Impaired glucose tolerance, beta cell function and lipid metabolism in HIV patients under treatment with protease inhibitors
G Behrens, A Dejam, H Schmidt, HJ Balks, G Brabant… - Aids, 1999 - journals.lww.com
G Behrens, A Dejam, H Schmidt, HJ Balks, G Brabant, T Körner, M Stoll, RE Schmidt
Aids, 1999•journals.lww.comObjectives: To evaluate metabolic abnormalities, beta-cell function, lipid profile and vascular
risk factors in HIV patients on protease inhibitors (PI). Design: Prospective cross-sectional
study. Methods: Thirty-eight HIV-1-infected patients receiving at least one PI were compared
with 17 PI-naive HIV patients in an oral glucose tolerance test (OGTT). Serum glucose,
insulin, proinsulin, and C-peptide were determined. The fasting lipid pattern was analysed
using electrophoresis and the assessment of apolipoproteins including lipoprotein (a) …
risk factors in HIV patients on protease inhibitors (PI). Design: Prospective cross-sectional
study. Methods: Thirty-eight HIV-1-infected patients receiving at least one PI were compared
with 17 PI-naive HIV patients in an oral glucose tolerance test (OGTT). Serum glucose,
insulin, proinsulin, and C-peptide were determined. The fasting lipid pattern was analysed
using electrophoresis and the assessment of apolipoproteins including lipoprotein (a) …
Abstract
Objectives:
To evaluate metabolic abnormalities, beta-cell function, lipid profile and vascular risk factors in HIV patients on protease inhibitors (PI).
Design:
Prospective cross-sectional study.
Methods:
Thirty-eight HIV-1-infected patients receiving at least one PI were compared with 17 PI-naive HIV patients in an oral glucose tolerance test (OGTT). Serum glucose, insulin, proinsulin, and C-peptide were determined. The fasting lipid pattern was analysed using electrophoresis and the assessment of apolipoproteins including lipoprotein (a). Fibrinogen, homocysteine, and anticardiolipin antibodies were also assessed.
Results:
Twenty-seven (71%) of the PI-treated group had detectable hyperlipidaemia. Isolated hypertriglyceridaemia was present in 12 patients (44%), two (7%) of them had type V and 10 (37%) subjects had type IV hyperlipidaemia (Frederickson classification). Type IIb hyperlipidaemia defined as an increase of both very-low-density lipoproteins (VLDL) and low-density lipoproteins (LDL) was found in 10 (36%) subjects, and five (18%) patients presented with isolated hypercholesterolaemia (type IIa). PI treatment was associated with significant higher fasting cholesterol, triglycerides, LDL and VLDL levels. Apolipoprotein B and E concentrations were significantly increased in patients receiving PI. Elevated concentrations of lipoprotein (a)(> 30mg/dl) were detected in six (16%) of the hyperlipidaemic patients on PI. Eighteen (46%) patients on PI had impaired oral glucose tolerance and five (13%) had diabetes. Although four (24%) of the PI-naive patients were glucose intolerant, none had diabetes. Fasting concentrations and secretion response of insulin, proinsulin, and C-peptide to glucose ingestion was significantly increased in the PI-treated group suggesting a beta-cell dysfunction in addition to peripheral insulin resistance. Beta-cell abnormalities were associated with the abnormal lipid pattern and PI treatment.
Conclusion:
Combination drug regimens including PI are accompanied by impaired glucose tolerance, hyperproinsulinaemia as an indicator for beta-cell dysfunction, and lipid abnormalities proved to be significant risk factors for coronary heart disease. Moreover, PI may have an impact on the processing of proinsulin to insulin.
Lippincott Williams & Wilkins