Fluconazole (800-1,000 mg i.v.) was administered to 14 consecutive patients with AIDS and cryptococcal meningitis. At 10 weeks the rate of clinical success was 54.5% (six of 11 patients responded to fluconazole); the Kaplan-Meier estimate of the response rate was 67.1%, and the overall mortality rate was 18.2% (two of 11 patients died). At the end of treatment, eight (72.7%) of 11 patients responded to fluconazole. The median time to the first negative cerebrospinal fluid (CSF) culture was 33.5 days (95% confidence interval, 18.3-67.3); the median time for patients with initial CSF cryptococcal antigen titers of > or = 1:1,024 was 66 days compared with 18 days for patients with initial CSF cryptococcal antigen titers of < 1:1,024 (P = .06). The median time to the first negative CSF culture for patients with an isolate for which the minimum inhibitory concentration (MIC) was 4 micrograms/mL was 56 days compared with 16 days for patients with an isolate for which the MIC was < 4 micrograms/mL (P = .11). The mean serum and CSF levels of fluconazole at steady state were 42.47 +/- 26.31 micrograms/mL and 36.63 +/- 21.08 micrograms/mL, respectively (ratio of CSF:serum, 0.86). No treatment was interrupted and no dose was tapered because of side effects. High-dose fluconazole might be an effective and well-tolerated therapeutic option for patients with AIDS and acute cryptococcal meningitis.

No abstract

To compare efficacy, tolerability, and cost of antibiotic prophylaxis with teicoplanin and cefazolin in clean prosthetic vascular surgery, a randomized, prospective, double-blind study was performed at the Vascular Surgery Unit of a tertiary-care university hospital. Two-hundred thirty-eight consecutive patients undergoing elective, clean, abdominal or lower-limb prosthetic vascular surgery were allocated to receive a single intravenous dose of teicoplanin (400 mg) or cefazolin (2 g) at the induction of anesthesia. Surgical-site infections occurred in 5.9% of teicoplanin recipients (4.2% wound infection, 1.7% graft infection) and 1.7% of cefazolin recipients (1.7% wound infection, 0% graft infection) (P=0.195). Other postoperative infections occurred in 10% of teicoplanin recipients (pneumonia 7%, urinary tract infection 3%) and 12% of cefazolin recipients (pneumonia 7%, urinary tract infection 2.5%, bloodstream infections 2.5%). Overall mortality rate was 3.4% in teicoplanin recipients (4 patients) and 2.5% in cefazolin recipients (3 patients). Infective deaths occurred in one patient for each group. The two prophylactic regimens were well tolerated. Cost savings of US $52,510 favoring cefazolin were related to the lower acquisition cost (US $1034 vs US $4740) and to the shorter duration of the hospital stay (1762 days vs 1928 days). Cefazolin can still be regarded as the drug of choice for prophylaxis in clean vascular surgery.

Objective To report a case of visceral leishmaniasis treated with liposomal amphotericin B (LAB) after probable failure with amphotericin B lipid complex (ABLC). Case Summary A 62-year-old white renal transplant recipient was admitted for pyrexia, hepato-splenomegaly, and pancytopenia. Leishmania amastigotes were detected from bone marrow aspirate and in circulating blood monocytes and neutrophils. The patient, who weighed 56 kg, received ABLC at a starting dose of 200 mg/d (3.6 mg/kg of body weight per day) for 13 days, achieving a total dose of 2,600 mg (46 mg/kg) without clinical improvement. The patient was switched to 100 mg/d (1.8 mg/kg) of LAB for 10 days, after which a dose of 250 mg (4.5 mg/kg) was repeated on days 17,24,31, and 38. Twenty-four hours after the first dose of LAB, the patient showed an excellent clinical response. On the following days, there was a progressive increase in hemoglobin concentration and leukocyte and platelet counts. Three months later, the patient was asymptomatic. Discussion Although treatment with ABLC appears to be effective for the treatment of Indian patients with visceral leishmaniasis, experience with immunocompromised patients is limited. This is the first case of a renal transplant recipient in which ABLC was used to treat visceral leishmaniasis without remarkable efficacy, but with infusion-related adverse effects perhaps due to the use of higher doses. Conclusions A randomized comparative trial is needed to compare LAB with ABLC in the treatment of visceral leishmaniasis in patients who have received kidney allografts.

Pituitary apoplexy is a rare and underdiagnosed clinical syndrome. It results from hemorrhagic infarction of the pituitary gland. In its classical form it is characterized by acute headache, ophthalmoplegia, visual loss and pituitary insufficiency. Meningeal irritation signs, clinically indistinguishable from infectious meningitis, are considered rare and have not been reported as presenting signs. We report a 53-yr-old man who was admitted to hospital following acute headache, fever, neck stiffness and paresis of the left oculomotor and abducent nerves. A lumbar puncture revealed an increased number of polymorphs but with a sterile cerebral spinal fluid. Magnetic resonance imaging (MRI) showed an intrasellar mass with central necrosis in an enlarged sella. Endocrinological evaluation demonstrated insufficient thyroid, adrenocortical, and gonadal function. Necrosis within a chromophobe adenoma was found upon surgical decompression of the sella. After surgery anterior panhypopituitarism did not recover, while ophthalmoplegia subsided. The patient is now in good health under appropriate hormonal replacement therapy.

No abstract

Hospital acquired blood stream infection by Ralstonia pickettii in 9 cancer patients related to the heparin solution contamination used to flush the central venous catheter.

TO THE EDITOR: Nonphenothiazine antipsychotic-induced hepatotoxicity is rare. 1,2 Risperidone is a nonphenothiazine benzisoxazole derivative that is structurally different from other antipsychotics associated with hepatotoxicity. Although hepatotoxicity is listed in the product information 3 as a potential adverse effect, there have been no reports of hepatotoxicity in patients receiving less than 25 days of therapy. To our knowledge, there are only two published letters 4,5 reporting possible risperidone-induced hepatotoxicity in adults. In the first report, 4 one patient had greater than 6 months' exposure, and a second patient had 6 weeks' exposure to risperidone 6 mg/d; both developed liver enzyme abnormalities consistent with hepatocellular toxicity. The second report 5 described a 54-year-old man with dementia who developed jaundice with an isolated increase in total bilirubin on day 25 after starting risperidone 1 mg bid. We describe suspected drug-induced hepatitis in a man who received only two doses of risperidone 0.5 mg po.Case Report. An 81-year-old white man was admitted to the hospital January 16, 1997, because of a history of paranoid delusions and a significant decline in his level of functioning. His medical history was significant for Parkinson's disease, dementia, depression, hypothyroidism, and peptic ulcer disease. He reported no history of alcoholism. Medications on admission included enteric-coated aspirin, diltiazem, sublingual nitroglycerin, levothyroxine, and doxepin. He had been taking stable dosages of all of these medications for at least 6 months; doxepin was not continued in the hospital. He was prescribed lorazepam prn on January 16, which he continued to receive throughout his hospital stay. Baseline liver function test results on admission were normal, with aspartate aminotransferase (AST) 20 units/L (normal <37), alanine aminotransferase (ALT) 13 units/L (<40), alkaline phosphatase 90 units/L (40-120), and total bilirubin 0.7 mg/dL (0.1-1.2). Risperidone was started on January 20. He received two doses of 0.5 mg po. On January 21, 1997, he was noted to be jaundiced and the risperidone was discontinued. Other than mild right upper quadrant pain, the patient reported no other symptoms. Similarly, physical examination revealed jaundice and some tenderness on palpation of the right upper quadrant. Liver function test results at that time revealed AST 434 units/L, ALT 101 units/L, total bilirubin 3.6 mg/dL, and alkaline phosphatase 244 units/L. Complete blood count, electrolytes, and serum creatinine were all normal. An ultrasound scan of the abdomen on January 22, 1997, revealed mild splenomegaly (14.1 cm) and small gallstones without any dilation of the biliary tree. Repeat liver function test results 2 weeks later (February 2, 1997) had returned to baseline (AST 19 units/L, ALT 5 units/L, alkaline phosphatase 114 units/L). Similarly, follow-up liver enzymes on April 17 and 24 were normal. Viral hepatitis serology (hepatitis A, B, and C) was negative. He continued to do well and re...