Das Megacolon
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Zusammenfassung
Es wurden histologisch und enzymhistochemisch verschiedene Formen des Megacolon untersucht:
Bei Morbus Hirschsprung zeigt der spastische Teil des Dickdarms neben einer Aplasie der intramuralen Ganglien eine Hyperplasie des extramuralen Parasympathicus. Dieser hyperplastische Parasympathicus ist durch eine vermehrte Acetylcholinausschüttung mit reaktiver Steigerung der Acetylcholinesterase-Aktivität charakterisiert. Die erhöhte Enzymaktivität der Acetylcholinesterase gestattet eine einfache und sichere Diagnosestellung bereits an oberflächlichen Schleimhautbiopsien des Colon. Das aganglionäre Colonsegment zeigt eine spastische Kontraktion der Ringmuskulatur infolge Fehlens einer Modulation der Exzitation des extramuralen Parasympathicus durch Ganglienzellen des Plexus myentericus und submucosus.
Dem sekundären Megacolon liegt eine symptomatische Dilatation des Colon infolge eines distal stenosierenden Prozesses zugrunde. Es kommt hierbei zu einer Arbeitshypertrophie der Darmwandmuskulatur sowie einer mäßig starken Aktivierung der Enzymaktivitäten in den Ganglienzellen der Darmwand.
Für das erworbene Megacolon ist eine Läsion in der neuralen Darminnervation typisch. So kann ein hypoxämischer Schaden des Colon nach chirurgischen Eingriffen, unter dem Bilde einer totalen oder subtotalen Atrophie der neuralen Strukturen, zu einem Megacolon acquisitum führen. Andere Ursachen sind die chronische Colitis ulcerosa, die Chagaskrankheit etc.
Pseudo-Hirschsprung und Hypoganglionose werden als gleichartige Krankheiten angesehen. Die kongenitale Hypoganglionose ist ein typisches Beispiel für das funktionelle Megacolon. Es ist durch eine Hypoplasie des das distale Colon versorgende Nervensystem ausgezeichnet.
The diagnosis and pathophysiology of megacolon
Summary
Different types of megacolon were investigated by histological and enzyme histochemical methods.
The spastic part of the bowel in Hirschsprung's disease shows, in addition to aplasia of the intramural ganglion cells, hyperplasia of the extramural parasympathicus. The latter is characterized by an extreme increase in acetylcholinesterase activity. This increased enzyme activity permits easy and confident diagnosis from superficial biopsies of the colonic mucosa. The spasticity of the distal, aganglionic colon segment can be explained by the permanent parasympathetic excitation of the circular muscle in the absence of modulation of the extramural parasympathetic stimulation by the intramural ganglion cells (myenteric and submucosal).
Secondary megacolon is a symptomatic dilatation of the colon by a stenosing process of the lower bowel. There is compensatory hypertrophy of the muscle of the intestinal wall and moderate enzyme activity in the ganglion cells of the parasympathetic plexus.
Lesions of the neural structures of the intestinal wall are typical of acquired megacolon. Hypoxemic damage of the colon after surgical intervention in the lower bowel, a infrequent cause of acquired megacolon, is characterized by total or subtotal atrophy of the ganglion cell plexus. Signs of degeneration of the ganglion cells and smooth muscles may commonly be observed in Chaga's disease and in chronic ulcerative colitis etc., when there is the clinical picture of megacolon.
Pseudo-Hirschsprung's disease and hypoganglionosis are regarded as identical conditions. Congenital hypoganglionosis is a typical example of functional megacolon with hypoplasia of the neural structures of the bowel wall.
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