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hypophosphatemia/phosphatase
Линкът е запазен в клипборда
Страница 1 от 296 резултата
Low neutrophil alkaline phosphatase in renal tubular acidosis with hypophosphatemia after toluene sniffing.
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Selective renal involvement in the early development of hypercalcemia and hypophosphatemia in VX-2 carcinoma-bearing rabbits: studies on serum and tissues alkaline phosphatase and renal handling of phosphorus.
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Effect of paricalcitol on circulating parathyroid hormone in X-linked hypophosphatemia: a randomized, double-blind, placebo-controlled study.
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BACKGROUND
Hyperparathyroidism occurs frequently in X-linked hypophosphatemia (XLH) and may exacerbate phosphaturia, potentially affecting skeletal abnormalities.
OBJECTIVE
The objective of the study was to suppress elevated PTH levels in XLH patients.
METHODS
This was a prospective, randomized,
Osteopetrosis, hypophosphatemia, and phosphaturia in a young man: a case presentation and differential diagnosis.
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We report the case of a 30-year-old African-American male with osteopetrosis and hypophosphatemia, presenting with diffuse myalgias. Laboratory evaluation performed revealed a low serum phosphorus level with urinary phosphate wasting, low calcium, and 25-hydroxyvitamin D concentrations, as well as
Hypophosphatemia in breast-fed low-birth-weight infants following initial hospital discharge.
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The present study evaluated 12 infants with birth weights less than 2000 g who received human milk plus a multivitamin supplement and 20 similar infants who received standard cow's milk formula for 16 weeks from the time of initial hospital discharge. Examination at birth, at hospital discharge
Dosage effect of a Phex mutation in a murine model of X-linked hypophosphatemia.
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X-linked hypophosphatemia (XLH) is caused by mutations in the PHEX gene, which increase circulating levels of the phosphaturic hormone, fibroblast growth factor 23 (FGF23). Because XLH is a dominant disease, one mutant allele is sufficient for manifestation of the disease. However, the dosage effect
Effect of dipyridamole on serum and urinary phosphate in X-linked hypophosphatemia.
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X-linked hypophosphatemia (XLH) is characterized clinically by rickets, hypophosphatemia and hyperphosphaturia. Conventional treatment of XLH with oral phosphate and vitamin D is associated with hypercalcuria and nephrocalcinosis. Recently, intravenous and oral dipyridamole has been reported to
X-Linked Hypophosphatemia: Uniquely Mild Disease Associated With PHEX 3'-UTR Mutation c.*231A>G (A Retrospective Case-Control Study).
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X-linked hypophosphatemia (XLH), the most prevalent heritable renal phosphate (Pi) wasting disorder, is caused by deactivating mutations of PHEX. Consequently, circulating phosphatonin FGF23 becomes elevated and hypophosphatemia in affected children leads to rickets with skeletal deformity and
High iFGF23 level despite hypophosphatemia is one of the clinical indicators to make diagnosis of XLH.
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X-linked hypophosphatemic rickets (XLH) is caused by inactivating mutations in the phosphate-regulating gene with homologies to endopeptidases on the X chromosome (PHEX) gene. Deletion of Phex leads to increased serum fibroblast growth factor23 (FGF23) levels in mouse. The aim is to assure the
Severe muscle weakness secondary to paraneoplastic hypophosphatemia in neuroblastoma.
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We report a 28-year-old woman who presented with severe proximal muscle weakness secondary to paraneoplastic hypophosphatemia and associated with recurrent neuroblastoma. The biochemical findings included hyperphosphaturia, a reduced serum level of 1,25-dihydroxyvitamin-D3, elevated alkaline
Hypophosphatemia predicts a failure to recover from adefovir-related renal injury after dose reduction in lamivudine-resistant hepatitis B patients.
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OBJECTIVE
In chronic hepatitis B patients receiving 10 mg adefovir, dose reduction is recommended when renal injury appears. However, recovery is not always achieved and markers that recommend switching to another antiviral agent are unknown. We investigated adefovir-related renal injury, recovery
Oncogenic osteomalacia should be considered in hypophosphatemia, bone pain and pathological fractures.
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The clinical manifestation of oncogenic osteomalacia includes bone pain, pathological fractures, general fatigue and muscle weakness. Such unspecific symptoms hinder the establishment of a proper diagnosis which very often requires long-lasting investigations with many diagnostic imaging methods.
Up-regulation of liver glucose-6-phosphatase in x-linked hypophosphatemic mice.
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We previously showed that a phosphate-deficient diet resulting in hypophosphatemia upregulated the catalytic subunit p36 of rat liver glucose-6-phosphatase, which is responsible for hepatic glucose production. A possible association between phosphate and glucose homeostasis was now further evaluated
Hypophosphatemic rickets accompanying McCune-Albright syndrome: evidence that a humoral factor causes hypophosphatemia.
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McCune-Albright syndrome (MAS) is sometimes complicated by hypophosphatemia. However, it remains unclear whether a humoral factor is associated with the cause of hypophosphatemia. We isolated cells with mutations of the Gsalpha gene from fibrous bone dysplasia tissues of two MAS patients (MAS
Extracellular matrix mineralization in periodontal tissues: Noncollagenous matrix proteins, enzymes, and relationship to hypophosphatasia and X-linked hypophosphatemia.
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As broadly demonstrated for the formation of a functional skeleton, proper mineralization of periodontal alveolar bone and teeth - where calcium phosphate crystals are deposited and grow within an extracellular matrix - is essential for dental function. Mineralization defects in tooth dentin and
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