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DI-051 Rifampicin-induced systemic lupus erythematosus
  1. S Khettar1,
  2. A Clerc2,
  3. JC Lega2,
  4. S Durupt3
  1. 1Pharmacie Centrale Des Hospices Civils de Lyon, Pharmacie, Saint Genis Laval, France
  2. 2Centre Hopistalier de Lyon Sud, Internal Medicine, Saint Genis Laval, France
  3. 3Centre Hopistalier de Lyon Sud, Internal Medicine and Cystic Fibrosis Department, Saint Genis Laval, France

Abstract

Background Rifampicin is usually a well tolerated antimicrobial agent, but it can, rarely, cause systemic lupus erythematosus (SLE). We report a case of SLE in a man treated by rifampicin for a hip prosthesis infection.

Drug-induced SLE (DISLE) represents 10% of all SLE. DISLE has been reported with over 40 drugs. It is important to diagnose DISLE because stopping the drug allows the disease to be controlled.

Purpose To describe this unusual adverse effect caused by rifampicin and to highlight what had to be done to diagnose it.

Materials and methods A seventy year-old man was hospitalised in March 2005 for oligo-arthritis of the interphalangeal joints, with pleuro-pericarditis. For four months he was treated for an E. faecalis infection of a hip prosthesis with amoxicillin and rifampicin (1200 mg every 12 h).

Rifampicin is usually a well-tolerated antibiotic. Drug-drug interactions, nausea and hypertransaminasaemia are the main problem in clinical practice. Only few cases of rifampicin-induced SLE have been reported in the literature. HLA-DR4 allele and slow acetylator phenotype are two groups of genetic factors associated with DISLE. Antihistone antibodies are positive in 75 to 95% of those with DISLE, while they are found only in 20% of idiopathic SLE. Mechanisms of DISLE are complex and differ from one drug to another.

Results Laboratory tests showed: haemoglobin 10.2 g/dl, white cell count 4.41giga/l, platelet count 233 giga/l, creatinine 300 mmol/l. Antinuclear antibodies (ANA) were positive at a titre of 1/1280 with homogeneous pattern; double-stranded DNA antibodies were 177 IU (N < 75 IU). Antihistone antibodies were 52 kU/l (N < 20 kU/l). Pleural and pericardial fluid analysis revealed no microbial agent or neoplastic cells. Rifampicin-induced SLE was diagnosed.

Rifampicin was stopped. Corticosteroids were used for the systemic signs for 6 months. In October 2007 the patient was free of symptom.

Conclusions There is no predictor for the occurrence of DISLE. It is important to know that rifampicin can cause SLE. When DISLE is suspected, it is necessary to measure ANA and antihistone antibodies to confirm the diagnosis and to stop the treatment promptly.

No conflict of interest.

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