RESUMO
Some patients with undiagnosed celiac disease have minor mucosal lesions that may not be apparent during routine histological analysis. Twenty-five such patients of our institution were discharged to their primary-care physicians despite having positive endomysial antibody serology. To re-evaluate diagnosis for these patients, immunohistological staining with antibodies to CD2, CD3, CD7, CD8, CD69, and Ki67 was conducted on original biopsies from twenty patients. Clinical, serological, and histological investigations were offered to all fourteen patients who attended for review. We observed a significantly greater (P < 0.0001) numbers of intraepithelial lymphocytes and Ki67-positive enterocytes in sections from these twenty patients than for normal controls. Of the fourteen patients who attended for further review, firm diagnosis of celiac disease was made for seven patients and diagnosis was likely for another two. Our study clearly revealed that over-reliance on standard histological findings results in failure to diagnose celiac disease.
Assuntos
Doença Celíaca/diagnóstico , Duodeno/patologia , Mucosa Intestinal/patologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Antígenos CD/imunologia , Biópsia , Doença Celíaca/imunologia , Diagnóstico Diferencial , Duodeno/imunologia , Feminino , Seguimentos , Humanos , Imuno-Histoquímica , Mucosa Intestinal/imunologia , Masculino , Pessoa de Meia-Idade , Estudos RetrospectivosRESUMO
Gluten-sensitive enteropathy is characterized by small intestinal damage. The pathogenic mechanisms involved are not precisely understood. There is recent interest in the possibility that matrix metalloproteinases might play a pathogenic role. Using immunohistochemistry technique, we examined the protein expression of matrix metalloproteinases-1, -3, and -9 and the tissue inhibitor metalloproteinase-1 in duodenal biopsies from 30 patients with celiac disease and dermatitis herpetiformis. We demonstrated that the percentage of cells expressing these enzymes and their inhibitor in all patients was significantly greater than in the normal controls (P < 0.0001). This was evident even in patients with a minimal lesion but was most marked in patients with severe damage, mirroring the degree of inflammation in the small intestinal tissue. The increased expression of these enzymes and their inhibitor in the duodenal mucosa of patients with gluten-sensitive enteropathy suggests a role for these enzymes in the tissue remodeling which is a feature of these disorders.