Antinuclear factor in rapid and slow acetylator patients treated with isoniazid.

Evans, David A.; Bullen, Margaret; Houston, J. Brian; Hopkins, C. A.; Vetters, J. M.

doi:10.1136/jmg.9.1.53

Cited by 36 publications

(5 citation statements)

References 7 publications

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“…Interestingly, the risk of developing DILE is about the same in patients with the same serum concentration of procainamide, regardless of the acetylator phenotype [64]. Unlike the findings in procainamide and hydralazine, isoniazid-implicated DILE seems to be less related to acetylator phenotype though isoniazid is also metabolized by acetylation [65,66]. In addition, associations between DILE occurrence and certain human leukocyte antigen (HLA), like HLA-DR2, HLA-DR3, class III C4A and C4B null complement alleles, have been suggested by some studies, but these findings were not always consistent [67][68][69].…”

Section: Genetic Predispositionmentioning

confidence: 90%

Drug-induced lupus erythematosus: an update on drugs and mechanisms

Sawalha

2018

Current Opinion in Rheumatology

116

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Section: Genetic Predispositionmentioning

confidence: 90%

Drug-induced lupus erythematosus: an update on drugs and mechanisms

Sawalha

2018

Current Opinion in Rheumatology

116

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“…The method of Price-Evans et a1 was used (6). Fasting patients ingested 160 mg of sulfamethazine/kg of metabolically active mass (i.e., body weight by 0.7) as powder with water.…”

Section: Sulfamethazine Typingmentioning

confidence: 99%

Acetylator phenotype in systemic lupus erythematosus

Foad

Litwin

Zimmer

et al. 1977

Arthritis & Rheumatism

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The acetylation rate of sulfamethazine was studied in 25 patients with systemic lupus erythematosus (SLE). Seventeen of 25 SLE patients, 6896, were slow acetylators compared to the reported incidence of 52% in the general population. There was no correlation between the acetylator phenotype in SLE patients and the various clinical manifestations or the activity of the disease. Lupus patients who were slow acetylators had a lower lymphocyte response to phytomitogens compared to rapid acetylators.Following the administration of certain drugs, a number of patients develop a disease which presents many of the clinical and laboratory characteristics of systemic lupus erythematosus (SLE). The drugs most clearly associated with this lupus-like syndrome are hydralazine, procainamide, anticonvulsants, and isoniazid (1 ). Prolonged therapy with hydralazine, a frequently used antihypertensive agent, induces antinuclear factors (ANF) in 54% of patients (2). Approximately 12% of

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“…Segovia et al (2) and Evans et al (9) did not find a significant difference between slow and rapid acetylators in the incidence of positive ANF during long-term treatment with INH. Recent studies suggest that procaine amide may induce a lupoid syndrome not only in slow (20) but also in rapid acetylators (6,17).…”

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confidence: 89%

Acetylator Phenotype in Patients with Hydralazine‐induced Lupoid Syndrome

Boman

Hassler

et al. 1976

Journal of Internal Medicine

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The acetylator phenotype has been determined (isoniazid half-life) in 31 patients, 25 of them women, who had exhibited a lupus erythematosus-like syndrome during treatment with hydralmine. Twenty-nine patients were slow acetylators, one was rapid (probably spontaneous SLE) and one uncertain. Only two patients had been given more than 200 mg of hydralazine daily. The mean duration of therapy was 32 months at the onset of symptoms. These were not serious but rather long-standing. Our study confirms that patients who risk developing hydralazine lupus are slow acetylators, especially females, treated with more than 100 mg daily. Rapid acetylators seem to develop this side-effect rarely, if at all.Hydralazine (Apresolin@) was the first drug reported to induce a syndrome similar to systemic lupus erythematosus (SLE) (20). An important pathway for the metabolism of hydralazine is acetylation, which is under polymorphic genetic control (12,26). The enzyme involved also acetylates other drugs, such as isoniazid (INH) (II), certain sulfonamides (12, 29) and procaine amide (13,19,27). Slow acetylators are more prone to develop side-effects on conventional doses of INH (7), phenelzine (lo), sulphapyridine (5, 29) and dapsone (8) . Perry (25) found that nearly all patients who developed a lupoid syndrome during treatment with hydralazine were slow acetylators and that positive antinuclear factor (ANF) preceded the clinical symptoms. By contrast, Alarc6n-

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Antinuclear factor in rapid and slow acetylator patients treated with isoniazid.

Cited by 36 publications

References 7 publications

Drug-induced lupus erythematosus: an update on drugs and mechanisms

Drug-induced lupus erythematosus: an update on drugs and mechanisms

Acetylator phenotype in systemic lupus erythematosus

Acetylator Phenotype in Patients with Hydralazine‐induced Lupoid Syndrome

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