HIV antibodies in a remote rural area in Rwanda, Central Africa: an analysis of potential risk factors for HIV seropositivity.

Detection of HIV antibodies by means of an immunoenzymatic assay, an indirect immunofluorescence technique and Western blot was attempted on 375 serum samples collected in the Murunda area, a remote rural area situated in Rwanda, central Africa. Two out of 147 (1.4%) adults from a strict rural area, five out of 59 (8.5%) adults from an adjacent market place, and 49 out of 169 (30%) STD clinic attenders from the same area were HIV seropositive. In the first two groups, HIV seropositivity was associated with a history of sexually transmitted disease (STD) in the previous 2 years (P less than 0.001) and with a history of travel to a Rwandese urban centre in the previous 5 years (P less than 0.05). This study suggests that HIV seroprevalence is low in rural central Africa compared with urban centres. Risk factors for HIV seropositivity are similar in rural and urban-based adults in Rwanda, i.e. heterosexual promiscuity and STDs. Many HIV seropositive rural subjects from this study are likely to have acquired HIV infection through sexual contacts in Rwandese cities.

PIP: 375 serum samples collected from youth and adults in Murunda, a remote rural area in Rwanda, were analyzed for antibodies to human immunodeficiency virus (HIV). Study subjects were drawn from 3 selected populations: those from the village of Rulimba, a strictly rural area; adults from Gisiza, an adjacent rural market place that is connected by roads to 2 other cities; and patients from the same district who attended the Murunda health center for treatment of a sexually transmitted disease during the study period. The prevalence of HIV seropositivity was 2/147 (1.4%) in the strictly rural group, 5/59 (8.5%) in the market place area, and 49/169 (30%) among patients receiving treatment for sexually transmitted diseases. No significant differences existed between male and female subjects in terms of HIV seropositivity. HIV seropositivity was also associated with a history of venereal diseases in the market place sample. These results suggest that Rwanda's rural population (93%) is at lower risk of HIV infection that the urban population. Where HIV infection does exist in rural areas, it is transmitted mainly by heterosexual contact with persons from urban centers. The relatively high rate of HIV infection observed in adults living in a rural market place accessible from most of the Rwandan main cities, together with the association between HIV seropositivity and past residency or travel in urban centers, indicates that most of the rural-based seropositive adults identified in this study were infected elsewhere. These findings also contradict the popular assumption that HIV was present in an unrecognized form for many years in rural Central Africa.

Clonidine combined with sufentanil and bupivacaine with adrenaline for obstetric analgesia.

Clonidine produces analgesia via a non-opioid mechanism and it may be used as an interesting adjuvant to local anaesthetics and opioids in obstetric analgesia. To examine the effects of the addition of clonidine to bolus injections of bupivacaine, adrenaline and sufentanil, we enrolled 50 women receiving extradural analgesia for vaginal delivery into a double-blind study. They were allocated randomly to two groups: group A received a 10-ml extradural solution of bupivacaine 12.5 mg combined with adrenaline 25 micrograms and sufentanil 10 micrograms; group B received the same solution with clonidine 30 micrograms. Each patient was allowed two subsequent injections of the chosen solution. Subsequently, if still in the first stage of labour, analgesia was augmented with additional 10-ml injections of bupivacaine 12.5 mg with adrenaline 25 micrograms, without sufentanil or clonidine. The latter solution was used for perineal analgesia in group A; clonidine 30 micrograms was added in group B. During the first and second stages of labour, there was no difference between the two groups in duration of analgesia after the first injection (142 min in group A; 127 min in group B), number of injections (1.8 in group A; 1.9 in group B) and the total bupivacaine requirements (33.9 mg in group A; 34 mg in group B). The quality of analgesia was evaluated as very good in both groups (23/25 in group A; 24/25 in group B). The degree of motor block or the frequency of other side effects were not enhanced by clonidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Clonidine pretreatment reduces the systemic toxicity of intravenous bupivacaine in rats.

BACKGROUND: Clonidine prolongs the duration of sensory and motor block induced by bupivacaine, and this association, in constant infusion by the epidural route, is used for postoperative analgesia. After a near-fatal intravenous bolus of bupivacaine in dogs, clonidine improves ventricular electrophysiologic parameters, but probably worsens bupivacaine-induced bradycardia and depression of the myocardial contractility. The current study, using a rodent animal model, evaluated the influence of clonidine pretreatment on the systemic toxic effects of bupivacaine overdose induced by a constant intravenous infusion. METHODS: Twenty Wistar male rats were anesthetized with thiopental, and controlled ventilation was started with an equal mixture of O2 and N2O. Electrocardiogram (ECG), electroencephalogram (EEG), and invasive arterial blood pressure were continuously recorded. Clonidine (5 micrograms/kg) or saline was injected intravenously in a randomized fashion. After 15 min, an intravenous infusion of bupivacaine was started at 2 mg.kg-1 x min-1. The time of occurrence of the bupivacaine-induced toxic events was recorded and the doses were calculated. Ten (five in each group) additional rats, pretreated according to the same protocol, were killed at the time of the first dysrhythmia, for blood sampling and plasma bupivacaine concentration measurement. RESULTS: Clonidine reduced heart rate and arterial blood pressure before bupivacaine infusion (P < 0.05). The threshold doses at the first QRS modification (11.3 +/- 5.6 vs. 2.1 +/- 0.9 mg/kg) and the first dysrhythmia (40.6 +/- 15.3 vs. 8.48 +/- 3.7 mg/kg), the increase in EEG total spectral power (33.3 +/- 21.9 vs. 8.2 +/- 5.1 mg/kg), the 25 and 50% reduction in baseline mean arterial pressure and heart rate, the isoelectric EEG (58.6 +/- 14 vs. 22 +/- 6.6 mg/kg), and the final systole (99 +/- 16 vs. 51.8 +/- 14.5 mg/kg) were significantly greater in the clonidine group than in the saline group (P < 0.01). The time between the first dysrhythmia and 50% reduction of baseline mean arterial blood pressure was not different between the groups. In the additional series, the first dysrhythmia occurred later (10.9 +/- 4.5 vs. 3.2 +/- 1.0 min, P < 0.01) and plasma bupivacaine levels were greater (18.7 +/- 8.0 vs. 7.8 +/- 3.2 micrograms/ml, P < 0.01) in the clonidine group than in the saline group. CONCLUSIONS: In this model, clonidine given prophylactically delays the toxic manifestations of bupivacaine overdose and does not accentuate the subsequent hypotension.