BACKGROUND: Low high-density lipoprotein cholesterol (HDL-C) is a risk
factor for coronary artery disease. Investigating mechanisms underlying
acquired severe HDL deficiency in noncritically ill patients
(”disappearing EIDL syndrome”) could provide new insights into HDL
metabolism. OBJECTIVE: To determine the cause of low HDL-C in patients
with severe acquired HDL deficiency.
METHODS AND RESULTS: Patients with intravascular large B-cell lymphoma
(n = 2), diffuse large B-cell lymphoma (n = 1), and autoimmune
lymphoproliferative syndrome (n = 1) presenting with markedly decreased
EIDL-C, low low-density lipoprotein cholesterol (LDL-C), and elevated
triglycerides were identified. The abnormal lipoprotein profile returned
to normal after therapy in all 4 patients. All patients were found to
have markedly elevated serum interleukin-10 (IL-10) levels that also
normalized after therapy. In a cohort of autoimmune lymphoproliferative
syndrome patients (n = 93), IL-10 showed a strong inverse correlation
with HDL-C (R-2 = 0.3720, P < .0001). A direct causal role for increased
serum IL-10 in inducing the observed changes in lipoproteins was
established in a randomized, placebo-controlled clinical trial of
recombinant human IL-10 in psoriatic arthritis patients (n = 18). Within
a week of initiating subcutaneous recombinant human IL-10 injections,
HDL-C precipitously decreased to near-undetectable levels. LDL-C also
decreased by more than 50% (P < .0001) and triglycerides increased by
approximately 2-fold (P < .005). All values returned to baseline after
discontinuing IL-10 therapy.
CONCLUSION: Increased IL-10 causes severe HDL-C deficiency, low LDL-C,
and elevated triglycerides. IL-10 is thus a potent modulator of
lipoprotein levels, a potential new biomarker for B-cell disorders, and
a novel cause of disappearing HDL syndrome. Published by Elsevier Inc.
on behalf of National Lipid Association
