Hepatobiliary and pancreatic ascariasis.

Ascariasis is a helminthic infection of global distribution with more than 1.4 billion persons infected throughout the world. The majority of infections occur in the developing countries of Asia and Latin America. Of 4 million people infected in the United States, a large percentage are immigrants from developing countries. Ascaris-related clinical disease is restricted to subjects with heavy worm load, and an estimated 1.2 to 2 million such cases, with 20,000 deaths, occur in endemic areas per year. More often, recurring moderate infections cause stunting of linear growth, cause reduced cognitive function, and contribute to existing malnutrition in children in endemic areas. HPA is a frequent cause of biliary and pancreatic disease in endemic areas. It occurs in adult women and can cause biliary colic, acute cholecystitis, acute cholangitis, acute pancreatitis, and hepatic abscess. RPC causing hepatic duct calculi is possibly an aftermath of recurrent biliary invasion in such areas. Ultrasonography can detect worms in the biliary tract and pancreas and is a useful noninvasive technique for diagnosis and follow-up of such patients. ERCP can help diagnose biliary and pancreatic ascariasis, including ascaris in the duodenum. Also, ERCP can be used to extract worms from the biliary and pancreatic ducts when indicated. Pyrantel pamoate, mebendazole, albendazole and levamisole are effective drugs and can be used for mass therapy to control ascariasis in endemic areas.

Hepatitis E: evidence for person-to-person transmission and inability of low dose immune serum globulin from an Indian source to prevent it.

This study was undertaken to assess the role of person-to-person transmission in hepatitis E and the ability of immune serum globulin (ISG) from an Indian source to prevent such transmission. Seventy six subjects (62 household contacts of patients with sporadic hepatitis E and 14 controls with no household contacts) were studied clinically, biochemically and serologically at entry and fortnightly thereafter for the next 8 weeks. Thirty two household contacts received 2 mL of 16.5% ISG 16.5% while the other 30 household contacts and 14 controls received 2 mL of normal saline intramuscularly at entry. Eighteen (29%) household contacts and none of the control subjects developed biochemical evidence of acute hepatitis E (p less than 0.01). The enzyme elevation occurred after a mean interval of 31.0 +/- 4.5 days from the onset of disease in the index case. This suggested that the disease in the case contacts had been contracted by household contact with the index case and not by simultaneous infection of the index case and the household contact. The incidence of disease was similar in the household contacts receiving ISG and normal saline (25% and 33.3% respectively, p = ns). ISG had no effect on the time interval to SGPT rise or on the severity of disease in household contacts.