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CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2010;8:4–6

BSTRACTS FROM AROUND THE WORLD

Visit CGH online at www.cghjournal.org to link to these articles and additional articles of interest.

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s It Time to Revisit How Fellowshipraining Is Constructed?

riedman LS, Brandt LJ, Elta GH, et al. Special Report: Reportf the Multisociety Task Force on GI Training. Gastrointestndosc 2009;70:823– 827. Hepatology 2009;50:1325–1329. Gas-

roenterology 2009;137:1839 –1843.

Summary. Last year, our societies created a 9 memberask force to evaluate the current gastroenterology train-ng model and to make appropriate recommendations.he rationale for revisiting our current training practiceas the emergence of certification in transplant hepatol-gy and the perception that the current curriculum mayot adequately prepare trainees for other focused prac-ices, like inflammatory bowel disease (IBD) or oncology.

number of important recommendations were prof-ered. The task force did not support separate trainingnd certification in hepatology distinct from gastroenter-logy. However, recommendation was given to provide aodel for focused recognition in transplant hepatology,hich could be acquired during the 36 months of fellow-

hip training. Overall, the task force felt that training inocused areas of practice, such as motility, oncology, IBD,nd endoscopy, could be obtained during the final 18onths of fellowship training. Regarding research, fel-

ows should devote 6 months of their training to some typef research, though there was agreement that time devotedo research for those considering a community practice

ight be better spent in other relevant scholarly activities.ore than 6 months of training and research, of course,ould be required of those wishing to become fully fledged

esearchers. Lastly, considering the current climate, the re-ision of the gastroenterology core curriculum as a compe-ency-based document was recommended.

Editor’s comment. It doesn’t seem that long ago thatellowship training changed overnight from 2 to 3 years.he explanation for such a lengthening was that themount of information digestive disease specialistseeded to know was burgeoning, that nutrition shoulde included in the curriculum, and that research shoulde an important component. At many fellowship pro-rams, particularly the “clinical” programs, however, theesearch experience has been neither particularly strongor emphasized; thus, a 6 month block has been left for

ellows, quite frankly, to perform rather meaningless re-earch. The third year of fellowship then became “moref the same” unless the program offered advanced pro-edures or areas of focused practice. However, aroundhat time, it became clear that, given the complexity ofdvanced procedures, a dedicated additional year of ad-

anced training was warranted and adopted at most large c

cademic programs. Such was the thought for hepatol-gy as well. With further experience, it has become clearhat, in order to practice community based general gas-roenterology, 3 years is really unnecessary. I have nevereen particularly convinced that the research componentdded anything to one’s practice. It has become evident,hough, that the removal of research and advanced train-ng from the advanced 3 years allows other subspecialtieso be learned, such that the 3-year fellowship could thenonceivably incorporate hepatology or perhaps even IBD.ut what curriculum would you use and would IBDpecialists agree on what one needs? I think this is ap-ropriate, as a hepatologist could receive more than ad-quate training with 2 years of gastroenterology plus thedditional year of dedicated hepatology. If, however, oneanted to obtain additional research training, then fur-

her training beyond the 3 years would be required foruccess. Whether it is best to train second year fellows foryear in advanced procedures or wait until after the thirdill be debated. Let’s see how authorities such as theesidency Review Committee and American Board of

nternal Medicine respond to these suggestions.

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ssociation of Lymphomas Withhiopurine Use in Inflammatory Bowelisease

eaugerie L, Brousse N, Bouvier AM, et al. Lymphoproliferativeisorders in patients receiving thiopurines for inflammatoryowel disease: a prospective observational cohort study. Lancet009;374:1617–1625.

Summary. There has been concern regarding an in-reased risk for lymphoproliferative diseases in IBD pa-ients using thiopurines, although this risk has nevereen well quantified. This prospective cohort study ex-mined the incidence rate of lymphoproliferative disor-ers in IBD patients treated and not treated with thio-urines during a 3-year follow-up interval. Comparisonas made with the number of cases expected in theeneral population with the same age and sex distribu-ions. Of the total study population, 19,486 patients94%) were included in the analysis. At study entry, 30%f patients were receiving thiopurines, 14% had discon-inued thiopurines, and 56% had never received thiopu-ines. During almost 50,000 patient years of follow-up,3 patients were diagnosed with incident lymphoprolif-rative disorders (1 case of Hodgkin’s lymphoma and 22ases of non-Hodgkin’s lymphoma). Of these 23 patients,5 (including the patient with Hodgkin’s lymphoma)ere receiving thiopurines at symptom onset, 2 had dis-

ontinued thiopurine therapy, and 6 had never received

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hese agents. Nine patients were diagnosed during therst year of follow-up, 5 during the second year, and 9eyond the second year. The incidence rates were 0.9 per000 for those receiving the agent. The unadjusted haz-rd ratios were 3.45 (1.34 – 8.89; P � .0106) for patientsho received these agents vs those who had never re-

eived these agents and 0.74 (0.15–3.68, P � .7) foratients who discontinued thiopurines vs those who hadever received the drug. No increase in lymphomas wasetected in those patients who had never received thio-urines relative to the general population. Eight patientsied from causes related to the lymphoma within thetudy period. In general, patients who were receivingmmunosuppressive therapy had a post-transplant–typeymphoproliferative disorder histologically.

Editor’s comment. Conflicting data regarding the usef thiopurines and risk of lymphoproliferative diseases exist.his large well done study from Europe demonstrates aigher rate of such disorders in IBD patients receivinghiopurines, which can be fatal. As with any other therapy,isks and benefit must be balanced. For many of our pa-ients, the benefit of these drugs in reducing the need fororticosteroids—which have significant morbidity in and ofhemselves—is likely worth the small (5 times the back-round rate) but definite risk. These findings call us toemain vigilant for early diagnosis of such disorders so thatreatment can be appropriately instituted at an early stage.t this juncture, we also need to alert our patients to the

ncreased risk, not to frighten them or dissuade them fromsing these effective agents, but for presumed medical legaleasons and for education.

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o Ahead and Have Another Cup of Joereedman ND, Everhart JE, Lindsay KL, et al. Coffee intake isssociated with lower rates of liver disease progression inhronic hepatitis C. Hepatology 2009;50:1360 –1369.

Summary. Population-based studies have shown thatersons regularly drinking coffee have a lower risk ofirrhosis and other liver diseases. Laboratory-based inves-igations also demonstrate that components in coffeeave beneficial effects. This study using data from theALT-C (Hepatitis C Antiviral Long-term Treatment

gainst Cirrhosis) Trial (a study of patients with bridgingbrosis or cirrhosis on liver biopsy who failed to achieve austained virologic response to peginterferon plus ribavirinreatment) specifically examined coffee intake and impor-ant endpoints, such as liver tests, histology, and progres-ion of liver disease, including development of carcinoma.f the 766 participants, 233 had outcomes. Outcome rateseclined with increasing coffee intake, but no such associ-tion was observed in those who consumed tea. Drinkers ofor more cups of coffee per day had a 53% lower risk of liverisease progression when compared to non-coffee drinkers.

nterestingly, they also found that coffee drinking at base- e

ine was associated with better status for markers of liverisease and portal hypertension.

Editor’s comment. This is an interesting observation,ut one must remember that this is only an association.everal different mechanisms for a positive effect of cof-ee consumption on progression of liver disease haveeen offered. Whether further identification of the ben-ficial component in coffee is worthy of further studyemains to be determined, given that coffee contains over000 chemical compounds.

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atty Liver on Ultrasound Is Associatedith Higher Death Rates

aring R, Wallaschofski H, Nauck M, et al. Ultrasonographicepatic steatosis increases prediction of mortality risk fromlevated serum gamma-glutamyl transpeptidase levels. Hepatol-gy 2009;50:1403–1411.

Summary. Recent epidemiologic studies have foundhat elevation of the gamma-glutamyl transpeptidaseGGT) level is an independent predictor of mortality.

ata were collected from 4160 subjects without viral liverisease or cirrhosis recruited for a population-basedtudy of health. Hepatic steatosis was defined by elevatedGT levels in the presence of a hyperechogenic liver onltrasound. During almost 30,000 person years of follow-p, 7.5% of the cohort died. Elevated GGT levels weressociated with increased risk of mortality in men, butot in women. This association was even stronger in menith hepatic steatosis (hazard ratio, 1.98; 95% confidence

nterval, 1.21–3.27). Cardiovascular mortality was a fre-uent cause of death in those with fatty liver.

Editor’s comment. This study adds further evidenceo the potential mortality of fatty liver disease principallys a marker for cardiovascular morbidity and mortality.hus, an elevation of GGT and hepatic steatosis onltrasound is associated with all-cause mortality in men,nd the predictability of GGT is better for mortalityompared to liver ultrasound. In our male patients withatty liver on ultrasound, further education regarding itsmplications is warranted and may provide an additional

arker for cardiovascular risk.

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onalcoholic Fatty Liver Disease inhildren Is Associated With End Stageiver Disease and High Mortality

eldstein AE, Charatcharoenwitthaya P, Treeprasertsuk S, et al.he natural history of non-alcoholic fatty liver disease in chil-ren: a follow-up study for up to 20 years. Gut 2009;58:1538 –544.

Summary. The burgeoning obesity epidemic has

aten its way into the young population. Autopsy studies

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6 ABSTRACTS FROM AROUND THE WORLD CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Vol. 8, No. 1

f children ages 2–19 years have demonstrated an alarm-ng rate of nonalcoholic fatty liver disease (NAFLD) inbese children approaching 40%. This retrospective lon-itudinal hospital-based cohort study examined 66 chil-ren with NAFLD (mean age, 13.9) who were followed upo 20 years. Of the cohort, 29% had the metabolic syn-rome at diagnosis. During follow-up, 2 children diednd 2 underwent liver transplantation for decompen-ated cirrhosis. The observed survival free of liver trans-lantation was significantly shorter in the NAFLD cohorts compared to the expected survival in the general USopulation of the same age and sex.

Editor’s comment. We are inundated daily with factselated to the obesity epidemic including involvement ofhildren. These data are alarming and suggest that ter-iary care centers may begin to see young people for

anagement of decompensated cirrhosis or liver trans-lantation from NAFLD. Such a study is a call to armsor what needs to be done regarding education of nutri-ion at the elementary school level. We have been negli-ent as a society in this regard, and parents, not schoolsr the vending machines, are to blame.

dditional Papers of Interest

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Ierardi E, Hassan C, Xullo Z, et al. Segmental colitisssociated with diverticula: a rare clinical entity and aew challenge for the gastroenterologist. Dig Liver Dis

009;41:794 –797. 2

Lees CW, Critchley J, Chee N, et al. Lack of associationetween cervical dysplasia and IBD: a large case-controltudy. Inflamm Bowel Dis 2009;15:1621–1629.

Abid A, Taha O, Nseir W, et al. Soft drink consump-ion is associated with fatty liver disease independent of

etabolic syndrome. J Hepatol 2009;51:918 –924.Allen PJ, Qin L-X, Tang L, et al. Pancreatic cyst fluid

rotein expression profiling for discriminating betweenerous cystadenoma and intraductal papillary mucinouseoplasm. Ann Surg 2009;50:754 –760.

Broeders JA, Rijnhart-de Jong H, Draaisma WA, et al.en-year outcome of laparoscopic and conventional Nis-

en fundoplication: randomized clinical trial. Ann Surg009;250:698 –706.

Gellad ZF, Almirall D, Provenzale D, et al. Time fromositive screening fecal occult blood test to colonoscopynd risk of neoplasia. Dig Dis Sci 2009;54:2497–2502.

Kim BJ, Park MK, Kim S-J, et al. Comparison of scoringystems for the prediction of outcomes in patients withonvariceal upper gastrointestinal bleeding: a prospectivetudy. Dig Dis Sci 2009;54:2523–2529.

Liebig C, Ayala G, Wilks J, et al. Perineural invasion isn independent predictor of outcome in colorectal can-er. J Clin Oncol 2009;27:5131–5137.

Ferrús JA, Zapardiel J, Sobreviela E. Management ofastroesophageal reflux disease in primary care settingsn Spain: SYMPATHY I study. Eur J Gastroenterol Hepa-ol 2009;21:1269 –1278.

Johnson CD. CT Colonography: Coming of age. AJR009;193;1239 –1242.

Kamisawa T, Shimosegawa T, Okazaki K, et al. Stan-ard steroid treatment for autoimmune pancreatitis. Gut

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