Frank P. Brooks

Sorbitol dehydrogenase in the diagnosis of liver disease

Summary and conclusionsIn an attempt to find a more useful clinical test for the diagnosis of liver disease, serum levels of the enzyme sorbitol dehydrogenase (SDH) were measured in patients with liver disease and patients with nonhepatic diseases. The majority of patients in both groups had concomitantly elevated serum levels of SGOT and SGPT. In the patients tested, SDH elevations were found to be specific for liver involvement, but much less sensitive than the transaminases. The serum sorbitol dehydrogenase test, in its present form, does not appear to offer any special advantages over the transaminase studies presently employed to detect hepatocellular disease. Certain conclusions can be drawn from the data: (1) SDH was found to be organ-specific but not disease-specific in the patients tested; (2) it was seen to be less sensitive than the transaminases; and (3) SDH levels remained elevated for much shorter periods of time than the transaminases.

Ileocecal endometriosis presenting with abdominal pain and gastrointestinal bleeding.

SummaryA 26-year-old woman with enteric endometriosis presenting with cecocolic intussusception, a cecal mass on barium enema, and gastrointestinal hemorrhage is described. Laparotomy revealed cecocolic intussusception, ileocecal endometrial implants, and cecal mucosal ulceration presumed secondary to ischemia of the intussuscepted bowel. Histopathology showed serosal and subserosal endometrial implants without mucosal invasion. A review of the literature of endometrial bowel disease is presented.

The Zollinger-Ellison syndrome in a 10-year-old boy

A 10-year-old boy with the Zollinger-Ellison syndrome is presented. Gastric secretory studies showed a 12 hour basal output of over 2 L.; with Histalog stimulation the acid output was 2 times normal. At laparotomy he was found to have nonbeta islet cell tumor metastases in the liver. No primary tumor was found in the pancreas. An extract of the tumor demonstrated secretory activity, and immunoassay of the patients blood revealed significant elevation of gastrin. Quantitative studies of the gastric mucosa showed an unusually large parietal cell mass. The boy is well and asymptomatic 2 years following total gastrectomy.

The secretion of bile

SummarySeparate active transport mechanisms may account for the entry of bile salts and bilirubin into the biliary canaliculi from the hepatic parenchymal cells. Extracellular fluid follows in response to osmotic gradients and possibly also by an independent secretory mechanism. This “primary bile” probably is modified, as it passes down the bile ducts, by bidirectional movements of electrolytes across the epithelium. At least one active transport process involving bicarbonate is involved in a secretory mechanism in the distal ducts. The control of bile secretion involves three major factors: the presence of bile salts, gastrointestinal hormones, and vagal innervation. It is likely that the hepatic circulation may also influence bile secretion; presumably, the bile salt concentration of portal venous blood determines the secretion of bile salts by the parenchymal cells, but the details of the mechanism are missing. Gastrin, secretin, cholecystokinin-pancreozymin, and glucagon all increase bile flow, particularly by increasing the flow of sodium chloride and bicarbonate solutions. Therefore, the control of bile secretion can be divided into the secretion of bile salts and the secretion and reabsorption of water and electrolyte. The latter seems to be particularly subject to neurohumoral influences. Factors determining the secretion of bilirubin are less well understood but may include the effects of glucagon.

Cholinergic control of rabbit pancreatic secretion.

Electrical stimulation of the vagus in anesthetized cats and rabbits increased the flow of pancreatic juice and the concentration of amylase, trypsin, and chymotrypsin. Similar stimulation to the rabbit pancreas in vitro was without effect. Adding physostigmine to the bath elicited a two to three-fold increase in the output of trypsin and chymotrypsin, with or without concomitant vagal stimulation. The effect was temperature-sensitive. Assay for acetylcholine activity in the bath fluid was negative, suggesting that physostigmine was prolonging the action of acetylcholine released within the pancreas.

Symptomatic treatment of duodenal ulcer

In this issue of the journal, Gustavsson et al report the results of a clinical trial of cimetidine in standard dosage of 200 mg three times a day and 400 mg at bedtime for four weeks, compared with the same dosage for at least a week and thereafter until symptoms (mainly pain) disappeared. On the average, patients in the symptom-treated group took their medication for another 10 days after the first two weeks of treatment. At endoscopy after four weeks, 20 of 26 patients in the standard treatment group had healed their ulcers, compared to 14 of 24 in the symptom-treated group. Both day and nighttime pain were more common in the fourth week of treatment in the patients whose ulcers failed to heal. Patients in the symptom-treated group saved 11 days of cimetidine therapy. The authors point out

Spontaneous Improvement in Pancreatic Function in Chronic Pancreatitis

Chronic pancreatitis is a disease with varying etiologic factors. It is relatively easy to diagnose in its later stages, but notoriously difficult early in its course. Treatment is often unsatisfactory. The clinical features of chronic pancreatitis are abdominal pain and the consequences of destruction of the exocrine and endocrine pancreas--steatorrhea and diabetes mellitus. Pain is less common in patients with chronic calcific pancreatitis than in chronic noncalcific pancreatitis. It may be absent even in patients continuing to abuse alcohol (1). Recently, a report appeared indicating that treatment with oral pancreatic extracts can relieve the pain of some patients with chronic pancreatitis (2). This has been attributed to a negative feedback mechanism in which trypsin in the duodenum inhibits the secretion of chymotrypsin by decreasing the release of cholecystokinin (3). The steatorrhea of chronic pancreatitis can usually be controlled by adequate replacement treatment with pancreatic extracts (4). However, fecal fat excretion is rarely reduced to normal levels. Inactivation of lipase by acid in the duodenum in the face of reduced duodenal bicarbonate secretion may account for failure of substitution therapy in some patients (5). In this issue of the journal Begley and RobertsThomas report three patients with chronic pancreatitis confirmed by ductal changes seen on ERCP who appear to have experienced a spontaneous reduction in the fecal excretion of fat; from 60 to 6 and 11 g/day in two patients and from 9 g while on substitution therapy to 3 g/day off treatment in the third. The duodenal bicarbonate concentration after secretin increased slightly as the steatorrhea decreased in one patient. The period of observation extended over 3, 22, and 27 years in the three patients. Diabetes was present in two patients, and the glucose tolerance test was mildly abnormal inChronic pancreatitis is a disease with varying etiologic factors. It is relatively easy to diagnose in its later stages, but notoriously difficult early in its course. Treatment is often unsatisfactory. The clinical features of chronic pancreatitis are abdominal pain and the consequences of destruction of the exocrine and endocrine pancreas--steatorrhea and diabetes mellitus. Pain is less common in patients with chronic calcific pancreatitis than in chronic noncalcific pancreatitis. It may be absent even in patients continuing to abuse alcohol (1). Recently, a report appeared indicating that treatment with oral pancreatic extracts can relieve the pain of some patients with chronic pancreatitis (2). This has been attributed to a negative feedback mechanism in which trypsin in the duodenum inhibits the secretion of chymotrypsin by decreasing the release of cholecystokinin (3). The steatorrhea of chronic pancreatitis can usually be controlled by adequate replacement treatment with pancreatic extracts (4). However, fecal fat excretion is rarely reduced to normal levels. Inactivation of lipase by acid in the duodenum in the face of reduced duodenal bicarbonate secretion may account for failure of substitution therapy in some patients (5). In this issue of the journal Begley and RobertsThomas report three patients with chronic pancreatitis confirmed by ductal changes seen on ERCP who appear to have experienced a spontaneous reduction in the fecal excretion of fat; from 60 to 6 and 11 g/day in two patients and from 9 g while on substitution therapy to 3 g/day off treatment in the third. The duodenal bicarbonate concentration after secretin increased slightly as the steatorrhea decreased in one patient. The period of observation extended over 3, 22, and 27 years in the three patients. Diabetes was present in two patients, and the glucose tolerance test was mildly abnormal in

Second International Conference on Gastrointestinal Hormones

The first group of papers emphasized the localization of biologically active peptides within cells of the gastrointestinal tract 9 Evidence was presented to indicate that individual cells, in the normal intestinal mucosa and in human gastroduodenal carcinoid tumors, may contain a peptide hormone and the biologically active amine, serotonin. Other cells contained more than one active peptide. Peptideproducing tumors may contain subsets of cells that produce peptides different from those responsible for symptoms 9 Progress was reported in the separation of individual gastrointestinal endocrine cells from the mucosa, by sedimentation techniques. A recurrent theme throughout the discussion was the need for antibodies with specificity for defined sequences of amtno acids; also emphasized was uncertainty as to the presence of hormones that were biologically active 9 The value of studying the development of endocrine cells was illustrated. A variety of peptides with immunoreactivities resembling ACTH, enkephalins, endorphins, somatostatin, neurotensin, growth hormone, and urogastrone have been localized by immunocytochemistry to the digestive tract 9 Many of these are not usually considered as gastrointestinal hormones. Their physiological significance remains to be determined 9 An alternative to immunological studies was proposed by Professor Mutt and his colleagues; they have developed an analytical technique for the

Alkaline gastritis following antrectomy—An elusive syndrome

Editorial. Le diagnostic de gastrite alcaline ou de reflux alcalin est delicat, la decision de realiser une diversion «Roux en Y» importante. Des explorations precises sont necessaires

A radioimmunoassay for cholecystokinin (CCK)

The availability of a suitable, sensitive, and specific radioimmunoassay for gastrin changed the entire diagnostic approach to the Zollinger-Ellison syndrome and opened up new directions in the pathophysiology of peptic ulcer disease. (1) It is of historical interest that the first antibodies produced to gastrin were to the C-terminal tetrapeptide of gastrin and hence failed to distinguish between gastrin and CCK (2, 3). Radioimmunoassays for secretin, although not yet commercially available, have been developed which can detect a rise in serum immunoreactivity after a meal. It was suggested recently that they could be used to follow the course of hyperacidity in response to antisecretory drugs (4). The third of the major classical gut peptides, CCK, has continued to elude the successful development o fa radioimmunoassay. Assays were developed, but their specificity and sensitivity were subject to criticism (5). In 1981 Byrnes et al reported a radioimmunoassay for CCK using antibodies raised against porcine CCK33 (6). This antibody bound CCK8 and C C K 3 3 with equimolar potency. Fasting plasma from human subjects gave a mean value of 6.3 pmol/liter. After a meal the level rose to 24.4 _+ 6.5 pmol/liter. Recently assays have been developed using multiple antibodies to different portions of the molecule (7, 8). The results were interpreted to indicate that the octapeptide of CCK (CCK-OP) was the principal molecular form of the hormone released into the blood in response to a meal. Nevertheless, the 33amino-acid peptide has been the form most commonly found in the gut.