Rheumatic Fever and Rheumatic Heart Disease: Where are we now in South Africa?

South Africa continues to face unacceptably high rates of rheumatic fever (RF) and rheumatic heart disease (RHD); despite readily available and inexpensive preventive measures. However; in the past several years; key players in South Africa's healthcare and political realms in addition to key players from many African nations have come together to acknowledge the persistent health burden attributable to RF/RHD and have agreed to a pledge of action to reduce it.The plan of action is a comprehensive RF/RHD prevention and treatment programme known as ASAP. The ASAP programme targets efforts to raise Awareness; establish surveillance systems; Advocate for increased resources for treatment; and to promote Prevention strategies. South Africa currently has a demonstration site where activities in all of these key areas are currently underway. Efforts in the area of surveillance include a RHD prevalence study that aims to screen 4 000 school-aged children through the use of a mobile echo-surveillance unit. In addition to local efforts; South Africa will join an international initiative to create a global RHD registry that will aid in all aspects of prevention and treatment to further reduce the burden of disease attributable to RF/RHD

Pituitary-adrenal function in uncomplicated falciparum malaria.

To investigate pituitary-adrenal function in acute uncomplicated falciparum malaria, we performed an overnight dexamethasone suppression test in 13 Vietnamese adults with acute malaria and 6 healthy controls. After blood samples were taken for serum cortisol and plasma ACTH at 23.00 hours on the admission day, 1 mg dexamethasone was given and further samples were taken at 08.00, 16.00 and 23.00 hours the next day. The patients received conventional antimalarial and supportive treatment. Baseline plasma ACTH concentrations in the patients [3.9 (0.2-41.2) pmol/l] and controls [3.4 (1.1-4.3) pmol/l] were similar (p=0.51), and exhibited a similar fall after dexamethasone to 0.6 (0.2-2.5) and 0.9 (0.7-1.6) pmol/l at 08.00 hours respectively (p<0.03 vs 23.00 hour values). Serum cortisol levels before dexamethasone were higher in the patients than in the controls [456 (102-821) vs 145 (64-183) nmol/l respectively; p=0.007] and the overnight fall was less in the patients [208 (26-340) and 23 (15-46) nmol/l at 08.00 hours respectively; p<0.001 vs 23.00 hour values and between groups]. Between 08.00 and 23.00 hours, plasma ACTH and serum cortisol remained suppressed in the controls. In the patients, the serum cortisol continued to fall progressively towards control values. These data suggest that there is a raised set point for cortisol inhibition of ACTH secretion but normal corticotrophin responsiveness to dexamethasone in uncomplicated malaria. A raised serum cortisol after dexamethasone in the patients might reflect the combination of a prolonged cortisol half-life and the stimulatory effects of cytokines on the adrenal cortex, with a consequent protective effect against complications such as hypoglycemia.