Vitamin replacement therapy

Makoff R. Vitamin replacement therapy in renal failure patients. Miner Electrolyte Metab 1999 25 349-351. 

KOMULAINEN M, KROGER H, TUPPURAINEN M T, HEIKKINEN A M, ALHAVA E, HONKANEN R, lURVELIN I and SAARiKOSKi s (1999) Prevention of femoral and lumbar bone loss with hormone replacement therapy and vitamin D3 in early postmenopausal women a population-based 5-year randomized trial. J Clin Endocrinol Metab 84, 546-52. 

Patients with abetalipoproteinaemia, a rare inborn disorder of lipoprotein metabolism, are totally deficient in vitamin E fiom birth and, if untreated, invariably develop a characteristic pigmentary retinopathy similar to that seen in retinitis pigmentosa and peroxisomal disorders. The same retinopathy has been observed in other patients with severe and chronic vitamin E deficiency. A essive vitamin E replacement therapy in all these patients has been shown either to prevent, to halt the progression of, or in some cases, to improve the characteristic visual abnormalities (Muller and Lloyd, 1982). 

Hormone-replacement therapy is also indicated for the prevention of osteoporosis but is not recommended for longterm use. Alternatives such as bisphosphonates or raloxifene should be considered as first-line therapy for the prevention of osteoporosis, in addition to appropriate doses of calcium and vitamin D. 

Osteoporosis Oral calcium supplementation (1000-5000 mg/day) Oral vitamin D Calcifediol (1000 lU/day) Calcitriol (0.5 mcg/day) Hormone-replacement therapy Calcitonin or oral bisphosphonates If daily intake less than 1000 mg elemental calcium Documented deficiency If kidney functioning If kidney not functioning Post-menopausal women without contraindications Documented loss in bone mineral density greater than 3% Data lacking for bisphosphonates in patients with Rl... 

The clinical problems that arise in the menopause are hot flushes, sweating, depression, decreased libido, increased risk of cardiovascular disease and osteoporosis. The latter results in increased incidence of hip, radial and vertebral fractures. Oestrogen is one factor controlling synthesis of active vitamin D and osteoporosis is in part due to a deficiency of vitamin D. Not surprisingly, to reduce these problems, administration of oestrogen is recommended (known as hormone replacement therapy or HRT). HRT reduces some of the risk factors for coronary artery disease since it reduces blood pressure and decreases the blood level of LDL-cholesterol and increases that of HDL-cholesterol. However, there is considerable debate about whether HRT increases the risk of breast or endometrial cancer. 

Oral As a dietary supplement when calcium intake may be inadequate. Conditions that may be associated with calcium deficiency include the following Vitamin D deficiency, sprue, pregnancy and lactation, achlorhydria, chronic diarrhea, hypoparathyroidism, steatorrhea, menopause, renal failure, pancreatitis, hyperphosphatemia, and alkalosis. Some diuretics and anticonvulsants may precipitate hypocalcemia, which may validate calcium replacement therapy. Calcium salt therapy should not preclude the use of other corrective measures intended to treat the underlying cause of calcium depletion. 

Sharabi A, Cohen E, Sulkes J, Garty M. Replacement therapy for vitamin B-12 deficiency comparison between the sublingual and oral route. Br J Clin Pharmacol 2003 56(6) 635-8. 

Other neurological syndromes (e.g., cerebral cortical atrophy, myopathy, cerebellar degeneration) are also associated with alcoholism, but their pathogenesis is less certain than that of nutritional deficiency disorders. Abstinence from alcohol plus vitamin replacement and physical therapy comprise the standard treatment approach for these conditions. 

Renal rickets (renal osteodystrophy) This disorder results from chronic renal failure and, thus, the decreased ability to form the active form of the vitamin. 1,25-diOH cholecalciferol (calcitriol) administration is effective replacement therapy. 

The reference values for human adults are in the range of 6 to 12 mM. Values exceeding 16 xM characterize hyperhomocysteinemia. Hyperhomocysteinemia can be fiuther subclassified as mild, intermediate, and severe [3,92]. Elevated homocysteine levels are found in 1-2% in the general population. Higher prevalence is associated with vascular diseases [3,93]. It increases with age. The vitamin deficiency, frequent in the elderly, contributes for the elevation of homocysteine levels [3,94]. Homocysteine levels increase in post-menopausal women, and are attenuated by hormone replacement therapy [3,94]. Hyperhomocysteinemia may result from [2,3,88,93] ... 

Formation of a blood clot results in a precipitous increase in the viscosity of the blood sample. The event of dotting is initiated by adding calcium ions, to replace those chelated by the citrate, and tissue factor. Tissue factor is a lipid-rich protein that activates the blood clotting cascade. The formahon of the viscous blood clot within seconds indicates normal vitamin K status. Delayed formation of the clot indicates a deficiency. Restoration of a normal clotting time with vitamin K therapy is required to prove that the subject had been deficient, that is, that the defect in the clotting assay was the result of K deficiency, rather than some other pnO blem. 

Vitamin D and its metabolites play an important role in the maintenance of extracellular calcium concentrations and in normal skeletal structure and mineralization. Vitamin D is necessary for the optimal absorption of calcium and phosphorus. On a worldwide basis, the most common cause of hypocalcemia is nutritional vitamin D deficiency. In malnourished populations, manifestations include rickets and osteomalacia. Nutritional vitamin D deficiency is uncommon in Western societies because of the fortification of miUc with ergocalciferol. " The most common cause of vitamin D deficiency in Western societies is gastrointestinal disease. Gastric surgery, chronic pancreatitis, small-bowel disease, intestinal resection, and bypass surgery are associated with decreased concentrations of vitamin D and its metabolites. Vitamin D replacement therapy may need to be administered by the intravenous route if poor oral bioavailability is noted. Decreased production of 1,25-dihydroxyvitamin D3 may occur as a result of a hereditary defect resulting in vitamin D-dependent rickets. It also can occur secondary to chronic renal insufficiency if there is insufficient production of the 1 -a -hydroxylase enzyme for the... 

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