Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study was conducted to evaluate the anti-atherogenic potential of losartan and to assess the effects of hydrochlorothiazide and indapamide on losartan activity in rat. Cholesterol diet (0.5%) for 12 weeks led to significant hyperlipidemia, increased body weight and oxidative stress in erythrocyte. While, losartan, hydrochlorothiazide and indapamide treatment continued for next 12 weeks, losartan showed anti-atherogenic activity reflected by hypolipidemic effect and antioxidant effect in erythrocyte. This activity was abolished by addition of hydrochlorothiazide with losartan but remained unaltered by addition of indapamide with losartan. Atherosclerotic change and oxidative stress were not found in rat aorta, which may be due to short duration and low dose of cholesterol feeding. Hydrochlorothiazide treatment was associated with hypokalemia, which was not present in losartan or indapamide treatment. This study suggests that indapamide might be co-administered with losartan conserving the essential anti-atherogenic potential of losartan.
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PMID:Comparative study of hydrochlorothiazide and indapamide on the anti-atherogenic potential of losartan in cholesterol fed rat. 2128 May 53

BACKGROUND Drug induced lupus erythematosus is considered an autoimmune entity which is precipitated by medications. Hydrochlorothiazide has been recognized to cause subacute cutaneous lupus erythematosus, but very few cases of systemic drug induced lupus systemic erythematosus have been reported. CASE REPORT A 57-year-old Caucasian male with a past medical history of hypertension and hyperlipidemia presented with recurrent fevers, chest pain, and dyspnea. Initial evaluation revealed diffuse ST elevations, small pericardial effusion, anemia, and leukopenia. He was initially treated with nonsteroidal anti-inflammatory drugs and prednisone for pericarditis. Six months later, he reported fatigue, arthralgias, morning stiffness, weight loss, fevers, and night sweats. Laboratory tests revealed persistent anemia and leukopenia. Extensive workup, including bone marrow biopsy and infectious evaluations, was negative. Autoimmune workup, however, revealed positive antihistone and antichromatin antibodies despite negative antinuclear antibody. A diagnosis of drug induced lupus secondary to hydrochlorothiazide was made. The medication was stopped, and prednisone was initiated resulting in marked improvement in his symptoms and hematologic abnormalities. CONCLUSIONS This report is one of the few known cases of systemic lupus erythematosus most likely induced by hydrochlorothiazide. Based on our finding, hydrochlorothiazide should be considered a possible offending agent when a patient presents with symptoms suspicious of drug induced lupus.
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PMID:When Chest Pain Reveals More: A Case of Hydrochlorothiazide-Induced Systemic Lupus Erythematosus. 3061