osteomalacia/protease

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Extracts from tumors causing oncogenic osteomalacia inhibit phosphate uptake in opossum kidney cells.

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In oncogenic osteomalacia (OOM), a tumor produces an unknown substance that inhibits phosphate reabsorption in the proximal tubules. This causes urinary phosphate wasting and, as a consequence, hypophosphatemic osteomalacia. To characterize this poorly understood biological tumor activity we

Tenofovir-induced osteomalacia.

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We present an HIV-infected woman in whom antiretroviral treatment with tenofovir disoproxil fumarate (TDF) induced severe skeletal pain, synovial effusions and multiple fractures secondary to a Fanconi syndrome with hypophosphatemia and osteomalacia. TDF interferes with the replication of

Phosphate wasting in oncogenic osteomalacia: PHEX is normal and the tumor-derived factor has unique properties.

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Oncogenic osteomalacia (OOM) is characterized by renal phosphate wasting and abnormal metabolism of vitamin D, somewhat similar to the phenotype of X-linked hypophosphatemic rickets (HYP). DNA from OOM tumor cells was analyzed for mutations in the PHEX gene, which is mutated in HYP. Screening for

Adamts1 is highly induced in rachitic bones of FGF23 transgenic mice and participates in degradation of non-mineralized bone matrix collagen.

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Transgenic mice overexpressing fibroblast growth factor 23 (FGF23) in osteoblasts have a rachitic bone phenotype. These mice display hypomineralized bones, increased expression of osteoblast markers, but osteoclast numbers are unaltered or slightly reduced. Paradoxically, they show increased serum

Vitamin D deficiency in HIV: a shadow on long-term management?

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Vitamin D deficiency in HIV infection has attracted much interest. The best known clinical outcomes of vitamin D deficiency are rickets (children) and osteomalacia (adults). Several non-skeletal disorders have also been linked to suboptimal vitamin D levels in the general population. The prevalence

Serum MEPE-ASARM-peptides are elevated in X-linked rickets (HYP): implications for phosphaturia and rickets.

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MEPE (Matrix Extracellular PhosphoglycoprotEin) expression is markedly elevated in X-linked-hypophosphatemic-rickets (HYP) and tumor-induced osteomalacia (TIO). In normal individuals, circulating serum-levels of MEPE are tightly correlated with serum-phosphorus, parathyroid hormone (PTH) and bone

Disorders of phosphate metabolism--pathomechanisms and management of hypophosphataemic disorders.

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Hypophosphataemia does not necessarily indicate phosphate (Pi) depletion. In acute emergencies such as septicaemia, alkalosis or re-feeding, hypophosphataemia may result from redistribution of Pi from the extracellular to the intracellular space. Hypophosphataemia from true Pi depletion gives rise

Zidovudine, tenofovir or abacavir? Different adverse effect profiles.

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Current guidelines on first-line treatment of HIV infection recommend a combination of at least three antiretroviral drugs from two different pharmacological classes: at least two nucleoside or nucleotide reverse transcriptase inhibitors plus either a protease inhibitor or a non-nucleoside reverse

Expression and inactivation of osteopontin-degrading PHEX enzyme in squamous cell carcinoma.

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Proteolytic enzymes mediate the activation or inactivation of many physiologic and pathologic processes. The PHEX gene (Phosphate-regulating gene with homologies to endopeptidase on the X chromosome) encodes a metallopeptidase, which is mutated in patients with a prevalent form (1:20,000) of

Hyperparathyroidism and complications associated with vitamin D deficiency in HIV-infected adults in New York City, New York.

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Although recent studies report a high prevalence of vitamin D deficiency in HIV-infected adults similar to that in the general population, metabolic complications of vitamin D deficiency may be worsened with HIV infection and remain insufficiently characterized. We conducted a retrospective

Osteoclast polarization is not required for degradation of bone matrix in rachitic FGF23 transgenic mice.

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Hypophosphatemic transgenic (tg) mice overexpressing FGF23 in osteoblasts display disorganized growth plates and reduced bone mineral density characteristic of rickets/osteomalacia. These FGF23 tg mice were used as an in vivo model to examine the relation between osteoclast polarization, secretion

HIV Infection and Bone Abnormalities.

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More than 36 million people are living with human immunodeficiency virus (HIV) infection worldwide and 50% of them have access to antiretroviral therapy (ART). While recent advances in HIV therapy have reduced the viral load, restored CD4 T cell counts and decreased opportunistic infections, several

The autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potency.

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Missense mutations in fibroblast growth factor 23 (FGF23) are the cause of autosomal dominant hypophosphatemic rickets (ADHR). The mutations (R176Q, R179W, and R179Q) replace Arg residues within a subtilisin-like proprotein convertase (SPC) cleavage site (RXXR motif), leading to protease resistance

The wrickkened pathways of FGF23, MEPE and PHEX.

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The last 350 years since the publication of the first medical monograph on rickets (old English term wrickken) (Glisson et al., 1651) have seen spectacular advances in our understanding of mineral-homeostasis. Seminal and exciting discoveries have revealed the roles of PTH, vitamin D, and calcitonin

Transgenic mice overexpressing human fibroblast growth factor 23 (R176Q) delineate a putative role for parathyroid hormone in renal phosphate wasting disorders.

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Fibroblast growth factor 23 (FGF23) is a recently characterized protein likely involved in the regulation of serum phosphate homeostasis. Increased circulating levels of FGF23 have been reported in patients with renal phosphate-wasting disorders, but it is unclear whether FGF23 is the direct

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