Vasculitis associated with levamisole and circulating autoantibodies.

Delta hepatitis is caused by a dual infection with the hepatitis delta virus (HDV) and hepatitis B virus (HBV). HDV depends on the helper function of hepatitis B surface antigen (HBsAg) for its replication. Therefore, epidemiology of delta hepatitis usually follows that of HBV infection and it is particularly prevalent in endemic areas for HBV infection. The incidence of anti-HDV positivity appears to increase with age, especially among anti-HBe positive carriers.' Infection with HDV occurs either as coinfection with the HBV or as superinfection in a chronic HBV carrier. Although it is often associated with severe and progressive liver disease, the natural course may vary.2 To establish the prevalence of delta infection in children, we investigated total antidelta using an ELISA system (Organon Technica) in 206 children who were chronically infected with HBV (121 asymptomatic carriers, 59 with chronic persistent hepatitis, 13 with chronic active hepatitis, and 13 with cirrhosis) aged between 8 months and 17 years (mean (SD) 7.76 (3.70) years). We detected antidelta in only six patients (2.9%): in three with cirrhosis, two with chronic active hepatitis, and one with chronic persistent hepatitis. Their ages ranged between 8 and 13 years. Four of them were positive for serum HBeAg and two were positive for antiHBe. None of the asymptomatic carriers had antidelta. When we take into consideration the prevalence of antidelta in children with chronic liver disease it was 7.1% (six of 85 children with chronic hepatitis or cirrhosis). During four to seven years of follow up clinical and laboratory findings of our patients remained relatively stable. Turkey has an intermediate endemicity for HBV infection and the prevalence of HBsAg carriers varies from 4% to 10% 34 and antidelta positivity in adult patients with chronic hepatitis B has been found up to 36% in prevalence studies.5 Farci et al, in Italy, found a prevalence of 12.5% of antidelta in chronic hepatitis B infected children.6 However, in their study all children had chronic liver disease. The prevalence of antidelta in Turkish children is lower than that in Italian children, even ifwe consider only the patients with chronic hepatitis or cirrhosis (7.1% v 12.5%, respectively). There was no difference in the mean age of the patients and in the follow up duration between two studies. In Egypt a low prevalence of antidelta in children was reported (4.2%), 7 whereas Ruiz-Moreno et al found a high prevalence in Spain (13%).8 The prevalence of antidelta in adults in Italy 9 is similar to our country. The route of transmission of HDV infection in children might be different in various contries. The percentage of delta infection parallels the severity of the disease2 6; in our study antidelta positivity was also high in patients with cirrhosis (3/13) and chronic active hepatitis (2/13,) while none of asymptomatic carriers had antidelta. As previously shown in children and adults,56 a correlation between chronic delta infection and presence of anti-HBe was not observed in our patients. Although it was believed that delta infection usually worsened the course of the disease, clinical and laboratory findings of our patients were stable during follow up, similar to that found in the study of Bortolotti et al2 We conclude that in our country the prevalence of HDV infection is not high during childhood, and its prevalence increases with age suggesting that HDV infection is usually acquired as a superinfection rather than coinfection and vertical transmission is uncommon. The course of the disease is usually stable. The epidemiology of HDV infection is different in various countries. To explain the differences in geographical distribution of HDV infection further studies are needed.