2
Rapid Transit After Colectomy Basse L, Madsen JL, Kehlet H. Nor- mal gastrointestinal transit after co- lonic resection using epidural analge- sia, enforced oral nutrition and laxative. Br J Surg 2001;88:1498 –500. Postoperative ileus is an expected out- come of colonic surgery and usually lasts 2–5 days. There has been a long term interest in lessening this effect to promote earlier postoperative recov- ery. Techniques such as epidural an- algesia, early oral nutrition, and pa- tient mobilization appear to result in more rapid return of bowel function postoperatively. This is normally evaluated by such findings as the first defecation after operation. However, the sequence of recovery of the GI tract from ileus and its rapidity remain unclear. Basse et al. have studied GI transit time using 111 In-labeled dieth- ylenetriamine pentaacetic acid to evaluate transit after colectomy with use of these adjuvant techniques. The authors studied 12 consecutive patients undergoing open colon resec- tion and receiving continuous epi- dural analgesia for 48 h, with no na- sogastric tube, early postoperative oral nutrition and mobilization, and oral cisapride. Transit measurements were compared with 12 normal vol- unteers who had histories of normal defecation and no bowel motility modifiers. They found that 50% of the tracer was excreted in the feces within 48 h in the patients undergoing colec- tomy, compared to 53% in the volun- teers, indicating that GI transit was normal within that period of time. In addition, the regional distributions of the marker were also similar. Thus, they have demonstrated a return to normal full gut transit by scintigraphy within 48 h. Although the relative contribution of the epidural analgesia, early postoperative nutrition, cisa- pride, and mobilization cannot be sep- arated in the present study, regimens such as this clearly appear to be useful in hastening the resolution of postop- erative ileus. Jon S. Thompson, M.D. Increased Iron May Promote Alcoholic Liver Injury De Feo MT, Fargion S, Duca L, et al. Non-transferrin-bound iron in alco- hol abusers. Alcohol Clin Exp Res 2001;25:1494 –9. Although alcohol abuse and its result- ant medical problems are widespread both in the United States and world- wide, the mechanism(s) responsible for the pathological effects of this substance remain elusive. In the liver, alcohol has been shown to increase oxidative stress along with lipid per- oxidation and collagen production, leading to fibrosis, and these mecha- nisms have been widely examined in both animal and human models. In addition to alcohol, increased levels of iron (especially the “free iron” that is low molecular weight and not bound to transferrin) have been impli- cated in playing a role in oxidative stress and fibrosis, although no con- clusive data are available. Patients with hereditary hemochromatosis who show increased levels of free iron in the serum also have a higher inci- dence of fibrosis and cirrhosis if they consume alcohol than controls. In an- imal models of alcohol administra- tion, the addition of dietary iron has been shown to lead to increased he- patocyte (liver cell) damage. In the study performed in this report, the in- vestigators examined whether small THE AMERICAN JOURNAL OF GASTROENTEROLOGY Vol. 97, No. 4, 2002 © 2002 by Am. Coll. of Gastroenterology ISSN 0002-9270/02/$22.00 Published by Elsevier Science Inc. WHAT’S NEW IN GI EDITOR Jon S. Thompson, M.D. University of Nebraska Medical Center Omaha, Nebraska SURGERY Dmitry Oleynikov University of Nebraska Medical Center Omaha, Nebraska GASTROENTEROLOGY Randall E. Brand Hermant K. Roy Northwestern University Chicago, Illinois Rene ´e L. Young John K. DiBaise Timothy M. McCashland Mark E. Mailliard University of Nebraska Medical Center Omaha, Nebraska RADIOLOGY Aurelio Matamoros, Jr. M. D. Anderson Cancer Center Houston, Texas PATHOLOGY James L. Wisecarver James M. Gulizia University of Nebraska Medical Center Omaha, Nebraska BASIC SCIENCE Carol A. Casey University of Nebraska Medical Center Omaha, Nebraska PEDIATRIC GASTROENTEROLOGY David R. Mack Children’s Hospital of Eastern Ontario Ottawa, Ontario, Canada Simon Horslen University of Nebraska Medical Center Omaha, Nebraska WHAT’S NEW IN GI

Increased iron may promote alcoholic liver injury

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Page 1: Increased iron may promote alcoholic liver injury

Rapid TransitAfter Colectomy

Basse L, Madsen JL, Kehlet H. Nor-mal gastrointestinal transit after co-lonic resection using epidural analge-sia, enforced oral nutrition andlaxative. Br J Surg 2001;88:1498–500.

Postoperative ileus is an expected out-come of colonic surgery and usuallylasts 2–5 days. There has been a longterm interest in lessening this effect topromote earlier postoperative recov-ery. Techniques such as epidural an-algesia, early oral nutrition, and pa-tient mobilization appear to result inmore rapid return of bowel functionpostoperatively. This is normallyevaluated by such findings as the firstdefecation after operation. However,the sequence of recovery of the GItract from ileus and its rapidity remainunclear. Basseet al. have studied GItransit time using111In-labeled dieth-ylenetriamine pentaacetic acid toevaluate transit after colectomy withuse of these adjuvant techniques.

The authors studied 12 consecutivepatients undergoing open colon resec-tion and receiving continuous epi-dural analgesia for 48 h, with no na-sogastric tube, early postoperativeoral nutrition and mobilization, andoral cisapride. Transit measurementswere compared with 12 normal vol-unteers who had histories of normaldefecation and no bowel motilitymodifiers. They found that 50% of thetracer was excreted in the feces within48 h in the patients undergoing colec-tomy, compared to 53% in the volun-teers, indicating that GI transit wasnormal within that period of time. Inaddition, the regional distributions ofthe marker were also similar. Thus,they have demonstrated a return tonormal full gut transit by scintigraphywithin 48 h. Although the relative

contribution of the epidural analgesia,early postoperative nutrition, cisa-pride, and mobilization cannot be sep-arated in the present study, regimenssuch as this clearly appear to be usefulin hastening the resolution of postop-erative ileus.

Jon S. Thompson, M.D.

Increased Iron MayPromote AlcoholicLiver Injury

De Feo MT, Fargion S, Duca L, et al.Non-transferrin-bound iron in alco-hol abusers. Alcohol Clin Exp Res2001;25:1494–9.

Although alcohol abuse and its result-ant medical problems are widespreadboth in the United States and world-wide, the mechanism(s) responsiblefor the pathological effects of thissubstance remain elusive. In the liver,alcohol has been shown to increaseoxidative stress along with lipid per-oxidation and collagen production,leading to fibrosis, and these mecha-nisms have been widely examined inboth animal and human models. Inaddition to alcohol, increased levelsof iron (especially the “free iron” thatis low molecular weight and notbound to transferrin) have been impli-cated in playing a role in oxidativestress and fibrosis, although no con-clusive data are available. Patientswith hereditary hemochromatosiswho show increased levels of free ironin the serum also have a higher inci-dence of fibrosis and cirrhosis if theyconsume alcohol than controls. In an-imal models of alcohol administra-tion, the addition of dietary iron hasbeen shown to lead to increased he-patocyte (liver cell) damage. In thestudy performed in this report, the in-vestigators examined whether small

THE AMERICAN JOURNAL OF GASTROENTEROLOGY Vol. 97, No. 4, 2002© 2002 by Am. Coll. of Gastroenterology ISSN 0002-9270/02/$22.00Published by Elsevier Science Inc.

WHAT’S NEW IN GI

EDITORJon S. Thompson, M.D.University of Nebraska

Medical CenterOmaha, Nebraska

SURGERYDmitry OleynikovUniversity of Nebraska

Medical CenterOmaha, Nebraska

GASTROENTEROLOGYRandall E. BrandHermant K. RoyNorthwestern University

Chicago, IllinoisRenee L. YoungJohn K. DiBaiseTimothy M. McCashlandMark E. MailliardUniversity of Nebraska

Medical CenterOmaha, Nebraska

RADIOLOGYAurelio Matamoros, Jr.M. D. Anderson Cancer Center

Houston, Texas

PATHOLOGY

James L. WisecarverJames M. GuliziaUniversity of Nebraska

Medical CenterOmaha, Nebraska

BASIC SCIENCECarol A. CaseyUniversity of Nebraska

Medical CenterOmaha, Nebraska

PEDIATRICGASTROENTEROLOGYDavid R. MackChildren’s Hospital of

Eastern OntarioOttawa, Ontario, CanadaSimon HorslenUniversity of Nebraska

Medical CenterOmaha, Nebraska

WHAT’S

NEWIN

GI

Page 2: Increased iron may promote alcoholic liver injury

increases in body iron might increasesusceptibility in humans to alcoholicliver injury.

To address this issue, De Feo et al.studied a group of 76 chronic alco-holic patients with and without livercirrhosis both during alcohol intakeand after withdrawal. All patientswere negative for hepatitis B virussurface antigen and hepatitis C virusantibody. Forty-one patients had livercirrhosis, whereas 35 patients werefree of cirrhotic indicators. In somepatients a follow-up period where al-cohol intake was monitored carefullywas also included. Twenty healthysubjects with normal iron status andno apparent alcohol intake in themonth-long period before the studywere used as normal controls. Theinvestigators measured serum levelsof non–transferrin bound iron (NTBI),the low molecular weight fraction ofiron, in all subjects. In this study,NTBI was detectable in greater than80% of the active abusers, but in only21% of the abstainers. In the group ofalcohol abusers, the patients with cir-rhosis showed significantly higherNTBI levels than patients without cir-rhosis. Transferrin saturation did notappear to correlate with NTBI levels.

This study is important because itprovides new information on the pos-sible association of NTBI, alcoholabuse, and liver damage. Althoughthe mechanism by which alcohol af-fects NTBI remains unindentified, re-sults from this study indicate that highlevels of NTBI might play a role inthe development of liver disease. Per-haps, as the authors suggest, studiesexamining NTBI chelators may behelpful in the future in defining a rolefor this substance in the developmentof liver injury after alcohol abuse.

Carol Casey, M.D.

Risk Factors forH. pylori Resistance

Meyer JM, Silliman NP, Wang W, etal. Risk factors for Helicobacter py-

lori resistance in the United States:The surveillance of H. pylori anti-mocrobial resistance partnership(SHARP) study, 1993-1999. Ann In-tern Med 2001;136:13–24.

Identification of risk factors associ-ated with antibiotic resistance to Hel-icobacter pylori is important, as treat-ment is generally prescribed withoutknowledge of the susceptibility of theindividual patient’s isolate. Meyerand colleagues performed a meta-analysis using patient data collectedfrom 20 clinical trials of H. pylorieradication conducted in the UnitedStates between 1993 and 1999, to es-timate the prevalence of H. pylori re-sistance to clarithromycin, metronida-zole, and amoxicillin and tocharacterize the risk factors (geo-graphic region, age, gender, studyyear, ethnicity, ulcer status, testmethod, and study) associated withthis resistance. Resistance patternswere as follows: 10%, clarithromycin;37%, metronidazole; and 1%, amoxi-cillin. Clarithromycin resistance wasassociated with geographic region(Northeast and Mid-Atlantic), olderage, female sex, inactive ulcer dis-ease, and study. Metronidazole resis-tance was associated with female sex,earlier year of study enrollment,Asian ethnicity, use of an epsilometertest, and study. There was also a trendtowards younger age. Amoxicillin re-sistance was not associated with anyfactor. Dual resistance to clarithromy-cin and metronidazole was present inapproximately 4% of isolates and wassignificantly associated with femalesex, older age, Asian ethnicity, middleyears of study enrollment, and study.

Although the generalizability andvalidity of these findings remain un-proven, clinicians should considerthese factors when deciding which pa-tients should undergo susceptibilitytesting and when choosing empiricalH. pylori treatment. Additionally,given the high prevalence of antibi-otic resistance and the subsequent re-duced treatment efficacy, consider-ation should also be given todocumentation of eradication of H.

pylori in those treated empirically,particularly those with risk factors.

J. K. DiBaise, M.D.

SPECT Imaging andGastric Accommodation

Liau S-S, Camilleri M, Kim D-Y, et al.Pharmacological modulation of hu-man gastric volumes demonstratednoninvasively using SPECT imaging.Neurogastroenterol Motil 2001;13:533–42.

The clinical importance of proximalstomach function has received muchattention over the last several years. Inparticular, impaired fundic accommo-dation has been reported frequently inconditions such as diabetic gastropa-thy, postfundoplication dyspepsia,and functional dyspepsia, and hasbeen suggested to contribute to thedevelopment of postprandial symp-toms of bloating, nausea, early satiety,and epigastric pain. Thus, the devel-opment of a noninvasive, clinicallyacceptable means of measuring gas-tric accommodation would be usefulnot only to demonstrate normal or ab-normal pathophysiology but also, po-tentially, to assist with rational thera-peutic decision making. Liau andcolleagues have previously demon-strated the feasibility of three-dimen-sional single photon emission CT(SPECT) using the Analyse softwaresystem as a noninvasive test of thepostprandial gastric accommodationresponse in humans. In this study,they sought to further validate this testby determining whether SPECT isable to demonstrate effects of phar-macological modulations on pre- andpostprandial gastric volumes. Thirty-two healthy individuals were studied.Twenty received no medication (con-trols), whereas six each were random-ized to either i.v. erythromycin or sub-lingual isosorbide. After a 10-minpreprandial supine SPECT measure-ment, a standard 300-kcal liquid mealwas ingested, followed by a 20-minpostprandial measurement. No signif-

792 What’s New in GI AJG – Vol. 97, No. 4, 2002