ACQUIRED ABNORMALITIES OF PLATELET FUNCTION

To the Editor: The review of platelet dysfunction by George and Shattil is an excellent summary of the molecular and clinical aspects of acquired platelet dysfunction. Although a number of systemic disorders are described in which platelet function is altered, no mention is made of chronic liver disease.

The cause of the bleeding diathesis seen in patients with chronic liver disease is complex and may include qualitative and quantitative platelet deficiencies.¹ Platelets have a deficiency of platelet factor 3 and membrane glycoprotein I.² Abnormal primary and secondary aggregation responses are also seen.³ Bleeding time is often prolonged, irrespective of the platelet count.⁴ As in uremia,⁵ levels of factor VIII coagulant, von Willebrand factor, and ristocetin co-factor activity are normal to increased and are associated with a normal distribution of von Willebrand factor multimers.^4,6 Hemorrhage remains an important source of morbidity and mortality in those with chronic liver disease.

In one uncontrolled study⁷ and two controlled trials,^4,6 treatment with desmopressin (l-deamino-8-d-arginine vasopressin) was found to improve the bleeding time in patients with chronic liver disease. An improvement in bleeding time correlates with neither pretreatment levels of von Willebrand factor⁷ nor an observed post-treatment increase in the levels of von Willebrand factor large multimers.⁴ The exact mechanism by which desmopressin reduces the bleeding time in chronic liver disease has yet to be established. Although larger clinical trials are needed to define its precise value, the drug may have a role in the treatment of patients with chronic liver disease in the setting of spontaneous hemorrhage, biopsy, and surgery.