The Body Covers: The XIII International AIDS Conference
Lipodystrophy: Definition and Treatment
July 13, 2000
Lipodystrophy syndrome definition: a search for consistency (ThPp1436)Dr. Belloso from Argentina attempted to deal with this uncertainty regarding ascertaining what exactly is LD by combining clinical evaluation (CE) by a health care provider, with a self-questionnaire (Q) and then he attempted to quantitate the responses to arrive at some concordance. The clinical evaluations did not correlate with the questionnaire responses with more LD being reported by Q than by CE. The CE included bioimpedance, DEXA scans, and anthropometry. None of these clearly correlated with the patients' self-reports. So, who knows LD when he/she sees it? The patient? The doctor? The so-called objective measurement test?
The next posters concerning LD deal with specific areas of treatment intervention, growth hormone for fat accumulation, and a "statin" drug for elevated levels of cholesterol. There has been a lot of interest in the potential use of recombinant human growth hormone (GH) for fat accumulation since Gabriel Torres's report at the 6th Retrovirus Conference in 1999. GH is known to be lipolytic and encourage the acquisition of lean body mass (LBM), but is expensive and may require long-term use to maintain its effects.
Body composition changes during and after growth hormone therapy for lipodystrophy with truncal adiposity (ThPpB1437)Dr. Engleson from New York tested growth hormone at a dose of six mg/day for 24 weeks in 30 patients with increased visceral abdominal tissue (VAT; also known as "protease paunch"). They did report improvements in VAT (46% decrease) and in subcutaneous adipose tissue (SAT; 18% decrease) as well as in LBM. However after 12 weeks off GH all truncal fat and SAT returned and 85% of the VAT returned. All gains in lean tissue were reversed as well. Adverse events were common, including carpal tunnel syndrome and hyperglycemia.
A randomized open-label comparative trial of dietary advice with and without pravastatin for the management of protease inhibitor (PI)-associated hypercholesterolemia (ThPpB1438)We know that elevated levels of cholesterol and triglyceride are frequently seen in patients with HIV with and without antiretroviral therapy. We have seen few studies systematically looking at the use of a "statin" for cholesterol lowering. Statin drugs have revolutionized the treatment of hypercholesterolemia (HC) because of excellent efficacy, safety and ease of use (as well as the generally dismal results from non-pharmacologic intervention). Moyle's study compared six months of dietary advice (DA) with pravastatin, a statin likely not to have significant drug interactions with antiretroviral drugs. The 31 male patients were all on antiretroviral therapy, had undetectable viral loads (<500) and HC (>250mg/dl). Total cholesterol fell significantly (17%) in the pravastatin but not the DA group. This fall in cholesterol was accounted for entirely by reduction in LDL cholesterol, as HDL cholesterol did not fall significantly. No patients discontinued due to adverse effects.
So, we still don't know what lipodystrophy is. We don't even know if we should use the term LD, as most of what we see is not really LD. The fat accumulation that is the most common body shape manifestation is not generally thought to be due to the mechanism of lipodystrophy. As far as treatment of the varied manifestations associated with LD, we are making baby steps. GH has shown consistent activity in reducing fat accumulation whether intraabdominal (visceral) or subcutaneous, but has also shown consistent limitations in its efficacy. Whether lower doses will be effective for long-term control is as yet untested Whether this is important is neither unclear nor untested. I reported earlier from this conference about the impact of LD on patients with HIV. This impact is real and threatens to affect adherence in some people. This brings me back full circle to adherence. Without adherence, antiretroviral drugs have no efficacy.
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