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125I-Antithrombin III metabolism studies were performed in 2 patients with ischemic and ulcerative colitis, respectively. Both patients had acquired antithrombin III deficiency and objectively diagnosed deep venous thrombosis. A decreased 125I-antithrombin III plasma disappearance halflife and an increased fractional catabolic rate was found in both patients. The transcapillary flux ratio was elevated in the patient with ischemic colitis. A follow-up study of the first patient during a period when no signs of an ischemic colitis were present and no medication was taken showed completely normal tracer data. The data are consistent with both gastrointestinal loss and intravascular consumption of antithrombin III. The antithrombin III deficiency could not be explained by other causes such as proteinuria, liver dysfunction, or obvious disseminated intravascular coagulation. Reduced antithrombin III plasma levels were considered to have contributed to the development of deep venous thrombosis in both patients.
E A Knot, and
J W ten Cate, and
T Bruin, and
A H Iburg, and
G N Tytgat
February 1992,
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A H Iburg, and
G N Tytgat
January 1978,
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E A Knot, and
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A H Iburg, and
G N Tytgat
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E A Knot, and
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G N Tytgat
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E A Knot, and
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T Bruin, and
A H Iburg, and
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E A Knot, and
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E A Knot, and
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A H Iburg, and
G N Tytgat
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E A Knot, and
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A H Iburg, and
G N Tytgat
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E A Knot, and
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G N Tytgat
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