[Electron microscopic study of the liver in chronic viral hepatitis C complicated by alcoholic liver disease]. / Elektronno-mikroskopicheskoe issledovanie pecheni pri khronicheskom virusnom gepatite C v sochetanii s alkogol'noi bolezn'iu pecheni.

Combination of HCV-infection and alcoholic liver disease is associated with enhancement of hepatocellular damage (lipid and hydropic degeneration become diffuse), a decrease of hepatocyte necrotic foci and lymphomacrophagal infiltration, an increase of hepatocyte apoptosis and liver fibrosis, absence of lymphoid follicles. An important role in the genesis of these liver alterations is attributed to the combination of viral and alcoholic factors with persistence of hepatitis C virus and liver reticulo-endothelial system depression.

[Comparative morphologic characteristics of viral hepatitis B and C]. / Sravnitel'naia morfologicheskaia kharakteristika virusnykh gepatitov B i C.

Using liver biopsies in chronic HBV and HCV infections and their combination, the authors found between them morphological difference represented by nonspecific morphological markers. The combination of fat and hydropic hepatocytes degeneration, their heterogeneity, lymphoid follicles of various location and maturation degree, sinusoidal cell hyperplasia, accumulation of lymphocytes and macrophages in sinusoids, destruction, proliferation and sclerosis of ductules are of a high significance in hepatitis C. Etiological markers of hepatitis B are so-called ground-glass hepatocytes and "sand" nuclei. Various combination of these markers are characteristic for HBV and HCV co-infections with predominance among them of a replicating virus.

[Visceral manifestations of Wilson-Konovalov disease (analysis of 22 cases)]. / Vistseral'nye proiavleniia bolezni Vil'sona-Konovalova (analiz 22 nabliudenii).

Twenty-two patients with Wilson-Konovalov disease (WKD) had not only hepatic but also visceral symptoms: renal affection, cutaneous vasculitis, arthralgias, endocrine disorders, etc. In 8 of these 22 patients extrahepatic symptoms appeared 10 years before hepatic signs. The latter were distinguished by the frequency of edematic-ascitic syndrome, hemolytic episodes, hemorrhagic syndrome; low activity of serum aminotransferase. Initial neurological symptoms were registered in 6 patients only. 12 patients benefited from copper-eliminating therapy. 4 patients had advanced process which caused death. To detect WKD early, special diagnostic tests should be conducted in all subjects under 45 with hepatic symptoms or WKD-specific visceral manifestations. Examination of the patients' sibs is also desirable.