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Prevalence of HSD alone is unknown, though previous estimates have placed the combined prevalence of hEDS and HSD between 194.2 per 100 000 (0.19%) or 1 in 500 people. [7] The condition is relatively common in those attending musculoskeletal services.
While hEDS affects at least one in 5,000 people globally, [1] [14] other types occur at lower frequencies. [ 11 ] [ 8 ] The prognosis depends on the specific disorder. [ 4 ] Excess mobility was first described by Hippocrates in 400 BC. [ 15 ]
Ehlers–Danlos syndrome is a genetic disorder caused by mutations or hereditary genes, but the genetic defect that produced hEDS is largely unknown. In conjunction with joint hypermobility, a common symptom for hEDS is smooth, velvety, and stretchy skin; a symptom largely unique to the syndrome.
Cancer in children is rare in the UK, with an average of 1,800 diagnoses every year but contributing to less than 1% of all cancer-related deaths. [70] Age is not a confounding factor in mortality from the disease in the UK. From 2014 to 2016, approximately 230 children died from cancer, with brain/CNS cancers being the most commonly fatal type.
"What are the Differences Between Cancer in Adults and Children?." Cancer Reference Information. 14 May 2009. American Cancer Society. 17 November 2009 <www.cancer.org> Pöder U, Ljungman G, von Essen L (May 2008). "Posttraumatic stress disorder among parents of children on cancer treatment: a longitudinal study". Psycho-Oncology. 17 (5): 430– 7.
3β-HSD II mediates three parallel dehydrogenase/isomerase reactions in the adrenals that convert Δ 4 to Δ 5 steroids: pregnenolone to progesterone, 17α-hydroxypregnenolone to 17α-hydroxyprogesterone, and dehydroepiandrosterone (DHEA) to androstenedione. 3β-HSD II also mediates an alternate route of testosterone synthesis from androstenediol in the testes. 3β-HSD deficiency results in ...
17β-Hydroxysteroid dehydrogenase 1 (17β-HSD1) is an enzyme that in humans is encoded by the HSD17B1 gene. [ 5 ] [ 6 ] [ 7 ] This enzyme oxidizes or reduces the C17 hydroxy/keto group of androgens and estrogens and hence is able to regulate the potency of these sex steroids
17 alpha ketosteroid reductase deficiency of testis, [1] 46,XY difference of sex development due to 17-beta-hydroxysteroid dehydrogenase 3 deficiency, 17-ketoreductase deficiency, 17-ketosteroidreductase deficiency. Biochemical effects of 17β-hydroxysteroid deficiency-3 in testosterone biosynthesis.