Biomedical subjects
Publications and source records attributed to N O Berg.
Selective angiography of the superior mesenteric artery (SMA) was performed in 14 patients with coeliac disease and in 20 sex- and age-matched patients without malabsorption. In coeliac disease there was a significant increase in the SMA diameter and a significantly shortened intestinal circulation time as compared to controls, reflecting an increased blood flow and/or a reduced blood volume in the diseased intestine.
Two cases of verified abdominal angina are presented. Multiple, atypical ulcerations in the postbulbar duodenum were diagnosed endoscopically in both cases. Atypical gastric ulcers were also present in one case. The suggestion is made that such ulceration may not be uncommon in intestinal ischaemia. Such findings at endoscopy should arouse the suspicion of abdominal angina, especially when preceding diagnostic procedures, including biopsies, have failed to demonstrate other clear-cut gastrointestinal disease.
In 1977 several patients were seen with soft-tissue sarcomas and previous exposure to phenoxy acids. This clinical observation resulted in a cases-referent (case-control) study being undertaken which showed that exposure to phenoxy acids or chlorophenols, which are chemically related, gave a roughly six-fold increase in the risk for this type of tumour. A further case-referent study of soft-tissue sarcomas has now been performed to confirm these earlier findings and also to obtain further information on the effects of different phenoxy acids. This new investigation gave an increase of the same magnitude in the risk for soft-tissue sarcomas after exposure to phenoxy acids or chlorophenols, but this risk related also to exposure to phenoxy acids free from impurities, such as polychlorinated dibenzodioxins and dibenzofurans.
Tissue destruction was produced by electrolysis after insertion of electrodes into the rabbit lung. The anode was the active electrode and the best electrode material was platinum. The lesions formed around the electrode were well demarcated and their size varied in relation to the charge applied. Complications were few and the lesions healed quickly. Tissue injury occurs as the result of chlorine liberation at the anode, the basis for which is chloride ion oxidation.
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Treatment of 13 urban Ethiopian children with mild ascariasis did not produce any evidence of improved intestinal morphology and absorption or nutritional status. Ascariasis treatment had no impact on anthropometric measures in an additional study group of 84 children. A review of the literature reveals that the nutritional consequences of ascariasis are uncertain.
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The incidence of coeliac disease in children in the city of Malmö, South Sweden, was 1 : 982 during 1966 to 1975. The diagnostic criteria were: flat intestinal mucosa on gluten-containing diet, free of symptoms, and improvement in mucosal morphology on gluten-free diet, and morphological and/or evident clinical relapse (three times) on gluten challenge. 6 (12%) of 49 children with initially a flat mucosa still had a normal mucosa on a gluten-containing diet for two years or longer, having so-called transient gluten intolerance.
Twelve infants suspected of cow's milk protein intolerance were challenged with cow's milk after at least one month of cow's milk-free diet. The challenge was clinically positive in seven. Small intestinal biopsies were taken with a multipurpose capsule both pre- and postchallenge (at 24 h) in eight, prechallenge in three, and postchallenge in one. Two or three biopsy specimens were taken at the same time in 15 of the 20 biopsy occasions. The morphology of the mucosa could vary from normal to slight damage at the same biopsy occasion. No difference was found in morphology judged by light microscopy between pre- and postchallenged biopsies. Light microscopy of small intestinal biopsies taken before and at 24 h after milk challenge seems of doubtful value as a routine diagnostic means in cow's milk protein intolerance.
A 10-year-old boy with severe familial lactose intolerance in infancy (vomiting, failure to thrive, lactosuria (5.25 g/l), sucrosuria (12 g/l), and aminoaciduria. Intestinal disaccharidases (including lactase and sucrase) normal at age 6 and 20 weeks. Oral lactose tolerance test at this age resulted in lactosuria (4.6 g/l); sucrose tolerance test, in sucrosuria (18.5 g/l). In contrast, intraduodenal lactose tolerance test gave only low lactose excretion in urine (0.28 g/l). He improved rapidly and had no lactosuria on intraduodenal feeding with citric acid milk. The lactosuria diminished as age increased, but was still higher at age 6 years than that of controls. He tolerated normal disaccharide containing food after 1.5 years of age. At 5.5 to 6 years, he had symptoms of lactose malabsorption, and an isolated lactase deficiency was proved. At 10 years, he still tolerates only limited amounts of milk. The defect in severe familial infantile lactose intolerance seems to be localized in the gastric mucosa. Acquired lactase deficiency can appear later in childhood in this syndrome.
Using immunohistochemical techniques we studied duodenal biopsies from 18 patients with coeliac disease and 24 patients with normal duodenal morphology. We had access to antisera against the following gastrointestinal peptides: cholecystokinin (CCK), gastric inhibitory peptide (GIP), gastrin-17, glucagon-enteroglucagon, motilin, neurotensin, pancreatic peptide (PP), secretin, somatostatin, substance P and vasoactive intestinal peptide (VIP). The somatostatin, GIP, CCK, and glucagon cells were increased in number in coeliac disease. The number of motilin cells was slightly increased, while secretin cells were reduced. Cells storing gastrin-17, substance P, or neurotensin were rare in all patients regardless of diagnosis. No PP immunoreactive cells were found and VIP was localised to neurons only. In biopsies from patients having a mucosa with ridging of villi the number of the various endocrine cell types did not differ from that in the control group.
Five patients in whom small-intestinal bypass was performed for severe obesity had a second operation 11-19 months later because of insufficient weight loss. Mucosal enzyme activities and histological appearance were investigated in biopsies from different parts of the functioning and excluded small intestine. These were compared with biopsies form corresponding sites obtained at the first operation. In addition to a prominent increase in length, circumference, and mucosal thickness in the functioning shunt, the disaccharidases and two intracellular beta-galactosidases increased in specific activity,, especially in the distal ileal part of the shunt. In the excluded segment of the small intestine different enzymes showed a different response: trehalase increased and alkaline phosphate decreased significantly. Other enzymes that were measured showed a varied pattern. The results indicated that not only the luminal content but also other, presumably hormonal, factors regulated the enzyme activities, and that different regulating factors influenced the various enzymes differently. The marked adaptive increase in mucosal surface of the functioning shunt could be one factor in explaining the weight stabilisation and, in some cases, weight increase after the initial rapid weight loss after the operation for small-intestinal bypass. The increase in specific enzyme activities would further increase the digestive capacity of the shunt.
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In an attempt to determine the frequency of liver injury in adult coeliac disease (A.C.D.) the case records of 74 consecutive patients were examined. In 13 cases histological sections of the liver were available and in 5 of these there were signs of reactive hepatitis. Histological signs of distinct hepatic injury with cirrhosis and/or chronic active hepatitis were found in 7 other patients. In 5 of these serum-IgA was normal, whereas 16 out of 20 control patients with liver cirrhosis not associated with A.C.D. had raised serum-IgA. Serum-aspartate-aminotransferase and serum-alanine-aminotransferase were determined in 53 patients; 29 had raised concentrations. In 19 patients serum-aminotransferases were repeatedly determined before and during the dietary regimen and there was a significant reduction in enzyme concentrations during treatment. The median concentration of serum-alkaline-phosphatase was also reduced during treatment but not significantly. The histological evidence of liver injury in 16% and the abnormal liver-function tests in 39% of the patients indicate that hepatic injury is common in A.C.D. Since liver-function tests or liver biopsy specimens were available for only about two-thirds of the patients, liver damage in A.C.D. may be more common than indicated by these results. The effect of a gluten-free diet on aminotransferase concentrations indicates that the liver injury may be reversible and suggests that in some A.C.D. patients progressive liver damage may be prevented by suitable treatment. Since A.C.D. is not always recognised, the diagnosis should be considered in patients with liver disease of unknown aetiology.