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March 1976

Platelet Aggregation in Portal Cirrhosis

Author Affiliations

From the Hematology Section, New York Veterans Administration Hospital, the Department of Medicine, Columbia University College of Physicians and Surgeons, and the Department of Medicine, New York Hospital-Cornell Medical Center, New York.

Arch Intern Med. 1976;136(3):316-319. doi:10.1001/archinte.1976.03630030050009

Primary and secondary platelet aggregation in response to adenosine diphosphate was studied in 24 patients with portal (Laënnec) cirrhosis and compared with platelet aggregation in 14 normal subjects. In 12 patients with cirrhosis, platelet aggregation was diminished when compared to controls. Of the 12 patients with impaired aggregation, 6 had elevated levels of fibrinogen-fibrin degradation products (FDPs), 11 had thrombocytopenia, 10 had shortened euglobulin lysis times, 11 had prolonged bleeding times, 4 had hypofibrinogenemia, and all had prolonged thrombin clotting times.

The data suggest that elevated levels of serum FDPs do not explain fully the impairment of platelet aggregation or the prolongation of the thrombin clotting time that was noted in patients with advanced liver disease. A possible explanation for the prolongation of the thrombin clotting time is the presence of "altered" plasma fibrinogen.

(Arch Intern Med 136:316-319, 1976)

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