PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 7959646

Obstructive enterocolitis: a clinico-pathological discussion.

T S Levine·A B Price
View original source ↗Export metadata ↓

Abstract

Obstructive colitis is a condition that is not widely appreciated by pathologists. It is defined as an ulcero-inflammatory lesion(s) proximal to a colonic obstruction from which it is separated by a variable length of normal mucosa. Five cases are described which illustrate the clinico-pathological spectrum of the condition. All presented surgically as acute intestinal obstruction, secondary to adenocarcinoma in four cases and a diverticular stricture in one case. Pathologically, the severity of colitis ranged from a single discrete ulcer to an extensive area of fulminant colitis indistinguishable from colitis indeterminate. Furthermore, two cases represented 'obstructive enteritis', a variant of obstructive disease not previously reported. Microscopically, all cases were characterized by distinctive areas of localized ulceration and active inflammation, the features of which were quite unlike those of Crohn's disease or ischaemia, separated by islands of normal mucosa. The role of mural hypoperfusion and secondary localized ischaemia in the pathogenesis of this disorder is discussed. It is suggested that colitis indeterminate represents the final common pathological pathway of the intestine to a wide range of initial insults, be they obstructive or inflammatory.

Explore related subjects

AdenocarcinomaAdultAgedDiverticulumEnterocolitisFemaleHumansIntestinal DiseasesIntestinal NeoplasmsIntestinal ObstructionMaleMiddle AgedCase ReportsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

T S Levine, A B Price. 1994. Obstructive enterocolitis: a clinico-pathological discussion.. https://doi.org/10.1111/j.1365-2559.1994.tb00598.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2001

Heterogeneous distribution of P53 immunoreactivity in human lung adenocarcinoma correlates with MDM2 protein expression, rather than with P53 gene mutation.

Although the tumor suppressor p53 protein (P53) immunoreactivity and its gene (p53) mutation were reported to be significant prognostic indicators for human lung adenocarcinomas, little is known regarding the relationship between the heterogeneous distribution of P53 and its genetic status in each tumor focus and the clinicopathological significance. To determine how P53 is heterogeneously stabilized in patients, we compared P53 expression to both the p53 allelic mutation in exon 2 approximately 9 by polymerase chain reaction-single strand conformation polymorphism using microdissected DNA fractions, and the immunohistochemical MDM2 expression. Of the 48 positive to P53 in 118 lung adenocarcinomas examined, 10 with heterogeneous P53 expression were closely examined. The higher P53 expression foci in 7 of 10 cases were less differentiated, histologically in respective cases, and were frequently associated with fibrous stroma. Two had genetic mutations in exon 7 of the p53 gene in both the high and low P53 expression foci of cancer tissue indicating no apparent correlation between heterogeneous P53 expression and the occurrence of gene mutation. Immunohistochemical expression of MDM2 was significantly lower in high P53 expression areas (p < 0.05, the mean labeling indices of high and low P53 expression areas being 4.2 +/- 5.4% and 13.6 +/- 12.2%, respectively). In addition, among all the 118 cases examined, MDM2 expression was significantly suppressed in cases of p53 gene mutation, simultaneously with P53 overexpression, as compared with cases without both the p53 mutation and expression (p < 0.001). These findings suggest that the heterogeneous stabilization of P53 in human lung adenocarcinomas could be partly due to suppressed MDM2 expression. The overexpression of non-mutated P53 may afford a protective mechanism in human lung adenocarcinomas.

Adenocarcinoma↗
PubMed2001

Appropriate subcellular localisation of prodrug-activating enzymes has important consequences for suicide gene therapy.

Escherichia coli B nitroreductase (NR) has been expressed stably in MDA-MB-361 human breast adenocarcinoma cells either as the wild-type protein (wtNR), which is distributed evenly between the cytoplasmic and nuclear compartments, or targeted to the mitochondrion (mtNR). Whereas bacterial NR is active as a dimer, a proportion of wtNR is monomeric. In contrast, mtNR is mostly dimeric, suggesting that it adopts a more stable, native conformation. Despite this, when tested in gene-directed enzyme prodrug therapy cell cytotoxicity studies, cells expressing wtNR or mtNR had similar sensitivity to the prodrug CB1954 and mounted similar bystander killing effects. Furthermore, when short prodrug exposures were given, wtNR was more efficient at killing cells than mtNR. These data demonstrate that the site of enzyme expression and prodrug activation is an important variable that requires consideration in suicide gene therapy approaches.

Adenocarcinoma↗
PubMed2001

Family history of cancer and risk of esophageal and gastric cancers in the United States.

The worldwide rates for histology- and subsite-specific types of esophageal and gastric cancer reveal strikingly divergent patterns. The contribution of environmental and genetic factors has been explored in several high-incidence areas, but data on genetic influences are scarce for Western countries. Using data from a multicenter, population-based, case-control study on 1,143 cases and 695 controls in the United States, we evaluated whether a family history of digestive or other cancers was associated with an increased risk of esophageal adenocarcinoma (n = 293), esophageal squamous cell carcinoma (n = 221), gastric cardia adenocarcinoma (n = 261) or non-cardia gastric adenocarcinoma (n = 368). After adjusting for other risk factors, individuals reporting a family history of digestive cancers experienced no increased risk of either type of esophageal cancer but they were prone to adenocarcinomas of the gastric cardia [odds ratio (OR) = 1.34, 95% confidence interval (CI) 0.91-1.97] and non-cardia segments (OR =1.46, 95% CI 1.03-2.08). This familial tendency, particularly for non-cardia gastric tumors, was largely explained by an association with family history of stomach cancer (OR = 2.52, 95% CI 1.50-4.23). In addition, family history of breast cancer was associated with increased risks of esophageal adenocarcinoma (OR = 1.74, 95% CI 1.07-2.83) and non-cardia gastric adenocarcinoma (OR = 1.76, 95% CI 1.09-2.82). Also seen were non-significant familial associations of esophageal squamous-cell cancer with prostate cancer as well as non-cardia gastric cancer with leukemia and brain tumors, though these relationships must be interpreted with caution. Our data point to the role of familial susceptibility to gastric cancer, but not to any form of esophageal cancer, in the United States.

Adenocarcinoma↗