https://aasldpubs.onlinelibrary.wiley.com/doi/epdf/10.1002/hep.25762

The diagnosis and management of non-alcoholic fatty liver disease: practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

SUMMARY Background Non-alcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease, and its worldwide prevalence continues to increase with the growing obesity epidemic. This study assesses the epidemiology of NAFLD in adults based on clinical literature published over the past 30 years. Aim To review epidemiology and natural history of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in adults based on clinical literature published over the past 30 years. Methods An in-depth search of PubMed (1980–2010) was based on five search terms: ‘nonalcoholic fatty liver disease’ OR ‘non-alcoholic steatohepatitis’ OR ‘fatty liver’ OR ‘steatosis’ AND ‘incidence’ [MeSH Terms] OR ‘prevalence’ [MeSH Terms] OR ‘natural history’. Studies of paediatric cohorts were excluded. Articles were categorised by topic and summarised, noting generalisations concerning their content.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2036.2011.04724.x

Systematic review: the epidemiology and natural history of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in adults.

Background Sclerosing pancreatitis is a unique form of pancreatitis that is characterized by irregular narrowing of the main pancreatic duct, lymphoplasmacytic inflammation of the pancreas, and hypergammaglobulinemia and that responds to glucocorticoid treatment. Preliminary studies suggested that serum IgG4 concentrations are elevated in this disease but not in other diseases of the pancreas or biliary tract. Methods We measured serum IgG4 concentrations using single radial immunodiffusion and an enzyme-linked immunosorbent assay in 20 patients with sclerosing pancreatitis, 20 age- and sex-matched normal subjects, and 154 patients with pancreatic cancer, ordinary chronic pancreatitis, primary biliary cirrhosis, primary sclerosing cholangitis, or Sjogren's syndrome. Serum concentrations of immune complexes and the IgG4 subclass of immune complexes were determined by means of an enzyme-linked immunosorbent assay with monoclonal rheumatoid factor. Results The median serum IgG4 concentration in the patients ...

https://www.nejm.org/doi/pdf/10.1056/NEJM200103083441005

High serum IgG4 concentrations in patients with sclerosing pancreatitis.

https://aasldpubs.onlinelibrary.wiley.com/doi/epdf/10.1002/hep.20973

Nonalcoholic fatty liver disease: From steatosis to cirrhosis

/pdf/nccn-clinical-practice-guidelines-in-oncology-hepatobiliary-1kpacqqvi8.pdf

NCCN clinical practice guidelines in oncology: hepatobiliary cancers.

Recently, we have reported that several nonacid agents including phenylpentol, methanol extract of licorice root (FM 100), plaunotol, and teprenon stimulate release of endogenous secretin in humans, dogs, and rats. The latter three are antiulcer agents developed in Japan that have a protective effect on the gastric mucosa. We have clearly shown that plaunotol inhibits postprandial gastrin release and gastric acid secretion that parallel the increase in plasma secretin concentration. It has also been recently demonstrated that the secretin-induced inhibition of gastric acid secretion in rats is completely blocked by indomethacin, a potent inhibitor of prostaglandin synthesis. It appears that the inhibitory action of secretin on gastric acid secretion is mediated mainly by endogenous prostaglandins. Because the three antiulcer agents FM 100, plaunotol, and teprenon have been shown to increase the content of endogenous prostaglandins in the gastric mucosa, endogenous secretin released by these agents may play a significant role in their mucosal protective action. It is concluded that the antiulcer effect of these drugs could in part be attributable to their unique ability to release endogeneous secretin, and that secretin is a potential mediator of the antiulcer actions of mucosal protective agents.

Secretin as a potential mediator of antiulcer actions of mucosal protective agents.

OBJECTIVE Ornithine carbamoyltransferase (OCT) is a liver-specific mitochondrial matrix enzyme and potential biomarker of liver fibrosis. This study investigated the OCT levels in patients with chronic liver disease with or without cirrhosis in order to assess the usefulness of OCT as a biomarker of cirrhosis. METHODS The subjects included 440 Japanese patients with chronic liver disease and 80 control subjects. The patients were divided into two groups, those with and without cirrhosis, both of which were further stratified into high-OCT and low-OCT subgroups. RESULTS In the non-cirrhosis group, the patients with non-alcoholic steatohepatitis (NASH), alcoholic liver disease, primary biliary cirrhosis and primary sclerosing cholangitis (PSC) comprised the high-OCT subgroup, while the patients with hepatitis B, hepatitis C and autoimmune hepatitis formed the low-OCT subgroup. There were significant differences in the OCT levels, OCT/aspartate aminotransferase ratios and OCT/alanine transaminase (ALT) ratios between these two subgroups (p<0.001). The same findings were observed in the cirrhosis group. The OCT levels were markedly higher in the cirrhosis group than in the non-cirrhosis group, particularly among the patients with PSC (p<0.001). The most useful biomarker for predicting cirrhosis was the OCT/ALT ratio in the patients with hepatitis C and NASH and the OCT level in patients with PSC. CONCLUSION The OCT level differs among patients with different chronic liver diseases. The role of OCT should be further evaluated in order to improve our understanding of the pathogenesis of these diseases. The OCT level is a useful surrogate marker of cirrhosis, particularly in PSC patients.

Investigation of ornithine carbamoyltransferase as a biomarker of liver cirrhosis.

Plaunotol, an acyclic diterpene alcohol, is a new antiulcer agent derived from the “plau-noi” plant and has been reported to stimulate the release of endogenous secretin in humans. We investigated the effect of plaunotol on postprandial gastrin release, comparing it to the effect of exogenous secretin in a physiological dose in eight healthy volunteers. Four sets of experiments were performed in each volunteer: (1) meal alone, (2) meal after intravenous ranitidine (50 mg), (3) meal after oral administration of plaunotol (320 mg) in addition to ranitidine, and (4) meal after ranitidine with simultaneous intravenous infusion of secretin (0.03 CU/kg/hr). The postprandial increase in plasma secretin concentration was significantly reduced by ranitidine, while postprandial gastrin release was markedly exaggerated. Plaunotol in combination with ranitidine significantly increased secretin release and inhibited gastrin release after a meal. Intravenous infusion of secretin resulted in significant suppression of postprandial gastrin release exaggerated by ranitidine. The present study indicates that plaunotol inhibits postprandial gastrin release by its unique secretin-releasing action.

Plaunotol inhibits postprandial gastrin release by its unique secretin-releasing action in humans.

A novel IgM class autoantibody to a hepatocyte-related 190 kDa molecule in patients with type 1 autoimmune hepatitis

UNLABELLED: We evaluated clinical significance of fecal elastase-1(FE-1) in patients with pancreatic diseases and pancreatic dysfunction, in comparison with other tubeless test and secretin test. PATIENTS AND METHODS: FE-1 was determined in healthy controls(n = 131), chronic pancreatitis(CP) (n = 52), acute pancreatitis(AP) (n = 14), pancreatic cyst(Pcyst) (n = 20), pancreatic cancer(Pca) (n = 12), post pancreatic surgery(post P) (n = 28), biliary diseases(B) (n = 6), and gastro-duodenal ulcer(G) (n = 6). Fecal chymotrypsin(FCT) and BT-PABA test were performed in those patients digestive diseases. Secretin test collecting duodenal juice through a duodenal tube was performed in only 65 patients described above. RESULTS: FE-1 was 1504 +/- 100 micrograms/g(M +/- SE) in healthy controls. Using a cut off of 200 micrograms/g, 94.6% for healthy controls had FE-1 above this limit. FE-1 was 517 +/- 106 micrograms/g in CP, 1802 +/- 437 micrograms/g in AP, 525 +/- 109 micrograms/g in Pcyst, 528 +/- 126 micrograms/g in Pca, 135 +/- 36 micrograms/g in post P, 1435 +/- 506 micrograms/g in B, and 1115 +/- 325 micrograms/g in G, respectively. Sensitivity in the diagnosis of CP was 51.9%, 46.2% and 54.8% for FE-1, FCT, and BT-PABA test, respectively. Specificity of FE-1 and FCT was 81.3% and 78.7%, while that of BT-PABA test was 44.4%. Significant correlation was observed between FE-1 and secretory data including juice volume, maximum HCO3- concentration, and amylase output obtained form secretin test. In diagnosis of severe pancreatic dysfunction classified based on secretin test, the sensitivity was 86.7% for FE-1, 66.7% for FCT, and 66.7% for BT-PABA test. The specificity was also 70.0%, 80.0%, and 54.3%, for FE-1, FCT, and BT-PABA test, respectively. CONCLUSION: These results indicate that FE-1 may be recommended as a new, noninvasive tubeless test of pancreatic function.

Keiko Shiratori

Papers

Secretin as a potential mediator of antiulcer actions of mucosal protective agents.

Investigation of ornithine carbamoyltransferase as a biomarker of liver cirrhosis.

Plaunotol inhibits postprandial gastrin release by its unique secretin-releasing action in humans.

A novel IgM class autoantibody to a hepatocyte-related 190 kDa molecule in patients with type 1 autoimmune hepatitis

[Fecal elastase-1 test: clinical evaluation of a new noninvasive pancreatic function test].