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It is known that in patients with porphyria cutanea tarda (PCT) there is an increased prevalence of the hepatitis B virus (HBV) and the hepatitis C virus (HCV). The incidence of anti-HCV in PCT in our country is 21.7% in estimations by the second generation method, however, the incidence of HBV in PCT was not assessed so far.In 60 patients with PCT antigens and antibodies against HBV and HCV were assessed (by the anti-HCV third generation ELISA method) and in subjects with signs of HBV or HCV. HBV DNA and HCV RNA were assessed by the method of the polymerase chain reaction. PCT without detectable HBV or HCV infection was found in 45 subjects (68%). HBV infection only was confirmed in seven subjects (10.6%), however none of the patients had positive HBsAg in serum. All had only antibodies against HBV. HCV infection only was detected in seven patients (10.6%) and HBV and HCV co-infection also in seven patients (10.6%). In the group of patients with HBV and HCV co-infection there was not a single HBsAg positive subject. The mean ALT serum activity was significantly higher as compared with subjects with HBV or HCV infection only (p0.05) and the histological finding on liver biopsy was more serious.HBV (21%) and HCV (21%) infection participates significantly in the clinical picture of PCT. A special subgroup is formed by patients with PCT and HBV and HCV co-infection who have as a rule a higher ALT activity and more severe histological changes in the liver. The incidence of HBV and HCV infection in PCT in the Czech Republic is double as compared with Germany or Great Britain.

In 1994 the authors published first results of anti-HCV antibodies in the group of 92 porphyria cutanea tarda patients, tested with ELISA second generation enzymatic method. Positivity, found in 21.7 per cent of them, was significantly higher when compared with the results of healthy blood-donors. Anti-HCV reactivity thus ascertained can be, however, non-specific in some cases and need not necessarily indicate existence of an active replication of hepatitis C-virus. The authors have therefore subsequently tried to verify the above results by the more sensitive polymerase chain reaction (PCR), enabling the proof of viral RNA and thus an assessment of the replication-activity of HCV. This study completes their previous findings for the evidence of viraemia in anti-HCV reactive PCT-patients.21 of 92 PCT-patients were reactive when examined with the second generation ELISA method (Sanofi, Pasteur). HCV RNA was examined in 20 subjects from the above group (one patient died in the meantime) by means of PCR. Positive HCV RNA was found in 17 patients, i.e. in 85 percent of them. Percutaneous liver biopsy without visual control was performed in 17 anti-HCV reactive and HCV RNA positive patients and in 46 anti-HCV negative porphyrics. The biopsy-findings were significantly worse in the HCV RNA-positive group. Also the average activity of ALT and AST was significantly higher in the patients with positive HCV RNA when compared with anti HCV-negative subjects.High frequency of HCV-infection (21.7 percent) was found in our group of 92 PCT-patients. Viraemia was present in the vast majority (85 per cent) of them, for they had also positive HCV RNA besides anti-HCV reactivity. These patients had also higher ALT- and AST-activity and more severe histological liver-changes. HCV-infection is the main virological cause of their liver lesion, beside ethylism. Hepatocellular carcinoma is rather exceptional in our porphyria patients in spite of their frequent HCV-infection.

In the majority of patients with acute viral hepatitis C the early antibody IgM anti-HCV in serum is positive. However, a substantial portion of the patients with chronic hepatitis C has also positive IgM anti-HCV as a sign of the continuing replication of the virus. The objective of the work was to assess the presence of IgM anti-HCV in patients with confirmed chronic hepatitis C, in subjects with HBsAg negative chronic hepatitis and in excluded blood donors. Moreover, the authors assessed the relationship between IgM anti-HCV positivity and the activity of serum transaminases and whether the presence of IgM anti-HCV has an impact on the histological finding in the liver.88 patients were examined (44 women and 44 men), average age 48 years. In 47 subjects histological examinations of the liver were made. IgG anti-HCV were assessed by the Monolisa anti-HCV Sanofi Pasteur test and IgM anti-c22 by an Abbott kit IgM HCV EIA: With regard to the results of the serological examination the patients were divided into three groups which were mutually compared. Group 1 comprised 24 patients with a positive IgG and IgM anti-HCV, group 2 38 patients with a positive IgG anti-HCV only and group 3 26 patients with a negative IgG and IgM anti-HCV. Of 88 examined patients 62 had positive IgG anti-HCV (70%). Of 62 IgG anti-HCV positive subjects 24 (39%) had positive IgM anti-c22. A total of 24 patients had blood transfusions (39%) but only 9 of them had positive IgM anti-c22 (37.5%). The mean ALT serum activity was significantly higher in subjects with positive IgM than in those without IgM (p = 0.006), however, for AST the difference was not significant (p = 0.09). Comparison of patients with a confirmed histological finding in the liver revealed that two-thirds of patients with a positive IgM anti-c22 either suffered from cirrhosis or chronic active hepatitis, while anti-HCV positive patients without IgM anti-c22 had cirrhosis or chronic active hepatitis only in one third of the cases.The results suggest that in chronic hepatitis C some 40% of the patients have positive IgM anti-c22; these subjects have a significantly higher serum ALT activity and a more advanced histological finding in the liver than subjects without IgM anti-c22. Assessment of IgM anti-c22 is important not only for diagnosis but also for treatment of chronic HCV infection with antiviral drugs.

In the majority of patients with acute hepatitis C the anti-HCV IgM antibodies in serum were present, however, some patients with chronic hepatitis C were positive for anti-HCV IgM too. The aim of this study was to assess the presence of anti-c22 IgM in patients with chronic hepatitis C and to determine whether the positivity for anti-c22 IgM has an impact on the histological finding in the liver. A total of 88 patients were examined (44 women, 44 men), mean age 48 years. The first group comprised 24 patients positive for both anti-HCV IgG and anti-c22 IgM, the second group 38 patients positive for anti-HCV IgG only, and the third group 26 patients negative for both anti-HCV IgG and anti-c22 IgM. Of 62 anti-HCV-IgG-positive subjects 24 (39%) were positive also for anti-c22 IgM. Of 24 patients who received a blood transfusion 9 (37.5%) were positive for anti-c22 IgM. The mean serum alanine aminotransferase (ALT) activity was significantly higher in subjects with anti-c22 IgM than that in subjects without them (p = 0.006), however, the difference in aspartate aminotransferase (AST) was not significant (p = 0.09). Histological examination was performed in 46 patients. Two-thirds of the patients with anti-c22 IgM had either cirrhosis or chronic active hepatitis (CAH) while only one third of the anti-HCV-positive patients without anti-c22 IgM had CAH or cirrhosis. The results showed that approximately 40% of the patients with CAH and cirrhosis had anti-c22 IgM, a significantly higher serum ALT activity and more serious histological finding in the liver than anti-HCV-positive patients without anti-c22 IgM.

The authors analyzed acute exacerbations of chronic hepatitis B in 24 chronic HBsAg carriers (20 with positive HBeAg, 4 with anti-HBe), more than half of whom were treated with glucocorticoids, by examining specific antigens and antibodies of the hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis delta virus (HDV), Epstein-Barr virus (EBV) and cytomegalovirus (CMV). Of 38 observed exacerbations of the disease they found in 7 (18%) deterioration after discontinuation of glucocorticoids, in 7 (18%) seroconversion of HBeAg to anti-HBe, in 9 (24%) spontaneous exacerbation of chronic hepatitis B, in 11 (29%) chronic activation, reactivation of EBV superinfection, in 3 (8%) CMV reactivation or superinfection and in one (3%) HDV superinfection. In no instance HAV superinfection was observed. Exacerbations were found five times more frequently in subjects in the stage of active viral replication (in HBeAg+ subjects) than in subjects with anti-HBe. In eight patients EBV reactivation was found after glucocorticoids withdrawal: in five patients after an average period of 5 months (range 3-7) and in three patients after an average period of 33 months (range 22-48). The results provide evidence that in addition to already known causes of acute exacerbations of chronic hepatitis B in our geographical area probably an important cause of deterioration of hepatitis is reactivation or superinfection with EBV and CMV in some patients in conjunction with previous glucocorticoid treatment.

Electron microscopy of 57 needle biopsies from livers of 55 patients with chronic hepatitis, mostly of type B, revealed, in addition to typical hepatitis B virus nucleocapsids in 34 cases, also atypical intranuclear inclusions in 9 biopsies. These inclusions consisted of electron-dense particles similar in size to hepatitis B virus nucleocapsids. The possibility of an involvement of a hepatitis non-A non-B virus is discussed.