net)
  • Osteomalacia, which means bone softening, is a type of disease in which there are structural deformations and deformations in the bone tissue that usually occur due to vitamin D deficiency. (healthmedic24.com)
  • Osteomalacia is a bone softening disease that usually occurs due to vitamin D deficiency. (healthmedic24.com)
  • Most Osteomalacia-Associated Mesenchymal Tumors Are a Single Histopathologic Entity: An Analysis of 32 Cases and a Comprehensive Review of the Literature. (ke-i.org)
  • Letter: Hypophosphataemic osteomalacia in patients receiving haemodialysis. (bmj.com)
  • Ahmed K Y , Varghese Z , Wills M R , Meinhard E , Moorhead J F . Letter: Hypophosphataemic osteomalacia in patients receiving haemodialysis. (bmj.com)
  • Girgis CM, Wong T, Ngu MC, Emmett L, Archer KA, Chen RC et al (2011) Hypophosphataemic osteomalacia in patients on adefovir dipivoxil. (springer.com)
  • What causes osteomalacia in patients with type 2 renal tubular acidosis (RTA)? (medscape.com)
  • Patients with chronic renal failure can develop aluminum toxicity, which can lead to osteomalacia and encephalopathy. (unboundmedicine.com)
  • Several decades ago, aluminum encephalopathy associated with osteomalacia has been recognized as the major complication of chronic renal failure in dialyzed patients. (unboundmedicine.com)
  • renal tubular osteomalacia a type resulting from acidosis and hypercalciuria when deficient renal tubular activity has caused inability to produce acid urine or ammonia. (thefreedictionary.com)
  • Osteomalacia as a complication of renal failure and disorders of Vitamin D metabolism are not discussed. (psychiatryadvisor.com)
  • Call your health care provider if you have symptoms of osteomalacia, or if you think that you may be at risk for this disorder. (medlineplus.gov)
  • Since 20 to 25 million individuals in the U.S. have osteomalacia, let's look at the things we can do to prevent and treat this disorder. (healthcentral.com)
  • Osteomalacia is a generalized bone disorder characterized by impairment of mineralization, leading to accumulation of unmineralized matrix or osteoid in the skeleton. (schizepigenetics.com)
  • One of the more common symptoms of osteomalacia is an inability to stand from a squatting position and difficulty climbing stairs. (papermasters.com)
  • We analyzed clinical features of osteomalacia patients who visited the neurology department. (springer.com)
  • The clinical features of osteomalacia include musculoskeletal vague pain and muscle weakness. (schizepigenetics.com)
  • As osteomalacia progresses, you might develop bone pain and muscle weakness. (mayoclinic.org)
  • The treatments will generally cure osteomalacia, but easing bone pain and muscle weakness may take several months. (facty.com)
  • However, as osteomalacia progresses and increases its severity, bone pain and muscle weakness problems begin to occur. (healthmedic24.com)
  • Schott GD, Wills MR (1976) Muscle weakness in osteomalacia. (springer.com)
  • This article provides a brief overview of advances in the understanding of the pathogenesis of rickets, osteomalacia and age-related osteoporosis. (scielo.org.za)
  • Osteomalacia in children is known as rickets , and because of this, use of the term "osteomalacia" is often restricted to the milder, adult form of the disease. (wikipedia.org)
  • Osteomalacia is an adult version of rickets. (peacehealth.org)
  • vitamin D refractory osteomalacia), who differed from those with the hereditary form of the disease by onset of symptoms during adolescence or adult life, negative family history, and evidence of increased urinary excretion of glycine (2). (annals.org)
  • Osteomalacia in the adult is most commonly found in confined, dark-skinned, or diet-disbalanced subjects. (blogspot.com)
  • In the US and Europe, more than 40% of the adult population older than age 50 are vitamin D deficient, this being the most prominent cause of osteomalacia. (kieran101.com)
  • Children with severe cases of osteomalacia may have to wear braces or have surgery to correct bone deformation. (facty.com)
  • Doctors for Osteomalacia: This section presents information about some of the possible medical professionals that might be involved with Osteomalacia. (raacked.com)
  • The easy availability of vitamin D - fortified milk has reduced the incidence of osteomalacia in developed countries to 0.1 percent. (encyclopedia.com)
  • The markedly increased incidence of osteomalacia in the fluoridated group supports previous reports that fluoride is an important factor… Since our patients in the fluoridated group were living in widely separate areas with different water supplies it seems unlikely that there was another common factor other than fluoride responsible for the higher incidence of osteomalacia. (fluoridealert.org)
  • Four of 7 patients using fluoridated water developed florid osteomalacia, as opposed to none of the 34 patients in the non-fluoridated group… We conclude that the presence of fluoride in the dialysate, perhaps in conjunction with other substances, is associated with an increased incidence of osteomalacia. (fluoridealert.org)
  • Osteomalacia should not be confused with osteoporosis , which is a disease of normal mineralization but decreased amounts of bone. (encyclopedia.com)
  • Osteomalacia is specifically a defect in mineralization of the protein framework known as osteoid. (blogspot.com)

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