There is accumulating evidence that human immunodeficiency virus type 1 (HI
V-1) protease inhibitors (Pls) can induce hyperlipidaemia. To evaluate the
frequency and type of hyperlipidaemia in PI-treated patients, 98 outpatient
s were prospectively analysed for their lipoprotein characteristics at the
Medizinische Hochschule in Hannover, Germany. Fifty-seven percent of the pa
tients studied presented with hyperlipidaemia. Both hypertrigylceridaemia (
type IV and V hyperlipoproteinaemia, 33%) and hypercholesterolaemia (type I
Ia hyperlipoproteinaemia, 6%) were detectable. The remaining 18% had a type
IIb hyperlipoproteinaemia. Increased lipid levels were highly statisticall
y significant compared to a control group of PI-naive HIV-l-infected patien
ts [low-density lipoprotein (LDL) 146 mg/dl (range, 53-274 mg/dl) versus 10
5 mg/dl (range, 22-188 mg/dl; P=0.0006); very-low-density lipoprotein (VLDL
) 35.5 mg/dl (5-253 mg/dl) versus 18 mg/dl (range, 3-94 mg/dl; P=0.0002)].
All Pls used (saquinavir, indinavir, nelfinavir and ritonavir) were associa
ted with this variable form of hyperlipidaemia according to the Fredrickson
classification. There was no significant correlation of any determined lip
id value with the duration of treatment. A higher frequency of the apolipop
rotein E2 allele and E4 allele was observed in the hyperlipidaemic subjects
. Patients with excessive hypertriglyceridaemia showed a reduced lipoprotei
n lipase activity. Lipodystrophy was observed especially in hyperlipidaemic
patients and to a lesser extent in normolipidaemic subjects. The frequency
of hyperlipidaemic risk factors was surprisingly high in the group studied
, which in turn may explain the proposed increased risk of atherogenesis in
HIV-1 PI-treated patients. Therefore, PI-treated subjects should also be e
valuated for their lipoprotein pattern, which may require antihyperlipidaem
ic interventions.