Epidemiology

Fatty liver linked to high plasminogen inhibitor levels in HIV-related lipodystrophy

Last Updated: 2003-05-02 15:08:53 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Liver fat content appears to contribute to the elevated levels of plasminogen activator inhibitor-1 (PAI-1) seen in patients treated with highly active antiretroviral therapy (HAART), according to a report in the April issue of Arteriosclerosis, Thrombosis and Vascular Biology.

Dr. Jussi Sutinen, of Helsinki University Central Hospital, Finland, assessed 30 patients on HAART who had lipodystrophy (HAART+LD+) and 13 HAART-treated patients without lipodystrophy (HAART+LD-), as well as 15 HIV-negative control subjects.

Liver fart content was significantly higher in the HAART+LD+ group, at 7.6% compared with 2.1% in the HAART+LD- group and 3.6% in the HIV-negative group. Plasma levels of plasma tissue plasminogen activator (tPA), insulin and triglycerides were also higher in patients with lipodystrophy.

In addition, PAI-1 levels correlated with liver fat content but not with subcutaneous or intra-abdominal fat in the HAART+LD+ group.

The authors treated the HAART+LD+ patients for 24 weeks with rosiglitazone 8 mg daily or placebo. Rosiglitazone treatment, but not placebo, was associated with decreased plasma PAI-1, serum insulin and liver fat content (p < 0.05), and increased serum triglycerides. The agent had no effect on subcutaneous or intra-abdominal fat depots.

The authors theorize that "plasma PAI-1 concentration is likely to be regulated directly (through changes in production or uptake of PAI-1 by the liver) or indirectly (through alterations in serum insulin concentrations due to changes in hepatic insulin sensitivity) by the liver."

Arterioscler Thromb Vasc Biol 2003;23:688-694.