Intermuscular tissue is decreased in HIV infection

HIV Treat Bull - 2009 Nov/Dec;10(11/12): 05

Simon Collins, HIV i-Base

The first study in the main conference looked at a intermuscular adipose tissue (IMAT) - the distribution of fat that is beneath the muscle facia and muscle tissue–as a new parameter of metabolic disturbances. Led by Carl Grunfeld with the FRAM study, this group has provided important insight into the association of HIV to metabolic changes by using full body MRI to identify changes and including an HIV-negative control group. Results from the study concluded that fat loss and fat gain are separate unrelated dysfunctions and that fat loss rather than fat accumulation is the driving mechanism behind HIV-related changes.

This year the group hypothesised that IMAT, which has been reported as increasing in obese HIV-negative women and having a strong relationship to insulin sensitivity, would behave similarly to visceral adipose tissue (VAT) and would be increased in HIV positive patients. IMAT is preserved in familial and decreased in generalised congenital lipodystrophy.

In fact, they reported that IMAT was 51% lower when comparing 425 HIV-positive patients to 211 HIV-negative controls, even after adjusting for demographics and lifestyle (adjusted to -48%), although somewhat attenuated after controlling for VAT, SAT and skeletal muscle volume (adjusted to -21%). All comparisons were significant (p<0.0001).

In HIV-positive people but less so in controls, IMAT was associated with higher levels of VAT, trunk SAT and leg SAT.

As both IMAT and subcutaneous adipose tissue (SAT) were decreased with exposure to d4T, the study concluded that IMAT shared similar cellular origins to SAT. Although the clinical implications are less significant in countries that have moved away from using d4T and ddI, this finding is likely to be most relevant to those where it is still widely used.

Ref: Grunfeld C et al. Intermuscular tissue is decreased in HIV infection. 11th Intl Workshop on Adverse Drug Reactions — 26-28 October 2009, Philadelphia. Oral abstract O-01. Antiviral therapy 2009; 14 Suppl 2: A3.

2009-11-10
IB2009-11-05

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