Studies
on
the Effect of Small Bowel Bypass for Massive Obesity on Gastric Secretory Function LESLIE WISE, M.D.,* ROBERT VAUGHAN, M.D., THEODORE STEIN, M.S.
From the Departments of Surgery and Anesthesiology, Washington University School of Medicine, St. Louis, Missouri 63110
Gastric secretory function was studied in 20 morbidly obese patients both before and after jejuno-ileal bypass. The mean postoperative weight loss was 99.2 pounds during a mean postoperative followup period of 12.6 months. The gastric secretory values we studied induded basal and histalogstimulated volume, pH, concentration, and output. No statistically significant changes were observed in any of these
After an overnight fast, a radiopaque nasogastnic
variables. Therefore it is suggested that jejuno-ileal bypass, as tube (#18 Salem Sump Tube) was placed under fluoroperformed for morbid obesity, is probably not an ulcerogenic scopic control into a dependent position of the stomach. procedure.
Twenty morbidly obese patients scheduled for jejunoileal bypass were selected at random to participate in this study. The physical characteristics of these patients are presented in Table 1. The preoperative gastric secretory studies were performed approximately one week prior to operation. The interval between the jejuno-ileal bypass and the postoperative studies ranged from 6 to 23 months. Weight loss occurred in all patients following bypass; the mean weight loss was 99.2 pounds (45.1 kg) during a mean followup period of 12.6 months.
The tube was taped to the nose to prevent further migration. Patients were placed in a 450 left lateral position and the residual gastric contents were aspirated. A 30-min basal secretion was then collected using intermittent suction (Gumco pump). Six consecutive 15min collections were then obtained after the subcutaneous injection of 1.7 mg/kg Histalog (3-amino-ethylpyrazole dihydrochloride). The 15-min period with the highest acid output was regarded as the peak acid output (P.A.O.). In all collections the volumes, pH, and acid concentrations were measured, and the acid output was calculated. The pH of the samples was measured using a Corning Model 12 Research pH meter. Acid concentration (mEq/l) was measured by titration of the sample with 0.01 N NaOH to an end-point of pH 7.0. Acid output (mEq/hr) was calculated from the product of the volume and acid concentration. All these studies were performed by the same technician. The type of small bowel bypass procedure performed in these patients is illustrated in Fig. 1. Thirty-five cm of jejunum was anastomosed end-to-end to 10 cm of terminal ileum; the proximal end of the excluded segment was closed and the distal end was anastomosed end-to-side to the cecum. Student's paired t-test was used to evaluate the significance of the changes in gastric secretion.
Submitted for publication July 23, 1975. This work was supported in part by N. I. H. Grant AMI2333. * Address all correspondence to Leslie Wise, M.D., Dept. of Surgery, Long Island Jewish-Hillside Medical Center, New Hyde Park, New York, 11040.
Results In Table 2 the pre- and postoperative basal gastric secretory data are presented. Similarly, in Table 3, the histalog-stimulated peak pre- and postoperative gastric
S MALL BOWEL BYPASS for exogenous morbid obesity is performed with increasing frequency. The natural history and the complications of this procedure have recently been reviewed by us.10 The effect of small bowel bypass on gastric secretion is controversial. Salmon and Wright have observed no significant changes in gastric acid secretion following jejuno-ileal bypass.6 Buchwald and coworkers,' however, suggested that gastric hypersecretion occurs in 40%o of patients following
jejuno-ileal bypass. The purpose of this study was to further evaluate the effect of small bowel bypass on gastric secretion. Methods
259
260
WISE, VAUGHAN AND STEIN TABLE 1. Physical Characteristics of Patient Population
Patient, Age (yrs) RC, 16 PG, 22 JH, 49 LJ, 28 MM, 39 RM, 38 DM, 43 FM, 33 MR, 46 KN, 26 TP, 61 CY, 27 BG, 54 LW, 24 FW, 39 LW, 28 SW, 23 KW, 26 AS, 44 JS, 40 Mean 35.3 S.D. + 11.6 S.E.M. ± 2.6
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.
Sex, Height (cm) F, F, M, M, F, F, F, F, F, F, F, F, F, F, F, F, M, F, F, F,
163 170 173 183 165 170 173 160 168 163 168 168 160 160 163 150 160 173 165 163
165.9 ± 6.8 ± 1.5
Postop
Diff.
99 124 149 164 130 151 121 112 166 100 133 120 126 125 114 130 191 134 112 141
76 80 105 112 72 102
23 44 44 52 58 49
93 70 79 90 111 87 82 81 80 95 83 85 75 83 87.1 ± 12.0 ± 2.7
28 42 87 10 22 33 44 44 34 35 108 49 37 58
132.1 +22.4 ± 5.0
Time (Mons) 15 9 12 20 19 6 6 10 7 19 6 17 23 20 12 6 11 10 16 7
45.1
12.6
±21.4
± 5.5 ± 1.2
± 4.8
Surg. M March 1976
Discussion
Weight (kg) Preop
Ann.
secretory data are shown. The gastric response following small bowel bypass produced a variable response. A Student's t-test analysis of the paired preoperative and postoperative measurements did not demonstrate any statistically significant change. We also analyzed whether there was a correlation between the duration of time postoperatively and changes in basal or histalogstimulated volumes, acid concentrations, or acid outputs; no such correlation was found.
Gastric hypersecretion following partial resection of the small intestine was first reported by Stassoff in 1914.8 These findings have been confirmed by numerous experimental and clinical studies. In studies on dogs, we have shown that following resection or exclusion of the proximal third of the small bowel there was a marked increase in the total gastric acid output. The increase in gastric acid secretory response following exclusion or resection of the middle third of the small intestine was variable and there was no significant change after distal third exclusions or resections.7 The pathogenesis of the gastric hypersecretion associated with small bowel resections is not clear. It has been suggested that intestinal resection may cause prolonged gastric emptying with consequent antral distension and increased gastrin release. Osborne et al.4 found that gastric emptying was not prolonged after massive small bowel resections; however, both they and Quintana et al.5 were able to abolish the gastric hypersecretion by excision of the gastric antrum. There is evidence to suggest that the fasting gastric acid secretory rate is not increased after intestinal resection and that the hypersecretion is due to increased post-prandial secretion.4 This would suggest that postresectional hypersecretion is due to a decrease or loss of some inhibitory mechanism. Recently Junghanns et al.3 have shown that there was a significant increase in post-prandial serum gastrin levels after proximal small intestinal resections in dogs. The elevation was less pronounced after resection of the distal part. These authors suggested that this may be evidence that the proximal part of the small intestine, in addition to the
FIGS. la and b. Jejunoileal bypass as performed
:.~ 1
.
by the authors.
Vol. 183 . No. 3
261
GASTRIC SECRETORY FUNCTION
TABLE 2. Basal Gastric Acid Secretory Data
Vol (ml/hr)
Patient
Preop
Postop
RC PG JH LJ MM RM DM FM MR KN TP CY BG LW FW LW SW 18. KW 19. AS 20. JS Mean S.D. S.E.M.
114 70 106 150 60 54 50 132 36 110 26 80 142 144 44 100 106 170 80 72
44 76 114 200 70 102 90 114 90 40 62 40 88 128 140 70 134 80 124 70
92.3 ±40.4 ± 9.0
93.8 ±38.4 ± 8.6
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.
Conc. (mEq/1)
pH
Output (mEq/hr)
Preop
Postop
Preop
Postop
Preop
Postop
1.6 1.4 1.2 1.8 3.3 1.7 1.9 7.6 1.9 1.6 2.4 1.8 2.0 1.5 5.8 3.3 1.9 1.5 3.6 1.4
2.0 1.6 1.5 1.3 1.9 1.5 1.8 2.2 2.0 6.0 1.5 1.7 1.3 1.7 1.8 2.4 1.2 1.4 5.7 2.0 2.1 ± 1.3 ± 0.3
40 62 90 38 12 30 30 0 28 40 19 36 30 55 8 10 24 68 10 70 35 ±23 ±5
22 46 56 60 26 52 24 14 37 0 50 34 50 32 28 16 66 68 4 26 36 ±19 4
4.6 4.4 9.4 5.6 0.8 1.6 1.6 0 1.0 4.4 1.0 2.8 4.3 8.0 0.4 1.0 2.6 13.0 0.8 5.0 3.6 ± 3.3 ± 0.7
0.8 3.6 6.4 12.0 1.8 5.2 2.2 1.6 3.3 0 3.2 1.4 4.4 4.0 4.0 1.2 8.8 5.4 0.4 1.8 3.6 ± 2.9 ± 0.6
2.2 + 1.1 ± 0.3
liver and kidney, plays an important role in the inactivation of endogenous gastrin. We have suggested that postresectional hypersecretion is due to loss of an inhibitory mechanism, in which serotonin plays a major role.9 Caridis et al.2 suggested that histaminase is the missing factor. Both serotonin and histaminase are inhibitors of gastric secretion and are asymmetrically distributed in the
small bowel with a maximum concentration in the proximal portion. If our data in animals can be extrapolated to humans, then small bowel bypass for obesity, using our technique, should not lead to gastric hypersecretion since the proximal portion of the jejunum is not bypassed. The results of this study have shown no significant change
TABLE 3. Stimulated (Peak) Gastric Acid Secretory Data
Conc. (mEq/1)
pH
Vol (ml/hr)
Patient
Preop
Postop
Preop
Postop
RC PG JH LJ MM RM DM FM
246 166 228 468 330 300 328 280 142 178 252 164 344 136 382 204 320 288 192 242
268 226 302 492 476 140 360 266 156 100 152 182 296 226 244 226 296 288 208 172
1.0 1.1 1.0 1.3 1.0 1.0 1.0 1.3 1.1 1.2 1.1 0.9 1.0 1.0 1.0 1.1 1.1 1.1 1.1 0.9
1.0 1.1 1.0 0.9 1.1 1.0 0.9 1.1 1.1 1.1 0.9 0.8 0.9 1.0 0.9 1.0 1.0 1.0 0.9 1.2
260
254
± 85 ± 19
± 99 ± 22
1.1 + 0.1 ± 0.02
± 0.1 ± 0.02
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.
MR KN TP CY BG LW FW LW SW KW AS JS
Mean S.D. S.E.M.
1.0
Output (mEq/hr) Preop
Postop
125 136 130 126 112 122 143 103 136 91 134 133 135 106 123 116 110 124 125 106
31.4 22.1 29.0 54.6 27.7 36.3 43.6 21.2 19.3 20.5 22.9 22.6 39.7
119
122
±17 ±4
±13 ±3
30.3 +10.5
33.9 30.7 39.2 62.0 53.2 17.1 51.4 27.4 21.1 8.2 20.0 24.2 44.1 24.0 30.0 26.2 32.6 35.7 25.7 18.2 31.2
Preop 129 138 128 116 103 121 131 76 136 116 91 138 115 112 131 116 105 126 112 146
Postop
15.2 50.1 23.7 33.5 36.2 21.6 35.4
±2.3
±13.0
±2.9
262
Ann. Surg.
WISE, VAUGHAN AND STEIN
in basal or histalog-stimulated gastric secretion following small bowel bypass for massive obesity. These findings are similar to those of Salmon and Wright,6 who found no significant changes in basal or histalogstimulated gastric acid secretion in 9 patients following small bowel bypass. In Salmon and Wright's studies the jejuno-ileal bypass was constructed by joining the proximal 10 inches (25.4 cm) of the jejunum distal to the ligament of Treitz end-to-end to 20 inches (50.8 cm) of distal ileum. The bypassed bowel was closed proximally and anastomosed end-to-side to the colon. The postoperative gastric analyses were performed 4 to 6 months after the operation. Buchwald et al.1 suggested that gastric hypersecretion occurs in over 40% of patients following jejunoileal bypass for massive obesity. Their technique of jejuno-ileal bypass consisted of anastomosis of the proximal 40 cm of jejunum beyond the ligament of Treitz end-to-end to the terminal 4 cm of ileum. The intervening bypassed bowel was closed proximally and was anastomosed end-to-side to the cecum. They administered histalog subcutaneously at a dose of 2 mg/kg, with a maximum dose of 200 mg. As the indicator for titration they used Topfer's agent, which has an end-point of pH 3.5. Statistical analysis of their data on 14 patients demonstrated an increase in the histalog-stimulated gastric acid output from a preoperative 13.9 + 6.0 mEq acid/hour to a postoperative 17.9 ± 6.6 mEq acid/hour (P < 0.01). There was no significant change in basal acid output. Buchwald's statement that the incidence ofgastric hypersecretion following jejuno-ileal bypass is 43% is based on the assumption that patients with values greater than 2 S.E.M. above the mean may be used as the criteria for classifying patients as hypersecretors. Statistically this is not valid. It is legitimate to compare statistically two groups of data by evaluation of their means and S.E.M.'s. Singular data from a group, however, may only be compared to the mean ± S.D. On re-evaluating their data according to these criteria, there was one hypersecretor in their preoperative group; postoperatively, this patient had a small decrease in his acid output. In their postoperative group only two patients hau values above the preoperative mean ± 2 S.D.-s. Therefore, only 14% of their patients had values which were just above the 95% confidence limit. It should also be noted that in our own series of 100 patients of jejuno-ileal bypass for morbid exogenous obesity during a mean followup period of 23.6 months
*
March 1976
none developed a chronic duodenal ulcer. It should be mentioned, however, that one patient developed a bleeding stress ulcer on the seventh postoperative day following her bypass, was treated conservatively and had no further symptoms. Followup upper gastrointestinal series did not show evidence of peptic ulceration. A second patient developed symptoms suggestive of peptic ulceration with melena 10 months after bypass. Upper gastrointestinal series and gastroduodenoscopy showed only acute duodenitis and no evidence of ulceration. A third patient developed gastric ulceration 23 months following bypass; she was again treated conservatively. In conclusion, data presented in this communication suggest that small bowel bypass does not lead to an increase in basal or peak gastric acid secretion. Furthermore, careful followup of 100 patients postoperatively tends to question the suggested premise that jejunoileal bypass predisposes to chronic duodenal ulcer formation. It should be appreciated, however, that in. this paper we studied basal and peak gastric acid secretion, but did not study the effect of jejuno-ileal bypass on post-prandial gastric secretory activity. References 1. Buchwald, H., Coyle, J. J. and Varco, R. L.: Effect of Small Bowel Bypass on Gastric Secretory Function: Post-intestinal Exclusion Hypersecretion, A Phenomenon in Search of a Syndrome. Surgery, 75:821, 1974. 2. Caridis, D. T., Roberts, M. and Smith, G.: The Effect of Small Bowel Resection in the Rat. Surgery, 65:292, 1969. 3. Junghanns, K., Kaess, H., Dorner, M. and Encke, A.: The Influence of Resection of the Small Intestine on Gastrin Levels. Surg., Gynecol. Obstet., 140:27, 1975. 4. Osborne, M. P., Frederick, P. L., Sizer, J. S., et al.: Mechanism of Gastric Hypersecretion Following Massive Intestinal Resection. Clinical and Experimental Observations. Ann. Surg., 164:622, 1966. 5. Quintana, R., Kohatzu, S., Woodward, E. R. and Dragstedt, L.: Mechanism of Duodenal Inhibition of Gastric Secretion. Arch. Surg., 89:585, 1964. 6. Salmon, P. A. and Wright, W. J.: Effect of Small Bowel Bypass on Gastric Secretion in Obese Patients. Can. J. Surg., 11:365,
1968. 7. Santillana, M., Wise, L., Schuck, M. and Ballinger, W. F.: Changes in Gastric Acid Secretion Following Resection or Exclusion of Different Segments of the Small Intestine. Surgery, 65:777, 1969. 8. Stassoff, B.: Experimentelle Untersuchungen uber die kompensatorischen Vorgange bei Darmresektionen. Beitr. Klin. Chir., 89: 527, 1914. 9. Wise, L.: Peptic Ulcer: A Reappraisal of its Aetiology. Ann. Roy. Coll. Surg. (Eng.), 50:145, 1972. 10. Wise, L.: The latrogenic Short Bowel Syndrome. In Practice of Surgery, Ballinger, W. F. and Drapanas, T. (Ed.): Vol. 2, St. Louis, Mosby Co., 1975.
on
the Effect of Small Bowel Bypass for Massive Obesity on Gastric Secretory Function LESLIE WISE, M.D.,* ROBERT VAUGHAN, M.D., THEODORE STEIN, M.S.
From the Departments of Surgery and Anesthesiology, Washington University School of Medicine, St. Louis, Missouri 63110
Gastric secretory function was studied in 20 morbidly obese patients both before and after jejuno-ileal bypass. The mean postoperative weight loss was 99.2 pounds during a mean postoperative followup period of 12.6 months. The gastric secretory values we studied induded basal and histalogstimulated volume, pH, concentration, and output. No statistically significant changes were observed in any of these
After an overnight fast, a radiopaque nasogastnic
variables. Therefore it is suggested that jejuno-ileal bypass, as tube (#18 Salem Sump Tube) was placed under fluoroperformed for morbid obesity, is probably not an ulcerogenic scopic control into a dependent position of the stomach. procedure.
Twenty morbidly obese patients scheduled for jejunoileal bypass were selected at random to participate in this study. The physical characteristics of these patients are presented in Table 1. The preoperative gastric secretory studies were performed approximately one week prior to operation. The interval between the jejuno-ileal bypass and the postoperative studies ranged from 6 to 23 months. Weight loss occurred in all patients following bypass; the mean weight loss was 99.2 pounds (45.1 kg) during a mean followup period of 12.6 months.
The tube was taped to the nose to prevent further migration. Patients were placed in a 450 left lateral position and the residual gastric contents were aspirated. A 30-min basal secretion was then collected using intermittent suction (Gumco pump). Six consecutive 15min collections were then obtained after the subcutaneous injection of 1.7 mg/kg Histalog (3-amino-ethylpyrazole dihydrochloride). The 15-min period with the highest acid output was regarded as the peak acid output (P.A.O.). In all collections the volumes, pH, and acid concentrations were measured, and the acid output was calculated. The pH of the samples was measured using a Corning Model 12 Research pH meter. Acid concentration (mEq/l) was measured by titration of the sample with 0.01 N NaOH to an end-point of pH 7.0. Acid output (mEq/hr) was calculated from the product of the volume and acid concentration. All these studies were performed by the same technician. The type of small bowel bypass procedure performed in these patients is illustrated in Fig. 1. Thirty-five cm of jejunum was anastomosed end-to-end to 10 cm of terminal ileum; the proximal end of the excluded segment was closed and the distal end was anastomosed end-to-side to the cecum. Student's paired t-test was used to evaluate the significance of the changes in gastric secretion.
Submitted for publication July 23, 1975. This work was supported in part by N. I. H. Grant AMI2333. * Address all correspondence to Leslie Wise, M.D., Dept. of Surgery, Long Island Jewish-Hillside Medical Center, New Hyde Park, New York, 11040.
Results In Table 2 the pre- and postoperative basal gastric secretory data are presented. Similarly, in Table 3, the histalog-stimulated peak pre- and postoperative gastric
S MALL BOWEL BYPASS for exogenous morbid obesity is performed with increasing frequency. The natural history and the complications of this procedure have recently been reviewed by us.10 The effect of small bowel bypass on gastric secretion is controversial. Salmon and Wright have observed no significant changes in gastric acid secretion following jejuno-ileal bypass.6 Buchwald and coworkers,' however, suggested that gastric hypersecretion occurs in 40%o of patients following
jejuno-ileal bypass. The purpose of this study was to further evaluate the effect of small bowel bypass on gastric secretion. Methods
259
260
WISE, VAUGHAN AND STEIN TABLE 1. Physical Characteristics of Patient Population
Patient, Age (yrs) RC, 16 PG, 22 JH, 49 LJ, 28 MM, 39 RM, 38 DM, 43 FM, 33 MR, 46 KN, 26 TP, 61 CY, 27 BG, 54 LW, 24 FW, 39 LW, 28 SW, 23 KW, 26 AS, 44 JS, 40 Mean 35.3 S.D. + 11.6 S.E.M. ± 2.6
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.
Sex, Height (cm) F, F, M, M, F, F, F, F, F, F, F, F, F, F, F, F, M, F, F, F,
163 170 173 183 165 170 173 160 168 163 168 168 160 160 163 150 160 173 165 163
165.9 ± 6.8 ± 1.5
Postop
Diff.
99 124 149 164 130 151 121 112 166 100 133 120 126 125 114 130 191 134 112 141
76 80 105 112 72 102
23 44 44 52 58 49
93 70 79 90 111 87 82 81 80 95 83 85 75 83 87.1 ± 12.0 ± 2.7
28 42 87 10 22 33 44 44 34 35 108 49 37 58
132.1 +22.4 ± 5.0
Time (Mons) 15 9 12 20 19 6 6 10 7 19 6 17 23 20 12 6 11 10 16 7
45.1
12.6
±21.4
± 5.5 ± 1.2
± 4.8
Surg. M March 1976
Discussion
Weight (kg) Preop
Ann.
secretory data are shown. The gastric response following small bowel bypass produced a variable response. A Student's t-test analysis of the paired preoperative and postoperative measurements did not demonstrate any statistically significant change. We also analyzed whether there was a correlation between the duration of time postoperatively and changes in basal or histalogstimulated volumes, acid concentrations, or acid outputs; no such correlation was found.
Gastric hypersecretion following partial resection of the small intestine was first reported by Stassoff in 1914.8 These findings have been confirmed by numerous experimental and clinical studies. In studies on dogs, we have shown that following resection or exclusion of the proximal third of the small bowel there was a marked increase in the total gastric acid output. The increase in gastric acid secretory response following exclusion or resection of the middle third of the small intestine was variable and there was no significant change after distal third exclusions or resections.7 The pathogenesis of the gastric hypersecretion associated with small bowel resections is not clear. It has been suggested that intestinal resection may cause prolonged gastric emptying with consequent antral distension and increased gastrin release. Osborne et al.4 found that gastric emptying was not prolonged after massive small bowel resections; however, both they and Quintana et al.5 were able to abolish the gastric hypersecretion by excision of the gastric antrum. There is evidence to suggest that the fasting gastric acid secretory rate is not increased after intestinal resection and that the hypersecretion is due to increased post-prandial secretion.4 This would suggest that postresectional hypersecretion is due to a decrease or loss of some inhibitory mechanism. Recently Junghanns et al.3 have shown that there was a significant increase in post-prandial serum gastrin levels after proximal small intestinal resections in dogs. The elevation was less pronounced after resection of the distal part. These authors suggested that this may be evidence that the proximal part of the small intestine, in addition to the
FIGS. la and b. Jejunoileal bypass as performed
:.~ 1
.
by the authors.
Vol. 183 . No. 3
261
GASTRIC SECRETORY FUNCTION
TABLE 2. Basal Gastric Acid Secretory Data
Vol (ml/hr)
Patient
Preop
Postop
RC PG JH LJ MM RM DM FM MR KN TP CY BG LW FW LW SW 18. KW 19. AS 20. JS Mean S.D. S.E.M.
114 70 106 150 60 54 50 132 36 110 26 80 142 144 44 100 106 170 80 72
44 76 114 200 70 102 90 114 90 40 62 40 88 128 140 70 134 80 124 70
92.3 ±40.4 ± 9.0
93.8 ±38.4 ± 8.6
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.
Conc. (mEq/1)
pH
Output (mEq/hr)
Preop
Postop
Preop
Postop
Preop
Postop
1.6 1.4 1.2 1.8 3.3 1.7 1.9 7.6 1.9 1.6 2.4 1.8 2.0 1.5 5.8 3.3 1.9 1.5 3.6 1.4
2.0 1.6 1.5 1.3 1.9 1.5 1.8 2.2 2.0 6.0 1.5 1.7 1.3 1.7 1.8 2.4 1.2 1.4 5.7 2.0 2.1 ± 1.3 ± 0.3
40 62 90 38 12 30 30 0 28 40 19 36 30 55 8 10 24 68 10 70 35 ±23 ±5
22 46 56 60 26 52 24 14 37 0 50 34 50 32 28 16 66 68 4 26 36 ±19 4
4.6 4.4 9.4 5.6 0.8 1.6 1.6 0 1.0 4.4 1.0 2.8 4.3 8.0 0.4 1.0 2.6 13.0 0.8 5.0 3.6 ± 3.3 ± 0.7
0.8 3.6 6.4 12.0 1.8 5.2 2.2 1.6 3.3 0 3.2 1.4 4.4 4.0 4.0 1.2 8.8 5.4 0.4 1.8 3.6 ± 2.9 ± 0.6
2.2 + 1.1 ± 0.3
liver and kidney, plays an important role in the inactivation of endogenous gastrin. We have suggested that postresectional hypersecretion is due to loss of an inhibitory mechanism, in which serotonin plays a major role.9 Caridis et al.2 suggested that histaminase is the missing factor. Both serotonin and histaminase are inhibitors of gastric secretion and are asymmetrically distributed in the
small bowel with a maximum concentration in the proximal portion. If our data in animals can be extrapolated to humans, then small bowel bypass for obesity, using our technique, should not lead to gastric hypersecretion since the proximal portion of the jejunum is not bypassed. The results of this study have shown no significant change
TABLE 3. Stimulated (Peak) Gastric Acid Secretory Data
Conc. (mEq/1)
pH
Vol (ml/hr)
Patient
Preop
Postop
Preop
Postop
RC PG JH LJ MM RM DM FM
246 166 228 468 330 300 328 280 142 178 252 164 344 136 382 204 320 288 192 242
268 226 302 492 476 140 360 266 156 100 152 182 296 226 244 226 296 288 208 172
1.0 1.1 1.0 1.3 1.0 1.0 1.0 1.3 1.1 1.2 1.1 0.9 1.0 1.0 1.0 1.1 1.1 1.1 1.1 0.9
1.0 1.1 1.0 0.9 1.1 1.0 0.9 1.1 1.1 1.1 0.9 0.8 0.9 1.0 0.9 1.0 1.0 1.0 0.9 1.2
260
254
± 85 ± 19
± 99 ± 22
1.1 + 0.1 ± 0.02
± 0.1 ± 0.02
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.
MR KN TP CY BG LW FW LW SW KW AS JS
Mean S.D. S.E.M.
1.0
Output (mEq/hr) Preop
Postop
125 136 130 126 112 122 143 103 136 91 134 133 135 106 123 116 110 124 125 106
31.4 22.1 29.0 54.6 27.7 36.3 43.6 21.2 19.3 20.5 22.9 22.6 39.7
119
122
±17 ±4
±13 ±3
30.3 +10.5
33.9 30.7 39.2 62.0 53.2 17.1 51.4 27.4 21.1 8.2 20.0 24.2 44.1 24.0 30.0 26.2 32.6 35.7 25.7 18.2 31.2
Preop 129 138 128 116 103 121 131 76 136 116 91 138 115 112 131 116 105 126 112 146
Postop
15.2 50.1 23.7 33.5 36.2 21.6 35.4
±2.3
±13.0
±2.9
262
Ann. Surg.
WISE, VAUGHAN AND STEIN
in basal or histalog-stimulated gastric secretion following small bowel bypass for massive obesity. These findings are similar to those of Salmon and Wright,6 who found no significant changes in basal or histalogstimulated gastric acid secretion in 9 patients following small bowel bypass. In Salmon and Wright's studies the jejuno-ileal bypass was constructed by joining the proximal 10 inches (25.4 cm) of the jejunum distal to the ligament of Treitz end-to-end to 20 inches (50.8 cm) of distal ileum. The bypassed bowel was closed proximally and anastomosed end-to-side to the colon. The postoperative gastric analyses were performed 4 to 6 months after the operation. Buchwald et al.1 suggested that gastric hypersecretion occurs in over 40% of patients following jejunoileal bypass for massive obesity. Their technique of jejuno-ileal bypass consisted of anastomosis of the proximal 40 cm of jejunum beyond the ligament of Treitz end-to-end to the terminal 4 cm of ileum. The intervening bypassed bowel was closed proximally and was anastomosed end-to-side to the cecum. They administered histalog subcutaneously at a dose of 2 mg/kg, with a maximum dose of 200 mg. As the indicator for titration they used Topfer's agent, which has an end-point of pH 3.5. Statistical analysis of their data on 14 patients demonstrated an increase in the histalog-stimulated gastric acid output from a preoperative 13.9 + 6.0 mEq acid/hour to a postoperative 17.9 ± 6.6 mEq acid/hour (P < 0.01). There was no significant change in basal acid output. Buchwald's statement that the incidence ofgastric hypersecretion following jejuno-ileal bypass is 43% is based on the assumption that patients with values greater than 2 S.E.M. above the mean may be used as the criteria for classifying patients as hypersecretors. Statistically this is not valid. It is legitimate to compare statistically two groups of data by evaluation of their means and S.E.M.'s. Singular data from a group, however, may only be compared to the mean ± S.D. On re-evaluating their data according to these criteria, there was one hypersecretor in their preoperative group; postoperatively, this patient had a small decrease in his acid output. In their postoperative group only two patients hau values above the preoperative mean ± 2 S.D.-s. Therefore, only 14% of their patients had values which were just above the 95% confidence limit. It should also be noted that in our own series of 100 patients of jejuno-ileal bypass for morbid exogenous obesity during a mean followup period of 23.6 months
*
March 1976
none developed a chronic duodenal ulcer. It should be mentioned, however, that one patient developed a bleeding stress ulcer on the seventh postoperative day following her bypass, was treated conservatively and had no further symptoms. Followup upper gastrointestinal series did not show evidence of peptic ulceration. A second patient developed symptoms suggestive of peptic ulceration with melena 10 months after bypass. Upper gastrointestinal series and gastroduodenoscopy showed only acute duodenitis and no evidence of ulceration. A third patient developed gastric ulceration 23 months following bypass; she was again treated conservatively. In conclusion, data presented in this communication suggest that small bowel bypass does not lead to an increase in basal or peak gastric acid secretion. Furthermore, careful followup of 100 patients postoperatively tends to question the suggested premise that jejunoileal bypass predisposes to chronic duodenal ulcer formation. It should be appreciated, however, that in. this paper we studied basal and peak gastric acid secretion, but did not study the effect of jejuno-ileal bypass on post-prandial gastric secretory activity. References 1. Buchwald, H., Coyle, J. J. and Varco, R. L.: Effect of Small Bowel Bypass on Gastric Secretory Function: Post-intestinal Exclusion Hypersecretion, A Phenomenon in Search of a Syndrome. Surgery, 75:821, 1974. 2. Caridis, D. T., Roberts, M. and Smith, G.: The Effect of Small Bowel Resection in the Rat. Surgery, 65:292, 1969. 3. Junghanns, K., Kaess, H., Dorner, M. and Encke, A.: The Influence of Resection of the Small Intestine on Gastrin Levels. Surg., Gynecol. Obstet., 140:27, 1975. 4. Osborne, M. P., Frederick, P. L., Sizer, J. S., et al.: Mechanism of Gastric Hypersecretion Following Massive Intestinal Resection. Clinical and Experimental Observations. Ann. Surg., 164:622, 1966. 5. Quintana, R., Kohatzu, S., Woodward, E. R. and Dragstedt, L.: Mechanism of Duodenal Inhibition of Gastric Secretion. Arch. Surg., 89:585, 1964. 6. Salmon, P. A. and Wright, W. J.: Effect of Small Bowel Bypass on Gastric Secretion in Obese Patients. Can. J. Surg., 11:365,
1968. 7. Santillana, M., Wise, L., Schuck, M. and Ballinger, W. F.: Changes in Gastric Acid Secretion Following Resection or Exclusion of Different Segments of the Small Intestine. Surgery, 65:777, 1969. 8. Stassoff, B.: Experimentelle Untersuchungen uber die kompensatorischen Vorgange bei Darmresektionen. Beitr. Klin. Chir., 89: 527, 1914. 9. Wise, L.: Peptic Ulcer: A Reappraisal of its Aetiology. Ann. Roy. Coll. Surg. (Eng.), 50:145, 1972. 10. Wise, L.: The latrogenic Short Bowel Syndrome. In Practice of Surgery, Ballinger, W. F. and Drapanas, T. (Ed.): Vol. 2, St. Louis, Mosby Co., 1975.
