Health practitioners' state of knowledge and challenges to effective management of hypertension at primary level.

BACKGROUND: Patient- and physician-related factors impact on the management and control of hypertension. OBJECTIVES: To systematically examine: (1) South African primary care doctors' state of knowledge on the management of hypertension; (2) primary health practitioners' knowledge on the South African hypertension guidelines; (3) current approaches to management of hypertensive patients; and (4) challenges to effective management of hypertension at primary level. METHODS: A cross-sectional, observational study using a semi-structured questionnaire was carried out in two large community health centres (CHCs) in the Cape Town metropole. All 16 doctors employed at both CHCs were voluntarily enrolled, seven (43.7%) of whom were female, with 14 (87.5%) younger than 40 years of age. The majority (81.2%) of the doctors surveyed had been practicing for less than 10 years. RESULTS: Ten (62.5%) of the doctors surveyed aimed to treat hypertension to target, and recommendations on lifestyle modifications were reportedly poorly done. While 11 (68.8%) of the doctors were aware of the South African hypertension guidelines, were (81.8%) of them were not conversant with the contents thereof. Doctors estimated that only 35% of their patients are treated to target. Poor patient adherence to prescribed treatment, language difficulty, heavy patient load, medical staff shortages, and patient loss to follow up were identified by the doctors as significant impediments to the effective management of hypertension at the primary level of care. CONCLUSION: Primary healthcare practitioners' knowledge regarding hypertension and the South African hypertension guidelines is poor. Management of hypertension by these doctors is sub-optimal. There are significant challenges to effective management of hypertension at this level of care.

Progressive human immunodeficiency virus-associated vasculopathy: time to revise antiretroviral therapy guidelines?

Cardiovascular abnormalities were appreciated early in the epidemic of the acquired immunodeficiency syndrome (AIDS), even before the aetiological agent, human immunodeficiency virus (HIV) was isolated and characterised. The aetiology and pathogenesis of cardiovascular disease in HIV infection is still the subject of intense speculation, and is likely multi-factorial. HIV affects every aspect of the cardiac axis, causing pericarditis, myocarditis, cardiomyopathy, coronary artery disease and microvascular dysfunction, valvular heart disease, pulmonary vascular disease and pulmonary hypertension, stroke and peripheral vascular disease. HIV-associated vasculopathy is an increasingly recognised clinical entity, causing high morbidity and increasing mortality in southern Africa, particularly from stroke and cardiovascular disease. HIV causes disease of the vascular tree, either by a direct effect on vascular or perivascular tissue, or indirectly via immune complex-mediated mechanisms, associated opportunistic infections and malignancies. As a result, highly active antiretroviral therapy (HAART) may have an important role in controlling disease progression. We report a case of histologically defined primary HIV vasculopathy in which the chance to start HAART was initially missed and in which the patient progressed to require bilateral amputations, but obtained disease quiescence upon commencement of HAART.

KUVA (khellin plus ultraviolet A) stimulates proliferation and melanogenesis in normal human melanocytes and melanoma cells in vitro.

BACKGROUND: Khellin is a naturally occurring furochromone which, when combined with artificial ultraviolet (UV) A or solar irradiation (KUVA), is reported to repigment vitiligo skin as effectively as PUVA photochemotherapy. The exact mechanism of KUVA-induced repigmentation is unknown. OBJECTIVES: The aim of this study was to test the effect of khellin and KUVA on proliferation and melanogenesis of normal human melanocytes and Mel-1 melanoma cells in vitro. METHODS: Cultured normal human melanocytes, Mel-1 melanoma cells and fibroblasts were treated with khellin, UVA and KUVA and the effect on proliferation determined by cell counting. The effect on melanogenesis was determined by a radiometric melanin formation assay. Changes in gene expression and protein synthesis were determined by Northern blot, reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analyses. RESULTS: Khellin stimulated proliferation of Mel-1 melanoma cells and melanocytes at concentrations between 1 nmol L-1 and 0.5 mmol L-1 with a peak effect at 0.01 mmol L-1 khellin. In contrast, khellin inhibited proliferation of fibroblasts over the entire concentration range tested. At concentrations above 0.5 mmol L-1, khellin was cytotoxic to both melanocytic cells and fibroblasts. Exposure of khellin-treated cells to single doses of UVA between 150 and 280 mJ cm-2 resulted in an enhanced proliferative effect. Khellin and KUVA also stimulated the melanogenic enzyme activity of pigmented cells, with the most effective treatment being 0.01 mmol L-1 khellin with 250 mJ cm-2 UVA. Western blot, Northern blot and RT-PCR analysis revealed that these increases in melanogenic enzyme activity were not due to increases in gene expression or protein synthesis. UVA treatment resulted in an increase in enzyme glycosylation and this correlated with the increase in melanogenesis. CONCLUSIONS: We conclude that khellin activated by UVA stimulates melanocyte proliferation and melanogenesis. Our results point to the possibility that current treatment regimens might be improved if reduced khellin doses are applied and suggest that improved delivery vehicles be tested.