[Hyperhomocysteinemia: development of deep vein thrombosis in another location during heparin anticoagulation therapy].
A 45-year-old man was admitted complaining of chest pain and pain and edema in the left lower extremity. Ultrasonography and venography results yielded a diagnosis of left femoral vein thrombosis, and pulmonary embolism was diagnosed later. Intravenous heparin therapy (10,000 IU/day) improved the patient's clinical signs. During this therapy, however, pain and edema of the right lower extremity developed, leading to a diagnosis of right femoral vein thrombosis. The patient was admitted to our hospital. At that time, coagulation studies showed an FDP level of 44.7 micrograms/ml and an FDP-DD level of 24.5 micrograms/ml. We surmised that the bilateral deep vein thrombosis had been caused by hyperhomocysteinemia (17.8 mumol/l). Genetic and other acquired risk factors for thrombophilia were ruled out. The patient's clinical signs again improved as a result of intravenous heparin therapy (15,000 IU/day), and FDP and FDP-DD levels returned to normal. We concluded that hyperhomocysteinemia is a risk factor for thrombosis and that it can generate thrombosis in other locations even during heparin therapy.
Tsuda
H
H
Department of Neurology, Kanazawa University.
Asakura
H
H
Matsuda
T
T
D000925:Anticoagulants / Q000627:therapeutic use*; D005268:Femoral Vein; D006493:Heparin / Q000627:therapeutic use*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000150:complications*; D008297:Male; D008875:Middle Aged; D020246:Venous Thrombosis / Q000188:drug therapy* / Q000209:etiology*
D000925:Anticoagulants; D006493:Heparin