CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2012;10:97–99

ABSTRACTS FROM AROUND THE WORLD

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� Thalidomide to the RescueGe ZZ, Chen HM, Gao YJ, et al. Efficacy of thalidomide forrefractory gastrointestinal bleeding from vascular malforma-tion. Gastroenterology 2011;141:1629 –1637.

Summary. Recurrent bleeding from gastrointestinalvascular malformations remains a significant chal-lenge, especially when endoscopic therapy is eitherineffective or the full extent of the lesions cannot bereliably assessed or treated. Recent evidence has shownthat vascular ectasias express vascular endothelialgrowth factor. Because several case reports suggestthalidomide—which alters this growth factor—may beeffective in these patients, this open-label, randomizedtrial was performed. Consecutive patients with refrac-tory bleeding from vascular ectasias over a 4-year pe-riod were randomized to thalidomide 100 mg daily(n � 28) or 400 mg of iron (n � 27, controls) daily for4 months. Bleeding was defined as a positive resultfrom an immunoassay fecal occult blood test. A num-ber of secondary end points were also assessed forrecurrent bleeding. These were patients who had had ahistory of bleeding for an average of 5 or more years.Using an intent-to-treat analysis, the primary endpoint was the effective response rate defined as theproportion of patients in whom bleeding episodes haddecreased by �50% in the first year of follow-up. Sev-enty-one percent of patients compared to 3.7% of theiron-control group met the primary end point (P �0.000; 95% CI 54.7– 85.9). All of the secondary endpoints were also met and were markedly statisticallysignificantly different between the 2 groups. Forty-sixpercent of treated patients compared to 0% of controlshad cessation of bleeding, and 11% vs 48% of patientswere subsequently dependent on blood transfusions.While the plasma concentration of vascular endothe-lial growth factor decreased significantly in the thalid-omide group, there was no significant difference in the20 patients in whom thalidomide was effective com-pared to the 6 in whom no significant changes in theend points were met.

Editor’s comment. The results here are quite strikingand warrant replication. The drug was relatively welltolerated with fatigue and somnolence being the mostcommon side effects, which were anticipated. While thegrowth factor levels decreased following treatment, therewas no statistical difference in the post-treatment levelsbetween the effective and ineffective groups. At this stage,given the manageable side effects of the drug and thesignificant morbidity from recurrent bleeding, these re-

sults suggest that this drug may be worth a try. I am sure m

further studies will be undertaken in this setting, perhapsin comparison to those with severe small bowel disease inwhom double balloon enteroscopy with therapy is theonly other option.

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� Maybe Worth Another LookMazzoleni LE, Sander GB, de Magalhães Francesconi CF, et al.Helicobacter pylori eradication in functional dyspepsia. Arch In-tern Med 2011;171:1929 –1936.

Summary. The impact of Helicobactyer pylori on pep-tic ulcer incidence in developed countries continues towane. Nevertheless, there remains significant interestworldwide in H. pylori given the worldwide prevalence.

his well-done, large randomized study from Brazileaddresses the issue of eradication and its effect onyspepsia. Adult patients with dyspepsia fulfilling theome III consensus criteria were randomized to anti-iotic therapy with omeprazole, amoxicillin, and clari-hromycin or omeprazole plus a placebo for 10 days.ndoscopy and H. pylori tests were performed atcreening and at 1 year. The primary outcome measureas defined as at least a 50% symptomatic improve-ent at 12 months. Patients were also asked about

lobal assessment of their symptoms and quality ofife. Overall, 49% compared to 36.5% in the antibiotics control group met the primary end point. Totalyspepsia relief was seen in 18% of the antibiotic groupompared to 14% in the control group (P � .34).lobal improvement was reported in 78% of the anti-iotic group compared to 67.5% in the control group

P � .02). The number needed to treat to achieve therimary outcome was 8. At 1 year, 88.6% of patients inhe antibiotic group were negative for H. pylori com-ared to 7.4% in the control group. Multivariate anal-sis did not identify any factors predictive of thoseho would respond clinically.

Editor’s comment. Dyspepsia is an important andifficult to treat syndrome. In countries where the prev-lence of H. pylori is receding, treatment is relegated toroton pump inhibitor therapy and perhaps other med-

cations for functional disease. At least by this and othertudies, H. pylori infection should be evaluated for andreated in patients with bonafide functional dyspepsia,ecognizing that the overall benefit is modest at best. Inddition, this study once again shows that completeesolution of symptoms is very uncommon, suggesting a

ultifactorial cause for dyspepsia. It is unfortunate that

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98 ABSTRACTS FROM AROUND THE WORLD CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Vol. 10, No. 2

there remain no great predictors for patients who re-spond to antibiotic therapy.

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� Can NAC Help in Severe AlcoholicHepatitis?Nguyen-Khac E, Thevenot T, Piquet MA, et al. Glucocorticoidsplus N-Acetylcysteine in severe alcoholic hepatitis. N Engl J Med2011;365:1781–1789.

Summary. The high mortality rate associated withlcoholic hepatitis is well recognized. The use of cortico-teroids in patients who have a high Maddrey discrimi-ate function has been shown to improve survival. N-

Acetylcysteine (NAC) is commonly given to patients withacute liver failure, and the rationale for its use in alco-holic hepatitis could be the value of NAC’s antioxidantproperties and its ability to reduce levels of free radicals.This randomized multicenter trial of patients with alco-holic hepatitis compared prednisolone to the combina-tion of prednisolone plus NAC in patients with severealcoholic hepatitis in whom the Maddrey discriminatedysfunction was �32. Both groups received 40 mg of oralprednisolone per day for 28 days, while the combinationgroup received 5 days of intravenous NAC. The primaryoutcome measure was survival at 6 months. The overallmortality rate was 38% in the prednisolone-only groupcompared to 27% in the combination group (P � .07; 95%CI 0.37–1.06). The median time to death was slightlylonger in the prednisolone-only group (40 days comparedto 254 days). Both the 1 month and 3 month mortalityrates favored the combination group. In addition, hepa-torenal syndrome occurred in 22% of the prednisolone-only group compared to the 9% in the combinationgroup, while no differences were seen in the rate ofinfections resulting in death.

Editor’s comment. While not statistically significant,using the P � .05 rate, there was clear separation of the2 groups within 30 days when examining the Kaplan–Meier curves. However, the confidence intervals wouldsuggest this perhaps is not significant. NAC is widelyused in patients with acute liver failure even in the ab-sence of documented or highly suspected use of acet-aminophen. The drug is relatively inexpensive and welltolerated. While no statistically significant difference be-tween groups was seen in the study, I suspect that manymay actually be using this combination anyway given thealways real possibility of the use of acetaminophen, par-ticularly in patients who are alcoholic where the use ofacetaminophen in standard doses could lead to acuteliver injury. The 1-month improved survival in the NACgroup was likely due to the fact that there was less

hepatorenal syndrome.

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� Messed Up in the HeadFrøjær JB, Olesen SS, Gram M, et al. Altered brain microstruc-ture assessed by diffusion tensor imaging in patients withchronic pancreatitis. Gut 2011;60:1554 –1562.

Summary. It is well recognized that abdominal painin chronic pancreatitis is debilitating and difficult totreat. Using neurophysiologic studies, prior studies haveshown reorganization of brain areas involving visceralpain processing. This study uses a novel magnetic reso-nance diffusion tensor imaging to assess changes inwhite and gray matter microstructure not seen by con-ventional imaging technique. The authors hypothesizedthat patients with abdominal pain in chronic pancreatitishave changes in brain microstructure in areas involved inthe processing of visceral pain. Twenty-three patientswith the diagnosis of chronic pancreatitis were studiedand compared to 14 healthy volunteers serving as con-trols. The duration of chronic pancreatitis averaged ap-proximately 2 years. All healthy volunteers had a normalstructural brain MRI. In patients with chronic pancreati-tis, they identified abnormalities in the amygdala, cingu-late cortex, insular, and pre-frontal cortex. White matterchanges were likewise significantly different than con-trols. Furthermore, the microstructural changes appearedto be influenced by the patient’s pain pattern with acorrelation seen between the abnormalities in some ofthe brain structures compared to the daily pain score,maximum pain score and brief inventory pain scores.

Editor’s comment. The exact nature of the structuralchanges responsible for the identified abnormalities isnot clear and may be multifactorial. Prior studies using asimilar technique have also identified similar abnormal-ities in patients with fibromyalgia and patients with neu-ropathic pain. This study and similar studies from thisgroup further enhance our understanding of the com-plexity of pain processing in patients with chronic pan-creatitis and further underscores the fact that treatmentof pain locally (ie, in the pancreas and surroundingnerves) may be ineffective if the problem is pain process-ing in the central nervous system. Looks like we need totreat the “head” and the pancreas.

Additional Papers of Interest

� Zhang L, Chari S, Smyrk TC, et al. Autoimmunepancreatitis (AIP) type 1 and type 2: an internationalconsensus study on histopathologic diagnostic criteria.Pancreas 2011;40:1172–1179.� Nøjgaard C, Becker U, Matzen P, et al. Progressionfrom acute to chronic pancreatitis: prognostic factors,mortality, and natural course. Pancreas 2011;40:1195–1200.� Meining A, Chen YK, Pleskow D, et al. Direct visual-

ization of indeterminate pancreaticobiliary strictures

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with probe-based confocal laser endomicroscopy: a mul-ticenter experience. Gastrointest Endosc 2011;74:961–968.� Huang ES, Karsan S, Kanwal F, et al. Impact of naso-gastric lavage on outcomes in acute GI bleeding. Gastro-intest Endosc 2011;74:971–980.� Peyrin-Biroulet L, Khosrotehrani K, Carrat F, et al.Increased risk for nonmelanoma skin cancers in patientswho receive thiopurines for inflammatory bowel disease.Gastroenterology 2011;141:1621–1628.� Buchholz U, Bernard H, Werber D, et al. Germanoutbreak of Escherichia coli O104:h4 associated withsprouts. N Engl J Med 2011;365:1763–1770.� Frank C, Werber K, Cramer JP, et al. Epidemic profileof Shiga-toxin–producing Escherichia coli O104:H4 out-break in Germany. N Engl J Med 2011;365:1771–1780.� Mathurin P, Moreno C, Samuel D, et al. Early livertransplantation for severe alcoholic hepatitis. N EnglJ Med 2011;365:1790 –1800.� Hotouras A, Collins P, Speake W, et al. Diagnosticyield and economic implications of endoscopic colonicbiopsies in patients with chronic diarrhoea. ColorectalDis 2011 Oct 4 [Epub ahead of print].� Hsu YC, Yang TH, Liou JM, et al. Can clinical featuresstratify use of endoscopy for dyspeptic patients with highbackground prevalence of upper gastrointestinal cancer?Dig Liver Dis 2011 Nov 22 [Epub ahead of print].� Ho KS, Quah HM, Lim JF, et al. Endoscopic stenting

nd elective surgery versus emergency surgery for left-ided malignant colonic obstruction: a prospective ran-omized trial. Int J colorectal Dis 2011 Oct 28 [Epub

ahead of print].� Elmunzer BJ, Padhya KT, Lewis JJ, et al. Endoscopicfindings and clinical outcomes in ventricular assist devicerecipients with gastrointestinal bleeding. Dig Dis Sci2011;56:3241–3246.� Cornett DD, Spier BJ, Eggert AA, et al. The causes andoutcome of acute pancreatitis associated with serumlipase 10,000 U/L. Dig Dis Sci 2011;56:3376 –3381.� Wallace M, Lauwers GY, Chen Y, et al. Miami classifi-cation for probe-based confocal laser endomicroscopy.

Endoscopy 2011;43:882– 891.

� Merritt RE, Whyte RI, D’Arcy NT, et al. Morbidity andmortality after esophagectomy following neoadjuvantchemoradiation. Ann Thorac Surg 2011;92:2034 –2040.� Savarino E, Zentilin P, Marabotto E, et al. Overweightis a risk factor for both erosive and non-erosive refluxdisease. Dig Liver Dis 2011;43:940 –945.� Kahrilas PJ, Hughes N, Howden CW. Response ofunexplained chest pain to proton pump inhibitor treat-ment in patients with and without objective evidence ofgastro-oesophageal reflux disease. Gut 2011;60:1473–1478.� Ferrante JM, McCarthy EP, Gonzalez EC, et al. Primarycare utilization and colorectal cancer outcomes amongMedicare beneficiaries. Arch Intern Med 2011;171:1747–1757.� Mega JL, Hochholzer W, Frelinger AL, et al. Dosingclopidogrel based on CYP2C19 genotype and the effect onplatelet reactivity in patients with stable cardiovasculardisease. JAMA 2011;306:2221–2228.� Salerno F, Cazzaniga M, Merli M, et al. Diagnosis,treatment and survival of patients with hepatorenal syn-drome: a survey on daily medical practice. J Hepatol2011;55:1241–1248.� Trinchet JC, Chaffaut C, Bourcier V, et al. Ultrasono-graphic surveillance of hepatocellular carcinoma in cir-rhosis: a randomized trial comparing 3- and 6-monthperiodicities. Hepatology 2011;54:1987–1997.� Loehrer PJ, Feng Y, Cardenes H, et al. Gemcitabinealone versus gemcitabine plus radiotherapy in patientswith locally advanced pancreatic cancer: an Eastern Co-operative Oncology Group trial. J Clin Oncol 2011;29:4105– 4112.� Weiss JM, Pfau PR, O’Connor ES, et al. Mortality bystage for right- versus left-sided colon cancer: analysisof surveillance, epidemiology, and end results-Medicaredata. J Clin Oncol 2011;29:4401– 4409.� van Soest EM, Valkhoff VE, Mazzaglia G, et al. Sub-optimal gastroprotective coverage of NSAID use and therisk of upper gastrointestinal bleeding and ulcers: anobservational study using three European databases. Gut

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