Hepatitis: Ozaslan E

Ozaslan E, Yilmaz R, Simsek H, Tatar G. · Division of Gastroenterology, Hacettepe University Hospital, Ankara, Turkey. · Ann Pharmacother. · Pubmed #12398565 No free full text.

Abstract: OBJECTIVE: Due to their antiproliferative activity, the probable effects of interferons on a fetus are a concern. We report on a pregnant patient who developed acute hepatitis C during pregnancy and was treated with a short course of interferon alfa therapy with a successful outcome. CASE SUMMARY: A 26-year-old woman was diagnosed with acute hepatitis C at the 16th week of pregnancy. She received a total dose of 72 million units of interferon alfa-2b during a 2 1/2 month period. Although the therapy was discontinued due to adverse effects, a complete biochemical and virologic response was obtained. Premature labor occurred and healthy, but growth-restricted, twin infants were born transvaginally. At 18 months of age, they had normal development, with a negative hepatitis C serology. DISCUSSION: The rate of transmission of hepatitis C virus from mother to infant is within the range of 1-5%. Although acute hepatitis C during pregnancy is a very rare occurrence, the mother is at a great risk for chronic infection. There is scarce literature about the probable effects of interferon use during pregnancy due to a lack of controlled studies in this special population. A total of 8 infants, including ours, exposed to interferon alfa and/or ribavirin during pregnancy showed no congenital anomalies or malformations. CONCLUSIONS: Patients with chronic hepatitis whose therapy can be delayed should not be treated with interferon due to a lack of controlled studies. However, women exposed to interferon inadvertently during pregnancy may be encouraged to continue pregnancy. In patients with acute hepatitis C during pregnancy, the use of interferon therapy should be considered with close monitoring.

Ozaslan M, Ozaslan E, Barsgan A, Koruk M. · Department of Biology, University of Gaziantep, 27310 Gaziantep, Turkey. · J Genet. · Pubmed #18305339 links to  free full text

Abstract: The S gene region of the hepatitis B virus (HBV) is responsible for the expression of surface antigens and includes the 'a'-determinant region. Thus, mutation(s) in this region would afford HBV variants a distinct survival advantage, permitting the mutant virus to escape from the immune system. The aim of this study was to search for mutations of the S gene region in different patient groups infected with genotype D variants of HBV, and to analyse the biological significance of these mutations. Moreover, we investigated S gene mutation inductance among family members. Forty HBV-DNA-positive patients were determined among 132 hepatitis B surface antigen (HbsAg) carriers by the first stage of seminested PCR. Genotypes and subtypes were established by sequencing of the amplified S gene regions. Variants were compared with original sequences of these serotypes, and mutations were identified. All variants were designated as genotype D and subtype ayw3. Ten kinds of point mutations were identified within the S region. The highest rates of mutation were found in chronic hepatitis patients and their family members. The amino acid mutations 125 (M -> T) and 127 (T -> P) were found on the first loop of 'a'-determinant. The other consequence was mutation inductance in a family member. We found some mutations in the S gene region known to be stable and observed that some of these mutations affected S gene expression.

Topal F, Ozaslan E, Akbulut S, Küçükazman M, Yüksel O, Altiparmak E. · Department of Gastroenterology, Numune Education and Training Hospital, Ankara, Turkey. · Ann Pharmacother. · Pubmed #16926305 No free full text.

Abstract: OBJECTIVE: To report the third published case, as of April 8, 2006, of methylprednisolone-induced toxic hepatitis. CASE SUMMARY: A 47-year-old woman was admitted to our clinic with weakness, fatigue, pruritus, and scleral icterus that had developed 10 days prior to presentation. She had been taking topiramate for one year for treatment of chronic isolated central nervous system vasculitis. One week before her symptoms developed, she had completed a self-prescribed 7 day course of oral methylprednisolone for treatment of left arm weakness. She believed that methylprednisolone was appropriate since it had been used previously for acute episodes of vasculitis. Results of liver function tests performed on admission were alanine aminotransferase 2478 U/L, aspartate aminotransferase 1600 U/L, total bilirubin 10 mg/dL, direct bilirubin 8 mg/dL, alkaline phosphatase 138 U/L, and gamma-glutamyl transferase 242 U/L. Topiramate and methylprednisolone were the only drugs she had been taking before admission, and no other causes of liver dysfunction (eg, infection, ischemia, systemic disease) were identified. Topiramate was stopped, and enzyme levels decreased to normal values within 45 days without treatment. There had been no increase in enzyme levels during hospitalization upon the accidental use of topiramate. Based on the history and laboratory findings, the final diagnosis was mixed hepatocellular and cholestatic liver injury caused by methylprednisolone. DISCUSSION: Steroids have rarely been associated with hepatotoxicity; moreover, they are the treatment of choice for severe hepatitis. To date, only 2 cases of methylprednisolone-induced hepatotoxicity have previously been reported. Our case is similar to those with regard to mixed hepatocellular and cholestatic liver injury. Resolution of the hepatotoxicity occurred after discontinuation of the drug, with conservative treatment measures. An objective causality assessment based on the Naranjo scale suggests that hepatotoxicity was probably related to methylprednisolone. CONCLUSIONS: Although rare, hepatotoxicity related to methylprednisolone should be considered in patients who develop elevated enzyme levels while receiving this steroid.

Ozaslan E, Kiliçarslan A, Simşek H, Tatar G, Kirazli S. · Division of Gastroenterology, Hacettepe University Faculty of Medicine, Ankara, Turkey. · J Int Med Res. · Pubmed #14587305 No free full text.

Abstract: We aimed to determine serum soluble Fas antigen (sFas) levels at various stages of hepatitis C virus (HCV)-induced liver disease, and investigate correlations between serum sFas levels and clinical, biochemical and pathologic features. Sixty-five patients were categorized into five groups: 1, chronic active hepatitis C, elevated alanine aminotransferase (ALT), HCV-polymerase chain reaction (PCR) positive; 2, responders to interferon + ribavirin therapy; 3, cirrhosis; 4, chronic hepatitis C, normal ALT, HVC-PCR positive; and 5, sustained responders. Group 6 comprised 15 control individuals. Serum sFas levels were measured by enzyme-linked immunosorbent assay. Significant differences in serum sFas levels were found between the following groups: 1 and 2; 1 and 3; 1 and 4; 1 and 6; and 3 and 6. Serum sFas levels did not correlate with ALT, histological activity or HCV-PCR positivity within group 1. Serum sFas levels appear to increase in advanced stages of HCV-induced liver disease, as a result of host-related immunological factors.

Ozaslan E. · No affiliation provided · Liver Int. · Pubmed #19453947 No free full text.

This publication has no abstract.

Ozaslan E. · No affiliation provided · Eur J Gastroenterol Hepatol. · Pubmed #19436174 No free full text.

This publication has no abstract.