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Abstract Objective: In 150 hypercholesterolemic patients, unable to tolerate â‰¥1 statin because of myositis-myalgia, selected by low (<32â€‰ng/ml) serum 25 (OH) vitamin D, we prospectively assessed whether vitamin D supplementation with resolution of vitamin D deficiency would result in statin tolerance, free of myositis-myalgia. Research design and methods: We studied 74 men, 76 women, median age 60, 131 white, 17 black and 2 other. On no statins, 50,000 units of vitamin D was given twice a week for 3 weeks, and then continued once a week. After 3 weeks on vitamin D, statins were restarted. Patients were re-assessed on statins and vitamin D every 3 to 4 months, with serial measures of serum 25 (OH) vitamin D, creatine phosphokinase (CPK), LDL cholesterol (LDLC) and assessment of myositis-myalgia. Main outcome measures: Percentage of patients myalgia-free on vitamin D plus reinstituted statins, serum 25 (OH) vitamin D, CPK, and LDLC on reinstituted statins and concurrent vitamin D supplementation. Results: On vitamin D supplementation plus re-instituted statins for a median of 8.1 months, 131 of the 150 patients (87%) were free of myositis-myalgia and tolerated the statins well. Serum 25 (OH) vitamin D increased from median 21 to 40â€‰ng/ml (pâ€‰<â€‰0.001), and normalized (â‰¥32â€‰ng/ml) in 117 (78%) of 150 previously vitamin D deficient, statin-intolerant patients. Median LDLC decreased from 146â€‰mg/dl to 95â€‰mg/dl, pâ€‰<â€‰0.001. Conclusion: Symptomatic myositis-myalgia in hypercholesterolemic statin-treated patients with concurrent serum 25 (OH) vitamin D deficiency may reflect a reversible interaction between vitamin D deficiency and statins on skeletal muscle causing myalgia.
Cholesterol Center, Jewish Hospital of Cincinnati , Cincinnati, OH , USA.
This article was published in the following journal.
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A nutritional condition produced by a deficiency of VITAMIN E in the diet, characterized by posterior column and spinocerebellar tract abnormalities, areflexia, ophthalmoplegia, and disturbances of gait, proprioception, and vibration. In premature infants vitamin E deficiency is associated with hemolytic anemia, thrombocytosis, edema, intraventricular hemorrhage, and increasing risk of retrolental fibroplasia and bronchopulmonary dysplasia. An apparent inborn error of vitamin E metabolism, named familial isolated vitamin E deficiency, has recently been identified. (Cecil Textbook of Medicine, 19th ed, p1181)
A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)
A nutritional condition produced by a deficiency of VITAMIN B 12 in the diet, characterized by megaloblastic anemia. Since vitamin B 12 is not present in plants, humans have obtained their supply from animal products, from multivitamin supplements in the form of pills, and as additives to food preparations. A wide variety of neuropsychiatric abnormalities is also seen in vitamin B 12 deficiency and appears to be due to an undefined defect involving myelin synthesis. (From Cecil Textbook of Medicine, 19th ed, p848)
A nutritional condition produced by a deficiency of VITAMIN A in the diet, characterized by NIGHT BLINDNESS and other ocular manifestations such as dryness of the conjunctiva and later of the cornea (XEROPHTHALMIA). Vitamin A deficiency is a very common problem worldwide, particularly in developing countries as a consequence of famine or shortages of vitamin A-rich foods. In the United States it is found among the urban poor, the elderly, alcoholics, and patients with malabsorption. (From Cecil Textbook of Medicine, 19th ed, p1179)
A nutritional condition produced by a deficiency of VITAMIN B 6 in the diet, characterized by dermatitis, glossitis, cheilosis, and stomatitis. Marked deficiency causes irritability, weakness, depression, dizziness, peripheral neuropathy, and seizures. In infants and children typical manifestations are diarrhea, anemia, and seizures. Deficiency can be caused by certain medications, such as isoniazid.
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