[Routine x-ray examination of the thorax prior to surgical intervention under general anesthesia].
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Biomedical subjects
Publications and source records attributed to K B Jensen.
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Forty-five adult outpatients with endoscopically confirmed gastric ulceration completed a double-blind trial of either cimetidine (1 g/day) or placebo. After six weeks 18 of the 23 patients receiving cimetidine showed complete ulcer healing compared with only six of the 22 patients receiving placebo. The cimetidine group also had fewer days with pain than the placebo group but the difference was not statistically significant. Cimetidine therefore seems to promote healing of gastric ulcers without severe side effects, although its effect on pain is less pronounced than in patients with duodenal ulcers.
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The amount of immunoglobulin-containing cells in gastric mucosa from 6 patients with Ménétriér's disease was estimated. Furthermore, the rate of gastric epithelial cell proliferation was sutdied in 4 of the patients. Fluorescent antisera specifically reacting with IgA, IgG and IgM were applied, and accordingly the cells were differentiated and quantitated. Other biopsies were labelled in vitro with 3H-thymidine and autoradiographs were prepared. The percentage of DNA-synthesising cells in the progenitor cell region was estimated. The number of IgM-containing cells in the gastric fundic mucosa was markedly increased, while the rate of epithelial cell proliferation was increased in 2 cases and within normal range in the remaining 2 patients.
Fifty-eight outpatients with a clinical and radiological diagnosis of duodenal ulcer completed a double-blind randomized trial of the effect of cimetidine on ulcer symptoms. Patients normally treated in general practice were included in the trial. The patients in the treatment group received cimetidine 1 g daily and the controls received inactive tablets. The treatment period was four weeks. During the last nine days 18 (60%) of 30 cimetidine-treated patients were symptom-free against 5 (18%) of 28 controls (P less than 0.005). The antacid consumption, the number of days with pain and the number of hours with pain also differed significantly in the two groups. Apart from a transient rash in one patient no important clinical side-effects were noted. The serum creatinine rose slightly in the cimetidine-treated patients.
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Serum orosomucoid was compared with clinical activity, routine laboratory tests, intestinal protein loss, and albumin and IgG turnover in 22 cases of ulcerative colitis. Serum orosomucoid was well correlated with clinical activity, haemoglobin and leucocyte counts were not. A significant correlation was present between serum orosomucoid and intestinal protein loss (gastro-intestinal 59Fe-iron dextran clearance), serum albumin, fractional catabolic rates of albumin, and IgG and IgG synthesis rate. No correlation was found between serum orosomucoid and albumin synthesis rate or serum IgG. It is concluded that serum orosomucoid is a highly reliable indicator of disease activity in ulcerative colitis.
Fifty patients with renal glomerular diseases entered a double-blind cross-over study on the effect of cyclophosphamide; 38 had received neither corticosteroids nor cytostatic drugs before joining the study. Cyclophosphamide was given for 4 months in doses decreasing from 3 to 1.5 mg/kg b.wt. Cyclophosphamide caused a 46% decrease in the 24-hour excretion of urinary protein and a decrease in serum creatinine within the normal range. Albumin, transferrin and IgA in urine, as well as albumin clearance and the sieving coefficient of albumin, changed parallel to the total urinary protein. The initial values of proteinuria and serum complement were of prognostic significance for the effect of cyclophosphamide in serum creatinine. We were unable to demonstrate a prognostic significance for the variables: clinical diagnosis, renal histology, arterial BP, initial values of serum creatinine and IgG, IgA and IgM in serum and urine. ESR appeared to be the most reliable acute phase reactant. No differences were found between the changes in renal histology during cyclophosphamide or placebo.
Postprandial duodenal bile acids, intestinal protein loss, and albumin and IgG turnover were studied in 19 non-operated patients with Crohn's disease. A lesion of the terminal ileum was present in 18 of 19 patients, either alone or associated with regional colitis. Identical bile acid studies were made in a control group of 20 patients with chronic diarrhoea of undetermined origin. Duodenal bile acid concentration was decreased in 9 of 19 patients with Crohn's disease, and in 5 of 20 patients with unexplained diarrhoea. The glycine/taurine-ratio was increased in 8 of 17 patients with Crohn's disease, but in only one of the 20 control patients. Abnormal intestinal protein loss was present in 13 of 14 patients with Crohn's disease. The fractional catabolic rate of albumin and IgG was increased in all 17 cases of Crohn's disease studied, except the patient with no protein loss. A statistically significant and positive correlation was observed between glycine/taurine-ratio and fractional catabolic rate of both albumin and IgG. No patient with Crohn's disease harboured an abnormal bacterial flora in the proximal small intestine. It is concluded that, in the absence of abnormal bacterial flora in the proximal jejunum, the glycine/taurine-ratio is more valuable as an indicator of terminal ileopathy than postprandial duodenal bile acid concentration in nonoperated patients with terminal ileitis. Abnormal intestinal protein loss and increased catabolic rate of albumin and IgG are practically always present in active Crohn's disease and are strong evidence of an organic gastrointestinal lesion in patients with normal radiographic findings.
A biochemical characterization of the toxic action of human serum on murine Ehrlich ascites tumor cells was attempted. Some observations are consistent, other inconsistent, with the hypothesis of complement dependent antibodies reacting with ubiquitous antigens on these cells. Studies using various serum fractions, and with pure preparations of human serum proteins, have not given consistent results. Of particular interest is the puzzling observation that the toxic action of human serum fractions sometimes only appears some time after the fractionation.
Simultaneous studies with 131-I-albumin and 125-I-immunoglobulin G (IgG) were made in 48 cases of chronic inflammatory bowel disease. Twenty-one had ulcerative colitis and 27 had Crohn's disease which was confirmed at laparotomy in every case. Intestinal protein loss was measured simultaneously by means of 59-Fe-iron dextran in 44 patients. All patients had abnormal intestinal protein loss. A high correlation was shown between fecal 59-Fe clearance and fractional catabolic rate of albumin, confirming the validity of 59-Fe-iron dextran as a test substance to measure intestinal protein loss. Fecal radioiodide excretion of 131-I from 131-I-albumin (A) and 125-I from 125-I-IgG (G) was significantly different in ulcerative colitis and Crohn's disease. The ratio G/A was close to unity (smaller than 1.60) in ulcerative colitis and Crohn's disease with exclusive or predominant involvement of the colon, whereas it was high in Crohn's disease of the small intestine and highest in cases with jejunal involvement. Thus, the ratio may be valuable in topographic diagnosis of chronic inflammatory bowel disease. A high ratio was found in 2 patients with Crohn's disease of the small intestine and normal radiography of the small intestine, and a low ratio was present in 7 cases of ulcerative colitis with normal radiographic findings. In all 9 patients with normal radiography, fecal 59-Fe clearance was elevated as evidence of abnormal intestinal protein loss. No correlation was present between the size of protein loss and the pathoanatomic extent of the lesions on subsequent laparotomy in 25 patients with Crohn's disease. Fecal radioiodide excretion (131-I from 131-I-albumin and 125-I from 125-I-IgG) was positively correlated with diarrhea (daily stool mass) in both ulcerative colitis and Crohn's disease. Intestinal protein loss was not.
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