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E Veys

Publications and source records attributed to E Veys.

43 records · Page 3Linked to original sources
PubMedDate not supplied

Ileal mucosal mononuclear cells in patients with seronegative spondylarthropathy.

In order to study local immunoregulatory mechanisms in patients with seronegative spondylarthropathy and histological evidence of asymptomatic intestinal inflammation, we determined mononuclear cells in distal ileal mucosa with an indirect immunoperoxidase technique using a panel of monoclonal antibodies. The number of intraepithelial lymphocytes in inflamed mucosa was not significantly increased. They carried mainly the suppressor-cytotoxic CD8 marker (greater than 80%), less frequently the helper T cell marker CD4 and lacked the pan T epitope CD3 in greater than 50%. There were no intraepithelial B cells or natural killer cells. The lamina propria lymphocytes were T and B cells, the former being more numerous. Helper T cells were more frequent than suppressor-cytotoxic T cells. There were no alterations in the proportion of T cells in inflamed mucosa. Natural killer cells were scarce. They occurred in small numbers in a minority of cases with gut inflammation and spondylarthropathy and rarely in inflammatory bowel disease. It is concluded that although there is an increase of lamina propria monocytes, there is no immunoregulatory imbalance in the ileal mucosa of patients with seronegative spondylarthropathy.

Adolescent↗
PubMedDate not supplied

[Osteopoikilosis].

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Adolescent↗
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

Double-blind comparison of etodolac and piroxicam in the treatment of rheumatoid arthritis.

Etodolac is the first of a new class of nonsteroidal anti-inflammatory drugs--the pyranocarboxylic acids--and has potent analgesic and anti-inflammatory properties. Etodolac and piroxicam were compared in the treatment of patients with active rheumatoid arthritis. A total of 118 patients entered this double-blind parallel study and were randomly assigned to receive 200 mg of etodolac twice a day (60 patients) or 20 mg of piroxicam once a day (58 patients) for 12 weeks. After the baseline evaluation, efficacy and tolerability evaluations were made at 2, 4, 6, 8, and 12 weeks. Significant improvement from baseline was noted in both treatment groups in the patient's and physician's global evaluations, in the number of swollen and tender joints, and in the pain intensity scores. Improvement was noted at the first visit (week 2) and continued through week 12. Based on changes in the patient's global evaluation, 56% of the etodolac-treated patients and 47% of the piroxicam-treated patients showed improvement at the final evaluation. Based on changes in the physician's global evaluation, 47% of the etodolac-treated patients and 42% of the piroxicam-treated patients showed improvement at the final evaluation. Eight (13%) patients in the etodolac group and 7 (12%) patients in the piroxicam group withdrew from the study because of adverse events. Most adverse events were mild to moderate; gastrointestinal complaints were the most prevalent adverse events in both treatment groups. No clinically significant changes were seen in laboratory test results or vital signs. These results demonstrate that etodolac is well tolerated and effective in the treatment of the signs and symptoms of rheumatoid arthritis and compares favorably to piroxicam in safety and efficacy.

Adolescent↗