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1.
Vojnosanit Pregl ; 67(12): 1021-4, 2010 Dec.
Article in Serbian | MEDLINE | ID: mdl-21425560

ABSTRACT

BACKGROUND: Meckel's diverticulum (MD) is a congenital anomaly of the small intestine. It results from incomplete obliteration and resorption of the proximal omphaloenteric duct connecting yolk sac with primitive gut in the fetal period. CASE REPORT: A case of 20-year old female with ectopic pancreatic rests in a MD was reported. She was hospitalized with clinical signs of acute appendicitis. During surgery an inflamated Meckel's diverticulum was found and a clinoid resection of the diverticulum was performed. Histologic examination revealed pancreatic tissue in the removed diverticulum. Endocrine cells (EC) were detected with Masson staining and aberrant pancreatic tissue with immunocytochemical LSAB2 method using pan cytokeratin as epithelial marker. CONCLUSION: Most of MD are asymptomatic and accessory finding during laparothomias for different causes, but complications of undiagnozed MD can be serious (diverticulitis, perforation with peritonitis or intestinal obstruction caused by invagination). In unclear cases, additional cytochemical and immunocytochemical diagnostics could be done.


Subject(s)
Choristoma/pathology , Meckel Diverticulum/diagnosis , Pancreas , Female , Histocytochemistry , Humans , Immunohistochemistry , Keratins/metabolism , Meckel Diverticulum/complications , Meckel Diverticulum/metabolism , Meckel Diverticulum/pathology , Young Adult
5.
Gut ; 51(5): 628-33, 2002 Nov.
Article in English | MEDLINE | ID: mdl-12377798

ABSTRACT

BACKGROUND: Sonic hedgehog (Shh) is an important endodermal morphogenetic signal during the development of the vertebrate gut. It controls gastrointestinal patterning in general, and gastric gland formation in particular. We have previously shown that Shh regulates gastric gland proliferation in the adult but detailed analysis of its expression along the adult gastrointestinal tract has never been undertaken. We therefore studied Shh expression along the normal human and rodent adult gastrointestinal tract as well as in intestinal metaplasia of the stomach, gastric and intestinal metaplasia of the oesophagus, and gastric heterotopia in Meckel's diverticulum. METHODS: The studies were performed with in situ hybridisation and by immunohistochemistry using an antibody that recognises the Shh precursor form. RESULTS: We found that in the normal gastrointestinal tract, high levels of Shh were expressed in the fundic glands of the stomach. Shh expression was also found in fundic gland metaplasia and heterotopia. However, Shh expression was lost in intestinal metaplasia of the stomach. CONCLUSION: We found a strong correlation between Shh expression and fundic gland differentiation. Our current study therefore provides evidence that in addition to its role in gastric epithelial development, Shh plays a unique role in gastric epithelial differentiation in adults.


Subject(s)
Gastric Fundus/chemistry , Meckel Diverticulum/metabolism , RNA, Messenger/analysis , Trans-Activators/analysis , Adult , Cell Differentiation , Esophagus/metabolism , Esophagus/pathology , Gastric Fundus/cytology , Hedgehog Proteins , Humans , Immunohistochemistry/methods , In Situ Hybridization/methods , Intestinal Mucosa/metabolism , Intestines/pathology , Metaplasia , Trans-Activators/genetics
6.
Development ; 127(22): 4915-23, 2000 Nov.
Article in English | MEDLINE | ID: mdl-11044405

ABSTRACT

The midgut and hindgut endoderm of the mouse embryo give rise to the intestinal epithelium, yet it is not known how the intestinal program is chosen in contrast to other endoderm-derived cell types. Previous tissue explant studies with embryos at 8.5 to 11.5 days gestation (d) showed that when the gut mesoderm is removed from the prospective intestinal endoderm, the endoderm activates the expression of liver-specific genes such as serum albumin, demonstrating the endoderm's pluripotence. This reversible repression of liver genes does not affect the expression of the endodermal transcription factors HNF3 and GATA4, nor these factors' ability to engage target sites in chromatin. We have now found that at 13.5 d, the mesoderm gains a second inhibitory activity, resulting in the irreversible loss of expression of HNF3 (Foxa2) and GATA factors in the endoderm and the absence of factors binding to their target sites in chromatin. The second inhibitory activity causes the endoderm to lose the potential to activate a liver gene, and this restriction precedes the normal cytodifferentiation of the intestinal epithelium. In summary, two inhibitory interactions with mesoderm successively restrict the developmental potential of the gut endoderm, leading to intestinal differentiation. We also observed rare gut bud structures in midgestation embryos that appear to represent murine examples of Meckel's Diverticulum, a congenital abnormality in human development. The absence of restrictive mesodermal interactions could explain how Meckel's diverticula express diverse non-intestinal, endoderm-derived cell types.


Subject(s)
Digestive System/embryology , Endoderm/cytology , Meckel Diverticulum/embryology , Mesoderm/cytology , Albumins/genetics , Animals , DNA-Binding Proteins/genetics , DNA-Binding Proteins/metabolism , Digestive System/metabolism , Endoderm/metabolism , Enhancer Elements, Genetic , GATA4 Transcription Factor , Gene Expression Regulation, Developmental , Gestational Age , Hepatocyte Nuclear Factor 3-alpha , Liver/embryology , Liver/metabolism , Meckel Diverticulum/metabolism , Mesoderm/metabolism , Mice , Mice, Inbred C3H , Nuclear Proteins/genetics , Nuclear Proteins/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolism , Transcription Factors/genetics , Transcription Factors/metabolism
8.
Eur J Nucl Med ; 9(7): 316-9, 1984.
Article in English | MEDLINE | ID: mdl-6088239

ABSTRACT

The aim of this study was to investigate the effects of prior administration of cimetidine in radionuclide imaging of Meckel's diverticulum. In three groups of seven rats with artificial Meckel's diverticulum, containing ectopic gastric mucosa, the effects of pentagastrin + glucagon plus 99mTc-pertechnetate, as well as cimetidine premedication plus 99mTc-pertechnetate, and 99mTc-pertechnetate alone were compared to attain improved radionuclide imaging of Meckel's diverticulum. This experimental model suggests that the use of cimetidine seemed to have some advantages: (a) nontarget (intestinal) radioactivity was diminished by cimetidine, (b) the target to nontarget (Meckel's diverticulum to intestinal activity) ratio increased with cimetidine pretreatment. This resulted in an enhanced accumulation of pertechnetate in the ectopic gastric mucosa, and reduced excretion of the radionuclide into the lumen. Consequently, better scintiphotograms and a low rate of false results added to the validity of this method.


Subject(s)
Cimetidine/administration & dosage , Glucagon/administration & dosage , Meckel Diverticulum/diagnostic imaging , Pentagastrin/administration & dosage , Animals , Gastric Mucosa/metabolism , Humans , Male , Meckel Diverticulum/metabolism , Methods , Radionuclide Imaging , Rats , Rats, Inbred Strains , Sodium Pertechnetate Tc 99m , Technetium/metabolism
9.
Gastroenterology ; 75(4): 655-60, 1978 Oct.
Article in English | MEDLINE | ID: mdl-361486

ABSTRACT

Immunocytochemical techniques using antigastrin antibody were employed to localize G cells in ectopic gastric mucosa of metaplastic and congenital origins and to compare their distribution with that in normal gastric mucosa. Five examples of Barrett's esophagus, 8 Meckel's diverticula, and 2 small bowel duplications were studied. Although G cells were absent in the gastric mucosa from all cases of Barett's esophagus, four Meckel's diverticula and one small bowel duplication contained G cells. In all instances of congenitally derived ectopic gastric mucosa where G cells were demonstrable, the gastric mucosa showed areas of antropyloric differentiation, whereas in the remaining cases the ectopic gastric mucosa was exclusively of the body-fundic type. It is concluded that the presence of G cells within ectopic gastric mucosa of Meckel's diverticula and small bowel duplications in foci of antropyloric differentiation reflects their developmental origin, whereas the absence of G cells in Barrett's esophagus is in keeping with its metaplastic derivation.


Subject(s)
Choristoma/pathology , Esophageal Diseases/pathology , Gastric Mucosa/pathology , Gastrins/biosynthesis , Intestinal Neoplasms/pathology , Meckel Diverticulum/pathology , Choristoma/metabolism , Choristoma/physiopathology , Esophageal Diseases/metabolism , Esophageal Diseases/physiopathology , Esophagus/metabolism , Esophagus/pathology , Esophagus/physiopathology , Gastric Mucosa/metabolism , Gastrins/metabolism , Histological Techniques , Humans , Intestinal Neoplasms/metabolism , Intestinal Neoplasms/physiopathology , Intestine, Small/metabolism , Intestine, Small/pathology , Intestine, Small/physiopathology , Meckel Diverticulum/metabolism , Meckel Diverticulum/physiopathology , Metaplasia
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