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Background: Recent reports suggest a decline of delta hepatitis (DH) in the West as well as in the Far East. Aim: To study the DH seroepidemiology in Turkey. Methods: Statistical power analysis was utilized based on data available in a recent article using prevalence figure estimates. Binominal distribution was applied in order to assess the number of samples required to estimate the prevalence with a given precision. Results: Out of 62 studies in the original study, 32 were eliminated because of insufficient power. A total of 6734 patients (5231 with chronic hepatitis and 1503 with cirrhosis) were analysed. Anti-HDV seropositivity among patients with chronic hepatitis B (CHB) and hepatitis B-induced cirrhosis was lowest in the west of the country and highest in the southeast (5 vs. 27%, P

The pancreas. The clinical pre-sentation may vary from edematous pancreatitis, a milder form, to necroti-zing pancreatitis, which has an unfavorable clinical course. The most com-mon etiological agents are bile stones and alcohol. Hypertriglyceridemia can also cause acute pancreatitis. The risk of acute pancreatitis increases when se­rum triglyceride levels exceed 1000 mg/L. Herein, we present a case wth type I familial hyperlipidemia who presented with hypertriglyceridemia-induced acute pancreatitis, which did not respond to conservative treatment but only abated after plasmapheresis., Akut pankreatit pankreasın akut inflamasyonudur. Hastalığın hafif bir şekli olan ödematöz pankreatitten, ağır bir klinikle seyreden nekrotizan pankreati-te kadar farklı klinik şekillerde prezente olabilir. Etyolojide en sık sebep, saf­ra taşları ve alkoldür. Hipertrigliseridemi de akut pankreatite yol açabilir. Se­rum trigliserid düzeyi 1000 mgr/dl ve üstüne çıktığında akut pankreatit riski artar. Biz Tip I ailevi hiperlipidemisi olan, hipertrigliseridemiye bağlı akut pankreatitle başvuran, konservatif tedaviye rağmen akut pankreatit tablosu yatışmayan ve plazmaferez ile klinik düzelme sağlanan bir olgu sunacağız.

BACKGROUND Chronic infection with hepatitis B virus and hepatitis delta virus (HDV) results in the most severe form of viral hepatitis. There is no currently approved treatment. We investigated the safety and efficacy of 48 weeks of treatment with peginterferon alfa-2a plus adefovir dipivoxil, peginterferon alfa-2a alone, and adefovir dipivoxil alone. METHODS We conducted a randomized trial in which 31 patients with HDV infection received treatment with 180 mu g of peginterferon alfa-2a weekly plus 10 mg of adefovir daily, 29 received 180 mu g of peginterferon alfa-2a weekly plus placebo, and 30 received 10 mg of adefovir alone weekly for 48 weeks. Follow-up was conducted for an additional 24 weeks. Efficacy end points included clearance of HDV RNA, normalization of alanine aminotransferase levels, and a decline in levels of hepatitis B surface antigen (HBsAg). RESULTS The primary end point - normalization of alanine aminotransferase levels and clearance of HDV RNA at week 48 - was achieved in two patients in the group receiving peginterferon alfa-2a plus adefovir and two patients in the group receiving peginterferon alfa-2a plus placebo but in none of the patients in the group receiving adefovir alone. At week 48, the test for HDV RNA was negative in 23% of patients in the first group, 24% of patients in the second, and none of those in the third (P=0.006 for the comparison of the first and third groups; P=0.004 for the comparison of the second and third). The efficacy of peginterferon alfa-2a was sustained for 24 weeks after treatment, with 28% of the patients receiving peginterferon alfa-2a plus adefovir or peginterferon alfa-2a alone having negative results on HDV-RNA tests; none of the patients receiving adefovir alone had negative results. A decline in HBsAg levels of more than 1 log(10) IU per milliliter from baseline to week 48 was observed in 10 patients in the first group, 2 in the second, and none in the third (P

The objective of this study was to review the studies on hepatitis D virus-related liver diseases and to evaluate the national and regional outcomes in order to identify the hepatitis D virus infection in Turkey.This retrospective study included 2182 acute viral hepatitis, 6613 inactive HBsAg carriers, 5961 chronic hepatitis B, 1264 liver cirrhosis and 748 hepatocellular carcinoma cases, who were evaluated for anti-hepatitis D virus positivity at several centers in Turkey since 1980's. ELISA method was used and the results were statistically evaluated.The anti-hepatitis D virus positivity was 3.0% in 1416 acute viral hepatitis and 8.1% in 766 acute hepatitis B cases. This ratio was significantly higher in Diyarbakir than in Istanbul and Ankara for acute viral hepatitis (p0.001). The mean anti-hepatitis D virus was 4.9% in inactive HBsAg carriers and significantly decreased from 1980 to 2005 (4.1% and 2.9%, respectively p0.001). The anti- hepatitis D virus was 20% in chronic hepatitis B and 32.5% in liver cirrhosis cases. The positivity were significantly lower in Istanbul and Izmir compared to Diyarbakr and Van (p0.001). Antihepatitis D virus positivity was decreased in all regions for the last two decades (p0.001). The rates decreased from 31% to 11% for chronic hepatitis B and from 43.3% to 24% for liver cirrhosis (p0.001). The mean anti-hepatitis D virus was 23% in hepatocellular carcinoma cases, which was significantly lower in Istanbul and Izmir compared to Diyarbakr and Elaz currency (p0.0001).The hepatitis D virus infection is a critical problem in our country, particularly in the Eastern and Southeastern Anatolia. In recent years, the hepatitis D virus infection is decreasing countrywise, however the rate still remains to be critical.

HBeAg-positive patients with normal ALT levels are unlikely to respond to current therapy. In addition, there is a high risk of hepatocellular carcinoma in HBeAg-positive patients in the natural course of HBV infection. For this purpose, we aimed to investigate the clinical efficacy and safety of a three-month course of lamivudine therapy in HBeAg-positive hepatitis B patients with normal aminotransferase levels for assessing a more practical and economical approach to these patients.Forty-six patients were prospectively randomized into two groups. Group A consisted of 13 patients treated with lamivudine 100 mg/day, for 12 weeks [7 males, mean age 23.30+/-5.82 years, median ALT of 27 IU/L (21-40), median HBV DNA of 4116 pg/ml (2885-6628)]. Group B consisted of 33 patients without treatment [18 males, mean age 24.75+/-6.92 years, median ALT of 30 IU/L (19-39), median HBV DNA of 4094 pg/ml (782-7387)]. Main outcome measure was sustained virologic response, which was defined as loss of HBV DNA in serum with HBeAg seroconversion at least 12 months thereafter. Follow-up lasted 12 months after the first dose.No significant effects were observed in the treated population in the reduction of HBV DNA to undetectable levels, in HBeAg/anti-HBe seroconversion, or in transaminase levels. At the end of follow-up, sustained virologic response was almost similar in the study as well as control group (7.6% vs. 3.0%, p=0.502). None of the 13 patients who received lamivudine therapy had HBeAg seroconversion during the study period. In addition, the suppression of serum HBV DNA was temporary; prolonged suppression could be achieved in only one patient in the follow-up period. The median levels of HBV DNA and ALT values between baseline and month 12 did not differ significantly between groups. All patients remained HBsAg positive and none developed anti-HBs. The therapy was well tolerated and post-therapy flare was not observed in any patient after stopping lamivudine therapy.A short course of lamivudine therapy resulted mostly in only temporarily depressed serum HBV DNA levels without significant change in viral clearance. Whether permanent suppression of HBV DNA can be achieved in this special population of HBsAg carriers by long-term treatment with lamivudine awaits further controlled trials. New and safe modalities of therapy are needed for the satisfactory treatment of these asymptomatic but viremic patients.

Hepatitis B virus infection is among the most devastating health problems in the world, including Turkey. In this cross-sectional study, we aimed to investigate the correlations between hepatitis B virus genomic load and various measures of the progression of chronic hepatitis B virus infection.A total of 354 chronic HBsAg carriers [126 inactive HBsAg carriers, 50 asymptomatic replicative carriers (immune tolerant patients), 90 chronic hepatitis B patients and 88 patients with liver cirrhosis] were enrolled into the study. Eligible patients included males and females, 14-62 years of age, with detectable serum HBsAg, HBeAg or anti-HBe in serum at the time of screening and for at least six months before study entry. Serum hepatitis B virus DNA was detected by liquid hybridization, and results under the level of 1 pg/ml were additionally confirmed by polymerase chain reaction.Of 354 patients, 118 (33%) were HBeAg-positive and 236 (67%) HBeAg-negative. Of HBeAg-negative patients, 126 (53%) had normal alanine aminotransferase, 31 (13%) had elevated alanine aminotransferase (chronic hepatitis B) and 79 (33%) had evidence of cirrhosis; corresponding figures in the HBeAg-positive patients were 50 (42%), 59 (50%) and 9 (8%). There is a significant correlation between transaminase values and histological liver damage, whereas no correlation was found between viral replication and liver damage.Hepatitis B virus DNA is an important and specific marker for ongoing hepatitis B virus related liver disease, but alanine aninotransferase was shown to be the best marker for liver inflammation and not hepatitis B virus viral load. Although these findings are not new, they are of some utility since they prevent unnecessary and cost-intensive viral load determinations in chronic HBsAg carriers.

Hepatocellular carcinoma represents the 8th most frequent malignancy worldwide. The World Health Organization recognizes five histologic patterns and four cytologic variants of hepatocellular carcinoma. Clear cell carcinoma of the liver is a well-defined variant of hepatocellular carcinoma in which a large number of cells show clear cytoplasm that does not stain with hematoxylin and eosin. It can be confused with other clear-cell malignancies. A 52-year-old man presented with mild dyspeptic symptoms, right-sided upper abdominal pain, weakness, weight loss, abdominal mass and jaundice symptoms for nearly six weeks. After diagnostic procedures, an ultrasonography-guided liver biopsy was performed. In microscopic examination, malignant cells with vacuolated foamy to clear cytoplasm and central and eccentric nuclei, tumor composed of solid mass and cords, and clear cells were observed, and hepatocellular carcinoma, clear cell variant, is diagnosed. We report this rare case of primary clear cell carcinoma in the cirrhotic liver. The case was discussed in detail regarding histological presentation, with particular attention to histopathologic differential diagnosis.