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[Hyperhomocysteinemia complicated by myocardial infarction and portal vein thrombosis--case report]

Dorota Dworakowska1, Ewa Kazimierska, Jolanta Weyer-Hepka

  • 1Klinika Chorób Wewnetrznych, Endokrynologii i Zaburzeń Hemostazy, Akademia Medyczna w Gdańsku. ddw@amg.gda.pl

Polskie Archiwum Medycyny Wewnetrznej
|May 13, 2008
PubMed

Insights

High homocysteine (HHcy) levels, linked to vitamin deficiencies, increase thrombosis risk. Early vitamin B and folic acid supplementation can normalize HHcy and prevent serious vascular complications.

Area of Science:

  • Cardiology
  • Metabolic Disorders
  • Genetics

Background:

  • Hyperhomocysteinemia (HHcy) is associated with vitamin deficiencies (B vitamins, folic acid), renal insufficiency, diabetes, hypothyroidism, and malignancies.
  • HHcy elevates the risk of arterial and venous thrombosis.
  • Genetic mutations in homocysteine metabolism pathways can also cause HHcy.

Observation:

  • A 38-year-old woman with documented HHcy experienced recurrent myocardial infarction at ages 38 and 44, and portal vein thrombosis at age 48.
  • Her cholesterol levels were consistently normal, highlighting HHcy as a likely contributor to her thrombotic events.
  • Diagnostic workup excluded MTHFR and CBS gene mutations as the cause of HHcy.

Findings:

  • The patient's HHcy was successfully treated with folic acid, vitamin B12, and vitamin B6 supplementation.
  • Normalization of homocysteine levels was achieved through vitamin therapy.
  • No genetic mutations in key homocysteine metabolism enzymes were identified.

Implications:

  • This case underscores the critical role of vitamin supplementation in managing HHcy.
  • Early diagnosis and treatment of HHcy with vitamins can potentially prevent severe thromboembolic complications.
  • Vitamin therapy offers a viable strategy for reducing cardiovascular and thrombotic risks in HHcy patients.

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