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Biomedical subjects

D K Driman

Publications and source records attributed to D K Driman.

10 recordsLinked to original sources
PubMed2001

Basaloid carcinoma of the colon arising at the splenic flexure.

AIMS: Basaloid carcinomas typically arise in the anal canal and there are only three well-documented cases of this neoplasm reported outside the anal canal, none more proximally than the sigmoid colon. The first occurrence of a basaloid colonic carcinoma arising outside the sigmoid colon, at the splenic flexure, is presented. METHODS AND RESULTS: A splenic flexure mass was resected from a 54-year-old man with a 3-week history of abdominal discomfort, diarrhoea and weight loss. This tumour, like typical anal canal basaloid carcinomas, was composed of islands of basaloid cells with peripheral nuclear palisading; within many islands there was central necrosis and focal squamous differentiation. Ultrastructural and immunohistochemical studies confirmed the basaloid nature and focal squamous differentiation within this neoplasm. Basaloid carcinoma of the anal canal has been associated with human papilloma virus. Using in-situ hybridization, HPV DNA was not detected in this case. CONCLUSIONS: Outside the anal canal, it has been postulated that basaloid colonic carcinomas may arise from cloacogenic embryologic rests, squamous metaplastic epithelium, or totipotential basal cells. The location and pathological findings of this tumour suggest that this rare colonic neoplasm arises from a totipotential basal cell.

Carcinoma, Transitional Cell↗
PubMed2001

GEWF solution.

BACKGROUND: Lymph node status is an important prognostic factor in the staging of colorectal carcinoma. Several adjunctive solutions have been used to increase the yield of pericolic lymph nodes from colorectal cancer resection specimens. METHODS: During 1998 at the Grey Bruce Regional Health Centre (Owen Sound, Ontario), 67 colonic resections were performed for colorectal cancer. Lymph nodes were identified using GEWF solution (glacial acetic acid, ethanol, distilled water, and formaldehyde) in 35 cases, and by the conventional method of sectioning, inspection, and palpation in 32 cases. RESULTS: There were no significant differences between GEWF and non-GEWF cases with respect to patient age, length of resection, size of tumor, tumor histologic type, tumor differentiation, or depth of tumor penetration into the bowel wall. Use of GEWF led to a significant increase in the number of lymph nodes found (10.2 +/- 4.9 per case) compared with non-GEWF cases (6.8 +/- 3.9 per case) (P =.002). In GEWF cases 358 lymph nodes were identified, 82 with metastases, whereas in the non-GEWF cases 218 lymph nodes were found, 41 with metastases. The size of positive lymph nodes in the GEWF group (0.5 +/- 0.2 cm) was significantly smaller than in the non-GEWF group (0.7 +/- 0.4 cm) (P =.046). A greater percentage of positive lymph nodes in the GEWF cases (49/82, 60%) were 0.5 cm or smaller compared with the non-GEWF cases (17/41, 41%). CONCLUSIONS: GEWF increases the yield of lymph nodes recovered from colorectal cancer specimens and may lead to improved staging of this cancer; it is inexpensive and simple to use.

Acetic Acid↗
PubMed2000

Mucocele of the appendix secondary to endometriosis. Report of two cases, one with localized pseudomyxoma peritonei.

This report documents 2 cases of obstructive mucocele of the appendix secondary to endometriosis of the appendix. In 1 case, the tip of the mucocele was ruptured and associated with localized pseudomyxoma peritonei. Mucoceles of the appendix usually are associated with hyperplastic or neoplastic mucosal proliferation; obstruction, particularly that due to endometriosis, is an infrequent cause. Occurrence of localized pseudomyxoma peritonei associated with appendiceal endometriosis and mucocele has not been reported previously.

Adult↗
PubMed1999

Prevention of adhesion formation with use of sodium hyaluronate-based bioresorbable membrane in a rat model of ventral hernia repair with polypropylene mesh--a randomized, controlled study.

BACKGROUND: There is a high incidence of adhesions after ventral hernia repair with polypropylene mesh. Hyaluronic acid (HA)-based membrane has been shown to reduce the incidence of adhesions in the absence of prosthetic mesh. The purpose of this study was to determine the effect of HA membrane on the quantity and grade of adhesions and its effect on strength of repair after abdominal wall repair with polypropylene mesh. METHODS: In 61 rats a full-thickness abdominal wall defect (excluding skin) was created, and a section of small bowel was abraded. The animals were randomized, receiving either HA membrane to cover the viscera or no membrane. The fascial defect was repaired with polypropylene mesh. Equal numbers of animals from each group were killed at 4 weeks and 8 weeks after surgery. Adhesion severity and percentage of mesh surface covered with adhesions were estimated. Tensile strength between mesh and muscle from each animal was measured. Sections of the mesh-muscle interface were examined histologically and measured for thickness and graded for inflammation and fibrosis. RESULTS: Fifty-five animals survived until the end point. Animals in the HA membrane group had a significant reduction in (1) grade of adhesions between small bowel and mesh at 4 weeks (P = .009) and 8 weeks (P = .000001), (2) grade of adhesions between colon and mesh at 8 weeks (P = .00003), and (3) percentage of mesh covered with adhesions at 4 weeks (P = .01) and 8 weeks (P = .0000002). There was no difference between the 2 groups in tensile strength of the repairs, tissue thickness, degree of inflammation, or degree of fibrosis. CONCLUSIONS: HA membrane reduces the quantity and grade of adhesions of both small and large bowel, to polypropylene mesh in a rat model of ventral hernia repair, without compromising strength of the repair.

Animals↗
PubMed1998

Colorectal inflammation and increased cell proliferation associated with oral sodium phosphate bowel preparation solution.

Evidence is emerging that sodium phosphate (NaP), a commonly used oral cathartic agent, causes aphthoid ulcers or focal active colitis (FAC) in the colon and rectum. The aims of this study were (1) to assess the incidence of such ulcers diagnosed endoscopically ("aphthoid ulcers"), (2) to assess the incidence of histologically detected FAC and neutrophilic infiltration overlying lymphoid follicles ("aphthoid lesions"), and (3) to determine whether this effect of NaP is associated with epithelial cell proliferation. Aphthoid ulcers, unexplained by other diagnoses, were found in 18 of 687 consecutive patients (2.6%) who underwent colonoscopic examination after oral NaP preparation during a 12-month period; biopsy specimens showed FAC or aphthoid lesions. FAC was present in 11 of 316 patients (3.5%) who had biopsies but were endoscopically normal. Eight patients with aphthoid ulcers in the rectosigmoid showed no abnormalities when reexamined by flexible sigmoidoscopy after an interval as short as 7 days (range, 7 to 56 days). Mucosal biopsy specimens from these patients were assessed for apoptosis and epithelial proliferation by determining the MIB-1 labeling index (LI). The LI was increased by 136% after NaP preparation (55 +/- 6) compared with biopsy specimens obtained from the same patients during reexamination without NaP preparation (23 +/- 6, P = .01). This correlated with the number of apoptotic bodies per 10 colonic crypts (1.2 +/- 0.3 v 0.5 +/- 0.2, respectively). To determine whether these proliferative changes represent a response to mucosal ulceration, rectosigmoid biopsy specimens were compared in two additional patient groups: an NaP group in whom no gross lesions were evident and a no-NaP group who were not exposed to NaP. Although more modest, similar changes in the LI (42 +/- 4 and 30 +/- 3, respectively, P = .03) and in the occurrence of apoptotic bodies per 10 colonic crypts (1.3 +/- 0.4 and 0.4 +/- 0.1, respectively) were observed. We conclude that use of NaP is associated with increased colorectal crypt epithelial cell proliferation. This proliferative response to NaP exposure is evident in the absence of colonoscopically or other histologically recognizable abnormalities. In a proportion of patients, aphthoid ulcers, FAC, or aphthoid lesions serve as markers of mucosal damage by NaP.

Administration, Oral↗
PubMed1996

Omeprazole produces parietal cell hypertrophy and hyperplasia in humans.

While there is evidence that omeprazole may induce changes in parietal cells, the effect of acid suppression on parietal cells in humans is poorly documented. This study was undertaken to evaluate the effects of omeprazole in human parietal cells over time. The light microscopic morphology of parietal cells in gastric biopsies from 17 patients on omeprazole were compared with those from 13 patients on ranitidine and 20 patients on no acid-lowering medication. Light microscopic and ultrastructural morphology of parietal cells was also evaluated in an additional 14 patients before and after omeprazole administration. Objective measurements of parietal cell height, mass and number were analyzed using analyses of variance. Electron microscopy was used to evaluate parietal cell enlargement. Twenty-five of 31 biopsies from patients on omeprazole, 1 of 13 from patients on ranitidine, and 0 of 20 from patients on neither drug showed parietal cell enlargement. Parietal cell height, mass, and number were increased in omeprazole-treated patients compared with ranitidine-treated patients and those on neither drug, and with the group also evaluated prior to beginning omeprazole treatment. Parietal cell height and mass were increased in patients on omeprazole longer than 12 months compared with biopsies from patients on the drug for less than 12 months. Resin-embedded sections and electron microscopy showed enlarged parietal cells with prominence of cytoplasmic tubulovesicles with sparse secretory canaliculi. Parietal cell hypertrophy and hyperplasia develops in patients on chronic omeprazole therapy; this can be recognized on routine examination of histologic sections. These morphologic changes increase with duration of therapy.

Adolescent↗
PubMed1992

Transforming growth factor-alpha in normal and neoplastic human endocrine tissues.

Transforming growth factor-alpha (TGF-alpha) is a polypeptide growth factor that binds to the epidermal growth factor receptor and is though to stimulate cell proliferation. It has been believed to play a role in tumor initiation by inducing the reversible transformed phenotype; overexpression of TGF-alpha may be important for tumor progression via autocrine stimulation and oncogene overexpression. Expression of TGF-alpha and the epidermal growth factor receptor has been documented in several nontumorous tissues and in a variety of tumors. This study used immunohistochemistry to localize TGF-alpha expression in normal and neoplastic endocrine tissues. Transforming growth factor-alpha was found in nontumorous hypothalamus, pituitary, thyroid, parathyroid, adrenal cortex and medulla, and pancreatic islets. Immunoreactivity was detected in most benign and malignant tumors of these tissues, as well as in endocrine neoplasms of the lung and gastrointestinal tract. Hypothalamic gangliocytomas, pheochromocytomas, and adrenal cortical carcinomas showed consistently greater immunoreactivity than their normal counterpart, but there was no correlation between degree of reactivity and tumor grade, stage, or hormone content. These results suggest that in endocrine tissues, TGF-alpha is unlikely to prove useful as a tumor marker but that the growth factor may play a role in both normal physiology and tumorigenesis.

Adrenal Glands↗