Reply to Drs. Klaus and Weiss

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<ul><li><p>LETTERS TO THE EDITOR</p><p>Motility of the Roux-en-YHepaticojejunostomy inAsymptomatic PatientsTO THE EDITOR: We read with great interest the article byLe Blanc-Louvry et al. (1) regarding motility changes afterRoux-en-Y hepaticojejunostomy in asymptomatic patients.About one-third of all patients who undergo Roux-en-Yhepaticojejunostomy have slow upper gastrointestinal tran-sit after the operation, which sometimes leads to nausea,vomiting, and abdominal pain. Therefore, the analysis ofmanometric recordings of asymptomatic patients as com-parative data are unrenounceable. The authors report twopatients who did not show a migration of phase III contrac-tions across the lateral anastomosis (group Y/J).</p><p>We do not agree with their suggestion that an end-to-sideanastomosis creates a functional obstacle because of a dis-turbance of the intrinsic neural system. We are reminded ofPernthaler et al.s article (2) reporting that regeneration ofpacemaker frequencies after orthotopic small bowel trans-plantation did not occur in rats. Recently, we have shownthat even after a 3-month period, no reconnection of theintrinsic neural system occurs after small bowel transplan-tation (3). That indicates that 1025 days after the opera-tion, according to the published protocol, a disturbance dueto phase III contractions migrating from the duodenum isnearly impossible. Furthermore, the arrival of duodenal lu-minal contents as a reason for a functional obstacle andtherefore, for the broken migration of phase III contractionscan be excluded, because MMC measurements accuratelytake place during the fasting state.</p><p>Our experience with motility changes after Roux-en-Yhepaticojejunostomy has recently been published introduc-ing a new technique for biliodigestive anastomosis in rats(4). This technique consists of a loop of the proximal jeju-num with a side-to-side anastomosis at its base. Orally of thehepaticojejunostomy the lumen of the bowel was obliter-ated. In this experimental approach, phase III contractionsmigrated down the jejunum without any disturbance be-cause of the side-to-side anastomosis of the bowel, evenafter a 6-month course.</p><p>Finally, a disturbance of phase III migration from theproximal side of the lateral anastomosis to the distal sidewas observed in only 30% (two of four) of patients. How-ever, this might be due to incomplete endoluminal acquisi-tion of contractile signals.</p><p>Alexander Klaus, M.D.Helmut Weiss, M.D.</p><p>Department of SurgeryUniversity of Innsbruck-Austria</p><p>Innsbruck, Austria</p><p>REFERENCES</p><p>1. Le Blanc-Louvry I, Ducrotte Ph, Manouvrier JL, et al. Motilityof the Roux-en-Y hepaticojejunostomy in asymptomatic pa-tients. Am J Gastroenterol 1999;94:25018.</p><p>2. Pernthaler H, Kreczy A, Plattner R, et al. Myoelectric activityduring small bowel allograft rejection. Dig Dis Sci 1994;39:121621.</p><p>3. Klaus A, Margreiter R, Klima G, et al. Pacemaker frequenciesdo not regenerate after orthotopic rat small bowel allo- andisotransplantation. Presented at the ESOT 1997.</p><p>4. Klaus A, Weiss H, Kreczy A, et al. A new technique preventingmotility disorders following biliodigestive anastomosis. Pre-sented at the 9th European Symposium on Neurogastroenterol-ogy and Motility.</p><p>Reprint requests and correspondence: Alexander Klaus, M.D.,Department of Surgery, University of Innsbruck-Austria, Anich-strasse 35, 6020 Innsbruck, Austria.</p><p>Received Nov. 16, 1999; accepted Jan. 10, 2000.</p><p>Reply to Drs. Klaus and WeissTO THE EDITOR: We thank Drs. Klaus and Weiss for theirpertinent comments concerning our paper on motilitychanges after Roux-en-Y hepaticojejunostomy in asymp-tomatic patients (1). They contest our hypothesis that anend-to-side anastomosis could create a functional obstaclebecause of disturbances in the intrinsic neural system. Theybase this argument on their results obtained in a small boweltransplantation model, even if a single transection model (2)seems very different from the surgical transplantation pro-cedure (3).</p><p>We agree with these authors that, 3 wk after surgery, it isnearly impossible that a reconnection of the intrinsic neuralsystem could occur because total recovery of propagationacross transection and reanastomosis requires a postopera-tive delay of 3 months (2). However, in our article, wehypothesized only that the lack of propagation below theanastomosis of phase III contractions, initiated in the limb,could be disturbed by motor activity in the duodenum. Weare not in agreement with the hypothesis of a methodolog-ical artifact and an incomplete endoluminal acquisition ofthe signals because, in our study, contractile events werevery well recorded immediately above and below the anas-tomosis.</p><p>I. Le Blanc-Louvry, M.D.Hospital Charles Nicolle</p><p>Pavillon DerocqueService de Chirurgie Digestive</p><p>Rouen Cedex, France</p><p>THE AMERICAN JOURNAL OF GASTROENTEROLOGY Vol. 95, No. 6, 2000 2000 by Am. Coll. of Gastroenterology ISSN 0002-9270/00/$20.00Published by Elsevier Science Inc. PII S0002-9270(00)00890-X</p></li><li><p>REFERENCES</p><p>1. Le Blanc-Louvry I, Ducrotte PH, Manouvrier JL, et al. Motilityof the Roux-en-Y hepaticojejunostomy in asymptomatic pa-tients. Am J Gastroenterol 1999;94:25018.</p><p>2. Sarna SK, Condon RE, Cowles V. Enteric mechanisms ofinitiation of migrating myoelectric complexes in dogs. Gastro-enterology 1983;84:81422.</p><p>3. Quigley EMM, Spanta AD, Rose SG, Lof J, et al. Long-termeffects of jejunoileal autotransplantation on myoelectrical ac-tivity in canine small intestine. Dig Dis Sci 1990;12:150517.</p><p>Reprint requests and correspondence: I. Le Blanc-Louvry,M.D., Hospital Charles Nicolle, Pavillon Derocque, Service deChirurgie Digestive, 1 rue Germont, 76301 Rouen Cedex, France.</p><p>Received Jan. 10, 2000; accepted Jan. 10, 2000.</p><p>Re: Daniel et al.: Liver Biopsy WithoutClear Indication or Informed ConsentTO THE EDITOR: Daniel et al. performed liver biopsies in81 individuals with unexplained elevated liver blood tests(LFTs) (1). The authors state that the studys objectiveswere to establish the prevalence of steatosis/steatohepatitisin this cohort, determine the prevalence of associated dis-eases, and establish the clinical management impact of liverhistology.</p><p>Twenty-one patients were categorized as symptomaticby study criteria. Symptomatic was defined by the presenceof even one of seven listed symptoms which the authorsbelieved might be attributable to hepatic disease. As it is notstated, one cannot discern whether most of these 21 patientswere categorized as symptomatic on the basis of vaguesymptoms of nausea or fatigue. In addition, although vari-ous signs were sought (i.e., Dupuytrens contracture, ascites,etc.), physical findings were not documented. Marker-neg-ative patients with elevated liver enzymes presenting withnausea, fatigue, or even right upper quadrant pain generallydo not have a hepatic explanation for their symptoms.Therefore, I do not consider a liver biopsy to be an importantdiagnostic tool in these patients. My diagnostic algorithm isquite different for an icteric patient than for a nauseated one.We must be cautious before erroneously attributing func-tional bowel symptoms, i.e., to liver disease. The studysdivision, therefore, into symptomatic and asymptomaticgroups seems arbitrary.</p><p>In general, I discourage liver biopsy in marker-negativeindividuals with chronically abnormal LFTs, as the risksoutweigh the potential clinical gain. Despite earlier teach-ings in the 1970s and 1980s recommending liver biopsy onpatients with chronic LFT elevations, liver histology inthese circumstances only rarely contributes to clinical man-agement. The overriding majority of these patients will befound to have some degree of fatty change, an entity thatpresently has no defined therapy. This was confirmed againin the present study, which showed that 67 of 81 patients</p><p>demonstrated steatosis/steatohepatitis histologically. Of thestudy population, 10% had normal histology and only 1.5%were found to be cirrhotic. What benefits, therefore, didthese 81 patients achieve from the biopsy procedure? Isuggest that their liver histologys lack of clinical impactwas quite predictable.</p><p>More troubling than the above issues is that these patientsdid not provide informed consent for the procedure. Appar-ently, this requirement was waived by Henry Ford Hospi-tals human rights committee. Such a waiver, however, doesnot relieve physicians of their ethical obligation to obtaininformed consent for all procedures and interventions withrisk. Although the article states that patients consented toliver biopsy, it specifically states that informed consent waswaived. What were these patients told? Did they even knowthey were participating in a research project? I suspect thatpatients were advised of the procedures possible compli-cations, although this is not stated, but I doubt that they wereoffered a sober assessment of the potential benefits or thealternatives to a biopsy. Had these patients been given theopportunity to provide informed consent, as was their right,then I believe that the study group would have nearlyevaporated.</p><p>The doctrine of informed consent is paramount in allmedical research involving human subjects. Institutionalreview boards, clinical researchers, and medical editorsmust not sacrifice informed consent to promote researchand publications. Under the current circumstances,should this study have been conducted? Should informedconsent have been waived? Should this study have beenpublished?</p><p>Michael Kirsch, M.D., F.A.C.P.Highland Heights, Ohio</p><p>REFERENCE</p><p>1. Daniel S, Ben-Menachem T, Vasudevan G, et al. Prospectiveevaluation of unexplained liver transaminase abnormalities inasymptomatic and symptomatic patients. Am J Gastroenterol1999;94:301014.</p><p>Reprint requests and correspondence: Michael Kirsch, M.D.,F.A.C.P., 6221 Tourelle Drive, Highland Heights, OH 44143.</p><p>Received Oct. 21, 1999; accepted Jan. 12, 2000.</p><p>Response to Dr. KirschTO THE EDITOR: The division into symptomatic andasymptomatic groups was certainly not arbitrary. The symp-toms of liver disease are nonspecific, and we do not implythat these symptoms are indicative of liver disease. Wesought symptoms that have been well documented in hepa-tology textbooks, and that have been used in previous sim-ilar trials for the sake of comparison. As stated in the text,we found no association between the presence of symptoms</p><p>1588 Letters to the Editor AJG Vol. 95, No. 6, 2000</p></li></ul>