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CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2009;7:916–918

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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Selective Serotonin Reuptakenhibitors and Upper Gastrointestinalleeding: More Data

argownik LE, Bolton JM, Metge CJ, et al. Selective serotonineuptake inhibitors are associated with a modest increase in theisk of upper gastrointestinal bleeding. Am J Gastroenterol009;104:1475–1482.

Summary. Limited observation suggests that selectiveerotonin reuptake inhibitors (SSRIs) are associated withemorrhagic complications. Determination of such anssociation would be important given the widespread usef these medications. It is thought that serotonin is

ntegral in the promotion of platelet aggregation, therebylocking the uptake of serotonin into platelets could

mpair normal hemostasis. This study used the compre-ensive data repository from Manitoba, Canada. Patientsdmitted to the hospital with a diagnosis of upper gas-rointestinal bleeding were matched to a non-bleedingontrol group. A modest increase in the risk of upperastrointestinal bleeding was found (odds ratio [OR],.43; 95% confidence interval [CI], 1.09 –1.89). The addi-ion of SSRIs to non-steroidal anti-inflammatory drugsNSAIDs) did not significantly increase the risk over usef an NSAID alone. Proton pump inhibitor co-therapyignificantly reduced the risk of SSRI-associated upperastrointestinal bleeding (OR, 0.39; 95% CI, 0.16 – 0.94).

Editor’s comment. The data add to growing litera-ure suggesting an association between SSRI use andastrointestinal bleeding. This study focused on upperastrointestinal bleeding and demonstrated a 43% in-rease in the risk of bleeding. It is comforting that, ateast in this study, SSRI plus NSAIDs did not augmenthe rate over NSAIDs alone. One would like to see moreata examining this relationship given the widespreadse of both drugs. We also need to determine risk factors

or SSRI-related bleeding as we have done with NSAIDs.t would also be interesting to look at any associationetween these drugs and clopidogril or warfarin.

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Colonoscopy Complications Are Realn a Medicare Population

arren JL, Klabunde CN, Mariotto AB, et al. Adverse eventsfter outpatient colonoscopy in the Medicare population. Annntern Med 2009;150:849 – 857.

Summary. Medicare coverage of colon cancer screen-ng was adopted in 1998 for those �50 years of age, withcreening colonoscopy added in July of 2001. While

olonoscopy represents the most invasive modality for d

olorectal cancer screening, large population-based stud-es assessing complications have not been performed. Aandom 5% sample of Medicare beneficiaries ages 66 to 95ears who underwent colonoscopy over a 4-year period wereatched with beneficiaries who did not have colonos-

opy. Medicare claims were used to measure rates of seriousost-procedural events (bleeding and perforation), otherastrointestinal events, cardiovascular events, or emer-ency department visits within 30 days of the procedure.verall, patients having polypectomy had the highest risk

or all adverse events compared with matched beneficiaries,nd increased risk of adverse events was observed in thoseith co-morbid conditions. Specifically, those with a historyf stroke, chronic obstructive lung disease, atrial fibrillation,r congestive heart failure had the highest risk for seriousost-procedural gastrointestinal events. Rates of adversevents also increased with age. The relative risk for a seriousastrointestinal event following polypectomy was 9.4 andas also higher for cardiovascular events (risk 23.3 vs 12.5

or screening colonoscopy alone). The risk in those �85ears was also significantly higher than those 66 to 69 yearsf age. The risk of perforation was 0.6 per 1000.

Editor’s comment. This large population-basedtudy is helpful in assessing real complications followingolonoscopy not only gastrointestinal but others suchs cardiovascular events. Co-morbidity significantly in-reased the rate of post-procedural complications espe-ially following polypectomy as compared to screeninglone, which is interesting. Not surprisingly, those whoere much older had a higher complication rate asell. These data will be helpful in discussing compli-

ations of colonoscopy in an educated fashion withur elderly patients particularly those with underlyingo-morbidity. It would have been interesting to deter-ine if there was any association between anti-platelet

gents bleeding.

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Pancreatic Ductal Anatomy Predictsutcome of Pseudocyst Treatment

ealon WH, Bhutani M, Riall TS, et al. A unifying concept:ancreatic ductal anatomy both predicts and determines theajor complications resulting from pancreatitis. J Am Coll

urg 2009;208:790 – 801.

Summary. Symptomatic pancreatic pseudocysts may beanaged percutaneously, endoscopically, or surgically, and

he route of treatment is often dictated by local expertise.revious observations suggest that complications anduccess of therapy are dictated by underlying pancreatic

uctal anatomy. This study reports the outcome of 563

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September 2009 ABSTRACTS FROM AROUND THE WORLD 917

atients with pancreatic pseudocysts in whom either ret-ograde pancreatography or MRCP were performed. Fourifferent types of anatomy were characterized. Normaluctal anatomy associated with pseudocysts (type 1),uctal stricture with pseudocysts (type 2), ductal cut-off

type 3), and dilated duct in chronic pancreatitis (type 4)Figure). Long-term resolution as well as outcomes ofreatment was correlated with ductal anatomy. Sponta-eous regression was seen in 87% of those with a normaluct in contrast to 5% or less in the other 3 types. Successf percutaneous drainage failed in 36% of type I patientss compared to 62%–100% in types II and III. Persistentstula was seen in 50% or more of those with type II and00% in types III and IV.

Editor’s comment. Pathophysiologically, these ob-ervations make intuitive sense. That is, those who haveormal ductal architecture may have spontaneous reso-

ution of a pseudocyst. In contrast those who have stric-ures, ductal disruption, or chronic pancreatitis with dilateducts are much less likely, if at all, to have spontaneousesolution and percutaneous drainage in these patients wasot effective and had a much higher rate of later fistula

Figure. Differing pancreatic anatomy associated with pseudocysts.

ormation. Taken together, these findings suggest that r

efore treatment of a pancreatic pseudocyst is under-aken, delineation of ductal anatomy either with MRCPr pancreatography may be helpful in predicting out-ome especially if one elects to treat with percutaneousrainage. Such delineation could then best dictate theest course of therapy and avoid ineffective treatmentsith potential morbidity.

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A Low Serum Ascites Albuminradient Is Not Always Ominous

handwalla HE, Fasakin Y, El-Serag HB. The utility of evaluat-ng low serum albumin gradient ascites in patients with cirrho-is. Am J Gastroenterol 2009;104:1401–1405.

Summary. The serum ascites albumin gradient (SAAG)s one of the key components in the diagnostic evaluation ofscites. A level �1.1 gm/dl is often caused by non-portalypertension disorders such as malignancy. This retro-pective study identified 92 patients from a VA hospitalith a SAAG �1.1 during a 5-year period. Seventy-sixatients had cirrhosis. Of these, 38% had an identifiableause usually primary bacterial peritonitis. Malignantscites was found in 28% and nephrotic syndrome in 17%.he largest group, however (47 patients, 62%) had no cause

dentified. Thirty-two patients underwent follow-up para-entesis and 73% changed to a high SAAG. Of the 16atients with no cirrhosis, a cause was identified in 12, mostommonly peritoneal carcinomatosis.

Editor’s comment. Causes unrelated to portal hyper-ension, especially malignancy, are often considered inatients with a low SAAG. This study nicely differentiateshe findings based upon the presence or absence of cir-hosis. Not surprisingly those without cirrhosis almostniformly had a cause identified, most commonly cancer.onversely, those with cirrhosis more often than not didot have a cause found and on follow-up the SAAGhanged. The data suggest that a low SAAG in patientsith cirrhosis may not warrant extensive evaluation, but

ather close follow-up.

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ddition Papers of InterestArgo CK, Northup PG, Al-Osaimi A, et al. Systematic

eview of risk factors for fibrosis progression in non-lcoholic steatohepatitis. J Hepatol 2009;51:371–379.

La Mura V, Abraldes JG, Raffa S, et al. Prognostic valuef acute hemodynamic response to i.v. propranolol inatients with cirrhosis and portal hypertension. J Hepatol009;51:279 –287.

Rege D, Laudi C, Galatola G, et al. Diagnostic accuracyf computered tomographic colonography for the detec-ion of advanced neoplasia in individuals at increased

isk of colorectal cancer. JAMA 2009;301:2453–2461.

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918 ABSTRACTS FROM AROUND THE WORLD CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Vol. 7, No. 9

Li D, Morris JS, Liu J, et al. Body mass index and risk,ge of onset, and survival in patients with pancreaticancer. JAMA 2009;301:2553–2562.

Schenck AP, Peacock SC, Klabunde CN, et al. Trendsn colorectal cancer test use in the Medicare population,998 –2005. Am J Prev Med 2009;37:1–7.

Yadav D, Hawes RH, Brand RE, et al. Alcohol consump-ion, cigarette smoking, and the risk of recurrent acute andhronic pancreatitis. Arch Intern Med 2009;169:1035–1045.

Aksoz K, Unsal B, Yoruk G, et al. Endoscopic sphinc-erotomy alone in the management of low-grade biliaryeaks due to cholecystectomy. Dig Endosc 2009;21:158 –61.

Schnitzler F, Fidder H, Ferrante M, et al. Mucosalealing predicts long-term outcome of maintenance ther-

py with infliximab in Crohn’s diease. Inflamm Bowel Dis009 April 1 [Epub ahead of print].

Igarashi Y, Okano N, Ito K. Effectiveness of peroralholangioscopy and narrow band imaging for endoscop-cally diagnosing the bile duct cancer. Dig Endosc 2009;1:S101–S102.

Pickhardt PJ, Kim DH. Colorectal cancer screeningith CT colonography: key concepts regarding polyprevalence, size, histology, morphology, and natural his-ory. AJR 2009;193:40 – 46.

Taouli B, Ehman RL, Reeder SB. Advanced MRI methodsor assessment of chronic liver disease. AJR 2009;193:14–27.

Ly J, O’Grady G, Mittal A, et al. A systematic review ofethods to palliate malignant gastric outlet obstruction.

urg Endosc 2009 Jun 24 [Epub ahead of print].