Dr Nageshwar Reddy from Hyderabad, India, has written an excellent review on the genetic mutations of chronic pancreatitis. The pancreas has an inbuilt mechanism to prevent autodigestion of the pancreas by activated trypsin. Firstly, FDA approved Drug Library the pancreatic secretory trypsin inhibitor (PSTI)/serine protease inhibitor Kazal-type 1 (SPINK1), inhibits the action of activated trypsin. A second line of defense is the autolysis of activated trypsin by the cationic trypsinogen, protease serine

1 (PRSS1). Genetic mutations in these two genes result in pancreatitis. Based on his own studies from India, he has shown a key role of SPINK1 mutations in the pathogenesis of tropical calcific pancreatitis. He has also discussed the role of a new mutation—chymotrypsinogen-C gene—in the pathogenesis of pancreatitis. Dr Rungsun Rerknimitr from Bangkok, Thailand, has given an overview of the Trichostatin A chemical structure epidemiology of chronic pancreatitis in Asia, with particular emphasis on pancreatitis subtypes that are unique to Asia Pacific, i.e. calcific pancreatitis and autoimmune pancreatitis. Professor J. Enrique Domínguez-Muñoz from Santiago

de Compostela, Spain, focused on the treatment of chronic pancreatitis exocrine insufficiency. He has described the indication for pancreatic enzyme replacement therapy insufficiency and how it should be given. He has also explained in some detail augmentation of pancreatic enzyme therapy with dietary modifications, timing with meals and co-prescription with acid suppressive agents. These three

reviews cover various aspects of etiology, epidemiology and treatment of chronic pancreatitis in the Asia Pacific region, which will be an invaluable addition to the published medical literature on the subject. “
“A 72-year-old Korean male was admitted because of sudden onset of abdominal distension. He had been treated with amiodarone 200 mg, felodipine 5 mg, hydrochlorothiazide 25 mg, and aspirin 100 mg per day for hypertension with atrial fibrillation for 5 years. Before starting medication, he had undergone ultrasonography of the liver and serum biochemical tests including liver MCE chemistry and lipid profile, with all results being within the normal range. There was no evidence of hepatitis B and C, autoimmune hepatitis, or metabolic diseases such as nonalcoholic steatohepatitis, Wilson’s disease, hemochromatosis, or α1-antitrypsin deficiency. In addition, he had no history of heavy alcohol consumption. CAD, cationic amphiphilic drug. Physical examination revealed massive ascites, peripheral edema, and splenomegaly. Liver chemistry tests were abnormal: serum albumin = 2.7 g/dL, total bilirubin = 2.3 mg/dL, aspartate aminotransferase = 317 U/L, alanine aminotransferase = 237 U/L, alkaline phosphatase = 137 U/L, gamma-glutamyl transpeptidase = 185 U/L, and international normalized ratio = 1.32.