Etienne D. Martin

Quantitative Estimation of the Collagen Content in Normal and Pathologic Pancreas Tissue

The aims of the study were to measure the collagen content in pancreas using a colorimetric method and to compare the amount of collagen in normal pancreas (11 cases), diffuse fibrosing pancreatitis (17 cases), and chronic calcifying pancreatitis (11 cases). The procedure of fibrosis measurement was based on the selective capacity of two dyes, Sirius red and fast green, to set on collagen and noncollagenous proteins, respectively. After staining of sections, colors were eluted from the sections and the specific absorbance of each eluted dye was read on a spectrophotometer. The collagen content in normal pancreata was 26.5 +/- 7.2 micrograms collagen/mg protein. The amount of collagen increased with the age of patients: the mean value of the patients under the age of 50 was 18.2 +/- 4 micrograms collagen/mg protein whereas the mean value in older patients was 31.9 +/- 8 micrograms collagen/mg protein (p less than 0.01). The value of collagen in pancreas with a diffuse fibrosing pancreatitis was 44.7 +/- 7.5 micrograms collagen/mg protein. This value was significantly different from the collagen content in normal pancreas (p less than 0.001) and in pancreas with a chronic calcifying pancreatitis (77.9 +/- 8 micrograms collagen/mg protein, p less than 0.001). This method permits discrimination between different chronic diseases that can also be differentiated on a histopathologic basis.

Light chain deposition disease with liver dysfunction

Light and transmission electron microscopic study as well as immunohistochemical investigation were performed on three cases of light chain deposition disease (LCDD) with severe liver dysfunction. In two cases, the amount of light chain deposits in the liver was moderate and did not correlate with the severity of clinical and biological symptoms. Ultrastructural study demonstrated a collagenization of the Disses space, with basement membrane-like material in association with light chain deposits. Immunohistochemical investigation showed a marked increase of collagen types I, III, and IV, as well as fibronectin and laminin in perisinusoidal space. This study suggests that collagenization of the Disses space has a minor role in liver dysfunction. The analogy between kidney and liver lesions in diabetes and in LCDD is stressed, but the mechanism of this abnormal accumulation of matrix proteins remains unknown.

Les lésions précancéreuses de l’estomac

RésuméDeux lésions gastriques répondent à la définition des lésions pré-néoplasiques:- l’une, assez fréquente est la gastrite chronique avec atrophie gastrique progressive, qui survient avec une particulière fréquence chez les ulcéreux gastriques et duodénaux, chez les gastrectomisés et au cours des anémies pernicieuses;- l’autre, beaucoup plus rare, est le polyadénome. La voie d’évolution vers la cancérisation est dans les deux cas une métaplasie intestinale et surtout une dysplasie d’intensité variable. Seule la dysplasie sévère a une réelle signification pré-néoplasique et un risque élevé d’évolution vers le cancer.Cette filiation, qui semble évoluer sur des périodes longues (de 10 à 25 ans) peut aboutir à détecter des E.G.C., à un stade utile.Malheureusement, ces E.G.C. ne représentent encore au mieux, que 30% des G.C. opérés. Il persiste donc une grande zone d’ombre sur les voies évolutives de 70 à 80% des G.C. Il est probable qu’il existe des lésions latentes de gastrite chronique, peut-être tout à fait localisées et dont l’évolution lésionnelle est peut-être plus rapide, aboutissant d’emblée à des G.C. à forme invasive.Cette différence évolutive est peut-être liée à des facteurs héréditaires ou immunologiques généraux et locaux.SummaryTwo kinds of gastric lesions can be considered as pre-neoplasic:- the first, rather frequent, is chronic gastritis with progressive gastric atrophy. It is regularly found in ulcer patients (gastric or duodenal ulcers), in gastrectomy patients and in pernicious anemia patients;- the second, less frequent, is the poly-adenoma. In both cases, the malignant transformation follows the same evolution: intestinal metaplasia, with dysplasia of variable intensity. But only severe dysplasia can be considered truly pre-malignant, and a high risk lesion. This evolution taking several years (10 to 25), can permit us to detect cancer at a useful stage, i.e. E.G.C. or even at a pre-malignant stage. Unfortunately, E.G.C. represents to-day, at best, less than 30% of surgical interventions for G.C. Therefore there is a 70 to 80% unknown factor in the evolution of G.C. It is probable that some type of latent lesion of G.C. exists in localized foci. Its evolution is perhaps much faster, ending in Gastric Cancer without passing through all the necessary stages.This difference in evolution is perhaps linked to hereditary or immunological factors whether generalized or local.

Expression of histocompatibility antigens and characterization of the lymphocyte infiltrate in hyperplastic polyps of the large bowel

HLA-DR expression, lymphocyte subsets, and the distribution of proliferating cells were studied in hyperplastic polyps from the colorectum. The density of T-cells (CD5+) (mean of cells/mm2 of tissue +/- SEM) was higher in the lamina propria of hyperplastic polyps (64.2 +/- 4.2) than in normal colonic mucosa (36.7 +/- 2.6, P less than .001). The CD4/CD8 ratio was higher in hyperplastic polyps (6.3 +/- 0.9, P less than .0001) and in colonic adenomas (5.9 +/- 0.9, P less than .001) compared with normal mucosa (2.3 +/- 0.2). Lymphocytes of the lamina propria were never Ki-67 positive either in normal mucosa or in hyperplastic polyps or adenomas. The epithelial layer of hyperplastic polyps and of normal mucosa did not express the HLA-DR antigen, whereas pericryptal fibroblasts and most of the leukocytes of the lamina propria were strongly positive for this antigen. In the epithelial layer proliferating cells were localized exclusively in the lower part of epithelial crypts, as was the case in normal mucosa, whereas in adenomas Ki-67-positive cells were present throughout the entire height of the mucosa. Thus, in hyperplastic polyps lymphocytes are increased in the lamina propria, with a predominance of the CD4 subset in close contact with HLA-DR positive pericryptal fibroblasts.