Estimated versus measured basal energy requirements in patients with Crohn's disease.

Increased energy expenditure associated with active inflammation has been thought to be one cause of weight loss in patients with Crohn's disease. Our aim was to test this hypothesis by determining if resting energy expenditure (REE) measured by indirect calorimetry was greater than the predicted energy expenditure (PEE) calculated from the Harris-Benedict formula (variables--sex, age, height, and weight) in each patient. Fifty-four patients with radiographic evidence of Crohn's disease were studied. There was a highly significant relationship (p less than 0.001) between REE and PEE, which can be expressed as follows: REE = 39.40 + 0.99 (PEE). The mean REE was 1427 +/- 228 kcal/day, whereas the mean PEE was 1404 +/- 197 kcal/day. Patients with the lowest weights when expressed as percentages of ideal body weights had the greatest resting energy expenditure per kilogram of body weight (r = -0.73, p less than 0.001). The mean REE per kilogram per day was 25 +/- 4 kcal, and only 4 of 54 patients (7%) had REE greater than or equal to 30 kcal/kg X day. Thus, REE measured by indirect calorimetry in Crohn's disease patients was not significantly higher than PEE that can be estimated from the Harris-Benedict equation. These findings show that most Crohn's disease patients without fever or sepsis do not have increased REE.

Giant hypertrophic gastropathy (Ménétrier's disease): pharmacologic effects on protein leakage and mucosal ultrastructure.

Seven patients with giant hypertrophic gastropathy participated in a gastric intubation perfusion study to investigate the route and mechanism of protein leakage associated with this disease. All patients had gastric tight junctions wider than those in healthy controls. Acute administration of propantheline bromide reduced gastric albumin leakage (-50.7%, p less than 0.05) and concurrently decreased width of tight junctions (p less than 0.05) in all patients. Another antisecretory agent, cimetidine, had no consistent effect on protein leakage or on the width of tight junctions. Pentagastrin and bethanechol chloride increased protein loss but had no effect on the width of tight junctions. These results are consistent with the hypothesis that proteins may take a paracellular route via the tight junctions as they traverse the gastric mucosa and that this may have a cholinergic mechanism.

Zinc nutrition in Crohn's disease.

A prospective evaluation of zinc status was made in 63 randomly selected patients with Crohn's disease. In the patients, mean serum and 24-hr urinary zinc values--105 microgram/dl and 383 microgram/day, respectively--were not different from controls. However, 46% of these patients had less than normal serum zinc and 36% had low urinary zinc excretions. Simultaneous reductions in both serum and urinary zinc were detected in 19% of patients. A direct correlation (P = 0.01) was found between serum levels of zinc and the concentration of albumin, the major zinc-binding protein, in outpatients but not in hospitalized patients or patients with Crohn's disease as a whole. Intake of zinc was surprisingly good--a mean intake of 13.4 +/- 1.4 mg/day. A significant (P = 0.006) association was found between urinary zinc and the Crohn's disease activity index but not between serum zinc concentration and this index. No association was found between zinc measurements and the presence or absence of fistulas, use of prednisone or sulfasalazine (Azulfidine), large bowel resections, and length of small bowel resected.

Diarrhea due to Campylobacter fetus subspecies jejuni. A clinical review of 63 cases.

Campylobacter fetus subspecies jejuni was isolated fom the feces of 63 (3.2%) of the 1,953 patients who had stools cultured at the Mayo Clinic in 1979. In contrast, Salmonella and Shigella combined were isolated from 31 (1.6%) patients. Two patients had double infections with Salmonella species and C. fetus subsp jejuni. Three patients had no diarrhea at the time of stool culture. One patient, who had chronic lymphocytic leukemia, had both blood and stool cultures positive for C. fetus subsp jejuni. There was a seasonal incidence that peaked in July when 7.8% of all patients who had stools cultured had C. fetus subsp jejuni isolated. Thirteen cases occurred in children 5 years of age and younger and 29 cases occurred between the ages of 15 and 30 years. Clinical features often included a prodrome of malaise, which preceded the onset of abdominal cramps, diarrhea, anorexia, fever, nausea, and vomiting. Grossly bloody diarrhea occurred in 33 patients, and massive intestinal bleeding occurred in 1 patient as a late complication after diarrhea had resolved. Transient splenomegaly was attributed to C. fetus subsp jejuni on one occasion. Proctoscopic findings may be similar to those seen in inflammatory bowel disease or pseudomembranous colitis. Three patients were referred to this institution with newly diagnosed chronic ulcerative colitis, and one patient was referred with newly diagnosed Crohn's disease. C. fetus subsp jejuni was isolated from their stools, and the diagnosis of inflammatory bowel disease was subsequently dropped. A selected review of cases illustrates the variety of gastrointestinal manifestations seen with this organism.

Persistent Nausea without organic cause.

The onset of functional nausea among 77 patients was frequently related to an organic disease or to a psychophysiologic response to stress. Later, the nausea had obvious features of conversion, hypochondriasis, or an hallucination. The patients had significant psychiatric disorders as assessed by the Minnesota Multiphasic Personality Inventory (MMPI) and by clinical examination. While in the hospital most patients experienced symptomatic improvement but they did not accept a psychologic explanation for their nausea.

In vitro studies of inflammatory bowel disease. Surface receptors of the mononuclear cell required to lyse allogeneic colonic epithelial cells.

Peripheral blood mononuclear cells from patients with either Crohn's disease or ulcerative colitis (collectively referred to as inflammatory bowel disease) are cytotoxic in vitro for isologous or allogeneic colonic epithelial cells. Utilizing the ability of thymus-derived (T) lymphocytes to bind sheep red blood cells to their surface and the property of bone marrow-derived (B) lymphocytes to display easily detectable surface immunoglobulin determinants, the cytoxicity of these lymphocyte subpopulations was tested. The results indicate that the mononuclear cell required for the lysis of colonic epithelium was not included within the bulk of T or B lymphocytes. Indeed, enrichment for cytotoxicity correlated best with enrichment for a mononuclear cell population lacking classical T or B markers. Additionally, mononuclear cells specifically adhering to plastic petri dishes coated with heat-aggregated immunoglobulin, and thus presumably bearing a surface Fc receptor, were enriched in their cytotoxicity. Alternatively, cells not adhering to aggregated Ig-coated petri dishes were relatively depleted of cytotoxicity. The implications of these findings as they relate to possible interactions between cellular and humoral immune mechanisms as a pathogenic mechanism for the colonic inflammatory process noted in patients with inflammatory bowel disease are discussed.

Gastrointestinal dysfunction in immunoglobulin deficiency. Effect of corticosteroids and tetracycline.

Idiopathic late-onset immunoglobulin deficiency in a young man was associated with achlorhydria and a severe intestinal malabsorption syndrome that did not respond to conventional therapy. Combined therapy with high doses of prednisone and tetracycline hydrochloride resulted in weight gain, cessation of diarrhea, improved absorption of water, fat, and vitamin B12, and production of gastric acid after stimulation with histamine. Serum immunoglobulin levels, however, did not increase.