A 67-year-old white man presented with bloody diarrhea and passed a 22-cm long segment of full-thickness sigmoid colon following a barium enema. He had advanced peripheral and cerebral vascular disease and had undergone pelvic irradiation for a bladder cancer five years previously. He recovered uneventfully from the bowel sloughage. This was apparently due to an intussusception of the sigmoid colon followed by the formation of adhesions between the edges of the adjacent viable bowel.

This is the fourth report of a case showing an association between juvenile and adenomatous polyposis. Starting at age 14, this patient underwent multiple polypectomies and gastrointestinal resections over a 15-year period. Although initial biopsies were diagnosed as juvenile polyps, later biopsies showed both adenomatous polyps and large polypoid masses with a mixture of juvenile and adenomatous features. Several typical small hyperplastic polyps were also found in the stomach. This case contrasts with the previous three cases in that the gastrointestinal tract is more widely involved and in that there is an unusual marked hyperplasia of argentaffin- and argyrophil-positive cells. The case reported here strengthens the relation between adenomatous polyposis and juvenile polyposis.

Our aim was to determine if pacing a segment of jejunum backwards with electrical stimuli could increase absorption from it. In four dogs, 75-cm loops of jejunum were isolated from the intestinal stream. After recovery, fluid was infused into the proximal stoma of the loop and effluent collected from the distal stoma for three consecutive 30-min periods. In the second period electrical stimuli were applied to the distal end of the loop to drive the pacesetter potentials of the loop, hence its contractions, backwards. The output of water, glucose, and sodium from the loop was decreased, and the transit of content through the loop was slowed during backward pacing. We conclude that pacing a segment of jejunum backwards with electrical stimuli enhances absorption of water, glucose, and sodium from that segment.

The kinetics of cholic acid (C) and chenodeoxycholic acid (CD) were studied in six patients with portal liver cirrhosis. The studies were conducted both before and after 5-6 weeks of treatment with cholestyramine (12 g/day). In keeping with previous observations, the pool size and formation of C showed subnormal values during the pretreatment period, while the production of CD was within normal limits. The pool sizes of C and CD did not change upon treatment with cholestyramine, but the mean total bile acid formation increased by a factor of about 2.5. The ratio between the amounts of C and CD synthesized remained essentially unchanged. Considering the therapeutic response previously observed in normal subjects and in patients with hyper-beta-lipoproteinemia, the present results suggest a selective impairment of the biosynthesis of C in patients with portal liver cirrhosis. It is suggested that the primary defect may reside in the 12alpha-hydroxylase enzyme system.

Serum gastric inhibitory polypeptide was measured in dogs prepared with Heidenhain pouches and Mann-Bollman fistulae following the intraduodenal (ID) infusion of isotonic saline, 20% glucose, or 20% mannitol. Following ID 20% glucose, serum GIP concentrations rose significantly (P less than 0.05) between 30 and 120 min and there was a significant inhibition (P less than 0.05) of acid secretion in the Heidenhain pouches between 15 and 75 min. A good correlation (r = 0.925) was found between the rise in serum GIP and the inhibition of acid secretion. Although neither ID isotonic saline nor 20% mannitol stimulated GIP release, the latter produced a significant (P less than 0.05) inhibition of acid secretion between 60 and 105 min. We conclude: (1) the inhibitory effect of acid secretion following ID glucose is mediated in part by the release of endogenous GIP; (2) glucose and mannitol probably inhibit gastric acid secretion by different mechanisms.

The probable etiology and outcome of bridging hepatic necrosis found on a liver biopsy performed within three months of the onset of clinical illness was evaluated in 42 consecutive patients with this finding. Eighteen of the patients (43%) had a probable drug etiology for their hepatitis. Ten patients had HBSAG-positive acute hepatitis. Fourteen patients had neither drug-induced disease nor proven HBSAg-positive hepatitis. One patient from the drug-induced group died, but the other 17 had complete clinical recovery. Eight of ten in the hepatitis B antigen-postive group cleared their antigen and had complete clinical recovery. Chronic hepatitis developed in two who remained persistently HGSAg positive. Eight of the patients in the group with unknown etiology recovered, while six developed evidence of active chronic liver disease. This incidence of active chronic liver disease is significantly greater than that found in the drug-induced group (P less than 0.02). We conclude that drug-induced hepatitiis accounts for a significant proportion of patients of acute hepatitis who have bridging hepatic necrosis on liver biopsy. However, in these drug-induced cases the finding of bridging hepatic necrosis does not appear to be associated with an increased risk of development of active chronic liver disease.

Twenty patients with longstanding alcoholism and biopsy-proven alcoholic liver disease presented with marked elevation of serum alkaline phosphatase (in excess of four times the upper limit of normal). None had a past or present history to suggest pancreatitis or biliary tract disease, nor had any of these patients recently taken medication which could be implicated in cholestatic jaundice. Thirteen (65%) of this group either had radiologic or post mortem confirmation of nonobstructed biliary systems. The histologic findings in this group of patients were compared with those of a group of patients with alcoholic liver disease and normal or only mild elevation of serum alkaline phosphatase. Significantly more hepatocellular necrosis (P less than 0.05), alcoholic hyaline (P less than 0.02), and cholestasis (P less than 0.002) were noted in the severely hyperphosphatasemic group. Minimal degrees of steatosis were found in both groups. These data indicate that intrahepatic cholestasis occurs in patients with alcoholic liver disease, and this may often be secondary to alcoholic hepatitis. Overemphasis has previously been given to alcoholic fatty liver as a cause of this syndrome.

The possibility of rhythmicity in the intestinal absorption of lipids was explored by assessing the absorption of vitamin K-1 by the unanesthetized rat at 6 PM, 12 and 6 AM, and 12 PM. A marked variability in the absorption rate of vitamin K-1 was found throughout the 18-hr period. The highest rates of absorption occurred at midnight (139.8 +/- .22 and 134.4 +/- 9.1 pmol/min/10 cm of jejunum and ileum, respectively). The lowest rates of absorption occurred at 6 AM (54.5 +/- 1 and 81.4 +/- 7.4 pmol/min/10 cm of jejunum and ileum, respectively). Absorption rates at noon were not different from absorption at 6 AM but an initial increase in absorption was noted at 6 PM. Synchronization of the absorptive rate with time is most likely related to the time of feeding and not to changes in the pattern of illumination. The possibility of marked diurnal variability in the absorption rate should be considered in the design and execution of intestinal absorption experiments.

Ninety-nine patients suspected of having pancreatic carcinoma were studied prospectively for carbohydrate tolerance. Thirty-two patients were proven subsequently to have pancreatic carcinoma; the remainder served as a control group. There was an increased incidence of carbohydrate intolerance in patients with pancreatic carcinoma compared to the control group. Insulin and C-peptide measurements during glucose tolerance tests suggest abnormal beta cell function and possibly insulin resistance as causes for this abnormality. Although factors related to malignancy in general could partly account for the results, a specific factor occurring in patients with pancreatic carcinoma must also be considered as it could serve as a marker for the early detection of this disease.

The possible role of circulating immune complexes (IC) in the production gastrointestinal lesions was studied in rabbits with chronic serum sickness (CSS) induced by multiple daily injections of bovine serum albumin (BSA). All rabbits generating a marked antibody response developed IC glomerulonephritis. In approximately 50% of these rabbits granular deposits of BSA, rabbit IgG, and C3 were also found in the gastrointestinal tract. The immune deposits in the gastrointestinal tract were mainly present in the vessel walls, close to the intestinal glands and the surface epithelium, and between the smooth muscle cells. This was accompanied by slight to moderate edema of the mucosa and the submucosa and mild infiltration of inflammatory cells. Electron-densedeposits were found in a pattern corresponding to that observed for BSA, rabbit IgG, and C3. Degranulated neutrophils, basophils, and mast cells were noticed in the interstitium. The presence in the same areas of granular deposits of BSA, IgG, and C3, corresponding to electron-dense deposits, suggests that the deposits contain BSA-anti-BSA complexes. These findings show that in rabbits with CSS circulating IC may localize and induce injury in the gastrointestinal tract.

We compared the effects of exogenous pentagastrin and meal-stimulated gastrin on plasma immunoreactive calcitonin (iCT) in various studies of 13 normal adult men. Bolus intravenous injection of pentagastrin (0.5 microgram/kg) produced increases of iCT in 8 of 9 men. There was a linearly increasing response of iCT concentrations to increasing doses of pentagastrin (0.0625, 0.125, 0.25, and 0.5 microgram/kg) and to achieved serum immunoreactive pentagastrin concentrations (r = 0.72, P less than 0.01). To determine the effects of endogenous gastrin upon peripheral iCT concentrations, we measured serum immunoreactive gastrin (iG) and plasma iCT in four men at frequent intervals for 240 min after ingestion of low- (100 mg) and high- (400 mg) calcium meals. Serum iG increased in all subjects, with a peak at approximately 30 min. However, plasma iCT levels were unchanged from basal throughout the study. The increase of pentagastrin (0.3 pmol/ml) which caused a barely detectable increase of iCT was five- to tenfold greater than the mean maximal increases of gastrin after low- and high-calcium meals (0.04 and 0.06 pmol/ml, respectively). These results suggest that increases of plasma iCT concentrations after administration of pentagastrin in man reflect pharmacologic phenomena and that postprandial gastrin secretion may be insufficient to affect peripheral iCT concentrations.