[Impediment of cellular immune response under treatment with ticlopidine in a patient with Staphylococcus aureus endocarditis].

A 52-year-old male with coronary artery disease was admitted with acute aortic valve endocarditis and a temperature up to 39.5 degrees C caused by Staphylococcus aureus. The patient was treated with ticlopidine (Tiklyd) after percutaneous transluminal coronary angioplasties to reduce restenosis by inhibiting thrombocyte aggregation. Upon admission c-reactive protein (CRP) was 389 mg/l. Interleukin-6 (IL-6) and Interleukin-2-receptor (IL-2-rec) were distinctly increased. Monoclonal antimyocardial antibodies were found. Leukocyte count never exceeded 9.8 G/l; however, transesophageal echocardiography validated a soft vegetation of the aortic valve. Antibiotic therapy was initiated with imipenem, gentamicin and vancomycin; clarithromycin was added after five days. Temperature normalized after 24 days. The c-reactive protein decreased from 389 mg/l to 6 mg/l, and the elevated cytokine levels decreased accordingly. Agranulocytosis or pancytopenia by ticlopidine through a toxic mechanism have been described, which are normally reversible within three weeks; there has not yet been a description of a missing leukocyte response in endocarditis as in this case report. This is a special situation with lack of or impeded immunological response, which limits the use of ticlopidine, especially since a therapeutic alternative with clopidogrel is available.