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Biomedical subjects

K Geboes

Publications and source records attributed to K Geboes.

321 records · Page 18Linked to original sources
PubMedDate not supplied

The histopathology of reflux esophagitis.

The histological features of the esophageal mucosa in patients with gastroesophageal reflux are basal zone hyperplasia of the squamous epithelium, elongation of the papillae towards the epithelial surface, an increase in the transverse diameter of the papillae and the blood vessels, and an ingrowth of capillaries into the epithelial layers. The presence of polymorphonuclear leucocytes in the epithelium and the lamina propria clearly represents esophagitis. In the advanced stages, erosions and ulcerations can be seen. Intra-epithelial lymphocytes are present in the normal esophageal mucosa. They are mainly T-cytotoxic lymphocytes.

Animals↗
PubMedDate not supplied

From inflammation to lesion.

The gastrointestinal tract is continuously in contact with a multitude of antigens and therefore contains a well developed defense mechanism composed of nonspecific and specific elements. The gastrointestinal mucosa immune system (GALT) is the specific defense. Its cellular components firstly appear during the 11th week of pregnancy. Stimulation of the lymphoid tissue starts early after birth and depends upon bacterial colonization. During life the immune system is continuously bombarded by a multitude of antigens. The normal presence of the GALT is the expression of a controlled physiologic inflammation. Inflammation is a complex series of homeostatic reactions involving cellular and molecular mechanisms orchestrated in such a manner as to protect the organism, only yielding pathologic changes when there is overwhelming acute response or when chronicity leads to loss of function. Several phases can be distinguished in the inflammatory reaction. The initial vascular reaction, controlled by vasoactive mediators is followed by a cellular reaction with recruitment of inflammatory cells (immune competent leucocytes and neutrophils). This process requires cellular adhesion and migration and depends on the expression of "adhesion molecules". Leucocytes already present in the tissue (lymphocytes monocyte/macrophage cells, eosinophils, and mast cells) and newly recruited cells (neutrophils, eosinophils, monocyte/macrophage cells and lymphocytes) will release a variety of inflammatory mediators with both positive and negative (tissue destructive) effects. Epithelial cells, fibroblasts and smooth muscle cells are actively involved in the reaction. Normally inflammation ends by healing. In chronic inflammatory bowel diseases healing does not occur or is incomplete. Early lesions described thus far for the small capillary lesions described in Crohn's disease). Yet similar lesions not leading to chronicity have been described in experimental and human clinical conditions. The major question therefore in Crohn's disease and ulcerative colitis is why the early lesions do not heal but lead to chronic inflammation. Intrinsic defects (alterations of epithelial cells, increased permeability or genetic predisposition) are considered as possible causes. Persistent inflammation may also be due to the nature of an extrinsic agent as in tuberculosis. A specific agent has as yet not been demonstrated in chronic idiopathic inflammatory bowel disease. An inappropriate inflammatory reaction to components normally present in the lumen of the gastrointestinal tract must also be considered. Heat shock proteins (HSP) produced by bacterial agents may for instance induce an autoimmune reaction as there is molecular analogy between HSP from bacterial origin and human HSP.

Colitis, Ulcerative↗
PubMedDate not supplied

Vascular alterations of the colonic mucosa in schistosomiasis and portal colopathy.

BACKGROUND/AIM: Portal colopathy, the occurrence of vascular-ectasia like lesions has been observed in patients with portal hypertension of variable etiology. Schistosomiasis is a major cause of liver damage and portal hypertension. In colonic schistosomiasis, vascular alterations are commonly observed. It is therefore possible that schistosomiasis may induce portal colopathy in addition to inflammatory changes directly induced by oviposition. MATERIALS AND METHODS: In order to examine this possibility, we reviewed the endoscopic data obtained in 100 consecutive patients with established bilharziosis. In addition, endoscopic biopsies from all patients were examined for the presence of inflammation, parasite eggs, granulomas and mucosal vascular congestion. The latter was assessed using immunohistochemical staining for Ulex Europaeus. RESULTS: Endoscopic abnormalities were observed in 66/100 patients. The main lesions were abnormalities in vascularisation of the mucosa, especially hyperemia, defined as the presence of numerous, prominent and irregular vessels (62%) and telangiectasia (4%). The mucosal biopsies revealed prominent vascularisation in 60% of the cases. Positivity for ulex staining was significantly correlated with the finding of hyperemia during endoscopy and with the presence of ova. No good correlation was found with the clinical presentation. The lesions were not well correlated with the presence of an increased cellular infiltrate in mucosal biopsies. CONCLUSIONS: This observation suggests that portal colopathy may explain some of the endoscopic lesions observed in the colon of patients with Schistosomiasis.

Adolescent↗
PubMedDate not supplied

Diagnostic accuracy of ultrasonography and surgical decision-making in patients referred for suspicion of appendicitis.

Two groups of patients referred for suspicion of acute appendicitis were compared to evaluate the accuracy of preoperative ultrasonography (US) and surgical decision-making. In one retrospective study, US was performed by trainees using a 3.5 MHz probe (219 patients). In the second prospective study, US was performed by a resident radiologist using a 5 MHz probe (144 patients). US accuracy rose from 65% to 90%, especially due to an improved negative predictive value (from 52% to 92%). The positive predictive value of US was 89%. The sonographically adjusted clinical decision to operate was correct in 85%. Thus, all patients with positive US should be operated. In contrast, clinical judgment must prevail in case of negative US findings in order to prevent surgical delay in about 11%. The negative laparotomy rate decreased by 5% only. This is probably due to the limited influence of negative US findings on surgical decision. US is to be recommended in all patients suspected for acute appendicitis when performed with an appropriate probe by an experienced ultrasonographist. However, it may not, on it self, reduce the rate of unnecessary operative procedures.

Adolescent↗
PubMedDate not supplied

The 1998 national Belgian consensus meeting on HP-related diseases: an extensive summary. The HP Belgian contact group organized in CHU Brugmann, Brussels.

"HP testing must be regarded as ONE of the important elements of the proper diagnostic work-up of a DISEASE, managed in close cooperation between GP's and specialists": that's the key message of the national consensus meeting held in CHU Brugmann on February 6th and 7th 1998. HP testing (usually by 2 direct methods: RUT-histology) and eradication treatment (ER), in infected patients, are strongly recommended in: 1. Past or current GDU (absolute indication), regardless of activity, complication(s), NSAID intake; 2. Low-grade MALT Lymphomas (Stage IE1) unequivocally diagnosed, managed and followed-up in specialised centers; 3. Post endoscopic resection of EGC. ER is advisable in HP carriers with a family history of gastric cancer. Chronic atrophic-, lymphocytic-, giant folds gastritis and hyperplastic polyps are acceptable indications for ER as well as scheduled long-term NSAID treatment in individuals with known HP status. Systematic ER in HP+ patients with fully investigated NUD is not indicated but could be considered in individual patients. Extra alimentary disorders and auto immune gastritis are no indication and there was no consensus for a "test and treat" policy in patients under 45 yrs old without alarm symptoms. Systematic screening of asymptomatic individuals is not recommended. A correct monitoring of eradication after treatment is recommended, mainly by UBT. In severe or refractory PUD, symptom recurrence and follow-up of EGC and Maltomas, endoscopic follow-up with HP testing is mandatory. The recommended first line treatment course (except known allergy or intolerance) is PPI full dose bid, Clarithromycin 500 mg bid Amoxycillin 1000 mg bid (7 days minimal 10 days maximal). RBC-based schemes must be locally validated and quadruple therapy is proposed when retreatment is needed. Culture, optional after the first treatment failure, is strongly recommended after a second failure. Overall, ER therapies are safe and neither the decreased efficacy of acid-lowering drugs, nor the possible increased risk of peptic oesophagitis are considered as contra-indications to eradicate. ER is cost-effective and cost-beneficial in PUD and adjusted number of pills delivered would cut costs. No clear economic data are currently available for a potential benefit of ER in GC prevention or NUD management. A national monitoring of HP resistance (Macrolides and Imidazoles) must be organized by specialised centers.

Gastrointestinal Diseases↗