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Bone pain / iron induced D3 insufficiency
2006-01-11 09:12:52 PM
A search of the literature of iron related disease .. reveals low vitamin D . What significance is the fact iron destroys vitamin D or more precisely in those with iron overload .. vitamin D is decreased .. in those with supplemental iron induced iron overload .. vitamin D is decreased. Bleeding / venesection / bloodletting / phlebotomy .. RESTORES .. vitamin D . <<snip>> The results reveal that the low serum 25-OHD concentration in patients with hemochromatosis is directly related to the extent of iron loading and it is improved by venesection therapy. <<snip>> Iron induced decreased vitamin D. <<snip>> when transferrin is saturated with iron, may impair bone formation and aggravate osteomalacia. <<snip>> Saccharated ferric oxide (SFO)-induced osteomalacia: in vitro inhibition by SFO of bone formation and 1,25-dihydroxy-vitamin D production in renal tubules. Sato K, Nohtomi K, Demura H, Takeuchi A, Kobayashi T, Kazama J, Ozawa H Bone. 1997 Jul ; 21(1): 57-64 A 60-year-old man with portal hypertensive gastropathy due to type C liver cirrhosis developed severe bone pains, marked hypophosphatemia with inappropriately increased urinary excretion of phosphate (%TRP; 9.6%), and hyperalkaline phosphatasia, after intravenous administration of saccharated ferric oxide (SFO) at a dose of 80-240 mg/week over a period of more than 5 years. The total iron infused was estimated to be more than 25 g. On a diagnosis of SFO-induced osteomalacia, the infusion of iron was immediately discontinued, and phosphate and vitamin D2 (1000 IU/day) were administered. Serum levels of 25-OHD2 increased after 1 week, whereas levels of 1,25-(OH)2D2 did not increase until 3 months later, accompanied by improvement of renal tubular reabsorption of phosphate and gradual improvement of the bone pains. The patient has been doing well for the last 2 years, with normal serum levels of phosphate, calcium, and alkaline phosphatase, without any supplementation of phosphate, vitamin D, or iron-containing agents. In primary culture of neonatal mouse renal tubules, in which 1,25-(OH)2D3 was produced from 25-OHD3 in response to PTH, SFO significantly inhibited PTH-induced production of 1,25-(OH)2D3 at 30 mumol/L, which is attainable in the urine of patients receiving a therapeutic intravenous dose of SFO. Furthermore, SFO decreased the calcium content and inhibited 45Ca incorporation in cultured fetal mouse parietal bones at 3 mumol/L. Such SFO concentration may be transiently observed in the plasma of patients receiving excessive intravenous doses of SFO for a prolonged period. These in vitro findings together with the clinical observations suggest that SFO, after filtration through the glomerulus and reabsorption in the proximal renal tubules, impaired proximal renal tubular function, such as tubular reabsorption of phosphate and 1 alpha-hydroxylase activity, leading to hypophosphatemic osteomalacia. Furthermore, it is highly likely that SFO in the peripheral blood, when transferrin is saturated with iron, may impair bone formation and aggravate osteomalacia. Although SFO-induced osteomalacia is reversible simply by discontinuation of the agent, excessive and prolonged administration of SFO should be avoided. ------------------------------------------------------------------------------------------- 1: Gastroenterology. 1985 Apr;88(4):865-9. Related Articles, Links Low serum 25-hydroxyvitamin D in hereditary hemochromatosis: relation to iron status. Chow LH, Frei JV, Hodsman AB, Valberg LS. Under normal conditions, vitamin D absorbed from the diet or synthesized in the skin is transported to the liver where it undergoes hydroxylation. The purpose of this study was to determine whether excess hepatic iron affects this process and the subsequent production of 1,25-dihydroxyvitamin D (1,25-[OH]2D) in the kidney. Mean serum 25-hydroxyvitamin D (25-OHD) concentrations in untreated hereditary hemochromatosis were 13 +/- 6 (SD) in 9 patients with cirrhosis, 13 +/- 6 in 5 patients with hepatic fibrosis, and 22 +/- 6 in 10 patients with normal hepatic architecture aside from siderosis and were significantly lower than the levels found in 24 controls matched for age, sex, and season, p less than 0.05. The mean serum 25-OHD levels in the two groups with hemochromatosis and hepatic damage were significantly lower than the value in the group with normal hepatic architecture, p less than 0.05. Serum 25-OHD levels in individual patients were inversely related to the size of body iron stores as measured by exchangeable body iron, r = -0.64, or serum ferritin, r = -0.47, p less than 0.05. In 15 patients removal of excess body iron by venesection therapy produced a significant increase in the mean serum 25-OHD from 20 ng/ml to 30 ng/ml, p less than 0.05. In contrast, mean serum 1,25-[OH]2D levels were similar in iron-loaded and control subjects, indicating that the regulation of this metabolite was intact in patients with hemochromatosis. The results reveal that the low serum 25-OHD concentration in patients with hemochromatosis is directly related to the extent of iron loading and it is improved by venesection therapy. PMID: 3838288 [PubMed - indexed for MEDLINE] -------------------------------------------------------------------------------- health.enotes.com/genetic-disorders-encyclopedia/major-histoco... Major histocompatibility complex HLA disease associations Disease MHC allele Approximate relative risk Ankylosing spondylitis B27 77?90 Patients with ankylosing spondylitis may have extremely low levels of 25(OH)D. tinyurl.com/8tonv Celiac disease DR3 + DR7 5?10 A low 25-(OH)D vitamin concentration was a typical biochemical abnormality in our patients (64% of men and 71% of women). tinyurl.com/b7b9d Diabetes, Type 1 DR3 5 decreased zinc and 25OHD serum levels in poorly controlled insulin-dependent (Type I) diabetic patients tinyurl.com/73fsu Diabetes, Type 1 DR4 5?7 Diabetes, Type 1 DR3 + DR4 20?40 Graves disease DR3 5 [High prevalence of secondary hyperparathyroidism due to vitamin D insufficiency in Graves' disease] www.hubmed.org/search.cgi Hemochromatosis A3 6?20 Lupus DR3 1?3 There was a high prevalence of hypovitaminosis D (65.2%), tinyurl.com/8wfws Multiple sclerosis DR2 2?4 Vitamin D Defends Against MS www.hon.ch/News/HSN/516850.html Myasthenia gravis B8 2.5?4 Psoriasis vulgaris Cw6 8 These data suggest that exogenous active forms of vitamin D3 are effective for treatment of psoriasis and that the endogenous 1,25-dihydroxyvitamin D level also may be involved in the development of this skin disease. tinyurl.com/9c88e Rheumatoid arthritis DR4 3?6 We suggest that there is a disturbance in vitamin D metabolism in RA. tinyurl.com/df6zv --------------------------------------------------------------------------------------------- Prabhala, A., R. Garg, and P. Dandona, Severe myopathy associated with vitamin D deficiency in western New York. Arch Intern Med, 2000. 160(8): p. 1199-203. Five cases of severe myopathy associated with vitamin D deficiency are described. Each patient was confined to a wheelchair because of weakness and immobility. Two were elderly, 1 was a 37-year-old African American with type 1 diabetes mellitus, 1 was being treated for carcinoid syndrome, and 1 was severely malnourished due to poor oral intake. In each, weakness had previously been attributed to other causes, including old age, concomitant diabetic neuropathy, or general debility. Correct diagnosis was made initially by a high index of suspicion, following the demonstration of clinical proximal myopathy; confirmation was made by the demonstration of low 25-hydroxyvitamin D and elevated parathyroid hormone concentrations. Treatment with vitamin D caused a resolution of body aches and pains and a restoration of normal muscle strength in 4 to 6 weeks. Four patients became fully mobile and had normal 25-hydroxyvitamin D concentrations, and the fifth also became mobile. In the 4 fully recovered cases, parathyroid hormone levels on follow-up were lower but still elevated. This finding suggests a degree of autonomy of parathyroid secretion known to occur in cases of long-standing vitamin D deficiency. Myopathy, due to chronic vitamin D deficiency, probably contributes to immobility and ill health in a significant number of patients in the northern United States. An awareness of this condition may significantly improve mobility and quality of life in patient populations vulnerable to vitamin D deficiency. Who loves ya. 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