Delta Hepatitis

Hepatitis delta virus (HDV) is a defective RNA virus that requires HBsAg for replication and transmission. It can cause acute or chronic hepatitis. Chronic infection with HDV is one of the most severe and difficult to treat forms of viral hepatitis. It has been estimated that there is a total of 15-20 million HDV carriers in the world. This review focuses on two fundamental aspects of HDV infection. On the one hand, epidemiological data are summarized, which are essential to understand the real burden of this disease. After the HBV vaccination programs in many countries all over the world, HDV infection has decreased since 1980’s but this decline has not continued further in the last decade. Therefore, HDV infection is still an important public health problem in the world. On the other hand, therapeutic options are described. Currently, interferons are the only option for the treatment of chronic hepatitis delta infection, and pegylated-interferons have shown better results than conventional interferons (IFNs). Monotherapy of nucleos(t)ide analogs have been found ineffective against the HDV infection, but adefovir and pegylated-IFN combination therapy have had some advantages for reduction of HBsAg levels. Trials with more potent nucleoside analogs and pegylated-IFN could be effective in the treatment of chronic HDV infection. New agents like prenylation inhibitors, that can affect the interactions between the large HDV antigen and HBsAg in the HDV virion, will be a hope in treatment of HDV infection

Juvenile Delinquent and Unruly Proceedings in Ohio: Unconstitutional Adjudications

This article will focus on the constitutional defects of juvenile court adjudications under Ohio juvenile law. The arguments presented, however, are equally applicable in other jurisdictions since every state has some type of legislation granting juvenile court jurisdiction over both criminals and noncriminal misconduct of children

Thyrotoxic Vomiting: A Case Report and Possible Mechanisms

The symptoms related to gastrointestinal (GI) tract are sometimes chief complaints in patients with endocrine disease. Thyrotoxicosis is a rare, but notable cause for unexplained and repeated vomiting. Here, we report an adolescent patient with thyrotoxicosis who was initially presented with repeated vomiting and epigastric pain. A 13-year-old female was referred to a GI outpatient department for evaluation of vomiting and abdominal pain from a pediatric clinic. Esophagogastroduodenoscopy revealed acute gastritis with duodenogastric reflux and suspicious reflux esophagitis of minimal change, but there was no significant improvement after treatment and as a result she was admitted to the emergency room. She was subsequently diagnosed as Graves' disease because an initial laboratory test at the GI outpatient department revealed thyroid stimulating hormone < 0.01 µIU/mL and additional blood tests showed elevated thyroid hormones and positive thyroid stimulating hormone receptor antibody. The vomiting and epigastric pain improved remarkably after treatment with antithyroid drugs. Clinicians should consider the possibility of thyrotoxicosis in patient with unexplained and repeated vomiting

Serum procalcitonin and CRP levels in non-alcoholic fatty liver disease: a case control study

<p>Abstract</p> <p>Background</p> <p>Both C reactive protein (CRP) and procalcitonin (PCT) are well known acute phase reactant proteins. CRP was reported to increase in metabolic syndrome and type-2 diabetes. Similarly altered level of serum PCT was found in chronic liver diseases and cirrhosis. The liver is considered the main source of CRP and a source of PCT, however, the serum PCT and CRP levels in non-alcoholic fatty liver disease (NAFLD) were not compared previously. Therefore we aimed to study the diagnostic and discriminative role of serum PCT and CRP in NAFLD.</p> <p>Methods</p> <p>Fifty NAFLD cases and 50 healthy controls were included to the study. Liver function tests were measured, body mass index was calculated, and insulin resistance was determined by using a homeostasis model assessment (HOMA-IR). Ultrasound evaluation was performed for each subject. Serum CRP was measured with nephalometric method. Serum PCT was measured with Kryptor based system.</p> <p>Results</p> <p>Serum PCT levels were similar in steatohepatitis (n 20) and simple steatosis (n 27) patients, and were not different than the control group (0.06 ± 0.01, 0.04 ± 0.01 versus 0.06 ± 0.01 ng/ml respectively). Serum CRP levels were significantly higher in simple steatosis, and steatohepatitis groups compared to healthy controls (7.5 ± 1.6 and 5.2 ± 2.5 versus 2.9 ± 0.5 mg/dl respectively p < 0.01). CRP could not differentiate steatohepatitis from simple steatosis. Beside, three patients with focal fatty liver disease had normal serum CRP levels.</p> <p>Conclusion</p> <p>Serum PCT was within normal ranges in patients with simple steatosis or steatohepatitis and has no diagnostic value. Serum CRP level was increased in NAFLD compared to controls. CRP can be used as an additional marker for diagnosis of NAFLD but it has no value in discrimination of steatohepatitis from simple steatosis.</p

Genome Wide Association Study Identifies Genetic Variants Associated With Early And Sustained Response To (Peg)Interferon In Chronic Hepatitis B Patients: The GIANT-B Study

(Peg)interferon ((Peg)IFN) therapy leads to response in a minority of chronic hepatitis B (CHB) patients. Host genetic determinants of response are therefore in demand

Advances in short bowel syndrome: an updated review

Short bowel syndrome (SBS) continues to be an important clinical problem due to its high mortality and morbidity as well as its devastating socioeconomic effects. The past 3 years have witnessed many advances in the investigation of this condition, with the aim of elucidating the cellular and molecular mechanisms of intestinal adaptation. Such information may provide opportunities to exploit various factors that act as growth agents for the remaining bowel mucosa and may suggest new therapeutic strategies to maintain gut integrity, eliminate dependence on total parenteral nutrition, and avoid the need for intestinal transplantation. This review summarizes current research on SBS over the last few years.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47168/1/383_2005_Article_1500.pd

HEPATO-GASTROENTEROLOGY

Background/Aims: Total parenteral nutrition causes many complications such as cholestasis. Ursodeoxycholic acid is used for the treatment of several cholestatic problems. Metronidazole was investigated before for preventing some components of total parenteral nutrition-associated hepatic dysfunction. This study was designed to investigate the effects of ursodeoxycholic acid alone and ursodeoxycholic acid + metronidazole combination on total parenteral nutrition-associated cholestasis. Methodology: Eighteen rabbits were divided into three groups as follows: group A received a standard formula of total parenteral nutrition only, group B received total parenteral nutrition + ursodeoxycholic acid (3mg/kg/day), and group C were given total parenteral nutrition + ursodeoxycholic acid + metronidazole (25mg/kg/day) for eight days, respectively. Several parameters of liver function tests were compared among these groups. These were transaminases, alkaline phosphatase, total bilirubin, total cholesterol, triglycerides, and serum bile acids. Liver histology was detected in each group at the end of the experiment. Results: In group A, total parenteral nutrition administration resulted in remarkably higher serum values of transaminases, alkaline phosphatase, total cholesterol, total bilirubin, triglycerides, and free bile acids whereas ursodeoxycholic acid administration showed important improvements in the serum values of these parameters in group B animals. The metronidazole group showed nearer or similar laboratory values with group B, but significant differences appeared in bilirubin values (P<0.05) among these groups. Liver histology presented marked differences between group A and group B. Steatosis formed the main component of liver histology in 4 animals out of 6 in group A. Contrary to this, all of the specimens showed normal liver structure except one in group B. In the third group we did not see better morphology than in group B. Conclusions: These results suggested that oral ursodeoxycholic acid therapy during total parenteral nutrition reduces bilirubin levels and improves the other indicators of cholestasis and helps prevent disturbances of liver histology. When it is combined with metronidazole a significant decrease in bilirubin levels has been gained. With the help of ursodeoxycholic acid we can provide enterohepatic circulation of bile acids and regulate lipid metabolism. Metronidazole can be an antibiotic of choice during total parenteral nutrition when needed