Scandinavian Journal of Gastroenterology

ISSN: 0036-5521 (Print) 1502-7708 (Online) Journal homepage: http://www.tandfonline.com/loi/igas20

Effect of Misoprostol and Antacids on Gastric and Duodenal Mucosal Enzyme Activities in Duodenal Ulcer Patients K. Vetvik, E. Schrumpf, K.-J. Andersen, D. W. Skagen & O. J. Halvorsen To cite this article: K. Vetvik, E. Schrumpf, K.-J. Andersen, D. W. Skagen & O. J. Halvorsen (1991) Effect of Misoprostol and Antacids on Gastric and Duodenal Mucosal Enzyme Activities in Duodenal Ulcer Patients, Scandinavian Journal of Gastroenterology, 26:4, 385-391, DOI: 10.3109/00365529108996499 To link to this article: http://dx.doi.org/10.3109/00365529108996499

Published online: 08 Jul 2009.

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Effect of Misoprostol and Antacids on Gastric and Duodenal Mucosal Enzyme Activities in Duodenal Ulcer Patients K. VETVIK, E. SCHRUMPF, K.-J. ANDERSEN, D. W. SKAGEN & 0. J. HALVORSEN Mandal Hospital, Mandal; Medical Dept. A, Rikshospitalet, Oslo; and Medical Dept. A and The Gade Institute, Dept. of Pathology, Haukeland Hospital, Bergen; Norway

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Vetvik K, Schrumpf E, Andersen K-J, Skagen DW, Halvorsen OJ. Effect of misoprostol and antacids on gastric and duodenal mucosal enzyme activities in duodenal ulcer patients. Scand J Gastroenterol 1991, 26, 385-391 The activities of 11 marker enzymes from the gastric and duodenal mucosa were determined in 15 patients with active duodenal ulcer disease before therapy, after 4 weeks of therapy with the prostaglandin El analogue misoprostol, 400 pg twice daily, and after another 4 weeks without any therapy. Another 15 patients were given a high-dose liquid antacid regimen. The activities were measured in homogenized material obtained with forceps through an endoscope. The healing rates of the two groups at 4 weeks were 53% and 80%, respectively. No changes in mucosal inflammation were noted during therapy. During treatment with misoprostol the activities in the descending duodenum of the membrane enzymes alkaline phosphatase, leucyl-0-naphthylamidase, y-glutamyltransferase, and 5’-nucleotidase increased towards the values seen in normal controls. Despite a higher healing rate, no changes in the enzyme activities occurred in the group given high-dose antacid therapy. Four weeks after cessation of therapy the enzyme activities in the misoprostol group were not significantly different from the pretreatment values. In the biopsy specimens from the duodenal bulb the activities of monoamine oxidase fell during treatment with misoprostol and were restored to the pretreatment activity when therapy was stopped. In the stomach mucosa the enzyme activities were largely unchanged during treatment with both misoprostol and antacids. These results indicate that misoprostol and antacids have different mechanisms of action but may also suggest that the demonstrated enzymic changes are unrelated to the healing process.

Key words: Antacids; basolateral membrane; brush border; duodenal ulcer; duodenum; lysosomes; misoprostol; mitochondria; mucosal enzymes; prostaglandins; smoking; stomach K&e Vetvik, M.D., Mandal Sykehus, N-4500 Mandal, Norway

Recently we reported alteration of enzyme activities in gastric and duodenal mucosa in patients with active duodenal ulcer (DU) compared with controls (1,2). The decreased enzyme activities in the duodenal mucosa tended to normalize on ranitidine therapy ( 3 ) . After cessation of treatment the enzyme activities returned to pretreatment levels. These changes seemed independent of ulcer healing and were interpreted

by us as being mediated directly or indirectly by ranitidine ( 3 ) . So far the effect of ranitidine in the ulcer-healing process has been ascribed to reduced gastric acid secretion. In the present study we wanted to compare the effects on mucosal enzymes of two different ulcer healing regimens in which enhanced mucosal resistance as well as acid reduction are implicated.

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Table I. Characteristics of the patients and endoscopic findings in the two groups

No. Age, years (mean (SD)) Sex Men, n Women, n Previous DU, n Smokers, n Antacids before inclusion, n Ulcer size (longest diameter), mm Bulbar deformity, n

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MATERIALS AND METHODS Patients Thirty patients were included. Except for the use of antacids to relieve dyspeptic symptoms, no anti-ulcer medication had been taken during the last month before inclusion. Characteristics of the patients and endoscopic findings are given in Table I. Treatment Fifteen of the patients participated in a randomized double-blind trial in which the efficacy of the prostaglandin El analogue misoprostol, 400 pg twice daily, was tested against ranitidine, 150 mg twice daily (3). The other 15 patients were given an antacid suspension (Novaluzid@, Astra AB, Sweden) consisting of magnesium hydroxide, magnesium carbonate, and aluminum hydroxide. The neutralizing capacity is 85 mmol HC1/10 ml. The patients were prescribed 10 ml of the suspension 1h and 3 h after the meals and before they went to bed. Treatment was started within 72 h of the diagnostic endoscopy. All patients were allowed to take paracetamol for symptomatic relief. In the misoprostol group ingestion of antacid tablets (BalancidB, Astra), consisting of aluminum hydroxide and magnesium carbonate, was also allowed. The amounts were recorded. They were all encouraged to stop smoking. Control endoscopy was performed after 4 weeks of treatment. If the ulcer was healed, the treatment was stopped, and the patients were given an appointment for another endoscopy 4 weeks later. An

Misoprostol

Novaluzid

15 48.0 (18.2)

15 47.3 (17.7)

10 5 12 8

9 9 8

9 6 14 10 7 8 8

ulcer was judged to be healed when no break in the continuity of the mucosa was found at endoscopy. Sampling procedure At each endoscopy two adjacent forceps biopsy specimens were obtained from the lower duodenal flexure, the duodenal bulb (as far away from the ulcer as possible), and the antral and body part of the stomach along the greater curve. The endoscopies were performed after an overnight fast, and the patients were sedated intravenously with diazepam. To avoid possible circadian variations of enzyme activities (4),each patient was examined at the same hour every time. For the same reason all endoscopies in this series were performed between 0800 h and 1200 h. One biopsy specimen from each of the four positions was used for histologic examination. The other specimen was used for determination of the mucosal enzyme activities. They were handled as described earlier (5-7). The criteria for histologic assessment of duodenitis and gastritis are given in two previous papers (1,2). The histologic examinations were performed by one of us (0.J. Halvorsen), who had no information on endoscopic or clinical findings. All examinations were performed and biopsy specimens taken in the course of appropriate medical investigation and with informed consent. Enzyme assays We studied the activities of the membrane enzymes lactase, sucrase, neutral-a-glucosidase,

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Table 11. The number of biopsy specimens from the descending duodenum and the duodenal bulb showing duodenitis before, after 4 weeks of therapy, and 4 weeks after cessation of treatment with misoprostol or Novaluzid@. The total number of specimens from each site is given in parentheses Before treatment

During treatment

After treatment

Misoprostol Descending duodenum Duodenal bulb

2 (15) 7 (15)

3 (13) 8 (13)

0 (7) 3 (7)

Novaluzid Descending duodenum Duodenal bulb

1(15) 6 (15)

0 (14) 2 (14)

0 (11) 0 (11)

alkaline phosphatase, leucyl-P-naphthylamidase (LAP), y-glutamyltransferase (y-Gt), and 5’nucleotidase; the lysosomal enzymes acid phosphatase, N-acetyl-0-D-glucosaminidase (NAG), and acid P-glucuronidase; and the mitochondria1 enzyme monoamine oxidase (MAO). Details of the assay methods have been described elsewhere (5-7).

Calculations Student’s t tests (two-sided) for paired and unpaired samples were used (as appropriate) to localize differences between groups. Differences were considered significant when the P values were less than or equal to 0.05. Fisher’s exact tests were used to demonstrate independence among smoking, use of antacids, and healing of the ulcer. RESULTS

Response to treatment In the misoprostol group the ulcer was healed in 8 of the 15 patients (53%) at the control endoscopy after 4 weeks. After another 4 weeks without therapy, a relapse ulcer was demonstrated in two patients at endoscopy. One patient was withdrawn from the study because of increasing abdominal pain; another did not comply with the protocol and was excluded for this reason. Two of the responders took an average of 13 tablets of Balancid (acid-neutralizing capacity, 12.5 mmol/ tablet) during the 4 weeks of therapy, whereas one non-responder ingested 20 tablets over the same period of time. One non-responder used

seven paracetamol tablets for pain relief during the 4 weeks of treatment. In the Novaluzid group 12 (80%) of the 15 patients had their ulcers healed during the 4 weeks of therapy. One did not show up for the second endoscopy. None of the patients quit smoking during the study.

Histologic findings The results of the histologic examinations of the biopsy specimens from all the four sites before treatment, after 4 weeks of treatment, and after another 4 weeks without therapy are given in Tables I1 and 111. Enzyme activities in the descending duodenum In the misoprostol group the activities of all the membrane enzymes on an average increased during therapy. The increase was significant for alkaline phosphatase, LAP, y-Gt, and 5’-nucleotidase when compared with the activities determined before treatment. The lysosomal enzyme acid phosphatase also increased significantly during therapy when compared with the pretreatment activities. The activities measured 4 weeks after the treatment ended were not significantly different from the activities seen before therapy started (Table IV). In the Novaluzid group the only change noted was an increase in alkaline phosphatase ( P < 0.005) activity among the smokers during the period of therapy when compared with the activities measured before start of therapy.

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Table 111. Histologic findings in the biopsy specimens from the antral and body part of the stomach in duodenal ulcer patients before treatment, after 4 weeks of treatment, and 4 weeks after cessation of therapy with misoprostol or Novaluzid@ Before treatment N Misoprostol Gastric antrum Gastric corpus

0 10

Novaluzid Gastric antrum Gastric corpus

0 10

S

I

During treatment

A

N

4

3 1

1 7

n = 15 3 7 3 2

5 0

1 9

n = 15 9 3

0

S

I

After treatment

A

N

S

I

A

1 1

0 6

n=7 5 2 1 0

0 0

0 0

6 6

n = 11 5 0 5 0

0 0

n = 13

7 5 1

4 0

n = 14 0 3 4 1

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N = normal mucosa; S = superficial gastritis; I = 'intermediate' gastritis; A = atrophic gastritis.

Table IV. Protein to DNA ratio and enzyme activities in mucosa of the duodenum descendens in duodenal ulcer patients before treatment, after 4 weeks of treatment, and 4 weeks after cessation of therapy with misoprostol. The values are given as mean SEM (units per gram of protein). The number of patients is given in parentheses Assay

Before treatment

Protein to DNA ratio Membrane enzymes Lactase Sucrase Neutral-a-glucosidase Alkaline phosphatase Leucyl-P-naphthylamidase y-Glutamyltransferase 5'-Nucleo tidase Lysosomal enzymes Acid phosphatases N-acetyl-0-D-glucosaminidase Acid P-glucuronidase Mitochondria1 enzyme Monoamine oxidase

46.01 2 5.84 (15)

During treatment

43.39? 6.10 (13)

* *

After treatment

38.32 f 10.72 (6)

165.50 2 23.50 (15) 246.42 2 20.17 (15) 18.87 t 3.15 (15) 80.83 2 8.99 (15) 54.21 t 7.03 (12) 11.45 t 1.31 (14) 22.15 t 2.12 (15)

217.30 21.30 (13) 288.59 k 19.78 (13) 20.38 3.13 (13) 98.75 2 9.94 (13)*** 60.04 ? 7.63 (lo)** 12.80 4 1.53 (12)** 26.90 2.95 (13)**

210.40 f 42.53 (7) 254.23 2 32.55 (7) 20.47 2 3.31 (6) 93.43 f 12.85 (7) 54.24 5 2.35 (5) 11.35 2 1.81 (7) 25.57 3.12 (7)

39.88 -t_ 3.44 (15) 12.62 t 1.14 (15) 19.05 +- 0.79 (15)

43.92 ? 3.12 (13)* 13.56 2 1.08 (13) 1.57 (13) 18.05

41.36 2 5.54 (7) 14.15 2 1.23 (7) 23.35 ? 4.71 (7)

5.19 t 1.46 (15)

*

* 4.62 *

0.48 (13)

5.05

*

0.77 (7)

' P < 0.05, * * P < 0.025, and * * * P < 0.005 compared with before treatment.

Enzyme activities in the duodenal bulb

Enzyme activities in the antral mucosa

In the duodenal bulb, however, there was an opposite tendency among the membrane-bound enzymes in the misoprostol group, but the decrease was significant only for sucrase ( P < 0.05). M A 0 (P < 0.05) activities also decreased during misoprostol therapy compared with pretreatment activities. The enzyme activities determined 4 weeks after cessation of therapy were not different from the activities measured before start of therapy (Table V). In the Novaluzid group no changes in enzyme activities were detected at this site.

No alteration in enzyme activity was detected in the misoprostol group in this region. The activities of acid phosphatase ( P < 0.01) were enhanced during Novaluzid treatment when compared with the prestudy activities.

Enzyme activities in the mucosa of the gastric body The activities of alkaline phosphatase ( P < 0.05) were enhanced during the treatment period when compared with the activities determined before treatment in the misoprostol group. Four weeks after treatment stopped the activities were

Misoprostol, Antacids, and Mucosal Enzymes

389

Table V. Protein to DNA ratio and enzyme activities in the mucosa of the duodenal bulb in duodenal ulcer patients before treatment, after 4 weeks of treatment, and 4 weeks after cessation of therapy with misoprostol. The values are given as mean t SEM (units per gram of protein). The number of patients is given in parentheses Assay

Before treatment

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~

Protein to DNA ratio Membrane enzymes Lactase Sucrase Neutral-a-glucosidase Alkaline phosphatase Leucyl-P-naphthylamidase y-Glutamyltransferase 5'-Nucleotidase Lysosomal enzymes Acid phosphatases N-acetyl- P-D-glucosaminidase Acid (J-glucuronidase Mitochondria1 enzyme Monoamine oxidase

54.05

*

8.60 (15)

During treatment 41.10

*

7.88 (13)

After treatment 44.45 ? 13.97 (6)

58.20 2 10.68 (15) 134.46 f 23.70 (15) 7.09 t 0.99 (15) 39.81 f 5.72 (15) 38.17" 5.24 (12) 11.88 2 1.09 (13) 20.25 f 1.86 (15)

40.01 f 5.55 (13) 82.83 f 22.82 (13)* 5.71 t 1.69 (13) 36.52 2 8.13 (13) 35.97 t 10.79 (10) 11.93? 0.99 (11) 17.35 2 1.40 (13)

71.41 2 21.88 (8) 102.54 36.71 (7) 6.41 2 2.21 (6) 39.15 t 9.01 (7) 32.36 f 8.41 (5) 1.76 (7) 11.65 1.26 (7) 16.85

44.39 ? 1.86 (15) 16.07 2 0.97 (15) 17.03 f 1.07 (15)

43.45 -+ 2.30 (13) 15.95 f 1.22 (13) 15.58? 1.44 (13)

43.09 f 4.06 (7) 16.42 t 1.06 (7) 15.18 f 1.55 (7)

4.47 5 0.94 (15)

2.68 2 0.36 (13)*

*

* *

4.39 f 0.84 (7)t

* P < 0.05 compared with before treatment. t P < 0.05 compared with during treatment.

significantly lower ( P < 0.005) than during therapy. NAG activities ( P < 0.05) were also significantly decreased after end of therapy compared with the activities determined during treatment with misoprostol. In the Novaluzid group LAP activities ( P < 0.01) rose significantly during the treatment period when compared with the prestudy activities.

mucosa of patients with active D U compared with controls (1,2). During ranitidine therapy in DU patients we demonstrated an increase in duodenal membrane enzyme activity towards the values noted in controls without D U (3). Four weeks after the end of ranitidine treatment the activities were decreased and not different from those determined before start of therapy. The reasons for these findings are not clear. In the present study we demonstrated a significant increase of membrane-bound enzyme activiUlcer healing, mucosal inflammation, cigarette ties in the second part of duodenum during smoking, ingestion of antacids or paracetamol Ulcer healing, mucosal inflammation, cigarette treatment with the prostaglandin analogue misosmoking, and ingestion of antacids or paracetamol prostol in spite of an ulcer-healing rate of only did not significantly influence the therapy-related 50%. The enzymic changes seemed unrelated to enzyme activity changes noted in this study, ulcer healing. The activities determined 4 weeks except for raised alkaline phosphatase activities after cessation of therapy were not significantly in the descending duodenum among smokers in different from the values measured in biopsy specimens obtained before start of treatment. the Novaluzid group. We could not demonstrate any dependence Somewhat unexpectedly, no enzymic changes among cigarette smoking, use of antacids before emerged in the group of patients given high-dose inclusion, and healing of the ulcer in any of the antacid therapy despite excellent effect on ulcer healing. The changes in enzyme activities in the therapy groups ( P > 0.2). misoprostol group in this study are found among the enzymes localized to the brush border and DISCUSSION basolateral membrane, whereas the changes In two previous papers we have reported altered demonstrated during ranitidine treatment were enzyme activities both in gastric and duodenal found among the enzymes localized predomi-

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nantly to the brush border (3). Moreover, during treatment with misoprostol, changes in enzymic activities showed an increase in the descending duodenum and a tendency towards decrease in the duodenal bulb, whereas we demonstrated an increase both in the descending duodenum and the duodenal bulb during ranitidine treatment. In the gastric mucosa only minor changes were noted. Endogenous and synthetic prostaglandins of the E class are recognized as effective inhibitors of acid secretion (8,9). The properties of acid secretion inhibition seem linked to interference with CAMP formation in the parietal cells (10). This action is probably mediated through a specific receptor on the cell membrane (10). The prostaglandins also exert mucosal cytoprotection in the stomach and duodenum (11). The mechanisms of mucosal cytoprotection demonstrated against toxic agents such as ethanol, taurocholate, and non-steroidal anti-inflammatory drugs are poorly understood. They are independent of acid secretion. A wide range of possible explanations have been offered; among them stimulation of mucus secretion, stimulation of bicarbonate secretion, prevention of mucosal barrier disruption, and enhancement of blood flow seem to be the most widely recognized (12). Recent studies in man have shown reduced prostaglandin synthesis in duodenal and gastric mucosa of D U patients (13). This finding points towards a possible defect of mucosal metabolism. The noted enzyme activity changes during misoprostol treatment are not easily explained. It could, for example, be linked to the reduction in acid secretion. It is, however, uncertain whether changes in duodenal acidity per se influence the mucosal enzyme activity, although there is an association between the activity of alkaline phosphatases, basal and stimulated acid secretion, and an inverse association between NAG and basal acid secretion in the gastric mucosa (5). Furthermore, the enzymic changes seen after misoprostol were different from those seen after ranitidine, which is supposed to act chiefly by acid reduction. Inflammation, on the other hand, is shown to reduce the activity of several mucosal enzymes in the duodenum (1). In this study, how-

ever, we could not demonstrate any effect of treatment on mucosal inflammation. Alkaline phosphatase and bicarbonate-stimulated ATPase are proposed to be the same enzyme in the duodenal mucosa (14). The latter enzyme is implicated in bicarbonate secretion in the duodenum. Isenberg et al. (15) have shown reduced proximal duodenal bicarbonate secretion in D U patients. In the third part of the duodenum no reduction of bicarbonate secretion was demonstrated. As misoprostol has been shown to stimulate bicarbonate secretion in both the proximal and the distal part of the duodenum (16, 17), an increase in alkaline phosphatase activity during misoprostol treatment might reflect the mechanism through which enhanced mucosal protection is achieved. However, our findings of increased alkaline phosphatase activity in the mucosa of the second part of the duodenum and unaltered activity of the duodenal bulb during misoprostol treatment do not fit entirely with this theory. The fact that misoprostol therapy did not significantly influence the enzyme activities in the mucosa of the duodenal bulb, where the ulcers were located, suggests that there is no connection between ulcer healing and the enzyme activity pattern. M A 0 activity has been linked to the intracellular regulation of gastrin release (18). In a previous paper we have reported decreased duodenal M A 0 activity among the same D U patients as reported in this study (1). The finding in these patients of a further decrease in M A 0 activity in the duodenal bulb during treatment with misoprostol could indicate an increase of gastrin release. The finding is, however, somewhat unexpected, as we did not demonstrate any M A 0 activity changes during Novaluzid and ranitidine treatment (3). The effect of low-dose antacid therapy on ulcer healing has been ascribed to stimulation of cytoprotective forces (19). Aluminum-containing antacids have been shown to stimulate mucosal prostaglandin synthesis in human stomach and duodenum (20). In this study the effect of the applied high-dose aluminum-containing antacid regimen on the healing of the ulcer was excellent. High-dose antacid therapy also reduces duodenal

Misoprostol, Antacids, and Mucosal Enzymes

acidity (21). The lack of changes in duodenal mucosal enzyme activity during therapy with Novaluzid shows that a reduction of acidity does not automatically increase mucosal enzyme aCtivity in DU patients. The finding of only sporadic gastric mucosal enzyme activity changes in this study is not easily understood. Gastric mucosal inflammation is shown to have an impact on the enzyme activities in patients with and without peptic ulcer disease (2,22). The lack of change in mucosal inflammatory state seen during therapy might to some extent provide an explanation. It should, however, be emphasized that the enzyme activities of the gastric body mucosa in DU patients with normal light microscopic findings also were unaltered during treatment. In conclusion, during misoprostol treatment there is an increase in the activities of some membrane-bound enzymes of the mucosa in the descending duodenum towards the values seen in patients without DU. N o mucosal enzymic changes in the duodenum are noted when the DU is healed by high-dose antacid therapy. The different effects of ranitidine, misoprostol, and antacids on duodenal mucosal enzyme activities may indicate different mechanisms of action but may also suggest that the demonstrated enzymic changes are unrelated to the healing process.

from eastric mucosa. Scand J Gastroenterol 1986. 21? 161-1O57 6. B0rkje B, Skagen DW, Andersen K-J, Schrumpf E, Longit,,dinal distribution of mucosal enzymes in the human large bowel. Scand J Gastroenterol1986. 21, 919-927 7. B0rkje B, Bdegaard S, Vetvik K, Skagen DW, Andersen K-J. Lzrum OD. Influence of remote cancer and obesity on, and distribution of mucosal enzymes, in upper small intestine. Scand J Gastroenterol 1986, 21, 928-934 8. Bauer RF. Misoprostol. Preclinical pharmacology. Dig Dis Sci 1985, ll(suppl), 118s-125s 9. Wilson DE, Winnan J, Quertermus J, Tao P. Effect of an orally administered prostaglandin analogue: 16,16-dimethyl prostaglandin E2 on human gastric secretion. Gastroenterology 1975, 69, 607-611 10. Lewin MJM. Cell biology of gastric acid secretion and mechanisms of action of acid secretion inhibitors. John Libbey Eurotext, Paris, 1988, 3-12 11. Isenberg JI. Overview of clinical cytoprotection. Dig Dis Sci 1985, ll(suppl), 81s-82s 12. Miller TA. Protective effects of prostaglandins against gastric mucosal damage: Current knowledge and proposed mechanism. Am J Physiol 1983, 245, G601-G622 13. Pugh S, Williams SE, Lewin MR, et al. Duodenal and antral mucosal prostaglandin E2 synthesis in a study of normal subjects and all stages of duodenal ulcer disease treated by Hz receptor antagonists. Gut 1989, 30, 161-165 14. Wilkes JM, Garner A , Peters TJ. Studies on the localization and proprieties of rat duodenal HCOyATPase with special relation to alkaline phosphatase. Biochim Biophys Acta 1987, 924, 159-166 15. Isenberger JL, Selling JA, Hogan DL, Koss MA. Impaired proximal duodenal bicarbonate secretion in patients with duodenal ulcer. N Engl J Med 1987, 316, 374-379 16. Isenberg JI, Hogan DL, Selling JA, Koss MA. Duodenal bicarbonate secretion in humans. Role of REFERENCES prostaglandins. Dig Dis Sci 1986, 3l(suppl), 130s 1. Vetvik K, Schrumpf E , Andersen K-J, Borkje 9, 17. Smedfors B, Johansson C. Stimulation of duodenal bicarbonate secretion by misoprostol. Dig Dis Sci Skagen DW, Halvorsen OJ. Enzyme activities in 1986, ~ ~ ( s u P P96s-100s ~), the duodenal mucosa in duodenal ulcer patients. 18. Dial EJ, Huang J, Delansorne R, Lichtenberger Scand J Gastroenterol 1989, 24, 244-250 LM. Monoamine oxidase; An important intra2. Vetvik K, Schrumpf E, Andersen K-J, et al. Enzyme cellular regulator of gastrin release in the rat. activities in the gastric rnucosa in duodenal ulcer Gastroenterology 1986, 90, 1018-1023 patients. Scand J Gastroenterol 1990, 25, 594-600 3. Vetvik K, SchrumpfE, Andersen K-J, Skagen DW, 19. Hollander D, Tarnawski A. Are antacids cytoprotective? Gut 1989, 30, 145-147 Halvorsen OJ. Effect of ranitidine on gastric and duodenal mucosal enzyme activities in duodenal 20. Preclik G , Stange EF, Gerber K, Ferzer G , Horn H, Ditschuneit H. Stimulation of mucosal prostaulcer patient. Scand J Gastroenteroll990,25,1123glandin synthesis in human stomach and duodenum 1128 by antacid treatment. Gut 1989, 30, 148-151 4. Markiewicz A, Kaminski M, Chocilowski W, Gomoluch T, Boldys H, Skrzypek 9. Circadian rhythms 21. Bendtsen F, Rune SJ. Effect of a single dose of antacids on gastric and duodenal bulb pH in duoof four marker enzymes activity of the jejunal villi denal ulcer patients. Scand J Gastroenterol 1988, in man. Acta Histochem 1983, 72, 91-99 23, 935-940 5 . Borkje B, 0degaard S, Skagen DW, Andersen K-J, Schrumpf E . Enzyme activities in biopsy specimens 22. Bdegaard S, Borkje B, Skagen DW, Laerum OD, Schrumpf E. Enzyme activities in human gastric mucosa in gastritis and resected stomachs. Scand J Received 31 July 1990 Gastroenterol 1986, 21, 1257-1264 Accepted 5 November 1990 -

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Effect of misoprostol and antacids on gastric and duodenal mucosal enzyme activities in duodenal ulcer patients.

The activities of 11 marker enzymes from the gastric and duodenal mucosa were determined in 15 patients with active duodenal ulcer disease before ther...
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