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In studies conducted in seven countries, 392 persons with acute diarrhea were enrolled and randomly assigned to one of three regimens. In order to compare the effectiveness of various therapies for acute gastroenteritis, patients were treated for five days with either norfloxacin, 400 mg twice daily, norfloxacin, 400 mg three times a day, or trimethoprim/sulfamethoxazole, (160 mg/800 mg) twice daily. Clinical cure occurred in 89 percent (lower dose) and 91 percent (higher dose) of those treated with norfloxacin, compared with 78 percent of those receiving trimethoprim/sulfamethoxazole; cure rates in each treatment group were greater when the patient's stool contained fecal leukocytes. In 105 of 106 (99 percent) patients treated with either dose of norfloxacin and in 49 of 52 (94 percent) trimethoprim/sulfamethoxazole-treated subjects, the bacterial enteropathogen identified in the pretreatment stool was eradicated on the posttreatment specimen. Two percent (two patients) of those receiving the lower dose of norfloxacin, 3 percent (two patients) of those receiving trimethoprim/sulfamethoxazole, and 4 percent (three patients) of those receiving the higher dose of norfloxacin experienced minor and transient adverse hematologic or blood chemistry reactions. In addition, mild cutaneous reactions that were attributed to the study medications developed in two patients receiving the higher dose of norfloxacin and in three patients who received trimethoprim/sulfamethoxazole. These studies indicate that norfloxacin is safe and effective therapy for bacterial diarrhea.
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We conducted a retrospective nested 1:2 case-control study in patients aged ≥18 years who underwent alloHSCT between 2001 and 2011 in 4 major allogeneic transplant centers. Controls were matched with IPD cases on the basis of conditioning intensity and donor relationship (related or unrelated). Demographics and clinical characteristics of cases and controls were summarized. Univariate analysis of risk factors in matched case-control sets, and multivariate conditional logistic regression to control for confounding, were performed.
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N asteroides is an aerobic, gram-positive, partially acid-fast, branching rod. Cell-mediated immunity via both macrophage activation and direct cytotoxicity represents the main host defense. While clinical infection most commonly occurs in immunocompromised hosts, Nocardia can infect and exist as a saprophyte in normal hosts. Diligence on the part of the treating physician is necessary to confirm the diagnosis. A combination of trimethoprim and sulfamethoxazole is the mainstay of treatment. With an aggressive approach to diagnosis and therapy, the prognosis in patients with nocardiosis appears to be dependent on their underlying disease process.
In this retrospective cohort study, 186 consecutive adult patients who received TMP-SMX as prophylaxis for pneumocystis pneumonia from January 2014 to January 2015 were evaluated. Data on the patients' age, gender, baseline estimated glomerular filtration rate (eGFR), baseline serum potassium, maximum serum potassium, duration reaching the maximal serum potassium level, dosage, and concomitant use of angiotensin-converting enzyme inhibitors (ACEi)/angiotensin receptor blockers (ARB), β-blockers, non-steroidal anti-inflammatory drugs and potassium-sparing diuretics were retrospectively collected. Hyperkalemia was defined as a serum potassium level ≥5 mEq/L. Univariate and multivariate analyses were performed.
A 14 year old boy developed the syndrome of Bickerstaff's brainstem encephalitis during the course of bacteriologically proved typhoid fever. The clinical course and the results of various neurological investigations are detailed. This report adds a further manifestation to the published neuropsychiatric complications of typhoid fever.
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Hypersensitivity to trimethoprim-sulphamethoxazole (TMP-SMX) in patients with HIV infection may be a result of either immune dysregulation, a direct cytotoxicity of the SMX-hydroxylamine metabolite (SMX-HA) (rather than SMX per se), or glutathione deficiency. We evaluated the in vitro cytotoxicity of SMX and SMX-HA to peripheral blood mononuclear cells (PBMC) of HIV-infected subjects to determine if the degree of in vitro cytotoxicity is associated with hypersensitivity, whether glutathione inhibits cytotoxicity, and whether in vitro cytotoxicity is predictive for the development of hypersensitivity. Given that fever is often a prominent feature of hypersensitivity, we also assessed whether SMX or SMX-HA could induce the in vitro production of IL-1 beta, IL-6 or tumour necrosis factor-alpha (TNF-alpha) by PBMC. The cytotoxicities of SMX and SMX-HA to PBMC were assessed in 45 HIV-infected patients with prior TMP-SMX therapy, and in eight HIV- controls. Twelve HIV-infected subjects were studied prospectively before primary Pneumocystis carinii pneumonia (PCP) therapy or rechallenge with TMP-SMX in previously hypersensitive subjects. Cytokine production was measured in four hypersensitive and two non-hypersensitive HIV-infected subjects, and three HIV-uninfected controls. The cytotoxicity of SMX-HA to PBMC was significantly greater in the 22 HIV-infected patients with prior hypersensitivity than both the 23 HIV-infected patients without hypersensitivity and the control group. Cytotoxicity was significantly reduced by glutathione only in the hypersensitive group. SMX did not induce cytotoxicity in any group. In 12 subjects studied prospectively, SMX-HA cytotoxicity was also significantly greater in those with subsequent hypersensitivity. Exposure of PBMC to SMX-HA resulted in a modest increase in the production of IL-6, IL-1 beta and TNF-alpha, although no major difference was detected between subjects with or without hypersensitivity. These data suggest that SMX-HA and glutathione deficiency are involved in the pathogenesis of hypersensitivity to TMP-SMX in HIV-infected patients, and that in vitro cytotoxicity could be useful in the diagnosis of hypersensitivity and predicting its likelihood.