OBJECTIVE - The purpose of this study was to investigate possible rela
tionships between lipoprotein (a) [Lp(a)] levels and NIDDM in African-
Americans. The objectives were to identify associations between Lp(a)
levels of subjects with and without NIDDM and to determine the influen
ce of glycemic control, determined by GHb, and of mode of therapy on L
p(a) levels. RESEARCH DESIGN AND METHODS - We studied 141 African-Amer
ican subjects, 103 with NIDDM and 38 without NIDDM. Their Lp(a) levels
, GHb levels, and apolipoprotein (a) [apo(a)] isoforms were determined
. Clinical information, including mode of therapy (sulfonylurea, insul
in, or no pharmacological therapy), date of diagnosis, and medical his
tory, was obtained by chart review and patient interview. RESULTS - Th
ere was no significant difference in median Lp(a) levels between the n
on-NIDDM (25.5 mg/dl) and NIDDM (24.0 mg/dl) study subjects. No statis
tically significant difference was found in Lp(a) levels when NIDDM pa
tients with GHb <12.3% were compared to those with GHb greater than or
equal to 12.3% (P = 0.096). An inverse relationship was found between
apo(a) root-mean-square isoform size and Lp(a) level (r(2) = 0.091, P
= 0.0035). Analysis of the cases by mode of therapy indicates that th
ere is evidence of an increased median level of Lp(a) in African-Ameri
cans with NIDDM on insulin therapy relative to those on sulfonylurea (
34.0 vs. 16.0 mg/dl; P = 0.013) and to nondiabetic subjects (34.0 vs.
25.5 mg/dl; P = 0.043). CONCLUSIONS - We conclude that the level of pl
asma Lp(a) is higher in African-Americans with NIDDM who are being tre
ated with insulin when compared to those on sulfonylurea therapy and t
o those who are non-NIDDM subjects, and this does not seem to be due t
o genetic variance or method bias.