Fat redistribution syndrome (FRS) in patients with HIV infection receiving treatment with combination antiretroviral therapy is more frequent in those who take protease inhibitors than in those who have never had these drugs, according to Dr Graeme Moyle (associate director of HIV research, Chelsea and Westminster hospital, London). However, it might occur with virtually any combination of therapy, with the prevalence ranging from 10 to 80 per cent. The likelihood of developing FRS increased over time, he said.
Presenting an overview of FRS at a Bristol-Myers Squibb press conference on February 9, Dr Moyle said that combination antiretroviral therapy caused metabolic abnormalities, including altered fat and sugar handling. This led to increased cholesterol and triglyceride levels and glucose intolerance or diabetes mellitus, respectively.
Physical changes included alteration in fat distribution. There was increased risk of atherogenic heart disease, although this was less than that posed by smoking, he commented. FRS was disfiguring, carried social stigma and could cause patients to stop taking their drugs. Consequently, virological control of HIV was lost. The syndrome was definitely drug-induced, Dr Moyle said, as it had been noted in healthy volunteers, as well as in patients with HIV.
In FRS, fat was lost in the periphery and the face, buttocks and limbs became emaciated. In males, there was increased fat deposition in the abdominal region, while, in females, deposition occurred around the breasts and upper body. FRS might be less common in black patients but was more likely to occur in those with histories of diabetes and hyperlipidaemia. It appeared to be progressive. There had been some speculation that protease inhibitors contributed to the increase in visceral fat deposition but not to the loss of fat in the periphery. Dr Moyle said that patients were unlikely to develop the syndrome within the first six months of treatment but metabolic disturbances became apparent during the first fortnight. He described a number of theories that had been put forward to explain FRS:
However, it was likely that the alteration in fat handling was multifactorial.
There was no "quick fix" to FRS and no established means of management. Reduced fat intake and increased exercise might help, as might lipid-lowering agents and drugs that improved insulin handling (such as metformin and the "glitazones"). Other treatments used were growth hormone, anabolic steroids, anti-TNF therapy and cosmetic treatment.
With regard to modifying existing regimes, Dr Moyle said that switching to other drugs, stopping all therapy and counselling were options. However, switching and stopping therapy were not without risk. Thus, the risk/benefit ratio must be assessed and management individualised, with a six-monthly evaluation of the outcome, he concluded.