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Effect of a New Drug on Coagulation Defects

JOHN C. HOAK, M.D.; JOHN R. CARTER, M.D.

Arch Intern Med. 1961;107(5):715-722.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

The patient with chronic liver disease leads a precarious existence. Metabolic function becomes impaired, and many complications arise which pose hazards to useful activity and even to life itself. Among these is the tendency to develop a hemorrhagic disorder. Since many blood clotting factors are produced in the liver, defects in its structure and function may play havoc with the hemostatic mechanism. Often such patients succumb to bleeding lesions which would not have been lethal if the blood clotting mechanism had been normal.

Several excellent reviews on coagulation defects in patients with liver disease have appeared recently.^1-3 The clotting defects are usually multiple. Deficiencies of platelets, prothrombin, Factor V, Factor VII, Factor X (Stuart-Prower), Factor IX (PTC), and fibrinogen have been observed. Fibrinolysis has been demonstrated in approximately 20% of patients with cirrhosis. Naeye⁴ maintains that PTA deficiency is a common finding in patients with liver disease. . . . [Full Text PDF of this Article]

Author Affiliations
IOWA CITY

From the Departments of Internal Medicine and Pathology, State University of Iowa College of Medicine.; Research Fellow, Department of Internal Medicine, State University of Iowa College of Medicine (Dr. Hoak); Professor and Head, Department of Pathology and Oncology, University of Kansas Medical Center, Kansas City, Kansas; formerly Professor, Department of Pathology, State University of Iowa College of Medicine (Dr. Carter).

Footnotes
Submitted for publication June 17, 1960.

This study was supported in part by Research Grant Number A-2464 from the National Institute of Arthritis and Metabolic Diseases, United States Public Health Service.

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