Morbidity and mortality patterns in HIV-1 seropositive/ seronegative women in Kampala and Harare during pregnancy and in the subsequent two years.

OBJECTIVE: To compare birth outcomes, hospital admissions and mortality amongst HIV-1 seropositive and HIV-1 seronegative pregnant women in Kampala, Uganda and Harare, Zimbabwe. DESIGN: In Kampala and Harare about 400 HIV-1 seropositive and 400 HIV-1 seronegative pregnant women were recruited at initial visit for antenatal care into a prospective study and followed for two years after delivery. The women were classified as HIV-1 seropositive at recruitment if initial and second ELISA tests were positive and confirmed by Western Blot assay. Data on demographic, reproductive, contraceptive and medical histories were obtained using a comprehensive questionnaire at entry, 32 and 36 weeks gestation, at delivery and at six, 12, and 24 months post delivery. In addition, a physical examination and various blood tests were performed at each antenatal and post natal visit. RESULTS: During the two years after delivery, HIV-1 seropositive women had higher hospital admission and death rates than HIV-1 seronegative women. HIV-1 seropositive mothers had a two-fold increase in risk of being admitted to hospital (Kampala: RR = 2.09; 95% CI = 0.95 to 4.59; Harare: RR = 1.98; 95% CI = 1.13 to 3.45). In the six weeks after delivery eight deaths occurred, six of which were among HIV-1 seropositive women and in the period from six weeks to two years after delivery, 53 deaths occurred, 51 of which were among HIV-1 seropositive women (Kampala: RR = 17.7; 95% CI = 4.3 to 73.2; Harare: RR = 10.0; 95% CI = 2.3 to 43.1). However, there was no difference in hospital admission rates between HIV-1 seropositive and seronegative women during pregnancy itself and there was only one death during that period (in a HIV-1 seronegative woman). There was no difference in the frequency of complications of delivery between HIV-1 seropositive and HIV-1 seronegative women and the outcome of births were also similar. CONCLUSIONS: A significant number of HIV-1 positive pregnant women presented at both Harare and Kampala although there was no difference in the number of hospital admissions or mortality between HIV-1 seropositive and HIV-1 seronegative women during pregnancy. Although there were no differences in complications during pregnancy or outcome at delivery, in the two years after delivery, HIV-1 seropositive women in both centres were at increased risk of being admitted to hospital and of dying.

Stevens - Johnson syndrome due to nevirapine.

A 25-year-old HIV-infected woman participating in a study of the effects of hormonal contraception on HIV disease progression was started on antiretroviral therapy-Combivir & Nevirapine (NVP) on May 27, 2004. NVP was 200mg daily initially for two weeks to be increased to 200mg bid thereafter. On day twelve, she presented with a mild skin rash on the trunk, purulent conjunctivitis, pharyngitis and fever. She was treated symptomatically and sent home. The following day she returned with a generalized erythematous eruption. She was admitted to JCRC (Joint Clinical and Research Centre) on June 14 and was diagnosed with Stevens - Johnson syndrome (SJS). Antiretroviral therapy was stopped. By July 05, 2004, she had improved and was discharged. After recovery she was restarted on Combivir and Efavirenz and is subsequently doing well on this regimen.

Placental membrane inflammation and risks of maternal-to-child transmission of HIV-1 in Uganda.

UNLABELLED: Prospective follow-up of 172 HIV-infected pregnant women and their infants was conducted at Mulago Hospital, Kampala, Uganda during 1990 to 1992. Information was collected on maternal immune status (CD4 counts or clinical AIDS), and concurrent infections with sexually transmitted diseases. Infants were observed on a follow-up basis to determine HIV infection, using polymerase chain reaction (PCR) under 15 months of age and enzyme immunoassay/Western blot for those older than 15 months. Placental membrane inflammation (chorioamnionitis and funisitis), and placental villous inflammation (villitis, intervillitis, and deciduitis) were diagnosed by histopathology. Mother-to-child HIV transmission rates were assessed, and adjusted odds ratios (OR) and 95% confidence intervals (95% CI) of transmission were estimated using women with no placental pathology or evidence of immune suppression as a reference group. RESULTS: The overall mother-to-child HIV transmission rate was 23.3%. Women with no placental membrane inflammation or immune suppression had a transmission rate of 11.3%; compared with 25.5% in women with placental inflammation and no immunosuppression (adjusted OR, 2.87; 95% CI, 1.04-7.90), and 37.0% in immunosuppressed women (OR, 3.07; 95% CI, 1.42-6.67). We estimate that 34% of HIV transmission could be prevented by treatment of placental membrane inflammation in nonimmunocompromised women. Transmission rates were 40.9% with genital ulcer disease (OR, 3.57; 95% CI, 1.28-9.66). Placental villous inflammation and artificial rupture of membranes did not increase transmission rates and cesarean section was associated with a nonsignificant reduction of risk (OR, 0.70; 95% CI 0.24-2.06). CONCLUSION: Placental membrane inflammation increases the rate of mother-to-child HIV transmission.