Eradication of esophageal varices by endoscopic sclerotherapy: how much is enough?

To clarify if complete eradication of varices from the lower esophagus by endoscopic sclerotherapy is really essential to prevent rebleeding, or if reduction of varices below a certain size can be considered a sufficient result, we compared the fate of 72 patients in whom sclerotherapy was stopped after one of the following endoscopic endpoints was reached: complete eradication (15 patients, group 1), partial eradication with residual small white varices (32 patients, group 2), and partial eradication with residual small blue varices (25 patients, group 3). The incidence of variceal recurrences and recurrent bleeding over a median follow-up of 17 months after stopping sclerotherapy did not differ significantly in the three groups. Analysis of the time course of variceal recurrences showed that the recurrence-free interval was almost identical in group 1 and group 2 patients (13 and 14 months, respectively). Group 3 patients had a shorter recurrence-free interval (8.3 months), but the difference was not statistically significant. We conclude that sclerotherapy can be stopped safely when either complete eradication or reduction of varices to small white columns is obtained.

Activation of coagulation in cirrhotics after endoscopic variceal schlerotherapy.

To investigate the occurrence and extent of activation of coagulation after endoscopic variceal sclerotherapy (EVS), we performed serial measurements of conventional coagulation tests [prothrombin time (PT), partial thromboplastin time (PTT), platelets, and fibrinogen], and of plasma fibrinopeptide A (FPA) in 39 cirrhotic patients undergoing 55 sessions of elective EVS. Thrombin (20 U/ml) and sodium morrhuate 5% were used in sequence as sclerosants on 34 occasions. In the remaining 21 sessions, sodium morrhuate 5% alone was used. Conventional coagulation tests did not change significantly after EVS, regardless of the type of treatment. Basal plasma FPA levels were abnormally high in about 50% of patients. After EVS, plasma FPA increased sharply in 37/39 patients (95%), returning to baseline values in most of them within 24 h. We conclude that transient systemic activation of blood coagulation occurs after EVS. Such activation can be detected only by sensitive methods such as FPA assay, and has no effect on conventional coagulation tests. This, and the absence of any clinical EVS-related coagulation disorder in our patients, suggests that activation of coagulation should not be a major concern for patients undergoing EVS.

[Natural history of the state of asymptomatic carrier of HBsAg: 7-year follow-up]. / Storia naturale della condizione di portatore asintomatico di HBsAg: sette anni di follow-up.

UNLABELLED: Ninety-six chronic asymptomatic HBsAg carriers underwent liver biopsy. Liver histology was normal in 5 cases, showed nonspecific changes in 67, chronic persistent hepatitis in 18, and chronic-active hepatitis in 6. Seventy-four patients were followed for up to 105 months (mean 80 months) in order to evaluate the occurrence of clinical, biochemical, serological or histological changes. Only two patients cleared the HBsAg, respectively 10 and 96 months after undergoing liver biopsy; the latter patient became anti-HBs positive 6 months after he cleared HBsAg. All 10 patients who initially were negative for both HBeAg and anti-HBe became anti-HBe positive during follow-up. All 4 patients who were HBeAg positive at the time of liver biopsy cleared HBeAg 6 to 39 months thereafter. Two of them became anti-HBe positive. None of the patients initially HBeAg negative became positive for this antigen during follow-up. Significant increases of serum transaminases were observed in 5 patients; in one superinfection by delta agent was documented, the other 4 being constantly anti-delta negative. Three of the latter patients underwent repeat liver biopsy, which showed progression from minimal changes to chronic persistent hepatitis in one, and from minimal changes to chronic active hepatitis in another. In the third patient, repeat biopsy showed persistence of chronic persistent hepatitis. IN CONCLUSION: chronic hepatitis occurs in about 25% of chronic asymptomatic HBsAg carriers; clearance of HBsAg is a rare event among these patients; the HBe system has little diagnostic or prognostic value; delta superinfection is rare; however, deterioration of liver histology may occur even in the absence of delta superinfection.

Acute type B hepatitis in parenteral drug-addicts (PDA): prognostic value of circulating HBsAg/IgM complexes.

Fifty-three parenteral drug-addicts with acute viral hepatitis type B were tested by a solid-phase radioimmunoassay for circulating HBsAg/IgM complexes in the acute phase and in the follow-up. Among the 47 recovered patients HBsAg/IgM complexes were either absent from the onset of the disease, or disappeared from serum within 4 weeks of admission, long before HBsAg had cleared or serum alanine aminotransferase has returned to normal. On the contrary, HBsAg/IgM complexes persisted indefinitely among the 6 patients who developed a chronic HBsAg-positive hepatitis. These results indicate that sequential serum testing for HBsAg/IgM complexes might be of value in predicting the long-term outcome of acute type B hepatitis of parenteral drug-addicts.

Case-control study of hepatitis B virus infection in chronic liver disease and hepatocellular carcinoma.

The prevalence of serum hepatitis B virus markers was studied in three groups of age- and sex-matched patients: a. 31 patients with liver cirrhosis and hepatocellular carcinoma (c-HCC); b. 31 patients with chronic liver disease (CLD) and c. 62 hospitalized control subjects. The overall exposure rate to the hepatitis B virus was 90% in c-HCC, 80% in CLD and 58% in control subjects. The prevalence of hepatitis B surface antigen (HBsAg) was 29%, 13% and 1.6% in the three groups, respectively. The prevalence of hepatitis B surface antibody was significantly lower in c-HCC (9.6%) than CLD (42%) and control subjects (40%). The serological evidence of continuous viral replication (HBsAg positivity or isolated high titre hepatitis B core antibody positivity) was more common in c-HCC (39%) than CLD (12%) and control subjects (1.6%). The prevalence and patterns of aggregation of serum hepatitis B virus markers were similar in the 31 patients with c-HCC and in 11 patients with HCC without concomitant liver cirrhosis (n-HCC). In conclusion, the overall exposure rate to the hepatitis B virus is similar in c-HCC and CLD. However, serological evidence of continuous viral replication is more common in the former group. A defective clearance of the hepatitis B virus in hepatocellular carcinoma is a possible explanation of the phenomenon. The strength of the association between hepatitis B virus infection and hepatocellular carcinoma appears to be similar in c-HCC and n-HCC.