Pneumocystis carinii is a common cause of pneumonia in individuals who are immunosuppressed by HIV infection. Use of molecular biological techniques show that P. carinii is a fungus and that infection in man is not a zoonosis. Invasive tests such as sputum induction or bronchoscopy are used to make the diagnosis of P. carinii pneumonia. Life long primary prophylaxis is given to HIV positive individuals with CD4+ lymphocyte counts < 0.20 x 10(9)/L or a CD4: total lymphocyte ratio of < 1.5, constitutional symptoms, or with other AIDS defining diseases. Secondary prophylaxis is given after a first episode to prevent a recurrence. First choice for primary and secondary prophylaxis is oral co-trimoxazole 960 mg od or three times a week. In patients who are intolerant to co-trimoxazole, nebulised pentamidine or dapsone (with or without pyrimethamine) are second and third choices. In a patient with acute PCP disease, severity should be assessed using clinical, radiographic and blood gas criteria as those with moderate or severe disease will benefit from adjuvant glucocorticoids. Co-trimoxazole (120 mg/kg/day in divided doses for 21 days) is first choice therapy for PCP of all degrees of severity. In patients who fail to respond to co-trimoxazole or who are intolerant to it, second line treatment is iv pentamidine in those with severe disease and oral dapsone with trimethoprim, oral clindamycin with primaquine or iv pentamidine in those with mild or moderately severe disease.
Introduction and objectives Pre-treatment Vitamin D deficiency (VDD) is well described amongst adult TB patients in Malawi and has been associated with impaired mycobacterial immunity. Anti-TB drugs and antiretroviral therapy (ART) for HIV may induce hepatic Vitamin D metabolism, further reducing the serum concentration of active metabolites including 25-OH D3. This study identified risk factors for baseline VDD, assessed the effect of therapy on 25-OH D3 concentrations, and evaluated whether VDD deficiency has prognostic implications for treatment response. Methods Adults with pulmonary TB were treated with standard 6 month therapy. Serum 25-OH D3 concentrations were measured at baseline, 8 weeks and end of treatment. Serial sputum samples were used to model the rate of bacterial elimination for each patient. Patients were followed until 1 year post-treatment and final outcomes were defined as favourable (stable cure) or unfavourable (failure/relapse). Linear and logistic regression analyses were used to identify risk factors for VDD and assess relationships between VDD and treatment response. Results 133 patients were studied. 75 (56%) were HIV-infected and 24 (18%) were on ART. 118 (89%) had favourable and 15 (11%) had unfavourable outcomes. The median baseline 25-OH D3 concentration was 57.3 nmol/l. 47 (28%) patients had concentrations <50 nmol/l, representing VDD. On multivariate analysis, neither HIV status nor ART influenced baseline 25-OH D3 levels, but lower concentrations were reported in patients who were recruited during the cold months of July/August (p = 0.001), suffered food insecurity (p = 0.035) or had a lower baseline Body Mass Index (p = 0.047). Without specific supplementation, 25-OH D3 levels improved during TB therapy (see figure). There were no associations between 25-OH D3 levels at
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