270 Ataei B et al. infection with HDV tends to accelerate the progression of chronic HBV infection to chronic active hepatitis, cirrho- sis, and hepatocellular carcinoma and mediates fulmi- nant hepatitis. In addition, the response of HDV patients to antiviral therapy and the required dosages of thera- peutic regimens differ from those of chronic hepatitis B alone (4, 5). Approximately 5% of patients with chronic hepatitis B infection worldwide are infected with hepatitis D virus. Its prevalence in Italy, eastern Europe, and western Asia is higher than in the rest of the world, reaching 83.3%, 8.3%, and 12.5% in Romania, Italy, and Russia, respectively (5-7). HDV has a broad geographical distribution with two dominant patterns of transmission. In endemic regions, such as southern Italy, parts of Africa, and South Amer- ica, it is transferred through close personal contact in the absence of clear skin contact, such as close personal relationships among members of a family. In contrast, in areas that have a low prevalence, such as western Eu- rope and North America, HDV is seen more commonly in groups with frequent skin contact such as continual recipients of blood and blood products and intravenous drug users (8, 9). Sex and maternal-child transmission are other modes of transmission (1, 4). The most frequent method of diagnosis of HDV infec- tion is measurement of anti-HDV (IgM, IgG) in serum by ELISA. PCR can also be used to detect viral RNA in blood (10, 11). Acute HDV infection can occur simultaneously with acute HBV infection or can be superimposed onto chron- ic HBV infection. Fatal fulminant hepatitis occurs in 20% to 30% of coinfections of HDV and HBV in humans versus 2% of patients with acute hepatitis B without HDV coin- fection (1). More than 3% of the Iranian population is in- fected with HBV, and few studies have been conducted to determine the prevalence of HDV in chronic HBV patients in Iran. No study has examined this topic in Isfahan, the second largest city in Iran. Objectives This study was designed and performed in 2009 to de- tect anti-HDV in chronic HBV patients and related risk factors in this region. Patients and Methods This cross-sectional study was performed from April to November 2009. We included patients with chronic hep- atitis B virus infection who were in a carrier state (nor- mal ALT, normal sonography, normal physical exam, and negative for HBeAg) or exhibited immune tolerance (nor- mal ALT, normal sonography, normal physical exam, and HBeAg-positive) and under surveillance at the Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, with at least 6 months of diagnosis. In these patients, HBsAg was detected by in- dividual, familial, or disease-related follow-up, and they were tested periodically to measure viral activity and HDV infection in Isfahan liver function. Sampling was performed by nonprobability purposive technique. Consecutive patients of all ages and both genders were included in the study, and patients with thalassemia and frequent recipients of blood and blood products were excluded. Persons who did not consent to participation in the study were not enrolled. For all patients, demographics and risk factors were recorded and 5-mL blood samples were collected. Total HDV antibody was detected by ELISA (Diapro, Italy). Re- sults on HBsAb, HBeAg, HBeAb, and HBV DNA were ex- tracted from the patients’ records. Laboratory results on other variables, such as age, sex, duration of hepatitis, methods of diagnosis, and risk factors of hepatitis, were recorded for each patient. Data were analyzed using SPSS, version 15, using descriptive statistical methods and chi- square, Fisher’s exact, independent t, and logistic regres- sion tests. P-values of less than 0.05 were considered sig- nificant. Table 1. Frequency of risk factors of hepatitis B virus infection in participants Number Percentage Intravenous drug users Variable Surgery Blood transfusion Transplantation Uterine curettage Dialysis Dental manipulation History of hepatitis in the family 186 Table 2. Frequency of hepatitis B markers relative to HDV antibody HDV antibody p-value Positive [No. (%)] Negative [No. (%)] 2 (2.3%) 8 (3.1%) 8 (3.5%) 2 (1.7%) _ _ 1 (2.6%) 2 (11.1%) 86 (97.7%) 248 (96.9%) 221 (96.5%) 113 (98.3%) 26 (100%) 16 (100%) 38 (97.4%) 16 (88.9%) 0.68 0.36 _ 0.23 Tattoo Ear Piercing Circumcision High-risk sex Phlebotomy a only in females b only in males Marker HBe antigen Positive Negative HBe antibody Positive Negative HBs antibody Positive Negative HBV DNA Positive Negative Hepat Mon. 2011;11(4):269-272 20 144 40 1 12 13 292 54 91 243 6 60 5.8 41.6 11.6 0.3 53.8 11.9 a 3.8 84.4 15.6 26.3 99.2 b 1.7 17.3