Biomedical subjects
Publications and source records attributed to H Malchow.
The remission period of patients with ulcerative colitis was extended by long term treatment with 2-3 g sulphasalazine daily. Proctocolectomy should be performed if no remission can be obtained on continued medical therapy. Moreover, in these cases the operation is suggested to avoid the unwanted side effects of the drugs and the increased risk of cancer.
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In morphologically different biopsy specimens from fundic, antral and duodenal mucosa of 134 persons, basal and histamine stimulated adenylate cyclase activity was studied: Basal and stimulated adenylate cyclase activities were log-normally distributed. Only in the fundic but not in the antral and duodenal mucosa adenylate cyclase was sensitive to histamine. The mean basal activity in the fundic gastric mucosa was 148, in response to 10(-5) mol/l histamine 292 pmol cAMP/mg protein/20 min. In human fundic biopsy specimens histologically identified as normal gastric mucosa, the stimulatory effect of histamine on adenylate cyclase decreased with the individual's age. In bioptic material from patients suffering from histologically proven chronic gastritis the histamine effect decreased with the degree of atrophy. A similar loss of histamine sensitivity was found in gastric mucosal biopsies of antrectomized individuals operated at least 5 years before by the Billroth I or II method, whereas in the mucosa of patients with gastric or duodenal ulcer no loss occurred. In contrast, the most pronounced stimulatory action of histamine was found in this latter group. Since a histamine sensitive adenylate cyclase is localized only in the glandular area of the fundic mucosa and the histamine sensitivity depends on a morphological intact structure of the mucosa, it can be concluded, that the effects of histamine on adenylate cyclase and on hydrochloric acid acid secretion have to be considered as a mechanism linked together.
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In the peripheral blood of patients with Crohn's disease (CD) the numerical distribution of the three major B lymphocyte subsets was determined by the identification of surface immunoglobulins using F(ab)(2)-antibody fragments. T cell counts were also obtained and the number of null cells was calculated. Twenty-eight patients with Crohn's disease including 14 patients with previously untreated and very short-standing disease (group CD 1) and 14 patients with long-standing and/or previous drug treated disease (group CD 2) were compared with 28 sex and age-matched normals as well as with 13 patients with acute inflammatory bowel disease (group D). Patients in group D and inactive patients of group CD 1 showed a significant absolute lymphocytosis due to an increase in both the three B cell subsets and the T cells, without changes in the null cells. While the proportion of T cells was normal, there was a significant relative B lymphocytosis and a relative null cytopenia in these patients. Active CD 1 patients, however, showed significantly lower absolute lymphocyte and T cell numbers. In group CD 2, there was a significant absolute lymphopenia caused by an equal decrease in B and T cells. Highly active CD 2 patients showed higher absolute null cell counts than inactive patients. With increasing disease duration there was a significant decrease of the relative and absolute B cell concentrations. The data obtained suggest that T and B cell populations in the peripheral blood are reduced in certain patients with Crohn's disease and that this occurs secondarily to activity of disease, chronicity of disease, and the effects of therapy.
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A patient with intestinal lymphoma developed a gram-negative septicemia 48 hours following a peroral biopsy of the small intestine. The bacteriological examination of the instrument proved the same bacteria (Pseudomonas aeruginosa) which was the cause of septicemia. On the basis of our observation and of other reports it seems reasonable besides gassterilization or effective disinfection of the instruments to carry out cultural examinations of the instrument before and following endoscopic and bioptic investigations of patients with impaired resistance; it would then be possible to start an appropriate antibiotic treatment in case of a septic complication.
12% of the rectal biopsies (19% of the patients) showed epitheloid cell granulomas in clinically definite Crohn's disease. In colonic biopsies such granulomata were visible in 14% (22% of the patients). Granulomata were scarcely seen in normal or slightly inflamed mucosa. They were mostly found together with crypt abscesses and/or erosions and ulcers. The combination of local inflammation around crypts and crypt abscesses is rather characteristic for Crohn's disease. The inflammatory colonic alterations, visible in crohon's disease, may have the following pathogenetic sequence: Local colitis-crypt abscess--destruction of the crypt with proliferation of enlarged histiocytes--transformation histiocytes to epitheloid cells and Langhans cells--epitheloid cell granuloma.
A 19 year old patient developed signs of a "prestomal ileitis" 5 1/2 years following proctocolectomy for ulcerative colitis. A reoperation was necessary because of "toxic megaileum"; these signs were explained by recurrence of ulcerative colitis involving the terminal ileum. A first report from 1976 must be revised because of further observation of the patient: 1 1/2 year following this complication Crohn's disease in this patient could be proven by endoscopic and bioptic examination. This diagnosis was not possible at the time of first report: findings by x-ray, endoscopy and microscopy were lacking typical signs of Crohn's disease.
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The effect of 300 mg cimetidine q.i.d. on ulcer healing was studied in a controlled double-blind clinical trial of 71 in-patients with duodenal ulcer. Healing occurred in 48.5% of patients in the cimetidine group after two weeks, and in 20.6% in the placebo group (P less than 0.05). The healing rate was 88% in the cimetidine group at four weeks, 79.4% in the placebo group. Only during the first day was ulcer pain significantly reduced in the cimetidine-treated patients. Neither basal nor pentagastrin-stimulated acid and pepsin secretions were affected by 17-day administration of cimetidine. The drug had to be withdrawn in two patients because of elevated serum-creatinine levels. There was no other untoward effect.
In a controlled double-blind clinical trial of 39 in-patients with gastric ulcer the effect of cimetidine on ulcer healing, ulcer pain and pentagastrin-stimulated acid and pepsin secretion was measured. A faster healing rate in the cimetidine group was statistically not significant. Cimetidine had no effect on ulcer pain and pentagastrin-stimulated acid and pepsin secretion. There were no serious untoward reactions.
Proportions and absolute numbers of circulating leukocyte populations and lymphocyte subpopulations (T- and B-cells) were determined in 33 patients with Crohn's disease (group CD), and were compared with those of age- and sex-matched healthy subjects. Group CD comprised 15 patients with newly diagnosed, short-standing, and untreated CD (group CD 1) and 18 patients with long-standing, previously drug treated CD (group CD 2). All CD groups showed a significant absoulte leukocytosis, based on a significant absolute and relative increase of the neutrophils, and, as far as group CD and CD 1 were concerned, also of the absolute number of monocytes. In group CD 1, absolute lymphocyte and relative as well as absolute T-cell numbers were close to normal. In contrast, in group CD 2 absolute as well as relative numbers of lymphocytes and absolute numbers of T-cells were highly significantly reduced, whereas the reduction of the relative T-cell concentration barely reached significance. The proportion of B-cells was significantly above normal in all patient groups, the absolute number in group CD only. Also group CD 1 showed considerably, though statistically insignificantly, higher than normal absolute B-cell numbers. In group CD 1 , there was an inverse correlation between absolute T-cell numbers and disease activity, and between absolute lymphocyte numbers and duration of disease. These data indicate that there is no gross numerical reduction of the carriers of the cell-mediated immunity as a primary predisposing factor for CD, but that a reduction of these cells occurs in the circulation after the disease has started.
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