Article 25 ( OH ) Vitamin D Deficiency in Hemodialysis ( HD ) Patients and a Matching Sample of the General Population : Experience of One Center a Pilot Study
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25 (OH) vitamin D plays an important role in many places through the body. Its deficien- cy can cause rickets or osteomalacia. This is particularly im- portant in hemodialysis (HD) patients who are at icreased risk due to decreased sunlight exposure and deterioration of their mineral homeostasis.To determine the prevalence of 25 (OH) vitamin D deficiency in HD patients at Rafic Hariri University Hospital (RHUH), compared to a sample of the general population matched for gender and age, and to evaluate the effectiveness of 25 (OH) vitamin D supplementation in HD deficient group.This is a cross sectional study conducted since December 2012, comparing the prevalence of 25 (OH) vitamin D deficiency in HD patients in the dialysis center at RHUH, with patients from the general population who sought medical attention at RHUH for purposes other than HD, matched for age and gender. 25 (OH) vitamin D levels were measured with radio- immunoassay method (LOINC) at CIC European Lab, Bar- celona, Spain. A pilot study was conducted with the 34 HD patients who turned out to be deficient or insufficient in 25 (OH) vitamin D. We supplemented them with cholecalciferol over 6 months. We then assessed their vitamin D levels, and biochemistry parameters.The prevalence of 25 (OH) vitamin D deficiency in the sample of HD patients at baseline was 32% while that of insufficiency was 36%. The prevalence of 25 (OH) vitamin D deficiency in the sample of general population was 67%. No correlation was found be- tween 25 (OH) vitamin D levels and the studied parameters. In the pilot study, after six months of cholecalciferol supple- mentation, there was a significant improvement in 25 (OH) vitamin D levels in the deficient and insufficient groups.The sample studied in the general population showed high prevalence of 25 (OH) vitamin D deficiency (67%). The sample studied in HD patients showed a preva- lence of 25 (OH) vitamin D deficiency of 32% and insuffi- ciency of 36%. The pilot study showed that 25 (OH) vitamin D supplementation in the form of cholecalciferol is beneficial in HD patients.Keywords:
Osteomalacia
Hypovitaminosis
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Osteomalacia
Osteoid
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Osteomalacia
Bone disease
Metabolic bone disease
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Rickets and osteomalacia are two distinct clinical disorders of impaired bone mineralization. Rickets is arising throughout the growing skeleton, in infants and children, whilst osteomalacia is occulting after the growth plates have fused in adults. Rickets and osteomalacia are reported with increasing frequency in Saudi Arabia, with vitamin D deficiency, being the most common etiological cause. The major clinical features of rickets and osteomalacia include bone pain and tenderness, and fatigue, muscle weakness, skeletal deformities, and tetany, due to hypocalcemia, in infants. Hypocalcemia, hypophosphataemia, and raised alkaline phosphatase activity are often typically found together with radiological changes such as widening of growth plates in rickets and pseudofractures in osteomalacia. Serum concentration of 25-hydroxyvitamin D are usually low, however, it could be normal in chronic renal failure, or hereditary forms of rickets. Treatment with vitamin D, or its active metabolites and mineral supplementation will generally effective. Measures for prevention of rickets and osteomalacia at a nationwide level should be established.
Osteomalacia
Tetany
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Etiology
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Rickets and osteomalacia are diseases characterized by impaired mineralization of bone matrix. The same causes can result in rickets and osteomalacia. Of these, rickets develops before the closure of growth plates and presents bone deformities and growth retardation. Diagnostic criteria for rickets and osteomalacia have been published in Japan.
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Further causes of rickets or osteomalacia need to be added to the list previously published by the author. These include phosphate deficiency osteomalacia from prolonged consumption of aluminum hydroxide, rickets and osteomalacia from prolonged therapy by antiepileptic drugs, rickets associated with the severe form of osteopetrosis, further rare causes of the Fanconi syndrome, congenital rickets occurring when the mother has osteomalacia from dietary causes or has celiac disease and temporary neonatal rickets probably due to enzymic immaturity. The importance is stressed of defining as closely as possible the type of rickets or osteomalacia one is dealing with, especially when considering therapy and detailed pathogenesis.
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Rickets/osteomalacia is a disorder causing mineralization defect and bone and skeletal fragility, although production of bone matrix proteins and their architecture is not impaired. The disease is called rickets and osteomalacia in children during skeletal development and in adults, respectively. Pathophysiology in rickets/osteomalacia is defect in vitamin D actions and/or hypophosphatemia. Vitamin D deficiency, inability of activation of vitamin D in vivo or functional derangement in vitamin D receptor is involved in impaired actions of vitamin D. Common causes of hypophosphatemia are excessive actions of fibroblast growth factor (FGF) 23 and renal tubular dysfunction. Among them FGF23 could be a principal regulator for phosphate metabolism, and many investigators are engaged in exploration of physiological and pathophysiological roles of FGF23 in human.
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This chapter describes definition, etiology, pathophysiology, diagnosis, treatment and prevention of nutritional rickets and osteomalacia. Rickets and osteomalacia (from Greek osteon and malakia, bone softness) are diseases characterized by hypomineralization of bone matrix. Rickets occurs only in children (before epiphyseal closure) and additionally leads to abnormal growth plate development, stunting, and bone deformities. The causes of osteomalacia and rickets are similar and can be classified according to underlying mechanisms: Vitamin D deficiency or resistance; calcium deficiency independent of vitamin D; hypophosphatemic disorders; and mineralization inhibitors. Patients with rickets and osteomalacia related to vitamin D deficiency typically have very low serum 250-hydroxyvitamin D (25OHD) concentrations, that is below 15 to 30 nmol/L. Vitamin D deficiency rickets responds to small doses of vitamin D. Nutritional osteomalacia may be treated with remarkably low doses of calcium and vitamin D.
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Rickets is an important problem even in countries with adequate sun exposure. The causes of rickets/osteomalacia are varied and include nutritional deficiency, especially poor dietary intake of vitamin D and calcium. Non-nutritional causes include hypophosphatemic rickets primarily due to renal phosphate losses and rickets due to renal tubular acidosis. In addition, some varieties are due to inherited defects in vitamin D metabolism and are called vitamin D dependent rickets. This chapter highlights rickets/osteomalacia related to vitamin D deficiency or to inherited defects in vitamin D metabolism. Hypophosphatemic rickets and rickets due to renal tubular acidosis are discussed in other sections of the journal.
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Rickets in the growing child or adolescent and osteomalacia in the adult develop in a variety of clinical situations and have in common an absence or delay in the mineralization of growth cartilage and in newly formed bone collagen. Classically, deficiency of vitamin D, which is essential for the absorption of dietary calcium, has been the major cause. However, rickets is also seen as a result of hereditary defects in critical vitamin D signaling molecules. Disturbances of phosphate metabolism can also lead to signs of rickets and osteomalacia, notably X-linked hypophosphatemic rickets, and oncogenic osteomalacia. Extrarenal synthesis of 1,25-dihydroxyvitamin D, such as that associated with granulomatous disease, can also lead to disturbances in calcium metabolism, with associated skeletal and nonskeletal changes.
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Bone remodeling
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Rickets and osteomalacia is a metabolic bone disease due to a mineralization defect as principal pathophysiology. Since a variety of disorders cause insufficient mineralization of bone, treatment specific to each disorder should be applied to a patient with rickets/osteomalacia. Clinical consensus for medical treatment for rickets/osteomalacia is overviewed in this manuscript. Vitamin D as an anti-rachitic factor and its metabolites play a pivotal role for treatment of patients with rickets/osteomaracia.
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Metabolic bone disease
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