Search PubMed⌕ Search

Biomedical subjects

M De Vos

Publications and source records attributed to M De Vos.

139 records · Page 8Linked to original sources
PubMedDate not supplied

Idiopathic inflammatory bowel diseases: immunological hypothesis.

Circumstantial evidence indicates that immunological mechanisms are important in the pathogenesis of inflammatory bowel diseases. In Crohn's disease lesions the naive T cells are reduced and memory T cells are increased in number. Colonocytes of normal mucosa do not express MHC class II molecules but aberrant HLA-DR expression is induced in inflammatory conditions. Also in ileal epithelial cells there is increased MHC class II molecules expression suggesting augmented antigen presentation. Once the initiating event (environmental, dietary, infectious or enterobacterial products) has activated inflammatory cells, an auto-amplifying inflammatory immune cascade is induced by numerous agents such as cytokines, transforming growth factors, leukotrienes, prostaglandins and other mediators. Tissue injury may be caused by oxygen free radicals generated by neutrophils and macrophages. The inflammatory process can be perpetuated by a persistent antigenic stimulus or alternatively, by abnormal regulation of immune and inflammatory responses. This can mean exaggerated activation of inflammatory responses to "normal" stimuli or defective feedback mechanisms of down-regulation. The early lesions of inflammatory bowel disease are patchy necrosis of the surface epithelium, focal accumulations of leukocytes adjacent to crypts and an increased number of intraepithelial lymphocytes. In Crohn's disease the earliest lesions are aphthoid ulcers overlying lymphoid follicles in the terminal ileum. In patients with spondylarthropathy and asymptomatic intestinal inflammation we demonstrated lesions in the top of the follicle associated epithelium. The changes consist of increase in number of membranous (M) epithelial cells, ruptures, fissures and perforations of M cells. Aphthoid ulcers that may occur in the entire gastrointestinal tract are typically found at the M cell level.(ABSTRACT TRUNCATED AT 250 WORDS)

Colitis, Ulcerative↗
PubMedDate not supplied

M cells are damaged and increased in number in inflamed human ileal mucosa.

Ileocolonoscopy and biopsies of patients with spondylarthropathy revealed gut inflammation in 62% of the cases. In order to better understand the pathogenetic mechanisms of spondylarthropathy related gut inflammation the follicle associated epithelium was examined. Biopsies from 9 controls and 18 patients with spondylarthropathy were studied by electron microscopy. Membranous (M) cells were investigated in normal and inflamed ileum. In normal mucosa M cells were scarce whereas in inflamed mucosa their number was increased (up to 24% of follicle associated epithelial cells). They showed a thin rim of cytoplasm covering groups of lymphocytes. In chronic ileitis necrotic M cells, ruptures of M cell cytoplasm and lymphocytes entering the gut lumen were observed. The bursts of M cells at the top of the lymphoid follicles lead to interruption of the gut epithelial lining and give luminal content access to the lymphoid tissue. This pathogenetic mechanism may cause aphthoid ulcers.

Crohn Disease↗
PubMedDate not supplied

Short- and long-term efficacy of cyclosporin administration in patients with acute severe ulcerative colitis. Belgian IBD Group.

Cyclosporin (CsA) has been proposed in the management of patients with acute ulcerative colitis (UC) in whom standard therapy failed and who were candidates for colectomy. Seven academic hospitals contributed to this retrospective study that included 29 patients (median age: 33 y. (15-74 y.); 12 females and 17 males). The median duration of the disease was 4 y. (0.3 to 33 y.). Before initiating CsA, patients were unresponsive to treatment including i.v. corticosteroids (n = 29), 5-ASA or salazopyrine (n = 19), azathioprine (n = 3), antibiotics (n = 14). The i.v. mean dose was 4 mg/kg/day and was adapted to blood level. Concomitant treatment included corticosteroids (n = 27). The median duration of i.v. CsA administration was 10 days (4 to 41 days). At the end of CsA administration, a global improvement was described in 20 patients while a surgery had to be performed immediately in 8 patients because of exacerbation of symptoms (n = 7) or perforation (n = 1). One other patient (74 y.) died because of Pneumocystis carinii infection. For the responders, maintenance therapy included: tapering dose of steroids (n = 12), azathioprine (n = 12), 5-ASA or salazopyrine (n = 10), methotrexate (n = 1) or oral CsA (n = II). The median duration of follow-up was 12 months (4 to 48 months). Among the 20 responders, 7 were subsequently referred for colectomy either electively (n = 3) or because of recurrence of the disease (n = 4). Among the 12 patients treated by azathioprine as a maintenance therapy, only 3 had to be referred for surgery (25%). Among the 8 patients who did not receive azathioprine, 4 were subsequently referred for a colectomy (50%) (NS). In patients with acute refractory UC who received CsA, the short-term efficacy (avoidance of immediate colectomy) was obtained in 20 out of 29 patients (69%). However, after a median follow-up of 12 months, only 13 patients were colectomy free (45%).

Acute Disease↗
PubMedDate not supplied

Fundic gland polyps: three other case reports suggesting a possible association with acid suppressing therapy.

We describe three patients who developed fundic gland polyps after starting a treatment with acid suppressive agents. All three patients were treated for a long time with H2-blockers or proton pump inhibiting agents for reflux oesophagitis. In one patient the fundic gland polyps disappeared after discontinuation of the acid suppressing therapy. A possible causal role of these agents is suggested. A review of the literature about fundic gland polyps and their possible association with acid suppressive therapy and a short review about proton pump inhibiting agents and the appearance of gastric polyps in general is given.

Aged↗
PubMedDate not supplied

Altered expression of alpha E beta 7 integrin on intra-epithelial and lamina propria lymphocytes in patients with Crohn's disease.

OBJECTIVE: To compare the expression of adhesion molecules on intestinal intra-epithelial (IEL) and lamina propria T cells (LPL) from ileum and colon, in patients with Crohn's disease (CD) versus healthy controls, with special reference for the alpha E beta 7 integrin. METHODS: IEL and LPL were obtained from 18 CD patients and 20 controls by enzymatic extraction, and subsequently characterized by flow cytometry for CD3, CD4, CD8, CD25, LFA-1 alpha (CD11a), CD44, alpha 4 and alpha E beta 7 integrin. RESULTS: In LPL of controls, a decreased CD4/CD8 ratio was noted in ileum compared to colon. This regional difference was accompanied by a higher expression of alpha E beta 7 integrin in ileum versus colon. In LPL from left hemicolon of CD patients, a decreased CD4/CD8 ratio was noted versus controls. alpha E beta 7 expression on T cells of LPL did not discriminate CD from controls. However, an overexpression of this beta 7 integrin member was observed on CD25+ T cell subsets from lamina propria of left hemicolon, in CD versus controls. Moreover, in IEL, profound alterations in alpha E beta 7 integrin were observed in CD, compared to controls. A decreased expression of alpha E beta 7 was noted in IEL of ileum of CD patients. This was also apparent in non-inflamed mucosa. CONCLUSION: The observed changes of alpha E beta 7 integrin expression in CD patients versus controls are of pathogenic relevance, especially the decreased expression of alpha E beta 7 in IEL of non-inflamed CD mucosa. This may be one of the earliest events in the pathogenesis of this disease.

Adolescent↗
PubMedDate not supplied

Prolactin and colorectal cancer: is there a connection?

UNLABELLED: The purpose of this study was to confirm the reported incidence of hyperprolactinemia in colorectal cancer and to find further evidence for an ectopic prolactin production by the tumor. MATERIAL AND METHOD: Thirty two consecutive patients with an adenocarcinoma of the colon (n = 17) or the rectum (n = 15) were included. Preoperative serum prolactin concentrations were determined and correlated with CEA concentrations and tumor stages. To exclude an ectopic production by the colon cancer, prolactin concentrations were determined during the operation, in the peripheral blood and in the efferent venous drainage area of the tumor. After resection, immunohistochemical staining for prolactin was made in all resected tumors. RESULTS: In all except two patients with a rectal cancer, preoperative plasma prolactin concentrations were normal. Peroperative serum concentrations of prolactin were high in all patients. No significant gradient was found between the peripheral venous concentration and the local venous concentration in the drainage area of the tumor. Immunohistochemical staining for prolactin was positive in only one rectal cancer. Finally, no correlation was found between plasma prolactin concentrations and tumor stages or CEA concentrations. CONCLUSION: Our results do not support the hypothesis of an ectopic prolactin production by colon adenocarcinoma. Only in a subgroup of rectal cancers, an ectopic prolactin production remains probable. At present, prolactin cannot be recommended as a tumor marker in colorectal cancer.

Adenocarcinoma↗