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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
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Disease relevance of Hypophosphatemia


Psychiatry related information on Hypophosphatemia


High impact information on Hypophosphatemia

  • We conclude that the subjects with hypercalciuria and the patients with HHRH shared a hereditary renal phosphate leak that led to hypophosphatemia, elevated serum concentrations of 1,25-(OH)2D, increased intestinal calcium absorption, and hypercalciuria [8].
  • We propose that the pivotal defect in this syndrome is a renal phosphate leak resulting in hypophosphatemia with an appropriate elevation of 1,25-dihydroxyvitamin D levels, which causes increased calcium absorption, parathyroid suppression, and hypercalciuria [9].
  • Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess [10].
  • Thus, sFRP-4 displays phosphatonin-like properties, because it is a circulating protein that promotes phosphaturia and hypophosphatemia and blunts compensatory increases in 1alpha, 25-dihydroxyvitamin D [11].
  • The low phosphate diet led to hypophosphatemia, hypercalcemia, and increased serum 1,25(OH)2D3 together with decreased PTH mRNA levels (25 +/- 8% of controls, P < 0.01) and serum immunoreactive PTH (4.7 +/- 0.8: 22.1 +/- 3.7 pg/ml; low phosphate: control, P < 0.05) [12].

Chemical compound and disease context of Hypophosphatemia

  • These results indicate that hypophosphatemia is associated with impaired glucose metabolism in both the hyperglycemic and euglycemic states, and that this associated primarily reflects decreased tissue sensitivity to insulin [13].
  • The remaining two untreated patients (aged 2 and 37 yr) displayed characteristic hypophosphatemia before calcitriol therapy [14].
  • Mild hypophosphatemia was present in SH on +D (5.8 vs. 6.9 mg/dl, P less than 0.005) and -D diets (6.2 vs. 7.9 mg/dl, P less than 0.005), and was associated with higher rates of cyclic adenosine monophosphate excretion (32.8 vs. 26.9 and 48.5 vs. 41.0 nmol/mg of creatinine, respectively) [15].
  • These data demonstrate that hypophosphatemia is associated with an augmented glucose-stimulated insulin release, without any effect on tolbutamide-stimulated insulin release [16].
  • Complete remission of the leukemia and fibrosis was achieved with a single 3-week course of low-dose cytarabine and hydroxyurea, with resolution of the hypocalcemia and hypophosphatemia [17].

Biological context of Hypophosphatemia


Anatomical context of Hypophosphatemia


Gene context of Hypophosphatemia

  • At comparable circulating levels, the mutant form was more potent in inducing hypophosphatemia, in decreasing circulating concentrations of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), and in causing rickets and osteomalacia in these animals compared with wild type FGF23 [27].
  • These results demonstrate that MEPE elevation in Hyp mice does not contribute to the hypophosphatemia associated with inactivating Phex mutations and is therefore not phosphatonin [28].
  • In summary, the Gy mutation is associated with a recessively expressed mutation of the spermine synthase gene, leading to spermine deficiency, and a dominantly expressed mutation of the Pex gene, leading to hypophosphatemia [29].
  • The present results indicate that the low serum IGFBP-3 activity in Hyp mice is not related to hypophosphatemia per se [30].
  • Phosphate deprivation induced hypophosphatemia IGF-II [30].

Analytical, diagnostic and therapeutic context of Hypophosphatemia


  1. Proximal myopathy caused by latrogenic phosphate depletion. Ravid, M., Robson, M. JAMA (1976) [Pubmed]
  2. Long-term control of plasma calcitriol concentration in dogs and humans. Dominant role of plasma calcium concentration in experimental hyperparathyroidism. Hulter, H.N., Halloran, B.P., Toto, R.D., Peterson, J.C. J. Clin. Invest. (1985) [Pubmed]
  3. Metabolic and cellular analysis of alopecia in vitamin D receptor knockout mice. Sakai, Y., Kishimoto, J., Demay, M.B. J. Clin. Invest. (2001) [Pubmed]
  4. Chronic metabolic acidosis increases the serum concentration of 1,25-dihydroxyvitamin D in humans by stimulating its production rate. Critical role of acidosis-induced renal hypophosphatemia. Krapf, R., Vetsch, R., Vetsch, W., Hulter, H.N. J. Clin. Invest. (1992) [Pubmed]
  5. Recombinant human erythropoietin and hypophosphatemia in patients with cirrhosis. Kajikawa, M., Nonami, T., Kurokawa, T., Harada, A., Nakao, A., Takagi, H. Lancet (1993) [Pubmed]
  6. Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss. Derr, R.F., Zieve, L. J. Lab. Clin. Med. (1978) [Pubmed]
  7. Hypophosphatemia secondary to oral refeeding in anorexia nervosa. Fisher, M., Simpser, E., Schneider, M. The International journal of eating disorders. (2000) [Pubmed]
  8. "Idiopathic" hypercalciuria and hereditary hypophosphatemic rickets. Two phenotypical expressions of a common genetic defect. Tieder, M., Modai, D., Shaked, U., Samuel, R., Arie, R., Halabe, A., Maor, J., Weissgarten, J., Averbukh, Z., Cohen, N. N. Engl. J. Med. (1987) [Pubmed]
  9. Hereditary hypophosphatemic rickets with hypercalciuria. Tieder, M., Modai, D., Samuel, R., Arie, R., Halabe, A., Bab, I., Gabizon, D., Liberman, U.A. N. Engl. J. Med. (1985) [Pubmed]
  10. Hypophosphatemia in hospitalized patients. Juan, D., Elrazak, M.A. JAMA (1979) [Pubmed]
  11. Secreted frizzled-related protein 4 is a potent tumor-derived phosphaturic agent. Berndt, T., Craig, T.A., Bowe, A.E., Vassiliadis, J., Reczek, D., Finnegan, R., Jan De Beur, S.M., Schiavi, S.C., Kumar, R. J. Clin. Invest. (2003) [Pubmed]
  12. Parathyroid hormone gene expression in hypophosphatemic rats. Kilav, R., Silver, J., Naveh-Many, T. J. Clin. Invest. (1995) [Pubmed]
  13. Hypophosphatemia and glucose intolerance: evidence for tissue insensitivity to insulin. DeFronzo, R.A., Lang, R. N. Engl. J. Med. (1980) [Pubmed]
  14. Healing of bone disease in X-linked hypophosphatemic rickets/osteomalacia. Induction and maintenance with phosphorus and calcitriol. Harrell, R.M., Lyles, K.W., Harrelson, J.M., Friedman, N.E., Drezner, M.K. J. Clin. Invest. (1985) [Pubmed]
  15. Pathophysiology of spontaneous hypercalciuria in laboratory rats. Role of deranged vitamin D metabolism. Lau, K., Thomas, D., Langman, C., Eby, B. J. Clin. Invest. (1985) [Pubmed]
  16. The relative roles of calcium, phosphorus, and parathyroid hormone in glucose- and tolbutamide-mediated insulin release. Harter, H.R., Santiago, J.V., Rutherford, W.E., Slatopolsky, E., Klahr, S. J. Clin. Invest. (1976) [Pubmed]
  17. Accelerated bone formation causing profound hypocalcemia in acute leukemia. Schenkein, D.P., O'Neill, W.C., Shapiro, J., Miller, K.B. Ann. Intern. Med. (1986) [Pubmed]
  18. Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. Sabbagh, Y., Carpenter, T.O., Demay, M.B. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  19. The Gy mutation: another cause of X-linked hypophosphatemia in mouse. Lyon, M.F., Scriver, C.R., Baker, L.R., Tenenhouse, H.S., Kronick, J., Mandla, S. Proc. Natl. Acad. Sci. U.S.A. (1986) [Pubmed]
  20. RNA-Protein binding and post-transcriptional regulation of parathyroid hormone gene expression by calcium and phosphate. Moallem, E., Kilav, R., Silver, J., Naveh-Many, T. J. Biol. Chem. (1998) [Pubmed]
  21. An ethyl-nitrosourea-induced point mutation in phex causes exon skipping, x-linked hypophosphatemia, and rickets. Carpinelli, M.R., Wicks, I.P., Sims, N.A., O'Donnell, K., Hanzinikolas, K., Burt, R., Foote, S.J., Bahlo, M., Alexander, W.S., Hilton, D.J. Am. J. Pathol. (2002) [Pubmed]
  22. Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo. Shimada, T., Muto, T., Urakawa, I., Yoneya, T., Yamazaki, Y., Okawa, K., Takeuchi, Y., Fujita, T., Fukumoto, S., Yamashita, T. Endocrinology (2002) [Pubmed]
  23. Longitudinal study of urinary excretion of phosphate, calcium, and uric acid in mutant NHERF-1 null mice. Weinman, E.J., Mohanlal, V., Stoycheff, N., Wang, F., Steplock, D., Shenolikar, S., Cunningham, R. Am. J. Physiol. Renal Physiol. (2006) [Pubmed]
  24. Increased cathepsin D release by Hyp mouse osteoblast cells. Matsumoto, N., Jo, O.D., Shih, R.N., Brochmann, E.J., Murray, S.S., Hong, V., Yanagawa, J., Yanagawa, N. Am. J. Physiol. Endocrinol. Metab. (2005) [Pubmed]
  25. Effect of phosphate supplementation on the expression of the mutant phenotype in murine X-linked hypophosphatemic rickets. Tenenhouse, H.S., Martel, J., Rubin, J., Harvey, N. Bone (1994) [Pubmed]
  26. Erythrocyte adenosine triphosphate depletion during voluntary hyperventilation. Stäubli, M., Ott, P., Waber, U., Stäuble, U.P., Jeanneret, C., Peheim, E., Straub, P.W. J. Appl. Physiol. (1985) [Pubmed]
  27. The autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potency. Bai, X.Y., Miao, D., Goltzman, D., Karaplis, A.C. J. Biol. Chem. (2003) [Pubmed]
  28. Role of matrix extracellular phosphoglycoprotein in the pathogenesis of X-linked hypophosphatemia. Liu, S., Brown, T.A., Zhou, J., Xiao, Z.S., Awad, H., Guilak, F., Quarles, L.D. J. Am. Soc. Nephrol. (2005) [Pubmed]
  29. Partial deletion of both the spermine synthase gene and the Pex gene in the X-linked hypophosphatemic, gyro (Gy) mouse. Meyer, R.A., Henley, C.M., Meyer, M.H., Morgan, P.L., McDonald, A.G., Mills, C., Price, D.K. Genomics (1998) [Pubmed]
  30. Serum insulin-like growth factor binding protein-3 in the hypophosphatemic mouse: decreased activity and abnormal modulation by dietary phosphate. Moriwake, T., Abribat, T., Brazeau, P., Ecarot, B. J. Bone Miner. Res. (1995) [Pubmed]
  31. The renal phosphate transport defect in normal mice parabiosed to X-linked hypophosphatemic mice persists after parathyroidectomy. Meyer, R.A., Tenenhouse, H.S., Meyer, M.H., Klugerman, A.H. J. Bone Miner. Res. (1989) [Pubmed]
  32. Hemangiopericytoma-induced osteomalacia: tumor transplantation in nude mice causes hypophosphatemia and tumor extracts inhibit renal 25-hydroxyvitamin D 1-hydroxylase activity. Miyauchi, A., Fukase, M., Tsutsumi, M., Fujita, T. J. Clin. Endocrinol. Metab. (1988) [Pubmed]
  33. Secondary hyperparathyroidism in X-linked hypophosphatemic mice. Kiebzak, G.M., Roos, B.A., Meyer, R.A. Endocrinology (1982) [Pubmed]
  34. Preventing hypophosphatemia during total parenteral nutrition. Thompson, J.S., Hodges, R.E. JPEN. Journal of parenteral and enteral nutrition. (1984) [Pubmed]
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