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doi: 10.1111/j.1440-1746.2010.06517.xpmid: 21091988
See article in J. Gastroenterol. Hepatol. 2010; 25: 1855–1860.
doi: 10.1111/j.1440-1746.2010.06516.xpmid: 21091989
See article in J. Gastroenterol. Hepatol. 2010; 25: 1876–1882.
doi: 10.1111/j.1440-1746.2010.06513.xpmid: 21091990
See article in J. Gastroenterol. Hepatol. 2010; 25: 1844–1849.
Apte, Minoti V; Pirola, Romano C; Wilson, Jeremy S
doi: 10.1111/j.1440-1746.2010.06445.xpmid: 21091991
Alcoholic pancreatitis is a major complication of alcohol abuse. The risk of developing pancreatitis increases with increasing doses of alcohol, suggesting that alcohol exerts dose‐related toxic effects on the pancreas. However, it is also clear that only a minority of alcoholics develop the disease, indicating that an additional trigger may be required to initiate clinically evident pancreatic injury. It is now well established that alcohol is metabolized by the pancreas via both oxidative and non‐oxidative metabolites. Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol‐induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis. Efforts to identify clinically relevant factors that may explain the susceptibility of some alcoholics to pancreatitis have been underway for several years. An unequivocal, functionally characterized, association is yet to be identified in clinical studies, although in the experimental setting, endotoxin has been shown to trigger overt pancreatic injury and to promote disease progression in alcohol‐fed animals. Thus, while the molecular effects of alcohol on the pancreas have been increasingly clarified in recent years, identification of predisposing or triggering factors remains a challenge.
Narula, Neeraj; Marshall, John K
doi: 10.1111/j.1440-1746.2010.06444.xpmid: 21091992
Patients with diverticular disease may experience a variety of chronic symptoms, including abdominal discomfort, bloating, and altered bowel habit. They are also at risk of complications, including hemorrhage, diverticulitis, abscess, and fistula formation. The potential role of abnormal colonic microflora in the pathogenesis of diverticular inflammation has led to investigation of novel therapies such as probiotics. Probiotics are microorganisms that may be of net benefit to humans when consumed. The rationale and safety of their use in diverticular disease is discussed and current literature is reviewed.
Oh, Hyoung‐Chul; Kim, Myung‐Hwan; Lee, Kyu Taek; Lee, Jong Kyun; Moon, Sung‐Hoon; Song, Tae Jun; Eum, Junbum; Park, Do Hyun; Lee, Sang Soo; Seo, Dong‐Wan; Lee, Sung Koo
doi: 10.1111/j.1440-1746.2010.06299.xpmid: 21091994
Background and Aim: The incidence of gallbladder stones is higher in women during pregnancy than in men. Progesterone can inhibit gallbladder motility and facilitate gallstone formation. However, the ionic mechanisms have not been fully illuminated. This study sought to investigate the effects of progesterone on L‐type calcium currents and voltage‐dependent potassium currents in gallbladder smooth muscle cells. Methods: Gallbladder smooth muscle cells were isolated by enzymatic digestion from adult guinea pigs. Ionic currents were recorded by the whole‐cell patch clamp method. Results: Progesterone inhibited L‐type calcium currents in a concentration‐dependent manner. The characteristic of current‐voltage curve was not significantly altered. The amplitude of calcium currents was gradually suppressed, reached a steady‐state level within 4–6 min, and restored partly after washout. In the presence of protein kinase A (PKA) inhibitor, Rp‐cAMP, the inhibitory effect induced by progesterone was apparently attenuated, whereas forskolin, a direct activator of adenylate cyclase, could suppress L‐type calcium channel. However, progesterone did not significantly affect voltage‐dependent potassium currents. Conclusions: Progesterone inhibits L‐type calcium channel by cAMP/PKA pathway in gallbladder smooth muscle cells. This may be an important mechanism for the gallbladder hypomotility induced by progesterone.
Hanaoka, Noboru; Uedo, Noriya; Shiotani, Akiko; Inoue, Takuya; Takeuchi, Yoji; Higashino, Koji; Ishihara, Ryu; Iishi, Hiroyasu; Haruma, Ken; Tatsuta, Masaharu
doi: 10.1111/j.1440-1746.2010.06442.xpmid:
Showing 1 to 10 of 20 Articles
Background and Aim: This study aimed to determine the clinical characteristics of immunoglobulin G4 (IgG4)‐associated sclerosing cholangitis (ISC) and provide clinical clues differentiating ISC from primary sclerosing cholangitis (PSC) or hilar cholangiocarcinoma (CCC). Methods: Sixteen patients with ISC manifesting as hilar/intrahepatic strictures were analyzed for clinical characteristics and compared with patients with PSC and hilar CCC as disease controls for histology and serum IgG4 levels. Results: Distinguished biliary imaging findings of ISC included multifocal biliary tree involvement (n = 14), concentric bile duct thickening with preserved luminal patency (n = 13), and relatively mild proximal dilatation, despite prominent bile duct thickening (n = 11). Serum IgG4 levels were elevated in 12 patients (75%), but not in any of the 25 patients with hilar CCC. Ten patients (63%) had a past or concurrent history of autoimmune pancreatitis (AIP). The significant infiltration of IgG4‐positive cells was observed with endobiliary or liver biopsy in 11 of 16 patients (69%) with ISC, but not in any patients with PSC or hilar CCC. Extrabiliary organ involvement, including sialadenitis, inflammatory pseudotumor of the liver and kidney, and retroperitoneal fibrosis, was present in seven patients. Marked improvement of biliary strictures and/or extrabiliary involvement was observed in all ISC patients after steroid therapy. Conclusions: ISC should be considered in the differential diagnosis of hilar/intrahepatic biliary strictures. Past or concurrent AIP or extrabiliary organ involvement strongly suggests the possibility of ISC. Significant infiltration of IgG4‐positive cells on endobiliary or liver biopsy specimens, and/or elevated serum IgG4 levels, highly support the diagnosis of ISC and provide the rationale for steroid therapy.
Background and Aims: Although Helicobacter pylori eradication decreases the incidence of metachronous gastric cancer after endoscopic treatment for early gastric cancer (EGC), metachronous cancer still develops after successful eradication, particularly in patients with severe corpus gastritis. We investigated whether the extent of atrophic fundic gastritis diagnosed by autofluorescence imaging (AFI) videoendoscopy is predictive of development of metachronous gastric cancer after H. pylori eradication in patients treated with endoscopic submucosal dissection (ESD) for EGC. Patients and Methods: A total of 82 patients who underwent ESD for EGC from 2003 to 2006, who received eradication therapy participated in this study. The extent of chronic atrophic fundic gastritis was evaluated by AFI and categorized into closed and open type. The main outcome was the incidence of metachronous gastric cancer detected by annual surveillance endoscopy. Results: During a median observation period of 55 months, metachronous gastric cancer developed in 12 of 82 patients (14.6%). Multivariate Cox's proportional hazard analysis revealed that open‐type, atrophic fundic gastritis diagnosed by AFI was significantly associated with development of metachronous gastric cancer (hazard ratio: 4.88, 95% confidence interval (CI): 1.32–18.2, P = 0.018) after adjustment for age, sex, histological intestinal metaplasia, serum pepsinogen level, and H. pylori status. Conclusions: Metachronous EGC developed after successful H. pylori eradication, and extensive atrophic fundic gastritis diagnosed by AFI was a significant predictor, thus it could identify patients undergoing ESD for EGC who still required intensive surveillance after eradication.