Cirrhosis of the Liver

Cirrhosis of the Liver 

a chronic progressive disease involving destruction of the liver substance and injury to all its structural elements, including the parenchyma (with the death of many cells and the proliferation of connective tissue), the interstitial tissue, the reticuloendothelial system, bile ducts, blood vessels, and the serous membrane. The disease is manifested in humans by functional insufficiency of the liver and portal hypertension; other organs and systems may be involved in the pathological process.

The term “cirrhosis” was proposed by R. Laennec in 1819 to designate diseases in which the liver becomes tawny-colored, wrinkled, and compressed. The current understanding of the disease was arrived at by the Congress of Gastroenterologists that met in Havana in 1956. Classification is based on several features of the disease, including the cause, functional condition of the liver, and morphological picture of the lesions. Cirrhosis of the liver may be caused by infectious hepatitis or some other infectious disease, poisoning (including alcoholic intoxication), protein deficiency in the diet, and constitutional-genetic characteristics. It may also be caused by a combination of factors, and in many cases the etiology remains obscure (cryptogenic forms). Disturbance of intrahepatic circulation and autoimmune processes play an important part in the development of the disease. Morphological changes are produced by the inflammatory reaction, the proliferation of connective tissue, and the development of “nodules” of regenerating parenchyma.

The clinical symptoms of cirrhosis of the liver vary with the form and stage of the disease. They may include weakness, emaciation, abdominal pain, dyspepsia, meteorism, enlargement of the liver and spleen, jaundice, ascites, fever, and bleeding. Vascular spiders, palmar erythema, strawberry tongue, clubbed fingers, gynecomastia, and encephalopathy may also occur. Laboratory tests reveal anemia, leukopenia, thrombocytopenia, an accelerated erythrocyte sedimentation reaction, abnormal proportions of plasma fractions, a high concentration of some enzymes, and a low potassium concentration. Death results mainly from hepatic coma or hemorrhages from dilated veins of the esophagus and stomach.

Of considerable diagnostic importance are functional tests and instrumental methods of examination (laparoscopy, punch biopsy of the liver, scanning, angiography) to detect characteristic changes in the shape and color of the liver, to determine the exact morphological variant of the disease, and to establish the extent of activity of the process. Timely treatment can induce a remission or stabilize the patient’s condition. A regimen involving limited mental and physical stress and proper diet is indicated in compensated cirrhosis. If the process is active, chloroquines or corticosteroids, cytostatic agents, antilymphocyte globulin, diuretics, and other drugs are prescribed, as are injections of albumin, plasma, and protein hydrolysates. If intrahepatic cholestasis is pronounced, cholestyramine treatment may be warranted. Prevention of cirrhosis of the liver involves the control of diseases that may cause the disorder (mainly infectious hepatitis and alcoholism) and prompt treatment of acute and chronic hepatitis.

REFERENCES

Tareev, E. M., and I. E. Tareeva. “Khronicheskie gepatity i tsirrozy,” In Mnogotomnoe rukovodstvo po vnutrennim bolezniam, vol. 5, Moscow, 1965. Pages 306–477.
Bondar’, Z. A. Klinicheskaia gepatologiia. Moscow, 1970.
Endemicheskii gepatit. Moscow, 1970.
Osnovy gepatologii. Riga, 1975.
Schiff, L. (ed.). Diseases of the Liver. Philadelphia-Toronto, 1969.
The Liver and Its Diseases. Stuttgart, 1974.

M. E. SEMENDIAEVA