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GASTROENTEROLOGY
`Volume 78, January-June 1980
`GASTROENTEROLOGY
`Volume 78, January-June 1980
`
`Editor
`
`John S. Fordtran
`Department of Internal Medicine
`Baylor University Medical Center
`Editor
`3500 Gaston Avenue
`Dallas, Texas 75246
`John S. Fordtran
`Department of Internal Medicine
`Editor of Liver Section
`Baylor University Medical Center
`3500 Gaston Avenue
`Burton Combes
`Dallas, Texas 75246
`University of Texas
`Southwestern Medical School
`Editor of Liver Section
`5323 Harry Hines Boulevard
`Dallas, Texas 75235
`Burton Combes
`University of Texas
`Associate Editors
`Southwestern Medical School
`5323 Harry Hines Boulevard
`Raj K. Goyal
`Dallas, Texas 75235
`University of Texas
`Health Science Center
`Associate Editors
`7703 Floyd Curl Drive
`San Antonio, Texas 78284
`Raj K. Goyal
`University of Texas
`John H. Walsh
`Health Science Center
`Veterans Administration
`7703 Floyd Curl Drive
`Wadsworth Hospital Center
`San Antonio, Texas 78284
`Los Angeles, California 90073
`John H. Walsh
`Athol Ware.
`Veterans Administration
`University of Texas
`Wadsworth Hospital Center
`Southwestern Medical School
`Los Angeles, California 90073
`5323 Harry Hines Boulevard
`Dallas, Texas 75235
`Athol Ware.
`University of Texas
`Selected Summaries Editor
`Southwestern Medical School
`Jon I. Isenberg
`5323 Harry Hines Boulevard
`San Diego, California
`Dallas, Texas 75235
`Book Review Editor
`Selected Summaries Editor
`Armand Littman
`Jon I. Isenberg
`Hines, Illinois
`San Diego, California
`Audiovisual Editor
`Book Review Editor
`Marvin M. Schuster
`Armand Littman
`Baltimore, Maryland
`Hines, Illinois
`Chairperson of Editorial Board
`Audiovisual Editor
`Marvin M. Schuster
`Fred Kern, Jr.
`Baltimore, Maryland
`Denver, Colorado
`
`Chairperson of Editorial Board
`
`Fred Kern, Jr.
`Denver, Colorado
`
`Editorial Board
`
`James L. Boyer, Chicago, Illinois
`Harold 0. Conn, West Haven, Connecticut
`Allan R. Cooke, Kansas City, Kansas
`Editorial Board
`Edwin Englert, Jr., Salt Lake City, Utah
`Michael Field, Chicago, Illinois
`James L. Boyer, Chicago, Illinois
`Harvey Goldman, Boston, Massachusetts
`Harold 0. Conn, West Haven, Connecticut
`Alan F. Hofmann, San Diego, California
`Allan R. Cooke, Kansas City, Kansas
`Bernard M. Jaffe, St. Louis, Missouri
`Edwin Englert, Jr., Salt Lake City, Utah
`Ronald M. Katon, Portland, Oregon
`Michael Field, Chicago, Illinois
`Young S. Kim, San Francisco, California
`Harvey Goldman, Boston, Massachusetts
`Raymond S. Koff, Boston, Massachusetts
`Alan F. Hofmann, San Diego, California
`Sumner C. Kraft, Chicago, Illinois
`Bernard M. Jaffe, St. Louis, Missouri
`Gabriel M. Makhlouf, Richmond, Virginia
`Ronald M. Katon, Portland, Oregon
`Charles E. Pope II, Seattle, Washington
`Young S. Kim, San Francisco, California
`Allan G. Redeker, Downey, California
`Raymond S. Koff, Boston, Massachusetts
`Malcolm M. Stanley, Chicago, Illinois
`Sumner C. Kraft, Chicago, Illinois
`Jerry S. Trier, Boston, Massachusetts
`Gabriel M. Makhlouf, Richmond, Virginia
`Elliot Weser, San Antonio, Texas
`Charles E. Pope II, Seattle, Washington
`Jack Wittenberg, Boston, Massachusetts
`Allan G. Redeker, Downey, California
`Malcolm M. Stanley, Chicago, Illinois
`Officers of the American
`Jerry S. Trier, Boston, Massachusetts
`Gastroenterological Association
`Elliot Weser, San Antonio, Texas
`Jack Wittenberg, Boston, Massachusetts
`President
`Robert M. Donaldson, Jr.
`Officers of the American
`West Haven, Connecticut
`Gastroenterological Association
`President Elect
`President
`Frank P. Brooks
`Robert M. Donaldson, Jr.
`Philadelphia, Pennsylvania
`West Haven, Connecticut
`Vice-President
`President Elect
`Malcolm P. Tyor
`Frank P. Brooks
`Durham, North Carolina
`Philadelphia, Pennsylvania
`Secretary
`Vice-President
`Kenneth A. Hubel
`Malcolm P. Tyor
`Iowa City, Iowa
`Durham, North Carolina
`Treasurer
`Secretary
`James L. Borland
`Kenneth A. Hubel
`Jacksonville, Florida
`Iowa City, Iowa
`
`Treasurer
`James L. Borland
`Jacksonville, Florida
`
`

`

`GASTAB (1980) ISSN 0016-5085. © 1980 by the American Gastroenterological Associa-
`GASTAB (1980) ISSN 0016-5085. © 1980 by the American Gastroenterological Associa-
`tion. Issued monthly in two indexed volumes per year by Elsevier North-Holland, Inc.,
`tion. Issued monthly in two indexed volumes per year by Elsevier North-Holland, Inc.,
`52 Vanderbilt Avenue, New York, NY 10017.
`52 Vanderbilt Avenue, New York, NY 10017.
`
`This journal has been registered with the Copyright Clearance Center, Inc. Consent is
`This journal has been registered with the Copyright Clearance Center, Inc. Consent is
`given for the copying of articles for personal or internal use, or for the personal or inter-
`given for the copying of articles for personal or internal use, or for the personal or inter-
`nal use of specific. clients. This consent is given on the condition that the copier pay
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`through the Center the per copy fee stated in the code on the first page of each article
`through the Center the per copy fee stated in the code on the first page of each article
`for copying beyond that permitted by the US Copyright Law. If no code appears on an
`for copying beyond that permitted by the US Copyright Law. If no code appears on an
`article, the author has not given broad consent to copy, and permission to copy must be
`article, the author has not given broad consent to copy, and permission to copy must be
`obtained directly from the author. This consent does not extend to other kinds of copy-
`obtained directly from the author. This consent does not extend to other kinds of copy-
`ing, such as for general distribution, resale, advertising and promotional purposes, or
`ing, such as for general distribution, resale, advertising and promotional purposes, or
`for creating new collective works.
`for creating new collective works.
`
`C 0 NT]
`
`ALIMEN
`
`LIVER P
`
`

`

`January 1980 (cid:9)
`1. Sharon P, Ligumsky M, Rachmilewitz D, Zor U: Role of prosta-
`glandins in ulcerative colitis. Enhanced production during ac-
`tive disease and inhibition by sulfasalazine, Gastroenterology
`75:638-640, 1978
`1. Sharon P, Ligumsky M, Rachmilewitz D, Zor U: Role of prosta-
`2. Kimberg DV: The ubiquitous prostaglandins and their role in
`glandins in ulcerative colitis. Enhanced production during ac-
`ulcerative colitis. Gastroenterology 75:748-750, 1978
`tive disease and inhibition by sulfasalazine, Gastroenterology
`3. Edmonds CI: Absorption of sodium and water by human rec-
`75:638-640, 1978
`tum measured by a dialysis method. Gut 12:356-362, 1971
`2. Kimberg DV: The ubiquitous prostaglandins and their role in
`4. Rampton DS, Sladen GE, Bhakoo KK, Heinzelmann DE, Youl-
`ulcerative colitis. Gastroenterology 75:748-750, 1978
`ten LJF: Rectal mucosal prostaglandin E release and electrolyte
`3. Edmonds CI: Absorption of sodium and water by human rec-
`transport in ulcerative colitis. In: Advances in Prostaglandin
`tum measured by a dialysis method. Gut 12:356-362, 1971
`and Thromboxane Research (In press)
`4. Rampton DS, Sladen GE, Bhakoo KK, Heinzelmann DE, Youl-
`5. Gerber JG: Prostaglandins and ulcerative colitis, a warning.
`ten LJF: Rectal mucosal prostaglandin E release and electrolyte
`Gastroenterology 76:658, 1979
`transport in ulcerative colitis. In: Advances in Prostaglandin
`6. Edmonds CJ, Pilcher D: Electrical potential difference and so-
`and Thromboxane Research (In press)
`dium and potassium fluxes across rectal mucosa in ulcerative
`5. Gerber JG: Prostaglandins and ulcerative colitis, a warning.
`colitis. Gut 14:784-789, 1973
`Gastroenterology 76:658, 1979
`7. Rask-Madsen J, Brix Jensen P: Electrolyte transport capacity
`6. Edmonds CJ, Pilcher D: Electrical potential difference and so-
`and electrical potentials of the normal and inflamed human
`dium and potassium fluxes across rectal mucosa in ulcerative
`rectum in vivo. Scand J Gastroenter 8:169-175, 1973
`colitis. Gut 14:784-789, 1973
`8. Hoult IRS, Moore PK: Sulphasalazine is a potent inhibitor of
`7. Rask-Madsen J, Brix Jensen P: Electrolyte transport capacity
`prostaglandin 15-hydroxydehydrogenase: possible basis of
`and electrical potentials of the normal and inflamed human
`therapeutic action in ulcerative colitis. Br J Pharmacol 64:6-8
`rectum in vivo. Scand J Gastroenter 8:169-175, 1973
`8. Hoult IRS, Moore PK: Sulphasalazine is a potent inhibitor of
`prostaglandin 15-hydroxydehydrogenase: possible basis of
`therapeutic action in ulcerative colitis. Br J Pharmacol 64:6-8
`Prostaglandins, Indomethacin, and Ulcerative
`Colitis
`
`Dear Sir:
`Prostaglandins, Indomethacin, and Ulcerative
`We read with great interest the results of the pilot study testing
`the local effects of indomethacin in active distal ulcerative colitis
`Colitis
`reported by Gilat et al.1 We carried out a similar experiment to
`Dear Sir:
`the one reported by these authors, and our results were also not
`We read with great interest the results of the pilot study testing
`encouraging.
`the local effects of indomethacin in active distal ulcerative colitis
`In our experiments, two different preparations were used. (All
`reported by Gilat et al.1 We carried out a similar experiment to
`the enemas were prepared by Dr. A. Raitano, Dr, G. Damiani, and
`the one reported by these authors, and our results were also not
`Dr. S. Maselli, pharmacists at our hospital.) The first one con-
`encouraging.
`sisted of a solution containing 50mg meglumine indomethinate
`In our experiments, two different preparations were used. (All
`(Liometacen) dissolved in 100 ml of a gummy medium composed
`the enemas were prepared by Dr. A. Raitano, Dr, G. Damiani, and
`by a suspension of 0.4 g gum tragacanth in distilled water, which
`Dr. S. Maselli, pharmacists at our hospital.) The first one con-
`was adjusted to pH 7 and mildly hypertonic (800 mOsm/liter) by
`sisted of a solution containing 50mg meglumine indomethinate
`means of a saline solution. We conducted a preliminary study in
`(Liometacen) dissolved in 100 ml of a gummy medium composed
`order to exclude noxious effects on the colonic mucosa in 4 pa-
`by a suspension of 0.4 g gum tragacanth in distilled water, which
`tients with irritable bowel syndrome and 4 patients with ulcer-
`was adjusted to pH 7 and mildly hypertonic (800 mOsm/liter) by
`ative colitis in remission. We did not find any harmful effects as
`means of a saline solution. We conducted a preliminary study in
`controlled clinically, endoscopically, and histologically. We then
`order to exclude noxious effects on the colonic mucosa in 4 pa-
`gave these topical enemas to 4 outpatients with active distal dis-
`tients with irritable bowel syndrome and 4 patients with ulcer-
`ease for 15 days without improvement. After these discouraging
`ative colitis in remission. We did not find any harmful effects as
`results, we used another preparation with indomethacin sus-
`controlled clinically, endoscopically, and histologically. We then
`pended in microcrystaline cellulose and sodium-carboxy-methyl
`gave these topical enemas to 4 outpatients with active distal dis-
`cellulose combined with the same gummy medium as before. We
`ease for 15 days without improvement. After these discouraging
`started treatment with enemas containing 50 mg indomethacin at
`results, we used another preparation with indomethacin sus-
`the same time. Both patients' conditions worsened, but promptly
`pended in microcrystaline cellulose and sodium-carboxy-methyl
`improved with topical and systemic steroid .administration. We
`cellulose combined with the same gummy medium as before. We
`tried again with lower doses, treating three groups of 3 patients
`started treatment with enemas containing 50 mg indomethacin at
`with 5, 10, and 20 mg, respectively, without any appreciable im-
`the same time. Both patients' conditions worsened, but promptly
`provement. In addition, 1 patient's condition worsened after
`improved with topical and systemic steroid ,administration, We
`being given 20 mg of indomethacin, and we thought it not ethical
`tried again with lower doses, treating three groups of 3 patients
`to continue the experiment.
`with 5, 10, and 20 mg, respectively, without any appreciable im-
`It is difficult to understand the reasons for these negative re-
`provement. In addition, 1 patient's condition worsened after
`sults. We emphasize that they could be due to either the specific
`being given 20 mg of indomethacin, and we thought it not ethical
`characteristics of the drug or the preparation we used, These ob-
`to continue the experiment.
`servations do not disprove that inhibition of PGs synthesis is in-
`It is difficult to understand the reasons for these negative re-
`volved in reducing inflammation in ulcerative colitis, however,
`sults. We emphasize that they could be due to either the specific
`and, therefore, other anti-PGs agents could be useful.
`characteristics of the drug or the preparation we used, These ob-
`servations do not disprove that inhibition of PGs synthesis is in-
`volved in reducing inflammation in ulcerative colitis, however,
`and, therefore, other anti-PGs agents could be useful.
`
`CORRESPONDENCE (cid:9)
`
`193
`
`M. CAMPIERI, M.D.
`G. A. LANFRANCHI, M.D.
`G. BAZZOCCHI, M.D.
`C. BRIGNOLA, M.D.
`M. CAMPIERI, M.D.
`A. BENATTI, M.D.
`G. A. LANFRANCHI, M.D.
`S. BOCCIA, M.D.
`G. BAZZOCCHI, M.D.
`G. LABO', M.D.
`C. BRIGNOLA, M.D.
`Istituto di Clinica Medico e Gastroenterologia
`A. BENATTI, M.D.
`Policlinco S. Orsola
`S. BOCCIA, M.D.
`Bologna, Italy
`G. LABO', M.D.
`Istituto di Clinica Medico e Gastroenterologia
`1. Gilat T, et al: Prostaglandins and ulcerative colitis. Gastroen-
`Policlinco S. Orsola
`terology 76:1083, 1979
`Bologna, Italy
`
`1. Gilat T, et al: Prostaglandins and ulcerative colitis. Gastroen-
`terology 76:1083, 1979
`Gastrin and Intestinal Phase of Gastric
`Secretion
`
`Dear Sir:
`Gastrin and Intestinal Phase of Gastric
`I read with great interest the recent report of Kauffman and
`Grossman' showing that the intestinal perfusion with a liver ex-
`Secretion
`tract (LE) meal in the dog stimulates gastric acid secretion but
`Dear Sir:
`does not change serum gastrin concentration. These findings,
`I read with great interest the recent report of Kauffman and
`which apparently are at variance with previous studies of Gross-
`Grossman' showing that the intestinal perfusion with a liver ex-
`man's group' and with our observations,5-7 were obtained in
`tract (LE) meal in the dog stimulates gastric acid secretion but
`dogs with the LE meal instilled into the distal portion of the duo-
`does not change serum gastrin concentration. These findings,
`denum via duodenal fistula, the proximal duodenum being obtu-
`which apparently are at variance with previous studies of Gross-
`rated by balloon to prevent duodenogastric reflux. This procedure
`man's group' and with our observations,5-7 were obtained in
`probably explains, at least in part, both the rather poor gastric
`dogs with the LE meal instilled into the distal portion of the duo-
`acid stimulation and the lack of change in serum gastrin level
`denum via duodenal fistula, the proximal duodenum being obtu-
`during intestinal perfusion of the LE meal.
`rated by balloon to prevent duodenogastric reflux. This procedure
`In our studies on the physiologic significance of the intestinal
`probably explains, at least in part, both the rather poor gastric
`phase of gastric secretion,5 a special gastroduodenal cannula was
`acid stimulation and the lack of change in serum gastrin level
`designed (in fact, suggested in part by Dr. Grossman), which by-
`during intestinal perfusion of the LE meal.
`passed the pyloric sphincter (closed by a double-walled mucosal
`In our studies on the physiologic significance of the intestinal
`septum to avoid duodeno-gastric reflux) and allowed for the inter-
`phase of gastric secretion,5 a special gastroduodenal cannula was
`mittent access either into the stomach or to the upper duodenum,
`designed (in fact, suggested in part by Dr. Grossman), which by-
`and for the free flow of food from the stomach to the duodenum
`passed the pyloric sphincter (closed by a double-walled mucosal
`between feedings. According to our experience with gastric stim-
`septum to avoid duodeno-gastric reflux) and allowed for the inter-
`ulation by an intestinally perfused LE meal in such preparation,
`mittent access either into the stomach or to the upper duodenum,
`the gastric acid response may reach up to 30-50% of the histamine
`and for the free flow of food from the stomach to the duodenum
`maximum, and it is accompanied by a small but significant in
`between feedings. According to our experience with gastric stim-
`crease in serum gastrin. This has been confirmed by measuring
`ulation by an intestinally perfused LE meal in such preparation,
`serum gastrin level independently in three different laborato-
`the gastric acid response may reach up to 30-50% of the histamine
`ries.5-7 Important conditions required to achieve this high degree
`maximum, and it is accompanied by a small but significant in
`of gastric acid and serum gastrin stimulation appear to be the
`crease in serum gastrin. This has been confirmed by measuring
`preservation of the nerve connections between the stomach and
`serum gastrin level independently in three different laborato-
`duodenum and the intact antral portion of the stomach, as well as
`ries.5-7 Important conditions required to achieve this high degree
`the upper portion of the duodenum, The removal of the antral
`of gastric acid and serum gastrin stimulation appear to be the
`mucosa' or the resection of the upper part of the duodenum abol-
`preservation of the nerve connections between the stomach and
`ished almost completely both serum gastrin and gastric acid re-
`duodenum and the intact antral portion of the stomach, as well as
`sponses to an intestinal LE meal. In this way we obtained evi-
`the upper portion of the duodenum, The removal of the antral
`dence that antral gastrin may be involved in the intestinal phase
`mucosa' or the resection of the upper part of the duodenum abol-
`of gastric acid secretion in the dog. Direct measurement of serum
`ished almost completely both serum gastrin and gastric acid re-
`gastrin in venous antral and duodenal outflows showed that duo-
`sponses to an intestinal LE meal. In this way we obtained evi-
`denal instillation of the LE meal causes a significant release of
`dence that antral gastrin may be involved in the intestinal phase
`gastrin selectively from the antrum and the duodenum.'
`of gastric acid secretion in the dog. Direct measurement of serum
`Our results are in agreement with previous findings of the
`gastrin in venous antral and duodenal outflows showed that duo-
`Grossman's group,' which demonstrated that perfusion of a LE
`denal instillation of the LE meal causes a significant release of
`meal into the small intestine by way of the stomach remnant
`gastrin selectively from the antrum and the duodenum.'
`caused a marked increase in serum gastrin in dogs with antral
`Our results are in agreement with previous findings of the
`pouches, but not in antrectomized animals. The explanation that
`Grossman's group,' which demonstrated that perfusion of a LE
`this rise in serum gastrin might derive from the antral mucosa re-
`meal into the small intestine by way of the stomach remnant
`tained in the residual stomach is not convincing because it was
`caused a marked increase in serum gastrin in dogs with antral
`reported that this gastrin response may be abolished by the resec-
`pouches, but not in antrectomized animals. The explanation that
`tion of the antrum.
`this rise in serum gastrin might derive from the antral mucosa re-
`tained in the residual stomach is not convincing because it was
`reported that this gastrin response may be abolished by the resec-
`tion of the antrum.
`
`

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