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Gallbladder emptying response to sham feeding
CORRESPONDENCE
January 1987
hepatotoxicity
simulating
alcoholic liver disease. N Engl J Med
1984;311:167-72.
3. Rigas B, Rosenfeld LE, Barwick KW, et al. Amiodarone hepatotoxicity: a clinicopathologic study of five patients. Ann Intern Med 1986;104:348-51. 4. Rijntjes PJM, Moshage HJ, van Gemert PJL, de Waal R, Yap SH. Cryopreservation of adult human hepatocytes: the influence of deep freezing storage on the viability, cell seeding, survival, fine structures and albumin synthesis in primary cultures. J Hepatol 1986;3:7-18.
Gallbladder Emptying Response to Sham Feeding Dear Sir: We would like to make several comments about the report by Fisher et al. (1) regarding the gallbladder emptying response to sham feeding. We were surprised to note that all healthy subjects studied responded to sham feeding. In contrast, our own studies have suggested that only 53% of healthy subjects will respond to sham feeding even with a very appetizing meal of choice, possibly because as yet unclear inbibitory influences on gallbladder emptying might outweigh cephalic stimulatory influences (2). It is not clear from the study by Fisher et al. how they excluded interdigestive gallbladder emptying (attributed to the IMMC) in their studies as the cause of gallbladder emptying rather than the response to sham feeding. It is vital that the time of onset of gallbladder emptying relative to the onset of sham feeding be noted (not reported by Fisher et al. but measured as 3.4 + 6.9 min in our studies) since, in the intervals during which they monitored gallbladder emptying, interdigestive gallbladder emptying would be expected to occur at some stage. In our studies we corrected for this by (a) using a derived probability factor for interdigestive gallbladder emptying, and (b) also directly measuring the IMMC (2). We also performed sham feeding in 12 patients who had previously undergone a truncal vagotomy and pyloroplasty in whom the postoperative insulin-stimulated acid output test was negative. In contrast to the findings of Fisher et al. who found no response to sham feeding in their 10 patients, we found that 4 of our 12 patients responded, a result that was not significantly different from the control group. We interpreted this as possibly due to intact vagal fibers to the hepatic plexus (possible but unlikely] or the vagus having no role in the cephalic phase of gallbladder emptying. We think that the role of the vagus nerve in mediating the cephalic phase of gallbladder emptying still requires further study before the conclusion of Fisher et al. that truncal vagotomy ablates the gallbladder response to sham feeding can be justified. With respect to possible hormonal mechanisms mediating the cephalic phase, we measured cholecystokinin during our shamfeeding studies using a sensitive and specific assay for all subtypes of cholecystokinin. We found that sham feeding did not cause a rise in cholecystokinin levels and thus concluded that cholecystokinin, at least, could be eliminated as the final common pathway for causing cephalic-mediated gallbladder emptying. Finally, we are in agreement with Fisher et al. about the effects of prior atropinization on ablating the gallbladder emptying response to sham feeding, from which we concluded, as did Fisher et al., that cholinergic pathways mediating gallbladder
emptying are a neglected but important ling gallbladder emptying.
mechanism
273
for control-
S. ELLENBOGEN.F.R.C.S. C. R. MACKIE.M.D., F.R.C.S. J. N. BAXTER,F.R.A.C.S. The University of Liverpool Department of Surgery P.O. Box 147 Liverpool L69 3BX, United Kingdom 1. Fisher RS, Rock E, Malmud LS. Gallbladder emptying response to sham feeding in humans. Gastroenterology 1986;90:1854-7. 2. Ellenbogen S, Grime JS, Mackie CR, et al. Mechanisms responsible for the cephalic phase of gallbladder emptying. Gut 1986:27:A261.
ggmTc-Sulfur Colloid Studies in Hepatic Hydrothorax Dear Sir: Rubinstein et al. (1) suggest that hepatic hydrothorax without clinical ascites may be diagnosed by -y-camera, demopstrating migration of interperitoneal 99mTc-sulfur colloid into the thorax, and that these patients may have small amounts of abdominal free fluid which may be detectable by ultrasonography. We recently saw a 58-yr-old woman who presented with right pleural effusion. She had micronodular cirrhosis, diagnosed by liver biopsy during a cholecystectomy for gallstones 5 mo previously. No ascites had been reported during the cholecystectomy. The physical examination and the abdominal ultrasound examination failed to discover any fluid in the peritaneal cavity. There were no symptoms or signs of heart failure and the serum albumin was normal. The effusion was a transudate. An intraperitoneal injection of 99mTc-sulfur colloid showed no migration of radionuclide into the pleural cavity under y-camera. It is not clear, however, if prior cholecystectomy played a role in this negative result. The patient was treated with chest tube drainage. The patient’s course was complicated by an empyema of the right pleural space that was treated with antibiotics after which the drainage decreased dramatically to about 250 ml daily. Forty-eight hours later the patient started to develop ascites and edema of the lower extremities. Ascites was confirmed by ultrasonography. We speculate that our patient underwent a spontaneous pleurodesis due to the empyema and subsequent accumulation of ascites-a course that is consistent with hydrothorax of hepatic origin. This case sugests that both abdominal ultrasound for ascites and intraperitoneally injected 99mTc-sulfur colloid migration in the thorax may be negative in patients with hepatic hydrothorax. MAURIZIOBONACINI,M.D. CUMPENI RAMMOHAN,
M.D., F.A.C.P
Department of Medicine Booth Memorial Medical Center 56-45 Main Street Flushing, New York 11355 1. Rubinstein D, McInnes IE, Dudley FJ. Hepatic hydrothorax in the absence of clinical ascites: diagnosis and management. Gastroenterology 1985;88:188-91.
January 1987
hepatotoxicity
simulating
alcoholic liver disease. N Engl J Med
1984;311:167-72.
3. Rigas B, Rosenfeld LE, Barwick KW, et al. Amiodarone hepatotoxicity: a clinicopathologic study of five patients. Ann Intern Med 1986;104:348-51. 4. Rijntjes PJM, Moshage HJ, van Gemert PJL, de Waal R, Yap SH. Cryopreservation of adult human hepatocytes: the influence of deep freezing storage on the viability, cell seeding, survival, fine structures and albumin synthesis in primary cultures. J Hepatol 1986;3:7-18.
Gallbladder Emptying Response to Sham Feeding Dear Sir: We would like to make several comments about the report by Fisher et al. (1) regarding the gallbladder emptying response to sham feeding. We were surprised to note that all healthy subjects studied responded to sham feeding. In contrast, our own studies have suggested that only 53% of healthy subjects will respond to sham feeding even with a very appetizing meal of choice, possibly because as yet unclear inbibitory influences on gallbladder emptying might outweigh cephalic stimulatory influences (2). It is not clear from the study by Fisher et al. how they excluded interdigestive gallbladder emptying (attributed to the IMMC) in their studies as the cause of gallbladder emptying rather than the response to sham feeding. It is vital that the time of onset of gallbladder emptying relative to the onset of sham feeding be noted (not reported by Fisher et al. but measured as 3.4 + 6.9 min in our studies) since, in the intervals during which they monitored gallbladder emptying, interdigestive gallbladder emptying would be expected to occur at some stage. In our studies we corrected for this by (a) using a derived probability factor for interdigestive gallbladder emptying, and (b) also directly measuring the IMMC (2). We also performed sham feeding in 12 patients who had previously undergone a truncal vagotomy and pyloroplasty in whom the postoperative insulin-stimulated acid output test was negative. In contrast to the findings of Fisher et al. who found no response to sham feeding in their 10 patients, we found that 4 of our 12 patients responded, a result that was not significantly different from the control group. We interpreted this as possibly due to intact vagal fibers to the hepatic plexus (possible but unlikely] or the vagus having no role in the cephalic phase of gallbladder emptying. We think that the role of the vagus nerve in mediating the cephalic phase of gallbladder emptying still requires further study before the conclusion of Fisher et al. that truncal vagotomy ablates the gallbladder response to sham feeding can be justified. With respect to possible hormonal mechanisms mediating the cephalic phase, we measured cholecystokinin during our shamfeeding studies using a sensitive and specific assay for all subtypes of cholecystokinin. We found that sham feeding did not cause a rise in cholecystokinin levels and thus concluded that cholecystokinin, at least, could be eliminated as the final common pathway for causing cephalic-mediated gallbladder emptying. Finally, we are in agreement with Fisher et al. about the effects of prior atropinization on ablating the gallbladder emptying response to sham feeding, from which we concluded, as did Fisher et al., that cholinergic pathways mediating gallbladder
emptying are a neglected but important ling gallbladder emptying.
mechanism
273
for control-
S. ELLENBOGEN.F.R.C.S. C. R. MACKIE.M.D., F.R.C.S. J. N. BAXTER,F.R.A.C.S. The University of Liverpool Department of Surgery P.O. Box 147 Liverpool L69 3BX, United Kingdom 1. Fisher RS, Rock E, Malmud LS. Gallbladder emptying response to sham feeding in humans. Gastroenterology 1986;90:1854-7. 2. Ellenbogen S, Grime JS, Mackie CR, et al. Mechanisms responsible for the cephalic phase of gallbladder emptying. Gut 1986:27:A261.
ggmTc-Sulfur Colloid Studies in Hepatic Hydrothorax Dear Sir: Rubinstein et al. (1) suggest that hepatic hydrothorax without clinical ascites may be diagnosed by -y-camera, demopstrating migration of interperitoneal 99mTc-sulfur colloid into the thorax, and that these patients may have small amounts of abdominal free fluid which may be detectable by ultrasonography. We recently saw a 58-yr-old woman who presented with right pleural effusion. She had micronodular cirrhosis, diagnosed by liver biopsy during a cholecystectomy for gallstones 5 mo previously. No ascites had been reported during the cholecystectomy. The physical examination and the abdominal ultrasound examination failed to discover any fluid in the peritaneal cavity. There were no symptoms or signs of heart failure and the serum albumin was normal. The effusion was a transudate. An intraperitoneal injection of 99mTc-sulfur colloid showed no migration of radionuclide into the pleural cavity under y-camera. It is not clear, however, if prior cholecystectomy played a role in this negative result. The patient was treated with chest tube drainage. The patient’s course was complicated by an empyema of the right pleural space that was treated with antibiotics after which the drainage decreased dramatically to about 250 ml daily. Forty-eight hours later the patient started to develop ascites and edema of the lower extremities. Ascites was confirmed by ultrasonography. We speculate that our patient underwent a spontaneous pleurodesis due to the empyema and subsequent accumulation of ascites-a course that is consistent with hydrothorax of hepatic origin. This case sugests that both abdominal ultrasound for ascites and intraperitoneally injected 99mTc-sulfur colloid migration in the thorax may be negative in patients with hepatic hydrothorax. MAURIZIOBONACINI,M.D. CUMPENI RAMMOHAN,
M.D., F.A.C.P
Department of Medicine Booth Memorial Medical Center 56-45 Main Street Flushing, New York 11355 1. Rubinstein D, McInnes IE, Dudley FJ. Hepatic hydrothorax in the absence of clinical ascites: diagnosis and management. Gastroenterology 1985;88:188-91.