Evaluation of the Senegal leprosy endemic in 2002

The authors had for aim to assess the epidemiology of leprosy in Senegal after 7 years of efficient prevention. METHODS: A retrospective study was made on epidemiologic data in Senegal collected between January 1 and December 31, 2002. The indicators of eradication (total number of new cases diagnosed in that year compared to the country's population, expressed in cases per 100,00 inhabitants), the coverage rate (number of cases treated compared to the number of patients recorded for treatment), as well as the cure rate (percentage of patients having complied to the duration of treatment) were all noted. RESULTS: The mean detection rate was 0.5 case per 100,000 inhabitants with 434 new cases reported. The prevalence rate was 0.99 per 10,000 with 981 cases recorded for total management. The coverage rate for total management was 100%. The observed cure rate was 89% and 8% of the patients were lost to follow-up.     

A model HIV/AIDS risk reduction programme in the Philippines: a comprehensive community-based approach through participatory action research

A 3-year, longitudinal, quasi-experimental study using participatory action research (PAR) was conducted to determine the feasibility and efficiency of an expanded sexually transmitted infection (STI) HIV/AIDS prevention program among diverse high-risk male heterosexual populations in the southern Philippines. A total of 3389 participants ( approximately 200 males from each of 18 study groups) were recruited, and 221 were trained as peer counselors to develop educational materials and reinforce safe sexual practices among their peers. Condom usage (36.10% to 38.70% to 46.31%), attitudes towards condoms (21.67% to 24.55% to 25.15%) and knowledge about HIV/STI transmission (41.87% to 42.19% to 33.31%) increased significantly from baseline to post-test and 6-month follow up, respectively (p < 0.01). Furthermore, the reported STI incidence decreased significantly (7.4% to 4.6% to 2.4%, respectively). Changes differed significantly between the intervention and control group at post-test and follow up (p < 0.01). These findings illustrate the appropriateness of using PAR methodology in promoting and sustaining positive behavior change.     

Effects of pravastatin on cholesterol metabolism in Watanabe heritable hyperlipidemic rabbits.

Pravastatin, a competitive inhibitor of hydroxymethylglutaryl CoA reductase (HMG CoA reductase) is a potent hypocholesterolemic agent in humans as well as experimental animals, including the Watanabe heritable hyperlipidemic (WHHL) rabbit, lacking low density lipoprotein (LDL) receptor activity. We studied the effect of pravastatin on several aspects of cholesterol metabolism in WHHL rabbits. Cholesterol synthesis was measured by intraperitoneal injection of radioacetate and determination of its incorporation into the nonsaponifiable lipid fraction of liver, plasma, adrenal glands and gonads. A single dose of pravastatin (25 mg/kg) caused statistically significant inhibition of hepatic cholesterol synthesis at 2, 6, 12, and 24 hours following oral administration. By 48 hours, the inhibitory effect of the drug was no longer demonstrable. The pattern of radioactivity in the plasma was similar to that in the liver. The drug had no statistically significant effect on cholesterol synthesis in adrenal glands and gonads, suggesting a selective effect on the liver. Cholesterol absorption was studied after simultaneous oral administration of [3H] cholesterol and [14C] beta-sitosterol. Pravastatin, 50 mg/kg for 10 days had no effect on fecal excretion of the radiolabelled steroids over 4 days. At 24 hours the plasma level of [14C] cholesterol was 1/3 that of control in pravastatin treated animals (p < 0.05) but did not undergo an accelerated decline over 6 days. The activity of acyl CoA: cholesterol acyltransferase (ACAT) in intestinal mucosa and the concentration of hepatic cholesterol were similar in animals treated over one year with pravastatin 50 mg/kg/day or with placebo. Our data do not allow us to make definitive conclusions about the effect of pravastatin on cholesterol absorption but are compatible with the hypothesis that the drug inhibits the hepatic synthesis as well as the assembly of cholesterol into lipoproteins.     

Pravastatin decreases serum lipids and vascular cholesterol deposition in Watanabe heritable hyperlipidemic (WHHL) rabbits.

The effects of long term administration of pravastatin (a competitive inhibitor of hydroxymethylglutaryl CoA reductase) were assessed by measuring serum lipids and aortic and coronary atherosclerosis in Watanabe Heritable Hyperlipidemic (WHHL) rabbits. Six-month-old WHHL rabbits were given either 50 mg/kg/day of the drug or vehicle. The rabbits were sacrificed following 6 or 12 months of treatment and serum cholesterol and triglycerides and aortic cholesterol and hydroxyproline were measured. Atherosclerotic plaques in the aorta and coronary arteries were quantified with morphometric methods. Mean serum cholesterol +/- SEM (n) in the control vs. pravastatin groups after 6 months were: 535 +/- 34 (11) vs. 411 +/- 22 (12) (p less than 0.005) and after 12 months 458 +/- 43 (9) vs. 309 +/- 29 mg/dl (12) (p less than 0.005). In the pravastatin group, percent aortic area covered with plaque and aortic cholesterol content were reduced 35% (ns) and 55% (p less than 0.05) at 6 months, and 26% (ns) and 44% (ns) at 12 months, respectively. Little difference was found in serum triglycerides and aortic hydroxyproline in the 2 groups. There was strong correlation of serum cholesterol with aortic cholesterol content (r = 0.61, p less than 0.003) and with the percent aortic plaque area (r = 0.67, p less than 0.001), at 12 months. Morphometric analysis of wall thickness and lumen area of major coronary arteries revealed no significant differences in the 2 groups. In conclusion, pravastatin effectively lowered the serum cholesterol level in an animal model defective in low density lipoprotein receptors; this reduction was strongly correlated with amelioration of such atherosclerotic processes as lipid deposition and plaque formation.