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[Familial antithrombin III abnormality accompanied with progressing ischemic stroke].

Y Sasaki, H Ueyama, Y Hashimoto

Rinsho Shinkeigaku = Clinical Neurology

|April 1, 1989

Summary

Familial antithrombin III (AT-III) abnormality, a genetic condition, can lead to severe ischemic stroke. This case highlights how homozygous AT-III deficiency causes progressive strokes, treatable with AT-III concentrates.

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Area of Science:

Neurology
Hematology
Genetics

Background:

Familial antithrombin III (AT-III) deficiency is a rare inherited thrombophilia.
AT-III plays a crucial role in regulating coagulation.
Genetic defects in AT-III can predispose individuals to thromboembolic events.

Observation:

A 31-year-old female presented with progressive ischemic stroke, including hemiparesis and altered consciousness.
Imaging revealed extensive cerebral infarcts and arterial branch occlusions.
The patient exhibited decreased biological AT-III activity but normal immunological levels, suggesting a functional abnormality.

Findings:

Familial investigation confirmed AT-III abnormality, with the patient identified as a homozygote lacking heparin affinity.

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Her parents were heterozygotes, indicating an autosomal recessive inheritance pattern.

Treatment with AT-III concentrate transfusion led to symptom recovery and halted infarct progression.

Implications:

Homozygous AT-III abnormality is a significant risk factor for severe, progressive ischemic stroke.
Early diagnosis and AT-III concentrate therapy can be effective in managing such cases.
Understanding genetic thrombophilias is crucial for stroke prevention and management strategies.