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Abstract
Hyperhomocysteinemia, defined as an elevated concentration of homocysteine in the
fasting state or after methionine loading, is an independent risk factor for premature
atherosclerosis and venous thrombosis. The role of the methionine loading test (MLT)
is, however, controversial. To determine the additional value of the MLT for diagnosis
of hyperhomocysteinemia, we prospectively studied 281 patients with premature arterial
disease and 148 of their first-degree relatives in the outpatient clinic of a general
hospital. Total plasma homocysteine (fasting and 6 hours after methionine loading),
folic acid, cobalamin, pyridoxine, and creatinine concentrations were measured. Hyperhomocysteinemia
was defined as a fasting homocysteine concentration and/or an increase in homocysteine
concentration after methionine loading exceeding the 95th percentile of a healthy
control group. Hyperhomocysteinemia was found in 141 (33%) of the 429 subjects: 15%
were diagnosed by fasting homocysteine concentration and 18% by MLT. Seventy-eight
(55%) of the 141 hyperhomocysteinemic persons were diagnosed only by the MLT. Folic
acid was lower in the group with an elevated fasting homocysteine concentration than
in those with only an abnormal MLT result (11 versus 15 nmol/L, p = 0.002). Folic acid was significantly negatively correlated, and creatinine significantly
positively correlated, with both fasting homocysteine concentration and increase in
homocysteine concentration. Negative correlations of cobalamin and pyridoxine with
fasting homocysteine concentration were found. In conclusion, the MLT is necessary
for diagnosis of hyperhomocysteinemia, because a considerable number of hyperhomocysteinemic
persons (55%) remain undiagnosed with the determination of a fasting homocysteine
concentration alone.
Abbreviations:
HPLC (High performance liquid chromatography), MLT (methionine loading test)To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
March 11,
1998
Received in revised form:
February 4,
1998
Received:
October 29,
1997
Identification
Copyright
© 1998 Published by Elsevier Inc.