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Gout and HIV: a new facet of the fat redistribution syndrome?
  Researchers from the Mortimer Market Center and the University College of London, both in the UK, reported on gout at their clinics in HIV+ patients at the recently held 9th Annual British HIV Association Conference in Manchester, UK. Here is the abstract (Poster 12) presented in the program.
Since 1996 there has been one case report of gout in an HIV+ patient. Over a 2-year period, 18 cases of gout were seen at a single HIV centre. A restrospective analysis of patient records was conducted. Apparently 1800 patients' records were reviewed. All cases of hyperuricaemia (elevated uric acid) attending the Mortimer Market Centre, a large HIV Center, between 1 February 2000 and 1 February 2002 were identified from the hospital database. Notes were scrutinised using a standardised proforma, to identify predisposing factors for gout, HIV clinical history, lipodystrophy and laboratory markers.
18 cases were identified. All 18 cases had clinical manifestations of gout and elevated serum urate (mean 686, range 428-1552). 12 had stage C disease and six stage B. Mean CD4 was 356 cells/Ál (range 50-1100) and mean viral load (VL) 13,559 copies/ml (range below detection to 83,000).
16/18 were receiving highly active antiretroviral therapy (HAART) and had been on it for an average of 41 months (range 3-48). Eight had predisposing risk factors for gout (e.g. pyrazinamide therapy, haematological malignancy). 7/10 of the remainder were receiving a boosted protease inhibitor [ritonavir (RTV)/saquinavir (SQV) n=5, RTV/indinavir n=1, RTV/amprenavir n=1), they had dyslipidaemia (mean triglycerides 542 mg/dl, range 373-783) and proven features of lipodystrophy. Patients with gout were significantly more likely to be taking boosted SQV than the remainder of the clinic attenders (50% versus 10%, P<0.00001).
Author conclusions: we report a high level of gout in our HIV population from 2000 onwards, especially in patients receiving boosted protease inhibitors. Most of these patients had dyslipidaemia and clinical features of lipodystrophy. As gout is known to be associated with insulin resistance, atherosclerosis and visceral fat accumulation in the HIV-negative population, this suggests that gout may be another metabolic complication of HAART.
Editorial note: It would be helpful to know the diet patterns of these patients. Only 1% of the studied patients had gout. Granted their lipids were high but perhaps their diet was particularly high in fatty foods and certain foods that are known to be related to elevating uric acid. In addition, a side effect of ddI is elevated uric acid but this study does not appear to report if these patients used ddI. Frankly, I don't think this study is convincing that gout occurred in this HIV infected population significantly more than it might occur in an HIV negative population.
Reference: 9th Annual British HIV Association Conference. April 24-26, Manchester, UK. S Creighton 1 , GP Kasidas 2 , SG Edwards and P French 1 1 Mortimer Market Centre and 2 University College London, London UK
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