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Biomedical subjects

C A Rubio

Publications and source records attributed to C A Rubio.

At least 37 records · Page 2Linked to original sources
PubMed2002

Cryptal lymphocytic coloproctitis: a new phenotype of lymphocytic colitis?

BACKGROUND/AIMS: Lymphocytic colitis is a clinicopathological entity characterised by protracted watery diarrhoea and an increased number of intraepithelial lymphocytes (IELs) in the surface epithelium of the colonic mucosa. This report describes two patients with symptoms similar to those of lymphocytic colitis and an increased number of IELs, but within the cryptal epithelium. METHODS: The numbers of IELs were assessed in colorectal biopsies from the two patients. Sections were stained immunohistochemically for CD3, CD8, CD20, and TIA1. RESULTS: The colorectal biopsies had an abnormally high number of IELs in the epithelium of the crypts but not in the surface epithelium. The IELs in the crypts were CD3+++, CD8+, TIA1+, and CD20-. CONCLUSIONS: The histological diagnosis in these two patients was cryptal lymphocytic coloproctitis. Patients with similar symptoms and an increased number of IELs in the surface epithelium are now filed at this department as having surface lymphocytic coloproctitis. Immunohistochemistry showed that the cryptal IELs were cytotoxic suppressor T cells. Interestingly, a case of cryptal lymphocytic colitis was recently recorded in a non-human primate dying after years of protracted chronic diarrhoea. It is possible that antigens present in the lumen of the crypts elicit a lymphocytic reaction within the cryptal cells.

Adult↗
PubMed2002

A simple method to demonstrate duodenal gastric metaplasia.

AIMS: The diagnosis of duodenal gastric metaplasia (DGM) is based on the demonstration of periodic acid Schiff (PAS) positive mucin in duodenal columnar cells. Recently, groups of duodenal columnar cells were seen to be autofluorescent in haematoxylin and eosin (H&E) stained sections from a patient with DGM. MATERIALS AND METHODS: Consecutive archival gastric and duodenal H&E sections from 30 patients with chronic gastritis and DGM (CG+DGM), from 30 with chronic gastritis without DGM (control group I), from 30 with normal gastric and duodenal mucosa (control group II), and from five patients with coeliac disease (control group III) were reviewed on a fluorescent microscope. RESULTS: The surface epithelium of the gastric mucosa in all 95 cases had autofluorescent material. In 31 cases with DGM (including one unreported case in control group I), groups of columnar duodenal cells also had autofluorescent material. In the remaining 64 cases, duodenal columnar cells were not autofluorescent. Results were confirmed with the PAS stain. CONCLUSIONS: The method described detected apical mucin secretion in columnar cells, both in the stomach and in the duodenum from patients with DGM. The autofluorescence was induced by eosin (which binds to neutral mucin). Observing H&E stained duodenal biopsies under a fluorescence microscope may be sufficient to confirm DGM or to detect incipient DGM. Despite long observation periods and a long exposure time while photographing, the autofluorescence did not fade away. Because re-cuttings for special staining (PAS) are no longer required when this method is used, both final diagnosing time and laboratory costs can be reduced.

Adolescent↗
PubMed2001

Re-adaptation of the gastroduodenal mucosa to DNA synthesis during protracted stress.

BACKGROUND: Previous study showed that under the influence of protracted physical stress, the DNA synthesis (DS) of the gastroduodenal mucosa rises, the highest peak being reached at 4 weeks. At 8 stress weeks, the DS decreases to values similar to those recorded at the beginning of the experiment. The possibility that this DS adaptation (DSA) could be maintained beyond 8 weeks in animals allowed to subsequent resting (stress-free) weeks, was now explored. METHODS: Sixty-five rats were investigated. Sixty rats were transported to the stress laboratory. Thirty were water plunged and 30 sham handled once a day, 5 days a week, for 8 weeks. After 8 stress weeks, groups of 5 animals were allowed to rest for one, two, three and four weeks, ending with single water plunging or sham handling. All 65 animals received ip injection of 3H-thymidine before they were sacrificed. The ratio radioactive DNA/total DNA reflected the DS of the stomach and duodenum. RESULTS: DSA was achieved at 8 stress weeks (stomach). The DS in the stomach of stressed rats had significantly increased at 10 weeks (P < 0.05), but at 12 weeks it had decreased to 8 weeks values. The DS in the duodenum of stressed rats had significantly increased at 9, 10 and 11 weeks (P < 0.05), but at 12 weeks DS values had decreased to those of 8 weeks. CONCLUSIONS: The DSA at 8 stress weeks had not prevailed because the DS increased considerably in the following weeks. At 9-11 weeks, DS values had significantly increased (P < 0.05) in stressed rats, but at 12 weeks a DS re-adaptation (DSRA) had occurred. Thus, it took 8 weeks to achieve DSA (stomach), but only 4 weeks to accomplish DSRA. Animals experienced sham handling as an stressor (milder) as it also induced DS re-adjustments in the gastroduodenal mucosa. Autoradiography showed that the labelling in DNA synthesizing cells was limited almost exclusively to the mucosal layer. The model described may prove of value to studies aimed at abating the disparate fluctuations of DNA synthesis in the gastroduodenal mucosa during the various phases of protracted stress.

Adaptation, Physiological↗
PubMed2001

Serrated neoplasia of the stomach: a new entity.

AIM: Despite the fact that gastric carcinoma continues to be one of the most common cancers world wide, only dysplasia in flat mucosa and adenomas have been shown to evolve into invasive carcinoma. The aim of this paper is to report a novel histological phenotype of gastric adenoma with early invasive growth. MATERIAL AND RESULTS: The patient presented with gastric complaints. A barium examination revealed an ulcerated tumour in the corpus, apparently infiltrating the gastric wall. The endoscopic examination showed a pediculated protruding tumour in the greater curvature. Punch biopsies were reported as invasive adenocarcinoma. Because of the poor condition of the patient, a partial gastrectomy was performed. The histological examination revealed elongated fronds with lateral crenated, saw tooth-like notches as a result of scalloped epithelial indentations. Areas with high grade dysplasia, with carcinoma in situ, and invasive carcinoma at the tip of the adenoma were demonstrated. The pedicle of the protruding neoplasia "emerged" from a non-protruding serrated adenoma. CONCLUSIONS: The protruding serrated neoplasia had apparently evolved from a non-protruding serrated gastric adenoma. This appears to be the first case of gastric serrated neoplasia in the literature.

Adenoma↗
PubMed2000

Nonprotruding colorectal neoplasms: epidemiologic viewpoint.

Histologic sections from 781 nonprotruding colorectal neoplasias (adenomas and early carcinomas) recorded in Sweden and in Japan were reviewed by the same observer, using strict histologic criteria. Low grade dysplasia (LGD) was present in 82.8% (299/361) of the nonprotruding neoplasms recorded in Sweden but in only 42.6% (179/420) of those recorded in Japan. On the other hand, high grade dysplasia (HGD) was found in 42.4% (178/420) of the nonprotruding colorectal neoplasias in Japanese patients but in only 14.1% (51/361) of those in Swedish patients. Whereas 15.0% (63/420) of the nonprotruding neoplasms in Japan were intramucosal carcinomas (IMCs) or submucosal carcinomas (SMCs), only 3.0% (11/361) of those reviewed in Sweden were IMCs or SMCs. Thus in Japan the lesions were histologically more "advanced" (significantly more lesions had HGD) and more "aggressive" (significantly more lesions were IMC or SMC) than in Sweden. The cause(s) of that phenomenon remains elusive. The term nonpolypoid adenoma connotes a group of dysplastic lesions with different histologic phenotypes. Interestingly, similar phenotypes were recently found in overt colorectal carcinomas in both Sweden and Japan. Experimental and clinical findings indicate that nonprotruding colorectal adenomas are closely associated with colonic lymphoid nodules, suggesting that the lymphoid-associated colorectal mucosa might be the birthplace of many nonprotruding adenomas (and consequently of nonprotruding early colorectal carcinomas).

Adenoma↗
PubMed2000

The Vienna classification of gastrointestinal epithelial neoplasia.

BACKGROUND: Use of the conventional Western and Japanese classification systems of gastrointestinal epithelial neoplasia results in large differences among pathologists in the diagnosis of oesophageal, gastric, and colorectal neoplastic lesions. AIM: To develop common worldwide terminology for gastrointestinal epithelial neoplasia. METHODS: Thirty one pathologists from 12 countries reviewed 35 gastric, 20 colorectal, and 21 oesophageal biopsy and resection specimens. The extent of diagnostic agreement between those with Western and Japanese viewpoints was assessed by kappa statistics. The pathologists met in Vienna to discuss the results and to develop a new consensus terminology. RESULTS: The large differences between the conventional Western and Japanese diagnoses were confirmed (percentage of specimens for which there was agreement and kappa values: 37% and 0.16 for gastric; 45% and 0.27 for colorectal; and 14% and 0.01 for oesophageal lesions). There was much better agreement among pathologists (71% and 0.55 for gastric; 65% and 0.47 for colorectal; and 62% and 0.31 for oesophageal lesions) when the original assessments of the specimens were regrouped into the categories of the proposed Vienna classification of gastrointestinal epithelial neoplasia: (1) negative for neoplasia/dysplasia, (2) indefinite for neoplasia/dysplasia, (3) non-invasive low grade neoplasia (low grade adenoma/dysplasia), (4) non-invasive high grade neoplasia (high grade adenoma/dysplasia, non-invasive carcinoma and suspicion of invasive carcinoma), and (5) invasive neoplasia (intramucosal carcinoma, submucosal carcinoma or beyond). CONCLUSION: The differences between Western and Japanese pathologists in the diagnostic classification of gastrointestinal epithelial neoplastic lesions can be resolved largely by adopting the proposed terminology, which is based on cytological and architectural severity and invasion status.

Adenoma↗
PubMed2000

Qualitative and quantitative differences between bile ducts in chronic hepatitis and in primary biliary cirrhosis.

AIM: Lymphocytic infiltration in the portal triads usually conceals the detection--in haematoxylin and eosin (H&E) stained sections--of bile ducts in two liver diseases: chronic hepatitis and primary biliary cirrhosis. The aim was to assess the number and the characteristics of the bile ducts in those diseases with the aid of an antibody to cytokeratin 7 (CK7). METHODS: Consecutive sections from 99 liver biopsies were stained with H&E and anti-CK7. RESULTS: In H&E sections the total number of central bile ducts in the triads was 52 in primary biliary cirrhosis (n = 37), 69 in chronic hepatitis (n = 43), and 30 in miscellaneous cases (n = 19). Using anti-CK7, the number of central bile ducts was 276 in primary biliary cirrhosis, 348 in chronic hepatitis, and 96 in miscellaneous cases. Central bile ducts with lumen were found in 93.0% of chronic hepatitis cases and in 89.5% of the miscellaneous cases, but in only 13.5% of the primary biliary cirrhosis cases. Peripheral bile ducts in groups of > or = 4/triad were found in all cases of chronic hepatitis (100%) and in 75.7% primary biliary cirrhosis cases, but only in 10.5% of the miscellaneous cases. In 21.6% of primary biliary cirrhosis cases, no bile ducts (central and/or peripheral) were present. CONCLUSIONS: Anti-CK7 detects bile ducts in the triads that are concealed by chronic inflammatory cells. Central and peripheral bile ducts in groups of > or = 4 were significantly more common in primary biliary cirrhosis and chronic hepatitis than in other liver diseases. The lack of lumen in central bile ducts, as well as the absence of central and/or peripheral bile ducts in CK7 stained liver sections, seem to be valuable additional parameters in the differential diagnosis between primary biliary cirrhosis and chronic hepatitis.

Adult↗
PubMed1999

Non-polypoid adenomas of the colon are associated with subjacent lymphoid nodules. An experimental study in rats.

BACKGROUND: Subjacent lymphoid nodules (SLNs) have been found in 38% of non-polypoid colonic adenomas in humans. In the present work the presence of SLNs in experimentally induced colonic adenomas was investigated in rats. METHODS: 1,2-Dimethylhydrazine was injected subcutaneously in 290 Sprague-Dawley rats for 27 weeks. RESULTS: An SLN was present in 28.6% of the 84 adenomas, in 8.4% of the 119 adenocarcinomas, and in 9.7% of the 31 small carcinomas without remnant adenomatous tissue. An SLN was found in 35.6% of the 59 non-polypoid neoplasias but only in 9.1% of the 175 polypoid (that is, exophytic) neoplasias. When only adenomas were considered, SLNs were present in 50.0% of the 34 non-polypoid adenomas but only in 14.0% of the 50 polypoid adenomas. CONCLUSIONS: Non-polypoid colonic adenomas evolve preferentially from the minimal fraction of the colonic mucosa that overlays the few existing lymphoid nodules in rats.

Adenoma↗
PubMed1998

Somatically acquired genetic alterations in flat colorectal neoplasias.

Somatically acquired mutations in several genes have been reported as playing an important role during colorectal tumorigenesis. Two alternative groups of carcinomas, termed LOH+ and RER+, have been defined on the basis of their genetic anomalies, a biallelic inactivation of the APC or the TGF-betaRII genes, occurring as an alternative, in LOH+ or RER+ tumors. It is a generally accepted hypothesis that most of colorectal cancers (CRC) develop from a pre-existing adenomatous polyp. Such benign lesions are usually exophytic polyps, a small proportion of adenomas having been described as flat lesions. The latter histological category has thus been proposed to bear specific genetic alterations. In order to examine this hypothesis, we have characterized a series of 44 flat colorectal neoplasias for their RER status and for somatic APC, KRAS and TGF-betaRII genes mutations. Flat colorectal neoplasias were found to be of the RER+ subtype in 22% of cases, all of them exhibiting a TGF-betaRII mutation. A mutation of the APC and KRAS genes has been found in 42% and 4% of tumors, respectively, none of these tumors being of the RER+ subtype. With the exception of a low KRAS mutation rate, flat adenomas appear to follow tumorigenesis pathways very similar to those identified in exophytic adenomas and carcinomas.

Adenoma↗