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We aimed to compare the efficacy of interferon-alpha2b (IFN) induction treatment in combination with ribavirin to IFN induction alone in chronic hepatitis C. In total, 125 patients (66 male, 59 female, mean age: 48 +/- 9, range: 21-70) were enrolled and randomized into two arms: In the first, patients received 5 MU/day of IFN for 4 weeks followed by 3 MU/day for the next 4 weeks. Treatment was continued with 3 MU three times a week IFN for an additional 40 weeks. Ribavirin was administered 1000-1200 mg/day according to the body weight for the entire 48-week period. In the second arm, patients received placebo in addition to IFN. Fifty-nine patients were placed in the ribavirin arm and 66 in placebo arm. All patients were genotype 1. At week 48, 24/66 (36%) from the placebo and 31/59 (52%) from the ribavirin group responded (P > 0.05). However, during the 24-week untreated follow-up period, 13/24 (54%) from the placebo, and 8/31 (26%) from the ribavirin group relapsed (P = 0.002.), resulting in a sustained virologic response (SVR) rate of 17% in the placebo and 39% in the ribavirin group (P = 0.005.) In conclusion, IFN induction treatment in combination with ribavirin is superior to IFN induction treatment alone in genotype 1 patients, and the SVR rate of 39% is encouraging. [ABSTRACT FROM AUTHOR]

Compares the effectiveness of interferon-α[sub2b] (IFN) induction treatment in combination with ribavirin and IFN induction alone in chronic hepatitis C. Treatment parameters; Division of the group into ribavarin and placebo groupings; Comparison of figures on the response and relapse of the patients; Emergence of a sustained virologic response; Superiority of the combination treatment over the stand-alone treatment.

This study was planned to show the beneficial effects of prostacyclin (PGI2) on pulmonary function after heparin reversal with protamine. Twenty-eight patients entered the study. Half of these patients received prostacyclin, whereas the other patients did not.N-acetyl glucosaminidase (NAG) level was 37.6 ± 4.7 pmoL/mL in the con trol group and 19.7 ± 3.8 pmoL/mL in the PGI2 group (p < 0.001) five minutes after protamine administration. Leukotriene B 4 (LTB4) level was 118 ±13.7 pmoL/mL in the control group and 56 ± 13.8 pmoL/mL in the PGI2 group (p < 0.001). Alveolar-arterial oxygen difference was 69± 15 mmHg in the con trol group and 58 ± 11 mmHg in the PGI2 group (p < 0.05).As a result of this study it was concluded that PGI2 reduced the toxic mani festations of heparin-protamine complex and improved the pulmonary gas ex change. [ABSTRACT FROM PUBLISHER]

This study was planned to show the beneficial effects of prostacyclin (PGI2) utilization on adverse effects of protamine. PGI2 was administered at a rate of 5 ng/kg/min. Twenty patients entered this study. Half of them received PGI2 whereas the others did not.Right ventricular end-diastolic volume index and right ventricular stroke work index were 72 mL/m2 and 2.2 g.m/m2, respectively, after patients were weaned off the bypass and 79 and 1.5, respectively, at five minutes after pro tamine administration in the control group; these values were 88 and 3.2, re spectively, and 86 and 3, respectively, in the PGI2 group. Left ventricular stroke work index (g.m/m2) was 27.9 in the control group and 36.7 in the PGI2 group (p < 0.05) after protamine administration.Thromboxane B2 levels (pmoL/mL) in coronary sinus (CS) blood were 251 in the control group and 90 in the PGI2 group at five minutes after protamine administration (p < 0.05). Myocardial blood flow was 174 mL in the control group and 245 mL in the PGI2 group at five minutes after protamine adminis tration (p < 0.05). Cyclic adenosine monophosphate (cAMP) and cyclic guano- sine monophosphate (cGMP) levels in CS blood were 17 pmoL/mL and 2.1 pmoL/mL, respectively, in the control group and 36 and 0.3, respectively, in the PGI2 group at five minutes after protamine administration. Leukotriene B4 level was 129 and 57 pmoL/mL in the control and PGI2 groups, respectively (at the same time as the cAMP measurement) (p < 0.05).From the results of this study the authors conclude that adverse effects of heparin reversal with protamine can be reduced with the use of PGI2. [ABSTRACT FROM PUBLISHER]

Aim: To investigate the antifibrotic effects of peginterferon-alpha 2b and taurine on oxidative stress markers and hepatocellular apoptosis., Methods: Sixty rats with CCl4-induced liver fibrosis were divided into 4 groups (n=15). Group 1 was left for spontaneous recovery (SR). Groups 2-4 received peginterferon-alpha 2b, taurine, and their combination, respectively, for four weeks. Histological fibrosis scores, histomorphometric analysis, tissue hydroxyproline, tissue MDA, GPx and SOD activities were determined. Activated stellate cells and hepatocellular apoptosis were also evaluated., Results: The degree of fibrosis decreased in all treatment groups compared to spontaneous recovery group. Taurine alone and in combination with peginterferon-alpha 2b reduced oxidative stress markers, but peginterferon-alpha 2b alone did not. Apoptotic hepatocytes and activated stellate cells were higher in groups 2-4 than in group 1. Combined taurine and peginterferon-alpha 2b further reduced fibrosis and increased activated stellate cell apoptosis, but could not improve oxidative stress more than taurine alone., Conclusion: Peginterferon-alpha 2b exerts anti-fibrotic effects on rat liver fibrosis. It seems ineffective against oxidative stress in vivo. Peginterferon-alpha 2b in combination with taurine seems to be an antifibrotic strategy.

Fallot tetralogy (FT) is the most frequently observed conotruncal heart defect (CTHD) and accompanies 15% of the 22q11 deletion syndromes, DiGeorge/ velocardiofacial (DGS/VCFS) syndromes. TBX1 is a gene located in the 22q11 region and has a role in neural crest migration and conotruncal development. The mouse Tbx1 locus shows 98% homology with TBX1. DGS/VCFS-like aortic arch abnormalities in the mouse were attributed to deletions in this locus. The T-box region, common to both mice and humans, is part of TBX1 with proven effects on heart outflow track anomalies. The role of TBX1 in non-syndromic CTHDs is still unclear. In this study, we screened the TBX1 gene T-box region exons in 50 FT patients without 22q11 deletion and in 50 healthy volunteers. Our study did not show any disease causing mutations, but one polymorphic change. These results do not support a major role of the T-box region in the etiology of isolated FT. Furthermore, this study also confirms that mouse cardiac-development study models do not always provide an explanation for human phenotype-genotype correlations.

Background/aims: Thromboembolic events are more common in patients with inflammatory bowel disease than in the normal population; however, the reason for the increased prevalence is not clear. The aim of this study was to evaluate the prevalence of factor V Leiden, prothrombin G20210A and methylene tetrahydrofolate reductase (MTHFR) gene mutations in IBD patients followed in our outpatient clinic., Methods: Thirty-four patients with ulcerative colitis and 28 patients with Crohn's disease and 80 healthy controls were included in the study. No patient had a history of previous thromboembolism. Factor V Leiden, prothrombin G20210A and MTHFR gene mutations were studied., Results: Heterozygote factor V Leiden mutation was found in five (6.25%) control patients and in two (3.2%) IBD patients. Heterozygote MTHFR mutation was obtained in seven (11.3%) IBD patients and in five (6.25%) controls. Heterozygote prothrombin G20210A mutation was found in two (2.5%) and homozygote MTHFR mutation in one (1.25%) control patient. There was no statistical difference between the IBD group and healthy controls., Conclusions: Genetic mutations that could increase the thrombosis risk were not found to be different in IBD versus the normal population in our study.

A number of disorders for which an association with hepatitis C virus infection exist. These disorders include essential mixed cryoglobulinemia, membranoproliferative glomerulonephritis, and idiopathic pulmonary fibrosis. This study was initiated to investigate the cellular content and lymphocyte subpopulations of bronchoalveolar lavage fluid obtained from individuals with chronic hepatitis C and to compare the results to those of controls. Eighteen patients with chronic hepatitis C (male/female, 6/12) and 14 healthy volunteers (male/female, 6/8), were studied. Bronchoalveolar lavage fluid was obtained from each; and the lymphocyte subtypes and the presence of HCV-RNA in the bronchoalveolar lavage fluid were determined. All anti-HCV positive subjects were HCV-RNA positive in serum. One (5.6%) had a HCV-RNA positive bronchoalveolar lavage. The total cell and neutrophil counts of the bronchoalveolar lavage fluid were significantly greater in patients with chronic hepatitis C as compared to controls (5,799.6 +/- 957.4 x 10(3)/ml vs. 1,835.7 +/- 447.8 x 10(3)/ml, P = 0.001; 1,175.8 +/- 634.7 x 10(3)/ml vs. 53.1 +/- 28.1 x 10(3)/ml, P = 0.029). In contrast, the lymphocyte, macrophage and eosinophil counts did not differ. No difference in the percentage, median or range of individual T cell subsets or B cell numbers in the bronchoalveolar lavage fluid existed between the groups. It is concluded that hepatitis C virus infection may be associated with an occult pulmonary inflammatory reaction manifested by an increased number of polymorphonuclear neutrophils in bronchoalveolar lavage fluid. This finding may contribute to the process that leads to idiopathic pulmonary fibrosis seen in a minority of cases of chronic hepatitis C., (Copyright 2002 Wiley-Liss, Inc.)