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Detailed, country‐specific epidemiological data are needed to characterize the burden of chronic hepatitis C virus (HCV) infection around the world. With new treatment options available, policy makers and public health officials must reconsider national strategies for infection control. In this study of 15 countries, published and unpublished data on HCV prevalence, viraemia, genotype, age and gender distribution, liver transplants and diagnosis and treatment rates were gathered from the literature and validated by expert consensus in each country. Viraemic prevalence in this study ranged from 0.2% in Iran and Lebanon to 4.2% in Pakistan. The largest viraemic populations were in Pakistan (7001000 cases) and Indonesia (3187000 cases). Injection drug use (IDU) and a historically unsafe blood supply were major risk factors in most countries. Diagnosis, treatment and liver transplant rates varied widely between countries. However, comparison across countries was difficult as the number of cases changes over time. Access to reliable data on measures such as these is critical for the development of future strategies to manage the disease burden.

The total number, morbidity and mortality attributed to viraemic hepatitis C virus (HCV) infections change over time making it difficult to compare reported estimates from different years. Models were developed for 15 countries to quantify and characterize the viraemic population and forecast the changes in the infected population and the corresponding disease burden from 2014 to 2030. With the exception of Iceland, Iran, Latvia and Pakistan, the total number of viraemic HCV infections is expected to decline from 2014 to 2030, but the associated morbidity and mortality are expected to increase in all countries except for Japan and South Korea. In the latter two countries, mortality due to an ageing population will drive down prevalence, morbidity and mortality. On the other hand, both countries have already experienced a rapid increase in HCV‐related mortality and morbidity. HCV‐related morbidity and mortality are projected to increase between 2014 and 2030 in all other countries as result of an ageing HCV‐infected population. Thus, although the total number of HCV countries is expected to decline in most countries studied, the associated disease burden is expected to increase. The current treatment paradigm is inadequate if large reductions in HCV‐related morbidity and mortality are to be achieved.

Ulcerative colitis and experimental colitis are known to be associated with functional and structural abnormalities of the small intestine. The aim of this study was to determine whether experimental colitis in the rat has any effect on jejunal amino acid absorption and to investigate the neural mechanisms involved. In Sprague Dawley rats, colitis was induced by intracolonic administration of 0.1 ml of 6% iodoacetamide. Alanine absorption in the jejunum was measured using the single pass intraluminal perfusion technique in vivo and the three-compartment model in vitro. Experiments were done in normal and sham treated rats, as well as in rats that underwent neonatal capsaicin treatment, adult capsaicin treatment, or subdiaphragmatic vagotomy. Colitis was more severe in rats subjected to neonatal or adult capsaicin treatment, but was not affected by subdiaphragmatic vagotomy. In rats with colitis, jejunal alanine absorption was reduced by 2% (P0.05), 28%, 40%, and 18% (P0.001) at 1, 1.5, 2, and 3 days post rectal iodoacetamide administration. A rebound increase of 12% above baseline was noted at 4 days (P0.05). Similar results were noted in vitro. In rats that received two consecutive injections of iodoacetamide, the decrease in jejunal alanine absorption occurred earlier, was more severe, and persisted for more than 30 days. Neonatal as well as adult capsaicin treatment aggravated both the colitis and the decrease in jejunal alanine absorption. On the other hand, subdiaphragmatic vagotomy attenuated the decrease in jejunal alanine absorption, but had no significant effect on colitis severity. It is concluded that iodoacetamide induced colitis impairs jejunal amino acid absorption and that this effect involves vagal efferents as well as capsaicin sensitive primary afferents.

We report here a case of ticlopidine-induced aplastic anemia that responded to G-CSF and review the literature. An 83-year-old woman was started on ticlopidine for coronary artery disease after an episode of upper gastrointestinal bleeding secondary to aspirin. She developed aplastic anemia seven weeks after initiation of ticlopidine. She was hospitalised and received empiric antibiotic therapy and granulocyte colony stimulating factor (G-CSF). Her bone marrow started to recover quickly, and white blood cell and platelet counts returned to normal within three weeks. A review of medical literature revealed 20 similar cases of ticlopidine-induced aplastic anemia resulting in death in seven cases. G-CSF has been used previously with variable success. Ticlopidine is associated with serious, sometimes fatal hematological side effects. This risk should be seriously taken into consideration when prescribing ticlopidine. G-CSF may be helpful in the treatment of ticlopidine-induced aplastic anemia.

Laparoscopic instrumentation of the common bile duct (CBD) via the transcystic route or through direct choledochotomy seems to be safe, but in rare cases, complications such as pancreatitis, bile duct damage, and hemorrhage from cystic artery may occur. We report an unusual complication with this approach. A 62-year-old man with gallbladder stones presented with obstructive jaundice, mild pancreatitis, and a dilated CBD. He underwent laparoscopic cholecystectomy with an intraoperative cholangiogram through the cystic duct. A small stone seen in the CBD was removed using a 6-Fr vascular Fogarty catheter. Two days later, he became jaundiced again with a rising bilirubin. An endoscopic retrograde cholangiogram showed a 1.5-cm round filling defect floating in a dilated CBD. A sphincterotomy was performed, and a balloon catheter was inflated proximally and pulled down. To our surprise, the filling defect was a crystal clear object, which we finally realized was a fully inflated Fogarty catheter balloon. The balloon spontaneously deflated while being caught with a basket. Surgeons should be aware of this possible complication, and every effort should be made to verify that the balloon still is in place after removal of the embolectomy catheter. Whether vascular embolectomy catheter balloons are appropriate for stone removal or more rigid balloons should be used needs further evaluation.

An audit was carried out on the activities of a one stop clinic where patients referred by GPs for endoscopy are first interviewed by a gastroenterologist, directly before the procedure. Such a barrier to open access endoscopy did not seem to reduce the workload or the rate of normal examinations.

A 22-year-old Pakistani man presented with a 1-year history of recurrent attacks of pancreatitis of unknown etiology that had required hospitalization and extensive investigation in Pakistan. He was admitted with abdominal pain, fever, and weight loss. An ultrasound and computed tomographic scan of the abdomen revealed abdominal lymphadenopathy, bulky and inhomogeneous pancreas, and a large fluid collection anterior to the right lobe of the liver. The collection was aspirated but Gram-stain, Ziehl-Neelsen stain for acid-fast bacilli, and DNA analysis by a highly specific polymerase chain reaction-based assay were negative. Because of a strong clinical suspicion of tuberculosis, the patient was started on antituberculous chemotherapy; 4 weeks later the aspirate grew Mycobacterium tuberculosis (hominis). The patient improved rapidly and has remained well after 18 months follow-up. A high index of clinical suspicion and appropriate microbiological investigation is required for the diagnosis of this rare, but potentially curable cause of pancreatitis.