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Collagenous colitis is a clinicopathologic syndrome with chronic watery diarrhea, diffuse colitis with surface epithelial injury, and a distinctive collagen band beneath the surface epithelium especially in the proximal colon. The cases of seven patients (including six middle-aged women) with chronic, watery, noninfectious diarrhea were studied. Roentgenographic and endoscopic findings were not diagnostic. Two patients had rectal mucosal inflammation but sparing of the distal colon from subepithelial collagen. Other findings included thyroid disease (four patients), urethral fibrosis (three), elevated erythrocyte sedimentation rate (six), and eosinophilia (three). The colon was thought to be the main source of diarrheal fluid, but bile salt malabsorption, steatorrhea, and net small-bowel secretion were additive factors in some patients. With antiinflammatory treatment the diarrhea abated, the surface epithelial injury decreased, and the subepithelial collagen resolved (two patients), but lamina propria inflammation persisted. Collagenous colitis seems to be a chronic systemic, and perhaps autoimmune, disorder.

Diffuse mucosal granularity was reported recently in small bowel Crohn's disease. The radiographic appearance corresponded on histopathologic examination to villous hypertrophy, fusion, or epithelial bridge formation. We have observed similar granularity in Crohn's disease but also in several other conditions, including radiation enteritis, pancreatic glucagonoma, protein-losing enteropathy, and small bowel ischemia. Histopathologic examination demonstrated various alterations in villous morphology, such as edema, hyperplasia, clubbing, or fusion. In Crohn's disease, this appearance was sometimes an indication of early inflammatory disease but was also seen following extensive small bowel resection, possibly due to villous enlargement resulting from intestinal adaptation. These findings suggest that granular mucosa in the small bowel is a nonspecific finding reflecting an alteration in villous structure.

Lactose intolerant populations are heterogeneous with respect to their milk-drinking habits. A gradation of lactase activity in the intolerant population may result in sufficient lactose hydrolysis to obviate symptoms and lead to continued milk consumption. This paper reports on differences in maximum blood sugar rise in lactose intolerant children who are observed to consume or reject milk. Of the 89 black elementary school children, 48 (54 per cent) evidenced a flat lactose tolerance curve. Twenty-eight of these 48 children (58 per cent) were defined as nonmilk drinkers. The maximum blood sugar rise was 12.3 mg/100 in the 20 lactose malabsorbers who were defined as milk drinkers. It appears that some lactose malabsorbing children may have sufficient, albeit lower, levels of lactase to hydrolyze moderate amounts of milk.

A prominent submucosal layer of decreased attenuation was demonstrated on CT in three patients with inflammatory bowel disease. On pathologic examination this zone proved to be due to extensive submucosal fat accumulation and not active inflammation. The potential significance of this finding is discussed.

The ability of lactose-intolerant individuals to tolerate 8 ounces of milk was determined in healthy teen-agers. Thirty-two blacks were studied with 50-gm lactose tolerance tests. Nineteen (59%) had a flat blood sugar curve and 13 (39%) also developed bloating, cramps, loose stools, or diarrhea with the test. These latter 13 were defined as lactose-intolerant. Seven of the 13 lactose-intolerant teen-agers (54%) developed abdominal bloating and/or cramps after drinking 8 ounces of milk (half-pint). None had diarrhea. Eight were symptomatic with the equivalent amount of lactose (12 gm) while only one had symptoms with the monosaccharide components of lactose, glucose and galactose. The symptoms with milk and 12 gm of lactose were less severe than with the 50-gm tolerance test. A history of a prior awareness of milk intolerance was obtained from 11 of the 13 lactose-intolerant subjects. At least one half of lactose intolerant teen-agers might be expected to be symptomatic after drinking 8 ounces of milk without other food. Milk intolerance should be considered in the nutritional planning for teen-agers with special attention to members of population groups with a high prevalence of lactose intolerance.

Diamine oxidase (DAO; EC 1.4.3.6) is an enzyme found in high activity in the mature cells of the upper villus of rat small intestinal mucosa and in very much lower activity in all other tissues in the nonpregnant rat. This study was designed to determine whether a provocative test for increasing the level of plasma DAO activity by heparin administration could be used to monitor the extent and severity of acute, severe, small intestinal mucosal injury. In adult rats, small intestinal loops of varying lengths were perfused with 2,100 mosM sodium sulfate solution for 60 min to produce selective damage to villus epithelium. Plasma postheparin DAO (PHD) activity (180 min after 400 U/kg i.p. heparin) was measured 7 h after initiation of perfusion. With increasing length of intestinal mucosal injury, there was a progressive decrease in both basal and plasma PHD activity. The decrease in plasma PHD activity closely reflected the length of intestinal mucosa injured (n = 128, r = 0.86, P less than 0.001), and it was much more sensitive (threshold limit of detection = 13% of total length, range = 67 U/ml for 100% length of injury) than unstimulated basal levels of plasma DAO (threshold = 40%, range = 2.1 U/ml). Our previous data have suggested that DAO is unique among intestinal mucosal enzymes in that circulating levels can serve as a marker of mucosal injury; this study illustrates that the addition of a low-dose heparin administration enhances the use of DAO even further as a sensitive, quantitative, circulating marker for monitoring the extent of small intestinal mucosal injury in the rat.

Methylxanthines, being potent phosphodiesterase inhibitors, produce increased intestinal cyclic AMP levels and would be predicted to produce increased net intestinal fluid secretion. Their effect when presented to the intestinal lumen, which would be analogous to human ingestion, had not been previously determined. Isolated loops of rat jejunum were perfused with solutions of caffeine and theophylline in vivo. There was a decrease in net fluid absorption in both neonatal and mature animals exposed to theophylline. Mature animals exposed to caffeine developed a prompt secretory response, comparable to thax induced by cholera toxin. The data indicate that methylxanthines are potent intestinal secretagogues when administered intraluminally and suggest that secretory stimulation could be important in the gastrointestinal symptomatology elicited in man by these compounds.

Nineteen of 20 healthy Oriental adults living in the United States developed abdominal cramps and diarrhea after ingesting an amount of lactose equivalent to that in one quart of milk; 14 reported similar symptoms after one or two glasses of milk; all had consumed milk as infants without having such symptoms. Two of 20 Caucasians tested were intolerant to milk and lactose. Many Orientals therefore may have a genetically determined lactase deficiency that may lead to intolerance to milk. Since lactase deficiency is also common among Negroes, the bulk of the world's adult population is probably intolerant to milk.