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Acta Gastroenterologica Latinoamericana 1983

[Evaluation of Ig and muramidase (lysozyme) in unspecified chronic duodenitis (bulbitis)].

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
Povezava se shrani v odložišče
E Domenichini
A H Fontán
W Wynbergh
R Pissinis
H N Rubio

Ključne besede

Povzetek

In 158 patients with symptoms of non ulcerative dyspepsia, endoscopic, histologic and immunohystochemical studies were performed over three years with the aim of investigating the immunological involvement in the Chronic non specific Duodenitis (CND). After excluding 112 patients with associated pathologies of those not fulfilling technics requisites, a population of 46 subjects was selected and subsequently it was subdivided into four groups. A group of 15 patients with histologically normal duodeno served as control; the rest (31 patients) were grouped according to duodenal compromise into three groups of minor-major severity; Grade 1 (n=12); Grade 2 (n=12); Grade 3 (n=7). The number of immunoglobuline producing cells by mn2 of mucosal area and semiquantitative evaluation of mononucleated cells with cytoplasmatic activity to hydrolitic enzymes (lysozyme or muramidase) were compared among the 4 sub-groups. It was observed a variation in the immunoglobulines rate among controls (IgA: M: G=82, 52: 11, 01: 6,45) regarding the most severe degree (61, 56: 27,30: 11,14). The increase of IgMy G compared with controls was highly significant (p is less than 0.001) and it was noted a correlative IgA diminution. The contribution of hydrolitic enzymes through the presence of "activated" histiocytes was maximal in the most degree-coinciding with the increase of IgM and IgG. This findings indicated that a marked local activation of the Immunitary System type B is observed in the Chronic Nonspecific Duodenitis and its increment, expressed as quali-quantitative variations of the different immunologlobulines and muramidase producing cells, should have lythic activity in the highest degrees. We conclude, proposing this disease as a model of immunological aggression which affects bulbar mucosae.

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