title: [Impediment of cellular immune response under treatment with ticlopidine in a patient with Staphylococcus aureus endocarditis].
abstract: 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.
authors.affiliation: Abteilung für Innere Medizin-Kardiologie Philipps-Universität Marburg.
authors.forename: P
authors.initials: P
authors.lastname: Alter
authors.forename: J R
authors.initials: JR
authors.lastname: Schaefer
authors.forename: B
authors.initials: B
authors.lastname: Maisch
mesh_terms: D000380:Agranulocytosis / Q000139:chemically induced; D015906:Angioplasty, Balloon, Coronary; D000900:Anti-Bacterial Agents / Q000008:administration & dosage / Q000627:therapeutic use; D017291:Clarithromycin / Q000008:administration & dosage / Q000627:therapeutic use; D003327:Coronary Disease / Q000517:prevention & control / Q000628:therapy; D004359:Drug Therapy, Combination / Q000008:administration & dosage / Q000627:therapeutic use; D015150:Echocardiography, Doppler; D004697:Endocarditis, Bacterial / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology; D005343:Fibrinolytic Agents / Q000009:adverse effects*; D005839:Gentamicins / Q000008:administration & dosage / Q000627:therapeutic use; D006801:Humans; D015378:Imipenem / Q000008:administration & dosage / Q000627:therapeutic use; D007111:Immunity, Cellular / Q000187:drug effects* / Q000276:immunology; D007958:Leukocyte Count; D007962:Leukocytes / Q000187:drug effects / Q000276:immunology*; D007970:Leukopenia / Q000139:chemically induced; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects*; D013203:Staphylococcal Infections / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology; D013845:Thienamycins / Q000008:administration & dosage / Q000627:therapeutic use; D013988:Ticlopidine / Q000009:adverse effects*; D013997:Time Factors; D014640:Vancomycin / Q000008:administration & dosage / Q000627:therapeutic use
chemical_list: D000900:Anti-Bacterial Agents; D005343:Fibrinolytic Agents; D005839:Gentamicins; D010975:Platelet Aggregation Inhibitors; D013845:Thienamycins; D014640:Vancomycin; D015378:Imipenem; D017291:Clarithromycin; D013988:Ticlopidine