The immunological diagnosis of chronic viral hepatitis

Chronic viral diseases of the liver are associated with changes in immune reactions mediated by T and B lymphocytes and dependent in severity on etiological factor (virus of hepatitis B, delta, C, their combination), the disease stage (hepatitis, cirrhosis), the process activity, kind of immune correction. HBsAg, viral hepatitis B marker, was detected in 21.2% of 1400 cases with chronic active hepatitis and liver cirrhosis. 32% of HbsAg-seropositive patients had antibodies to delta-antigen. Antibodies to HBsAg, HCV were found in 27.7 and 14.9% of the above patients. Chronic viral diseases of the liver with persistence of HBV, HDV and HCV markers are characterized by a complex of immune disorders, including a moderate rise in peripheral blood of IgM, IgG, IgA, IgE, Ig kappa, lambda, immune complexes, cryoglobulins, autoantibodies to subcellular structures as well as changes in regulatory (suppressor, helper) and effector (lymphokine-producing) functions of T lymphocytes, inhibition of phagocytosing capacity. The above shifts in immune status, clinical and biochemical activity of the disease are more pronounced in chronic active hepatitis with HCV markers compared to BHV. Of maximal intensity they were in combined viral infection HBV+HDV or HBV+HCV.     

Colitis and hepatitis caused by methyldopa

Acute, severe colitis and hepatitis developed in a 55-year-old man on two occasions in relation to administration of methyldopa. He also had fever, skin rash, and eosinophilia, suggesting drug allergy. All symptoms and signs remitted after he stopped taking the drug. It appears that this agent is capable of producing acute colitis as well as the previously recognized hepatitis.     

HLA class II genes in chronic hepatitis C virus-infection and associated immunological disorders

To investigate the factors that may confer susceptibility or protection to hepatitis C virus (HCV) infection and to HCV-associated immunological disorders, we designed two studies on 420 Sardinian transfusion-dependent thalassemia patients followed in our department in Cagliari since 1974. The first one was an epidemiological survey aimed to evaluate the prevalence of HCV infection and HCV-associated immunological disorders. In the second study, the distribution of different HLA class II genes was examined by DNA analysis in 116 HCV positive patients, 30 HCV negative patients, and 606 healthy controls. Three hundred fourteen patients became infected with HCV (74.7%) after 5.6 +/- 2.8 years of regular transfusion program. Mixed cryoglobulinemia, purpura, arthritis, proteinuria, decreased complement levels, rheumatoid factor and anti-GOR, smooth muscle antibody (SMA), anti-nuclear antibody (ANA), and liver, kidney microsome (LKM) autoantibodies were significantly more represented in HCV positive patients than in negative ones (P < .05). A significant increase of HLA class II DR2 subtype (DRB1*1601,DQB1*0502) was observed in a group of 30 HCV negative patients who despite 10.3 +/- 2.2 years in a regular blood transfusion program did not show any evidence of HCV infection (Pc < .0092). Our results represent clear evidence for a relationship between HCV infection and immune extrahepatic abnormalities. A gene(s) located in the human major histocompatibility complex (MHC) region may play an important role in conferring protection against HCV infection.     

Fatal cholestatic hepatitis caused by D-penicillamine

A 37-yr-old woman with RF-positive RA developed cholestatic hepatitis after 10 days of D-penicillamine therapy. This was discontinued immediately. The cholestasis persisted for the remaining 14 months of her life. Severe hypercholesterolemia developed with xanthelasmata and eventually pancytopenia, which was caused by a massive infiltration of the bone marrow by lipid-containing foam cells. The patient died of sepsis. Review of the literature shows intrahepatic cholestasis to be a rare and idiosyncratic complication of D-penicillamine therapy. To our knowledge, ours is the first documented case of persistent cholestatic icterus.     

The cytological aspects of chronic pancreatitis

Biopsy material of pancreatic tissue using light-optical radioautography and electron microscopy, and the method of high-precise radioautography also, was investigated to study up the pancreatic gland (PG) pathology in chronic pancreatitis (CHP). It was established that CHP is a chronic proliferative-destructive process causing focal generalized fibrosis of PG. All the structural components of organ, and the duct epithelium first of all, are affected in CHP. It gives reason to regard a duct system as a complex independent morphofunctional unit of PG.     

Clinico-radiological and functional aspects of respiratory syndromes caused by collagen diseases

The clinical and radiological features in 100 patients with collagen diseases (rheumatoid arthritis, lupus, sclerodermia, dermatomyositis, and panarteritis nodosa) were compared with respiratory performance. 56 patients were drawn from the series of Pende et Al. and 44 from a personal series. The results are set out in tables and graphs. It was found that lung lesions due to collagen disease have no special clinical and radiological features. Respiratory performance is that of a restrictive syndrome that gradually progresses from A.R. to E.S., S. and P.M., accompanied by obstruction of the large airways, as shown by hyperinsufflation in sclerodermia and reduced specific conductance in rheumatoid arthritis.     

An evaluation of the degree of the morphological activity and the stage of the process in patients with chronic liver diseases caused by coinfection with the hepatitis B, C and/or D viruses

In order to determine the differences in histological grade of activity and the stage of fibrosis in patients with chronic liver diseases due to multiple hepatitis virus infection and single infection of HBV and HCV we assessed the 68 liver biopsies samples according to Knodell and Scheuer scoring systems. Retrospectively, 216 liver biopsies reports from consecutive patients with chronic viral hepatitis were analysed. Histological activity index (HAI) in HBV/HCV coinfection was higher than in a single HCV infection; it did not differ in groups of HBV/HBC and HBV. The difference was due to the interface hepatitis; lobular activity and portal inflammation were the same. In HDV superinfection HAI was high due to both portal-periportal and lobular hepatitis. HAI depended mainly upon the presence of HBV replication; in patients with chronic hepatitis C with HBV-DNA HAI was also higher than in single HCV group. No difference in HAI between triple and dual hepatitis virus infection was found. In patients with HBV/HCV coinfection and especially with HDV superinfection the advanced stages occurred more than often than in patients with single infections.