https://www.journal-of-hepatology.eu/article/S0168-8278(14)00933-7/pdf

NAFLD: A multisystem disease

https://www.gastrojournal.org/article/S0016-5085(13)00168-6/pdf

The Epidemiology of Pancreatitis and Pancreatic Cancer

Non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2DM) are common conditions that regularly co-exist and can act synergistically to drive adverse outcomes. The presence of both NAFLD and T2DM increases the likelihood of the development of complications of diabetes (including both macro- and micro- vascular complications) as well as augmenting the risk of more severe NAFLD, including cirrhosis, hepatocellular carcinoma and death.

The mainstay of NAFLD management is currently to reduce modifiable metabolic risk. Achieving good glycaemic control and optimising weight loss are pivotal to restricting disease progression. Once cirrhosis has developed, it is necessary to screen for complications and minimise the risk of hepatic decompensation.

Therapeutic disease modifying options for patients with NAFLD are currently limited. When diabetes and NAFLD co-exist, there are published data that can help inform the clinician as to the most appropriate oral hypoglycaemic agent or injectable therapy that may improve NAFLD, however most of these data are drawn from observations in retrospective series and there is a paucity of well-designed randomised double blind placebo controlled studies with gold-standard end-points. Furthermore, given the heterogeneity of inclusion criteria and primary outcomes, as well as duration of follow-up, it is difficult to draw robust conclusions that are applicable across the entire spectrum of NAFLD and diabetes. In this review, we have summarised and critically evaluated the available data, with the aim of helping to inform the reader as to the most pertinent issues when managing patients with co-existent NAFLD and T2DM.

Non-alcoholic fatty liver disease and diabetes

Organ Failure Due to Systemic Injury in Acute Pancreatitis

1757 Identification of Ocular Sebaceous Neoplasia with Evaluation for Mismatch Repair Proteins L Schoenfield, J Anthony, R Djohan, I Lalak, M Levine, P Ng, J Perry, A Singh, T Plesec. Cleveland Clinic, Cleveland, OH. Background: Recognizing sebaceous carcinoma is important because of its risk for metastasis and tumor death. Histopathology alone is often difficult because fresh tissue for oil red-O stain is not always available. Several immunohistochemical stains (IHC) have been evaluated but often the diagnosis is elusive. Furthermore, the diagnosis of a sebaceous adenoma or carcinoma raises the possibility of Lynch syndrome, a cancer predisposition syndrome. Mismatch repair protein(MMR) abnormalities are a feature of Lynch syndrome, and they can be detected with IHC for the MLH1, MSH2, PMS2, and MSH6 proteins. Design: 14 sebaceous carcinomas and 3 adenomas from the eyelid (17 specimens) from 14 patients were evaluated for oil red-O when possible as well as IHC for AR, EMA, BER-EP4, CAM5.2 for diagnosis. MMR for MLH1, MSH2, PMS2, and MSH6 by IHC were evaluated as a possible screening panel for Lynch syndrome. Two patients already had other tissue tested by PCR for microsatellite instability (MSI) for Lynch syndrome. Results: Oil red-O was done on 6 of 17 specimens and positive in 5 of the 6 (83%). AR was positive in 2 of 3 adenomas (67%) and 5 of 14 carcinomas (36%). EMA was positive in 2 of 3 adenomas (67%) and 11 of 14 carcinomas (79%). BER-EP4 was negative in all 3 adenomas and positive in 7 of 14 carcinomas (50%). CAM5.2 was positive in 1 of 3 adenomas (33%) and 8 of 14 carcinomas (57%). All 17 specimens(100%) showed positive nuclear staining for MLH1 and PMS2, indicative of normal protein expression. In 14 of 17 specimens from 12 patients, MSH2 and MSH6 were also normal. 3 specimens from 2 patients that had rare positive cells for MSH2 and MSH6. Both patients had previous colonic tumors tested for MSI and were found to be MSI-H, indicative of possible Lynch syndrome. Conclusions: Diagnosing sebaceous carcinoma is important prognostically but sometimes challenging with routine histopathology. In our experience androgen receptor (AR) was found to be confirmatory in only 36% of cases and not dependent on the size of the tumor available. The other IHC stains were of marginal benefit and not specific. While none of the cases showed complete loss of expression of a MMR protein, there were 2 patients in with only rare positive cells who had known MSI-H tumors in the colon, suggestive of Lynch syndrome. Additional studies of these eyelid tumors may elucidate the possible role of using them for screening for Lynch syndrome.

When the Pancreas

TNF-alpha gene (TNFA) variants increase risk for multi-organ dysfunction syndrome (MODS) in acute pancreatitis.

OBJECTIVES A risk association has been observed between non-O blood groups and pancreatic adenocarcinoma. Chronic pancreatitis also increases risk for pancreatic cancer, raising questions as to whether non-O blood groups are a risk for chronic pancreatitis and whether the pathophysiologic pathways are linked. Our goal was to determine whether ABO blood group may affect the risk of chronic pancreatitis. METHODS The study cohort included chronic pancreatitis patients (n = 499) and healthy controls (n = 631) from the North American Pancreatitis Study 2 study. Genotyping was performed using Sequenom assay of rs8176746 A/C and rs505922 C/T to classify participants into ABO blood groups. RESULTS O blood group was nonsignificantly more common among cases (44.7% vs 42.0%; P = 0.36), particularly among cases with alcohol-related chronic pancreatitis (49.3% vs 42%; P = 0.060). Alcoholic patients without coexisting high-risk PRSS1, CFTR, or SPINK1 variants had a significant overrepresentation of O blood type when compared with controls (odds ratio, 1.54; 95% confidence interval, 1.09-2.17; P = 0.01). CONCLUSIONS A, B, and AB blood groups were not associated with a greater likelihood of having chronic pancreatitis and may decrease the risk of chronic pancreatitis in individuals who are very heavy drinkers. These results suggest that the mechanism linking non-O blood type with pancreatic pathology is specific to carcinogenesis.

/pdf/abo-blood-group-and-chronic-pancreatitis-risk-in-the-naps2-3ma18l66eh.pdf

ABO blood group and chronic pancreatitis risk in the NAPS2 cohort

Background & Aims

Steatosis is a defining feature of nonalcoholic fatty liver disease (NAFLD). However, evidence that severity of steatosis can predict adverse outcomes in NAFLD or nonalcoholic steatohepatitis (NASH) is lacking. The aim of this study was to determine whether steatosis assessed by computed tomography (CT) imaging predicts adverse outcomes in diabetic patients at risk for NAFLD/NASH.



Methods

We studied deaths, liver-related and cardiovascular adverse outcomes in a 5-year retrospective observational cohort of 2343 type 2 diabetic patients in a large care network who had noncontrast CT imaging for clinical indications. We measured steatosis by subtraction of spleen from liver attenuation, a method that showed low sensitivity (0.417) and high specificity (0.882) compared with histopathological scoring. We evaluated outcomes prediction using multivariate Cox proportional hazards modelling of steatosis both as a categorical (≥30%) and continuous variable.



Results

Steatosis ≥30% was present in 233 (9.9%) of the cohort at baseline. Over 5 years, there were 372 total deaths, 18 liver-related and 99 cardiovascular deaths, 48 liver transplants, 51 occurrences of hepatic encephalopathy, 41 hepatocellular carcinomas, 653 myocardial infarctions, 66 strokes, 180 occurrences of angina, 735 occurrences of arrhythmia and 772 occurrences of congestive heart failure. Steatosis had no predictive value for any adverse outcome. Patients with steatosis averaged 8 years younger than those without it. Age had a strong covariate influence on occurrence of total deaths, cardiovascular deaths, myocardial infarctions, arrhythmias and congestive heart failure.



Conclusion

Although steatosis on imaging is often the abnormality that triggers diagnosis and assessment of NAFLD/NASH, it lacks predictive value for adverse clinical outcomes.

Hepatic steatosis in diabetic patients does not predict adverse liver-related or cardiovascular outcomes.

881 The Impact and Prevalence of Chymotrypsinogen C (CTRC) Gene Variants in Chronic Pancreatitis in North America

What is Causing the Increase in Incidence of Acute Pancreatitis (AP)

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