International controlled trials have demonstrated increasing sustained virological response (SVR) rates to interferon-based therapies in hepatitis-C-treated patients. Response rates of 6-20% in the era of interferon monotherapy are compared with 42-82% with pegylated interferon plus ribavirin. The virological durability of the SVR is unknown and the optimal follow-up for these patients is unclear. The aim of our study was to determine SVR rates and the durability of the response to interferon-based therapies in the clinical setting. From our database of 1540 hepatitis C patients, 344 treatment courses of at least 12 weeks duration were identified, including interferon monotherapy (175 patients), interferon plus ribavirin (96 patients) and peginterferon plus ribavirin (73 patients). Interferon monotherapy was associated with an SVR rate of 5% in 103 genotype 1 patients and 25% in 72 genotype 2/3 patients. Response rates were higher (P < 0.001) with interferon plus ribavirin-41% in 34 genotype 1 patients and 73% in 62 genotype 2/3 patients-and with peginterferon plus ribavirin-47% in 47 genotype 1 patients and 79% in 26 genotype 2/3 patients. Of 147 patients with an SVR, 146 (>99%) remained hepatitis C virus PCR negative during a mean 2.3 years (range 0.3-10.3) of follow-up. In conclusion, with advances in therapies, we are achieving higher response rates in hepatitis C patients treated in the clinical setting. We can now expect an SVR in over half of the treated patients. Importantly, the response is durable and medium and long-term follow-up of these patients are of low yield and largely unnecessary.

Liver disease in adults with CF is commonly complicated by portal hypertension, but morbidity and mortality associated with this in our small patient population were low. UDCA is associated with improvement in hepatobiliary symptoms and liver function tests.

HIV infection has a significant impact on the natural progression of hepatitis B virus (HBV) related liver disease. In HIV-HBV co-infected patients, little is known about mutations in the HBV genome, which can influence severity of liver disease. The aim of this study was to characterize and to determine the frequency of known clinically-significant mutations in the HBV genomes from HIV-HBV co-infected patients and from HBV mono-infected patients. To accomplish this, genomic length HBV sequencing was performed in highly-active anti-retroviral therapy (HAART) –naïve HIV-HBV co-infected patients (n= 74) and in anti-HBV therapy-naïve HBV mono-infected patients (n=55). The frequency of HBV mutations differed between the co-infected and mono-infected patients when comparing patients with the same genotype. BCP mutations A1762T and G1764A were significantly more frequent in HBV genotype C mono-infection and the −1G frameshift was significantly more frequent in co- infection and was only observed in HBV genotype A co-infection. PreS2 deletions were observed more frequently in the setting of co-infection. Further work is needed to determine if these mutational patterns influence the differences in liver disease progression in HIV-HBV co-infected and HBV mono-infected patients.

Abdominal pain related to exercise, often loosely referred to as 'stitch', is not uncommon, particularly among participants in sports that involve running. The cause of this typically transient pain is poorly understood with several aetiologies proposed including diaphragmatic ischaemia (1, 2). Other gastrointestinal symptoms that are common during prolonged or high-intensity exercise include nausea, diarrhoea and gastrointestinal bleeding (3, 4). These symptoms are also usually transient and are thought to protect against critical organ damage by promoting cessation of exercise. Decreased gastrointestinal blood flow, increased motility and altered neuroendocrine modulation are postulated disease mechanisms (3). We report here a case of an elite runner with exercise-related severe abdominal pain and diarrhoea related to compression of the coeliac axis by the median arcuate ligament. Complete symptom relief was achieved with surgical division of the constricting ligament. The clinical characteristics and pathogenesis of coeliac axis compression syndrome are discussed.

Hepatitis B virus (HBV)-specific T-cell responses are important in the natural history of HBV infection. The number of known HBV-specific T-cell epitopes is limited, and it is not clear whether viral evolution occurs in chronic HBV infection.We aimed to identify novel HBV T-cell epitopes by examining the relationship between HBV sequence variation and the human leukocyte antigen (HLA) type in a large prospective clinic-based cohort of Asian patients with chronic HBV infection recruited in Australia and China (n ‫؍‬ 119). High-resolution 4-digit HLA class I and II typing and full-length HBV sequencing were undertaken for treatment-naïve individuals (52% with genotype B, 48% with genotype C, 63% HBV e antigen [HBeAg] positive). Statistically significant associations between HLA types and HBV sequence variation were identified (n ‫؍‬ 49) at 41 sites in the HBV genome. Using prediction programs, we determined scores for binding between peptides containing these polymorphisms and associated HLA types. Among the regions that could be tested, HLA binding was predicted for 14/18 (78%). We identified several HLAassociated polymorphisms involving likely known anchor residues that resulted in altered predicted binding scores. Some HLAassociated polymorphisms fell within known T-cell epitopes with matching HLA restriction. Enhanced viral adaptation (defined as the presence of the relevant HLA and the escaped amino acid) was independently associated with HBeAg-negative disease (P ‫؍‬ 0.003). Thus, HBV appears to be under immune pressure in chronic HBV infection, particularly in HBeAg-negative disease. G lobally, infection with hepatitis B virus (HBV) is common, and despite an effective vaccine, the number of persons with chronic HBV infection is increasing (9). Broad and effective HBVspecific T-cell responses are required to clear acute HBV infection (7, 37), but circulating HBV-specific T cells are rarely detected in chronic HBV infection (7,8). It is therefore unclear whether the adaptive immune response plays a role in controlling viral replication in chronic HBV infection and whether changes or adaptations in HBV are selected due to immune pressure.In individuals with chronic HBV infection, as many as 10 11 virus particles are produced per day (21, 30). HBV reverse transcriptase lacks proofreading activity, resulting in mutation rates estimated at 1.5 ϫ 10 Ϫ5 to 5 ϫ 10 Ϫ5 nucleotide substitutions per site per year in HBV e antigen (HBeAg)-positive individuals (32).Due to overlapping open reading frames (ORF), HBV genome evolution is constrained to maintain essential protein functions required for replication (28). There is some evidence that changes in HBV sequences can be selected due to host immune pressure (2,5,23) and that the HBV mutation rate is even higher in HBeAgnegative individuals (15, 33), possibly due to increased immune pressure prior to HBeAg loss (4, 10, 15) or due to higher levels of virus replication in the absence of HBeAg, given the known inhibitory effect of HBeAg on HBV replication at the level of n...