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At least 253 records · Page 14Linked to original sources
PubMed2005

Profiling of resource use variation among six diseases treated at 82 Japanese special functioning hospitals, based on administrative data.

BACKGROUND: Profiling treatment in Japanese hospitals has rarely been conducted systematically with an administrative database. The study aims to present descriptive statistics of medical profiling and to examine the sources of variation in resource used for six common diseases. METHODS: Administrative records for 266,677 patients were analyzed to examine variation in length of stay (LOS) and total charge (TC) by hierarchical multiple linear regression for cases of ischemic stroke, ischemic heart disease (IHD), great vessel disease (GVD), respiratory neoplasm, gastric neoplasm and colonic neoplasm. RESULTS: Average LOS and TC increased with disease severity and invasiveness of surgical procedure. The coefficient of determination of the full model was highest for LOS in IHD (0.432), and for TC that was highest in GVD (0.702). Among various variable sets examined, surgical procedures explained largest variance in resource use. CONCLUSION: With a standardized database derived from claims data, wide audience of stakeholders in Japanese healthcare will be able to access the profiling of practice or disease variation concerned.

Aged↗
PubMed1994

Pattern and presentation of large bowel neoplasms in Nigerians.

It is generally believed that colonic neoplasms are uncommon amongst Blacks. One hundred and twenty seven cases of large bowel neoplasms were treated at Obafemi Awolowo University Teaching Hospitals Complex, Ile-Ife between 1981 and 1990. There were 84 males and 43 females. The mean age was 53 years. Duration of illness prior to presentation at the hospital varied between two weeks to three years with a mean time lag of 15 months. Intestinal obstruction was found in 83 patients and these also presented with anaemia. However massive rectal bleeding was noticed only in 38 cases. Most of the lesions were rectosigmoid. Some of these patients accounting for 87 cases (69 pc) refused permanent colostomy due to social embarrassment. Histopathologic appearance of the tumours were mostly adenocarcinoma in 97 cases. Thirty five patients died within the first year of their presentation and management. Twenty eight patients are still being followed up while other patients have been lost to follow up. This study shows that a sizeable number of patients suffer from colonic neoplasm in our community.

Adenocarcinoma↗
PubMed2004

Dietary seed oil rich in conjugated linolenic acid from bitter melon inhibits azoxymethane-induced rat colon carcinogenesis through elevation of colonic PPARgamma expression and alteration of lipid composition.

Our previous short-term experiment demonstrated that seed oil from bitter melon (Momordica charantia) (BMO), which is rich in cis(c)9, trans(t)11, t13-conjugated linolenic acid (CLN), inhibited the development of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF). In our study, the possible inhibitory effect of dietary administration of BMO on the development of colonic neoplasms was investigated using an animal colon carcinogenesis model initiated with a colon carcinogen AOM. Male F344 rats were given subcutaneous injections of AOM (20 mg/kg body weight) once a week for 2 weeks to induce colon neoplasms. They also received diets containing 0.01%, 0.1% or 1% BMO for 32 weeks, starting 1 week before the first dosing of AOM. At the termination of the study (32 weeks), AOM induced 83% incidence (15/18 rats) of colonic adenocarcinoma. Dietary supplementation with 0.01% and 0.1% BMO caused significant reduction in the incidence (47% inhibition by 0.01% BMO, p<0.02; 40% inhibition by 0.1% BMO, p<0.05; and 17% inhibition by 1% BMO) and the multiplicity (64% inhibition by 0.01% BMO, p<0.005; 58% inhibition by 0.1% BMO, p<0.02; and 48% inhibition by 1% BMO, p<0.05) of colonic adenocarcinoma, though a clear dose response was not observed. Such inhibition was associated with the increased content of CLA (c9,t11-18:2) in the lipid composition in colonic mucosa and liver. Also, BMO administration in diet enhanced expression of peroxisome proliferator-activated receptor (PPAR) gamma protein in the nonlesional colonic mucosa. These findings suggest that BMO rich in CLN can suppress AOM-induced colon carcinogenesis and the inhibition might be caused, in part, by modification of lipid composition in the colon and liver and/or increased expression of PPARgamma protein level in the colon mucosa.

Adenocarcinoma↗
PubMed1987

Peanut lectin binding sites in colons of patients with ulcerative colitis.

We studied peanut lectin (PNA) binding sites in patients with ulcerative colitis (UC) with various degrees of disease activity and dysplasia. Peanut lectin binds to B-D-galactose (1-3) N-acetyl-D-galactosamine, which is the purported determinant for the T-blood-group antigen and the immediate precursor of the MN-blood-group glycoprotein. In the normal colon, PNA binds to the supranuclear (SN) portion of goblet and columnar cells, representing nascent glycoproteins in the Golgi apparatus prior to the addition of terminal sialic acid. In severely active UC, PNA binds to the glycocalyx and/or apical portion of columnar cells, crypt goblet cells, and the total cytoplasm of "regenerating or hyperplastic" epithelium. These patterns have been previously reported in colonic cancers, adenomas, and fetal colons, indicating the synthesis of incomplete glycoproteins. Cases of inactive UC and mildly active UC expressed PNA binding in an SN distribution similar to controls. Cases with dysplasia showed PNA binding patterns similar to colonic neoplasms. In UC, the perturbation of cell kinetics similar to colonic neoplasms and the more rapid cell migration and turnover may be reflected as synthesis of incomplete glycoproteins, as expressed by abnormal PNA binding patterns. These findings indicate that the epithelial cells in patients with severely active UC synthesize incomplete glycoproteins similar to colonic neoplasms; however, this abnormal glycoprotein pattern is reversible when inflammation is more quiescent.

Arachis↗
PubMed1997

The incidence of aberrant crypt foci and colonic carcinoma in dimethylhydrazine-treated rats varies in a site-specific manner and depends on tumor histology.

In an attempt to demonstrate the relationship between aberrant crypt foci (ACF) and subsequent colonic neoplasms, we investigated the distribution of ACF in the dimethylhydrazine (DMH) model of colonic carcinogenesis in the rat. DMH was given to male Wistar rats by s.c. injection in a dosage of 15 mg/kg body weight once a week for 19 weeks. As a result, eight poorly differentiated, mucin-secreting carcinomas, two well-differentiated tubular adenocarcinomas, and four adenomas developed in 35 rats autopsied at 24 weeks after the first injection of DMH. The location of each type of tumor was site specific. Poorly differentiated, mucin-secreting carcinomas of signet-ring type occurred only in the proximal colon; the mean location of these lesions was 17.6 +/- 3.8% (SE; range, 0-39%) of the length of the colon. Well-differentiated tubular adenocarcinomas and adenomas developed in the distal colon; the mean location of these lesions was 76.7% +/- 4.9 (SE; range, 60-90%) of the length of the colon. There was a mean number of 276 +/- 29 (SE) ACF per colon; these were present at between 40 and 90% of the colonic length, peaking at 70%. We conclude that ACF are marker lesions for colonic neoplasms, but only in the distal colon where tumors follow the adenoma-carcinoma sequence; this is not so for the proximal colon, where poorly differentiated, mucin-secreting carcinomas are found. These findings suggest that these latter tumors well may arise de novo and indicate that studies that attempt to correlate ACF with subsequent tumor formation must take cognizance, not only of the site, but also of the tumor type.

Adenocarcinoma↗
PubMed1995

Colonic histiocytic neoplasm mimicking malignant histiocytosis and presenting as intussusception.

It is now apparent that distinction between the so-called malignant histiocytosis and lymphoma can be made using panels of established immunohistochemical markers and/or genotypic analysis. Many, if not all, of the previously diagnosed cases of malignant histiocytosis have been shown to be of lymphoid, rather than histiocytic, lineage. We report a rare case of colonic histiocytic neoplasm accompanied by a lymphoreticular dissemination that mimicked that of malignant histiocytosis. In addition, barium studies and computed axial tomography confirmed an intussusception that subsequently developed. The histiocytic nature of the neoplastic cells was supported by immunohistochemical, ultrastructural, and cytochemical studies. To our knowledge our case may represent the fifth documented case of a histiocytic malignancy reported in the literature. The relationship among the various cases will be discussed as well as the significance of the focal S-100 immunoreactivity observed in the present case.

Colonic Diseases↗
PubMed1977

The effect of surgical resection of experimental "primary" adenocarcinoma of the colon of survival and incidence of metastases.

The effect of surgical resection of "primary" tumors classified by size at the time of resection has been studied in two tumor cell lines derived from dimethylhydrazine-induced colonic neoplasms in the Buffalo strain rat. Surgical treatment of colon cancer in the rat yields results similar to those for human carcinoma. Some of the smallest tumors resected were associated with metastases and this finding suggests a need for effective postoperative adjuvant therapy. The incidence of metastases and the size of the tumor were inveresely related to survival, e.g., the smaller the tumor or the sooner the excision, the greater the survival of the animal. The operated animal model studied here could prove to be very useful for evaluating various forms of systemic therapy for the control of micrometastases associated with colonic neoplasms.

Adenocarcinoma↗
PubMed1997

Absence of p53 gene mutations in rat colon carcinomas induced through the synergistic interaction between methylazoxymethanol and X-irradiation.

p53 is one the most frequently mutated genes found in human colonic tumors. Because colonic neoplasms induced in rats by certain chemical carcinogens are similar to human colonic tumors in their histological features and proliferation characteristics, the rat has been used as an experimental model to study the pathogenesis of colon cancer. However, p53 mutations were not detected in the chemically induced colonic tumors analyzed for p53 mutations. X-irradiation has also been shown to induce colonic neoplasms in rats that resemble human colonic tumors histopathologically. Because the incidence of colonic tumors induced by methylazoxymethanol (MAM) in rats was shown to be enhanced by X-irradiation, we immunohistochemically analyzed these colonic carcinomas for the presence of p53 gene mutations. The immunohistochemical analyses clearly showed the absence of nuclear immunoreactivity in all ten tumors examined. The results from the present study indicate that point mutations in p53, at least in the coding region, are not involved in the development of colon cancer induced by the combination of MAM and X-irradiation. Our observations, together with the data from previous studies, further suggest that rat colon carcinogenesis, unlike human colon cancer, may not involve p53 mutation as an obligatory event.

Adenocarcinoma↗
PubMed1999

Structural studies of initial lymphatics adjacent to gastric and colonic malignant neoplasms.

Invasion and metastases are the main causes of death from cancer, and prognosis is best correlated with invasion of malignant cells into initial lymphatics and dissemination to regional lymph nodes. Using both light and transmission electron microscopy, we examined human gastric and colonic cancers and their relation to initial lymphatics. Invasion of malignant tumor cells into the initial lymphatics was characterized by interdigitating and overlapping endothelium giving way to open junctions as lymphatic endothelial cells were apparently dissolved and destroyed. Cytoplasmic vesicles, mitochondria, and rough endoplasmic reticulum were qualitatively increased as demonstrated by image analysis.

Colonic Neoplasms↗
PubMed1986

Antitumor immune response to colorectal cancer antigen detected by the leukocyte adherence inhibition test (LAI) in groups at high risk for colorectal cancer.

Colorectal cancer is the second leading cause of cancer death in western populations. As treatment outcome is highly correlated with stage at diagnosis, early detection is a very important task. Three high-risk groups for colorectal cancer (first-degree relatives of colorectal cancer patients; individuals with past history of colorectal neoplasms, polyps, or carcinoma; and patients with ulcerative colitis) were screened for colonic neoplasms. The study program included the leukocyte adherence inhibition test (LAI), a specific immune response test for colorectal cancer antigen; fiberoptic sigmoidoscopy or colonoscopy; and guaiac impregnated slide test. The main finding was the detection of 92 positive LAI tests out of 451 high-risk individuals tested (20%), compared to eight positive tests out of 194 (4.1%) in a control group. Fifty-six colonic neoplasms were found out of 344 (16%) colonoscopies performed, most of them adenomatous polyps and a few carcinomas. Our findings, compared with the expected 2-3% neoplasms in low-risk groups, would prove that the screenees were indeed at high risk. However, only 11/56 (19%) of the polyps identified were LAI positive. The number of polyps found among LAI positive individuals were, so far, 11/92 (11%). The guaiac impregnated slide test for occult blood in the stool was performed in 221 screenees. Of these only 10 were positive (4.5%) compared with the average of 1% positive tests in low-risk groups.

Antigens, Neoplasm↗
PubMed1989

Streptococcus bovis septicemia and large bowel neoplasia.

Streptococcus bovis septicemia is a relatively uncommon entity that is associated with an increased incidence of colonic neoplasms. Three of four patients with S. bovis endocarditis subsequent to septicemia underwent colonoscopy. The fourth patient underwent a barium enema and a proctoscopic examination. Polyps were found in three patients, and adenocarcinoma of the colon in one. Patients with S. bovis endocarditis should be considered at high risk for colonic neoplasms. Screening colonoscopy is recommended for these patients, and follow-up colonoscopy may be warranted.

Adenocarcinoma↗
PubMed1994

Expression of cytokines, TNF-alpha and IL-1 alpha, in MAM acetate and 1-hydroxyanthraquinone-induced colon carcinogenesis of rats.

The expression of cytokines, TNF-alpha and IL-1 alpha, was examined by means of a reverse transcription followed by PCR (RT-PCR) in rat colon carcinogenesis. Forty male F344 rats were used and divided into four groups. At the start of the experiment, 20 rats were treated with methylazoxymethanol (MAM) acetate (25 mg/kg body wt, one time, i.p.) and divided into two groups; group 1 was exposed to 1% 1-hydroxyanthraquinone (1-HAQ) and group 2 was fed a basal diet during the experiment (40 weeks). Other rats were also divided into two groups; group 3 was exposed to 1% 1-HAQ as group 1, and group 4 was used as control. Tumor incidence (100%) and multiplicity (5.00 +/- 2.05) in group 1 were significantly greater than those in group 2 (20% and 0.2 +/- 0.42) and group 3 (10% and 0.10 +/- 0.32) (P < 0.01 and P < 0.01 respectively). RT-PCR technique with RNA was applied to the tissues from colon neoplasms and mucosa in each group. Expression of TNF-alpha and IL-1 alpha in the colon neoplasms was much stronger than that in the colon mucosa of each group (P < 0.001 and P < 0.01 respectively). The expression of TNF-alpha was more remarkable in the colon mucosa of group 1 than that in corresponding tissue of groups 2 and 3 (P < 0.01). The expressions of TNF-alpha and IL-1 alpha were more increased in the colon mucosa of groups 1, 2 and 3 than that in group 4 as control (P < 0.01 and P < 0.05 respectively). The results indicate that TNF-alpha and IL-1 alpha may act as growth factors in rat colon carcinogenesis by MAM acetate and 1-HAQ. In addition, the synergistic effect of 1-HAQ with MAM acetate in colon carcinogenesis might be related to biological effects of the cytokines expressed in the inflammatory condition generated by 1-HAQ.

Adenocarcinoma↗
PubMed2003

Colonic polyps of acromegalic patients are not associated with mutations of the peroxisome proliferator activated receptor gamma gene.

Peroxisome proliferator activated receptor (PPAR)gamma plays a pivotal role in regulating adipocyte differentiation and metabolism, but also has an antiproliferative effect in several tissues, including colonic mucosa, where it is highly expressed. Loss-of-function mutations have been reported in about 10% of sporadic primary colon cancer. Acromegalic patients have an increased prevalence of colonic neoplasms and lower PPARgamma levels in the colonic mucosa. Thus, PPARgamma may act as a tumor suppressor gene, and its reduced expression or loss-of-function mutations may contribute to tumorigenesis. In this study the expression and mutations of the PPARgamma gene in the colonic polyps and mucosa outside polyps were investigated in 10 acromegalic and 17 non-acromegalic patients. PPARgamma expression was evaluated by RT-PCR. PPARgamma was expressed in each sample, but expression appeared to be lower in polyps than in mucosa outside polyps from either acromegalic or non-acromegalic patients. All exons of the PPARgamma gene were directly sequenced after PCR amplification: no mutations were found either in acromegalic or in non-acromegalic patients. In conclusion, the results of this preliminary study suggest that the lower expression of PPARgamma rather than somatic mutations of this gene is involved in colonic tumorigenesis.

Acromegaly↗