SUMMARY To assess the course of recovery ofgluten sensitive enteropathy in adults, histological and functional recovery was studied in 22 patients, aged 20-79 years. Biopsy specimens taken at the time of diagnosis were studied in 20; after adhering to a gluten free diet for nine to 19 (mean 14) months in 14; and after adhering to the same diet for 24-48 (mean 34) months in 10 patients. Histological recovery was assessed morphometrically in the proximal jejunum. Mucosal linings significantly improved over time, but did not completely return to normal with a gluten free diet: at diagnosis the surface:volume ratio was 22% of normal, increasing to 48% and 66% after nine to 19 and 24-48 months, respectively, ofa gluten free diet. Disaccharidase activities progressively increased. After 24-48 months maltase, sucrase, and isomaltase had returned to normal in the proximal jejunum; they were still significantly decreased in the distal duodenum. Duodenal and jejunal lactase activities were both below normal after 24 to 48 months.It is concluded that recovery of the intestinal mucosa of adults with gluten sensitive enteropathy during a gluten free diet continues beyond nine to 19 months and is still incomplete after two to four years. The recovery of disaccharidase activities extends from the distal to the proximal part of the small intestine, and is aligned to histological recovery.Gluten sensitive enteropathy or coeliac sprue is characterised by severe villous atrophy of the small intestinal mucosa; it responds favourably to the withdrawal of dietary gluten. Gross villous architecture and absorptive cells are severely damaged, and many enzymes, necessary for the digestive-absorptive process, are severely depleted. This is especially true for brush border enzymes like the disaccharidases maltase, sucrase, isomaltase, and lactase. To what degree the mucosa will recover during a gluten free diet is still a matter ofcontroversy: morphological changes occur and disaccharidases increase after gluten withdrawal. Most investigators have found that although some patients show complete histological and functional recovery during the diet, most still show some degree of histological and functional damage, even after adhering to the diet for several years.'Within days or weeks of starting a gluten free diet a clinical response can be detected. This is also true for some of the histological and functional abnormalities: soon after gluten withdrawal the height ofthe mucosal surface cells increases6 and partial return to normal of organelles is observed.7 The recovery of the villous Accepted for publication 17 March 1988 architecture is known to occur much more slowly, but so far no studies have emphasised the course of this slow recovery. Little is known with certainty about the rate and course of recovery of the disaccharidases and other brush border enzymes.There is good evidence to suggest that the most severe histological damage is found in the proximal small intestine in untreated coeliac disease28 and that during treatment, t...
Ethoxyacetylene I reacts with tertiary aliphatic amines and water to yield (a-ethoxyvinyl) -trialkylammonium hydroxides 11. Several crystalline salts of these bases were obtained. Catalytic hydrogenation of (a-ethoxyvinyl) -trimethylammonium iodide IIa yielded trimethylammonium iodide and diethyl ether.Reppel) found that by the reaction of acetylene with trimethylamine and water vinyl-trimethylammonium hydroxide was formed.W e observed that an analogous reaction can be performed with ethoxyacetylene. When this compound was shaken with a solution of trimethylamine in water, heat was evolved, and after some time a strongly alkaline solution resulted. W e could obtain several stable and crystalline salts from the base. The iodide, picrate, and perchlorate were not hygroscopic, whereas the chloride, bromide, and sulphate were deliquescent.The analysis of the salts indicated that the base had the com-
1. In zwei Versuchen wurden einmal 200 und einmal 500 Brockmannsche Körperchen von Pleuronectiden homogenisiert und fraktioniert zentrifugiert. In den verschiedenen Fraktionen wurden Stickstoff, Zink, Insulin und beim zweiten Versuch Succino-Dehydrogenase quantitativ untersucht. Dabei konnte Insulin nur im zweiten Versuch in allen Fraktionen mit ausreichender Genauigkeit bestimmt werden.2. Die Konzentrationen von Insulin und Succino-Dehydrogenase verhielten sich in den verschiedenen Fraktionen fast gleich. 63% des gesamten Insulins fanden sich im zweiten Versuch in einer Fraktion mit der weitaus höchsten Enzymaktivität. Es muß infolgedessen angenommen werden, daß der überwiegende Teil des Hormons in den Mitochondrien vorliegt oder an diese fixiert ist. Die Insulinkonzentration in der insulin-reichsten Fraktion, berechnet aus Stickstoffwerten, beträgt 4,7 Prozent. Sie ist aber unter Berücksichtigung der teilweisen Hormoninaktivierung und des Anteils an inselfremdem Gewebe wesentlich höher anzunehmen.3. Die Zinkkonzentrationen verhalten sich innerhalb der verschiedenen Zellfraktionen abweichend von denen des Insulins. Die in der reinsten Mitochondrienfraktion vorliegende Zinkkonzentration von 1,3%, bezogen auf das darin enthaltene Insulin, genügt, um dieses eventuell unter Mitwirkung von bestimmten Proteinen in eine schlecht lösliche Depotform zu überführen. Das in dieser Fraktion beobachtete Verhältnis entspricht 1,2 Atomen Zink auf 1 Insulinmolekül der Größe 6000. Die höchsten Zinkkonzentrationen fanden sich in den Mikrosomen enthaltenden Fraktionen. Hier lag ein Überschuß von Zink unter Berücksichtigung der maximalen Bindungsfähigkeit des darin enthaltenen Insulins vor.4. Die bei den beiden Versuchen beobachteten Unterschiede im Gesamtgehalt der Brockmannschen Körperchen an Insulin und Zink werden auf die unterschiedlichen Stoffwechselbedingungen der zu verschiedenen Jahreszeiten gefangenen Fische zurückgeführt.5. Die Befunde werden im Zusammenhang mit früher besprochenen Vorgängen bei der blutzucker-gesteuerten Insulinabgabe diskutiert. Die Lokalisierung des Insulins in der Mitochondrienfraktion gibt einen neuen Einblick in die spezifische Funktion der Inselzellen. Die Abgabe von Insulin infolge einer spezifischen Steigerung des Inselzellstoffwechsels - deren Ursache wiederum ein vermehrtes Glucoseangebot aus dem Blut ist - ist besser zu verstehen.
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