[Disseminated intravascular coagulation, perimyocarditis and bilateral pleural empyema in adult Still's disease]. / Disseminierte intravasale Gerinnung, Perimyokarditis und bilaterales Pleuraempyem bei adultem Still-Syndrom.

HISTORY: A 21-year-old man was admitted to the hospital because of high fever, arthralgias and myalgias. One week before he was treated with penicillin G orally because of cough and sore throat. PHYSICAL EXAMINATION: The critically ill patient presented with a red throat and cervical lymphadenopathy. Lung auscultation revealed reduced respiratory sounds at both base, heart auscultation revealed a pericardial friction rub. Dermatologic examinations were normal. INVESTIGATIONS: Laboratory findings were notable for anemia, thrombopenia and leukocytosis, disseminated intravascular coagulation and markedly elevated CRP (309 mg/l). Electrogram showed inferior and lateral ST segment depression. Echocardiography showed pericardial effusion. Chest CT scan revealed bilateral pleural effusion, a left-sided small infiltrate and enlarged mediastinal lymph nodes. Abdominal ultrasound confirmed hepatosplenomegaly and ascites. TREATMENT AND CLINICAL COURSE: A diagnosis of parapneumonic bilateral pleural empyema, perimyocarditis and disseminated intravascular coagulation was made. Despite institution of empiric antibiotic therapy, no clinical improvement was observed. After exclusion of infectious, autoimmune or malignant disease, clinical and laboratory data, especially marked hyperferritinemia, helped to establish the diagnosis of adult-onset Still's disease. Immunosuppressive treatment with prednisolone and azathioprin resulted in remission. CONCLUSION: Adult-onset Still's disease is a rare inflammatory disorder of unknown origin, which may affect multiple organs. The diagnosis is based on a diagnostic score, which includes a number of clinical and laboratory findings, published by Yamaguchi in 1992. Marked hyperferritinemia represents an additional diagnostic clue to the disease.

Trichosporon asahii infection of a dialysis PTFE arteriovenous graft.

Trichosporon species are the causative agents of superficial skin infections, such as white piedra. Immunocompromised hosts, particularly those with underlying hematological malignancy, are at risk of developing invasive infection, which usually progresses to disseminated life-threatening disease. Peritonitis caused by Trichosporon has been described in end-stage renal disease patients treated with continuous ambulatory peritoneal dialysis. Here, we report on a Trichosporon infection of an arteriovenous graft in a patient on chronic hemodialysis. The infection was successfully treated with fluconazole and total surgical resection of the graft.

Preferential COX-2 inhibitor, meloxicam, compromises renal perfusion in euvolemic and hypovolemic rats.

Nonsteroidal anti-inflammatory drugs can impair renal perfusion through inhibition of cyclooxygenase (COX)-mediated prostaglandin synthesis. We investigated the influence of the preferential COX-2 inhibitor, meloxicam (MELO), on renal hemodynamics in eu- and hypovolemic rats compared to the nonselective COX inhibitor indomethacin (INDO). The hypovolemic state was obtained in rats by three daily injections of furosemide (2 mg/kg i.p.) followed by a sodium-deficient diet for 7 days. In euvolemic rats (n = 6) neither INDO (5 mg/kg i.v.) nor MELO (1 or 2 mg/kg i.v.) influenced mean arterial blood pressure (MAP) or impaired renal (RBF) and cortical blood flow (CBF). Medullary blood flow (MBF) decreased after INDO (18%; p<0.05), and dose-dependently after MELO (1 mg, 10%; 2 mg, 18%; p<0.05). In hypovolemic rats (n = 6) INDO and MELO had no effect on MAP. RBF and CBF were reduced after INDO (11 or 20%; p<0. 05), but showed no changes after MELO. INDO induced a decrease in MBF (22%; p<0.05) which was less pronounced after MELO (12%; p <0.05). In conclusion the preferential COX-2 inhibitor MELO compromized renal perfusion in the outer medulla both in eu- and hypovolemic animals.