Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acebutolol is a beta blocking agent that induces in C57Bl/6 mice a polyclonal activation of lymphocytes (PAL). In this study, its effect on cellular parameters of spontaneous PAL and lupus disease in NZB x NZW female mice is investigated. A significant reduction of PAL is found in 10-week-old mice after only five injections of 50 mg/kg/day of acebutolol. This effect is also observed in 7- and 9-month-old mice after 12 weeks of treatment. In these chronically treated mice, a significant decrease in incidence and levels of proteinuria as compared with untreated mice is found. No statistically significant increase in survival is observed. In conclusion, acebutolol down modulates the spontaneous PAL which characterizes the NZB x NZW mouse lupus disease and might prevent to some extent the development of nephritis.
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PMID:The beta-blocker acebutolol down modulates the spontaneous polyclonal activation of lymphocytes in NZB X NZW lupus mice. 178 64

Few such observations of beta-blocker-induced lupus have been published in the medical literature. In the index case, the usual criteria were present. Acebutolol withdrawal resulted in rapid clinical improvement. Antinuclear antibodies are still present after nine months follow up. Pathogenic hypotheses are discussed.
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PMID:[A new case of lupus induced by acebutolol]. 387 7

Acebutolol may induce the development of antinuclear antibodies and, exceptionally, of a lupus-like syndrome. The purpose of this study was to evaluate the prevalence of antinuclear antibodies in hypertensive diabetics under long-term treatment with acebutolol. Seventy-eight normal subjects, 75 diabetics under antidiabetic therapy only, and 75 hypertensive diabetics who received acebutolol in mean doses of 478 +/- 242 mg/day for at least one year were investigated. The 3 groups were comparable with regard to age and sex. Antinuclear antibodies were detected in 18.6% of diabetics under acebutolol, as against 3.8% and 1.3% respectively of subjects in the other groups (p less than 0.01). There was no correlation between the levels of antinuclear antibodies and the dosage or duration of acebutolol treatment. None of the sera tested contained antinative DNA antibodies, and none of the hypertensive diabetics exhibited signs of lupus-like syndrome.
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PMID:[Prevalence of antinuclear antibodies in hypertensive diabetics treated with acebutolol]. 624 46

Acebutolol induces transient polyclonal B cell activation in C57B1/6 mice but down-modulates the spontaneous polyclonal activation of NZBxNZW lupus mice. The immunomodulatory effects of this beta-blocker were studied in C57l/6 mice injected with LPS or immunized with sheep red blood cells. The effect of acebutolol on the polyclonal activation of lymphocytes induced by LPS was also investigated in heterozygous and nu/nu C57BL/6 mice. Finally, the direct effect of acebutolol on spleen cells was studied in vitro. Acebutolol treatment for 15 days (50mg/kg/day) inhibited the polyclonal activation of lymphocytes induced by LPS in C57BL/6 and in C57BI/6 nu/nu mice, but increased the humoral response to sheep red blood cells in C57Bl/6 mice. Moreover, spleen cells from C57Bl/6 mice treated for 15 days with acebutolol showed an increased number of CD5+ and CD4+ lymphocytes, as well as an increased reactivity to concanavalin A but not to LPS. In vitro, acebutolol at 10(-5)-10(-7) M induced an increased reactivity of spleen cells from naive mice to concanavalin A, whereas it did not affect the B cell responsiveness to LPS. These results indicate that acebutolol modulates both T-cells and non T-cells in the immune system.
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PMID:Evidence for a dual effect of acebutolol, a beta blocker, on the mouse humoral immune response. 857 44

Beta-blocking medications are rarely associated with drug-induced lupus erythematosus syndrome and have never been incriminated as a cause of subacute lupus erythematosus (SCLE). We present herein the first case of SCLE induced by acebutolol. A 57-year-old woman presented with a 1-month history of a cutaneous eruption of the photo-exposed areas. One month ago, the patient had started a treatment with oral acebutolol to cure a hypertension of 1-year evolution. Physical examination revealed erythematous scaly annular plaques, involving the face, arms and trunk. Immunologic serology findings revealed a positive titer of antinuclear antibodies up to 1/1,280 with positivity of antihistone and Ro/SSA antibodies. Acebutolol was stopped, and the lesions cleared completely 4 months later. Literature data, along with our case, suggest a link between acebutolol therapy and the onset of a lupus syndrome. Although this is the first report of acebutolol-induced SCLE, we should be aware of this occurrence, and avoidance of acebutolol is recommended in patients with stigmata of lupus erythematosus.
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PMID:Acebutolol-induced subacute cutaneous lupus erythematosus. 1601 21