What’s Hot in the Red Journal This Month.
Am J Gastroenterol. 2012 Feb;107(2):151-3
Authors:
PMID: 22306936 [PubMed - in process]
Darwinian dyspepsia: an extraordinary scientist, an ordinary illness, great dignity.
Am J Gastroenterol. 2012 Feb;107(2):161-4
Authors: Shanahan F
PMID: 22306938 [PubMed - in process]
Use of a screening tool to determine nonadherent behavior in inflammatory bowel disease.
Am J Gastroenterol. 2012 Feb;107(2):154-60
Authors: Kane S, Becker B, Harmsen WS, Kurian A, Morisky DE, Zinsmeister AR
Abstract
OBJECTIVES: Nonadherence is an issue in the management of inflammatory bowel disease (IBD), and no validated screening tool is available. We aimed to determine whether scores from a self-reported adherence survey correlated with pharmacy refill data as a reliable measure of medication adherence.
METHODS: We used the eight item, self-reported Morisky Medication Adherence Scale. Each question is worth a point, with a maximum score of 8. Pharmacies were contacted for refill information for the previous 3 months, then 3 and 6 months from enrollment. Refill data were recorded for each time interval as the medication possession ratio (MPR); adherence was defined as >80%. Analysis of variance was used to determine the relationship between survey scores and MPR by drug class.
RESULTS: One hundred fifty outpatients were enrolled, of whom 94 had Crohn’s disease and 56 had ulcerative colitis; 89 were female. At baseline, 47% of patients were on 5-aminosalicylic acid (5-ASA), 54% an immunomodulator, 15% infliximab, 8% an injectable biologic, and 6% budesonide. The median adherence score was 7. Fifty-two percent stated they “rarely” missed a dose of medication. The median adherence score, as defined by refill data, ranged from 0% (injectable biologic) to 75% (infliximab) by drug class. Only those on an immunomodulator had a survey score that positively correlated with adherence.
CONCLUSIONS: Only those on a thiopurine were likely to have a score predicting adherence behavior. Adherence to therapy for IBD is complex and cannot be predicted reliably by a self-reported survey tool validated for other chronic conditions.
PMID: 22306937 [PubMed - in process]
Images of the month.
Am J Gastroenterol. 2012 Feb;107(2):165
Authors:
PMID: 22306939 [PubMed - in process]
Continuing medical education: february 2012.
Am J Gastroenterol. 2012 Feb;107(2):166
Authors:
PMID: 22306940 [PubMed - in process]
Continuing medical education questions: february 2012.
Am J Gastroenterol. 2012 Feb;107(2):177
Authors: Devault KR, Patel MK, Qumseya B
PMID: 22306941 [PubMed - in process]
Continuing medical education: february 2012.
Am J Gastroenterol. 2012 Feb;107(2):178
Authors:
PMID: 22306942 [PubMed - in process]
Continuing medical education questions: february 2012.
Am J Gastroenterol. 2012 Feb;107(2):195
Authors: Devault KR, Cooney W, Prabhu A
PMID: 22306943 [PubMed - in process]
Editorial: Serum IGF-1 Linking Visceral Obesity With Esophageal Adenocarcinoma: Unconvincing Evidence.
Am J Gastroenterol. 2012 Feb;107(2):205-6
Authors: McColl KE
Abstract
There is a strong positive association between body mass index (BMI) and risk of esophageal adenocarcinoma. This is likely to be largely or entirely explained by the established association between central obesity and gastroesophageal reflux and between the latter and risk of esophageal adenocarcinoma. Visceral fat is also metabolically active and there is interest in the possibility that humoral factors released by this fat might promote esophageal carcinogenesis. Insulin growth factor I (IGF-1) has been studied but current data do not support circulating total IGF-1 as a humoral factor linking BMI and esophageal carcinogenesis.
PMID: 22306944 [PubMed - in process]
Editorial: Pancreas Divisum Does Not Cause Pancreatitis, But Associates With CFTR Mutations.
Am J Gastroenterol. 2012 Feb;107(2):318-20
Authors: Dimagno MJ, Dimagno EP
Abstract
Bertin et al. partially dispel arguments that pancreas divisum (PD) causes pancreatitis, but fascinatingly indicate that PD associates with CFTR gene mutations predisposing to pancreatitis. This association, however, does not definitely confer a pathophysiological role for PD in pancreatitis but may denote that PD co-mingles with CFTR mutations without influencing pancreatitis or CFTR mutations influence pancreatic duct embryogenesis. We advise “idiopathic pancreatitis” patients with PD to undergo genetic testing. In lieu of CFTR mutations undertake no endoscopic/surgical procedure; if CFTR mutations are found, then refer patients for genetic counseling and withhold endoscopic/surgical therapy unless randomized studies show benefit.
PMID: 22306946 [PubMed - in process]
