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PubMed2006

Effect of gastric bypass on Barrett's esophagus and intestinal metaplasia of the cardia in patients with morbid obesity.

Gastric bypass in patients with morbid obesity should be an excellent antireflux procedure, because no acid is produced at the small gastric pouch and no duodenal reflux is present, due to the long Roux-en-Y limb. Five hundred fifty-seven patients with morbid obesity submitted to resectional gastric bypass, and routine preoperative upper endoscopy with biopsy samples demonstrated 12 patients with Barrett's esophagus (2.1%) and three patients with intestinal metaplasia of the cardia (CIM). An endoscopic procedure was repeated twice after surgery, producing seven patients with short-segment Barrett's esophagus (BE) and five patients with long-segment BE. Body mass index (BMI) decreased significantly, from 43.2 kg/m(2) to 29.4 kg/m(2) 2 years after surgery. Symptoms of reflux esophagitis, which were present in 14 of the 15 patients, disappeared in all patients 1 year after surgery. Preoperative erosive esophagitis and peptic ulcer of the esophagus healed in all patients. There was regression from intestinal metaplasia to cardiac mucosa in four patients (57%) with short-segment BE, and in one patient (20%) with long-segment BE. Two (67%) of three cases with CIM had regression to cardiac mucosa. There was no progression to low- or high-grade dysplasia. Gastric bypass in patients with Barrett's esophagus and morbid obesity is an excellent antireflux operation, proved by the disappearance of symptoms and the healing of endoscopic esophagitis or peptic ulcer in all patients, which is followed by an important regression to cardiac mucosa that is length-dependent and time-dependent.

Adult↗
PubMed2004

Distinction between intestinal metaplasia in the cardia and in Barrett's esophagus: the role of histology and immunohistochemistry.

Intestinal metaplasia in Barrett's esophagus (BIM) is a precancerous condition, whereas the carcinogenic potential of intestinal metaplasia of the cardia (CIM) is uncertain. Although clinically important, histological distinction between both conditions by endoscopic biopsies is considered problematic. In the present study, 4-mm samples of BIM (n=31) and CIM (n=9) were selected from esophagectomy specimens that had been resected for esophageal cancer. Slides were coded and stained with hematoxylin and eosin (H&E), Alcian blue-periodic acid-Schiff (PAS), cytokeratins (CK) 7 and 20, and CD10, which labels the intestinal brush border. The predictive value of these stains for the recognition of BIM and CIM was evaluated independently by two senior pathologists. With the use of H&E-stained slides exclusively, BIM samples were categorized correctly in 93.5% and 83.9% of cases (pathologists 1 and 2, respectively), and CIM samples, in 100% and 88.9% of cases. Alcian blue-PAS-positive goblet cells were identified by both investigators in all BIM and CIM samples. BIM-typical CK 7 and 20 immunostaining pattern was identified in 90.3%/83.9% of BIM but only in 11.1%/11.1% of CIM. CD10-positive brush border was present in 32.3%/25.8% of BIM and in 88.9%/88.9% of CIM. When HE-stained slides and immunohistologically stained slides were used together for tissue recognition, BIM were categorized correctly in 90.3%/80.6% of cases, and CIM, in 88.9%/88.9% of cases. In conclusion, BIM and CIM can be usually distinguished on the basis of HE sections. CK 7 and CK 20 expression pattern analysis discriminates correctly between BIM and CIM in the majority of cases. CD10-positive intestinal brush border is present in the majority of CIM but only in a minority of BIM. However, immunohistochemical investigations could not improve the diagnostic accuracy of HE histology alone.

Adult↗
PubMed2005

Guanylyl cyclase C is a marker of intestinal metaplasia, dysplasia, and adenocarcinoma of the gastrointestinal tract.

Gastrointestinal (GI) tumors continue to be major causes of cancer-related mortality, in part, reflecting metastases that escape detection by histopathology. Moreover, although approximately 10% of carcinomas arise from unknown locations, these tumors frequently originate in the GI tract. Guanylyl cyclase C (GC-C) is a receptor selectively expressed by intestinal epithelial cells whose persistent expression by colorectal carcinomas and ectopic expression by adenocarcinomas of the upper GI tract suggest its use as a marker for GI malignancies. Here, expression of GC-C protein, identified by immunohistochemistry, was examined in tissues and tumors arising from the human GI tract. Guanylyl cyclase C protein was expressed by epithelial cells from the duodenum to the rectum, but not by those in normal esophagus and stomach. Expression was retained in tubular adenomas, inflammatory bowel disease, premalignant lesions, and in primary and metastatic adenocarcinomas from the colon, including metastases to lymph nodes and liver. Moreover, GC-C was ectopically expressed in all cases of dysplasia and adenocarcinomas arising from intestinal metaplasia in esophagus and stomach. Thus, GC-C appears to be an immunohistochemical marker for identifying adenocarcinomas of unknown origin, metastases in patients undergoing staging for GI adenocarcinomas, and intestinal metaplasia, dysplasia, and tumors arising therein in the upper GI tract.

Adenocarcinoma↗
PubMed2004

Enhanced expression of decay-accelerating factor, a complement-regulatory protein, in the specialized intestinal metaplasia of Barrett's esophagus.

Intestinal-type epithelium in Barrett's esophagus, so-called specialized intestinal metaplasia (SIM), is a risk factor for the development of esophageal adenocarcinoma. Surface expression of decay-accelerating factor (DAF), a complement-regulatory protein, is markedly enhanced in intestinal metaplasia of the gastric mucosa. We therefore examined DAF expression in areas of SIM in Barrett's esophagus in an attempt to determine whether DAF is a biomarker of SIM. We obtained 53 endoscopic biopsy specimens from the esophageal columnar mucosae of 45 patients. We immunohistochemically examined the distribution of DAF and 2 other complement-regulatory proteins: homologous restriction factor-20 and membrane cofactor protein. We also examined the expression of DAF messenger RNA in SIM with the use of laser-capture microdissection and reverse transcription-polymerase chain reaction. Of the 53 specimens, 10 were found histologically to involve areas of SIM, 41 were SIM-negative epithelium, and 2 comprised areas of SIM and SIM-negative epithelium. DAF staining was negligible in 35 of 43 specimens of the SIM-negative columnar epithelium, but DAF was strongly stained on the apical surface in all 12 SIM-positive specimens (P <.0001). In the 2 biopsy specimens in which both SIM and SIM-negative columnar epithelium were present, DAF staining was confined to the area of SIM. The expression of DAF messenger RNA was detected significantly more often in SIM than in SIM-negative columnar epithelium (P =.022). We conclude that DAF may be a surface marker for SIM and therefore useful in the identification of areas of the mucosa at risk for the development of adenocarcinoma in Barrett's esophagus.

Adult↗
PubMed2005

Massive squamous metaplasia of the thyroid gland-- report of three cases.

Three cases of massive squamous cell metaplasia in Hashimoto's thyroiditis are reported. The patients were two men and one woman aged 24, 52, and 55 years, respectively. In all three patients, the glandular parenchyma was replaced by hypocellular fibrous tissue with scattered chronic inflammatory infiltrate. Follicular cells were almost absent; the majority of residual epithelial cells formed squamous nests that were partly solid and partly cystic. There were three types of epithelial cells - squamous, basaloid, and follicular, with oncocytic differentiation. The squamous and basaloid cells showed strong positivity high molecular weight (HMW) cytokeratin, moderate to strong expression of galectin-3 (2/3), and nuclear expression of p63 protein (2/3). The staining pattern of p63 was identical to that of HMW, with predominant positivity at the periphery of cell nests. In one case, weak but unequivocal positivity of thyroid transcription factor-1 also was present. We believe that metaplasia was caused by Hashimoto's thyroiditis. The cases presented here are extremely rare, and only two convincing similar cases have been reported in the English literature so far. They may represent a diagnostic pitfall and should not be misdiagnosed as a malignancy, in particular as squamous cell or mucoepidermoid carcinoma.

Adult↗
PubMed2006

Regression of intestinal metaplasia to cardiac or fundic mucosa in patients with Barrett's esophagus submitted to vagotomy, partial gastrectomy and duodenal diversion. A prospective study of 78 patients with more than 5 years of follow up.

BACKGROUND: Regression of intestinal metaplasia to cardiac mucosa in patients with Barrett's (BE) esophagus could alter the natural history of BE. OBJECTIVE: To determine the regression of intestinal metaplasia to cardiac mucosa in patients followed more than 5 years after operation, by repeated endoscopy with biopsy. MATERIAL AND METHODS: This prospective study included 78 patients with BE submitted to combined vagotomy, antrectomy (an antireflux procedure), and Roux-en-Y gastrointestinal reconstruction with more than 60 months follow up. Patients were divided in 3 groups: (1) 31 with short-segment BE (< or =30 mm length); (2) 42 with long-segment BE (31 to 99 mm length); and (3) 5 with extra-long-segment BE (> or =100 mm). Each patient had at least three endoscopic procedures with multiple biopsies during a mean follow up of 95 months (range, 60-220 months). Acid and duodenal reflux were also evaluated. RESULTS: Sixty-four percent of patients with short segment BE had regression to cardiac mucosa at a mean of 40 months after operation. Sixty-two percent of patients with long segment BE had regression to cardiac mucosa at a mean of 47 months postoperatively. No regression occurred in the 5 patients with extra-long segment BE. In 20% of patients, regression to fundic mucosa occurred between 78 to 94 months after surgery. One patient progressed to low grade dysplasia, but no patient progressed to high-grade dysplasia or adenocarcinoma. Acid and duodenal reflux studies demonstrated that in asymptomatic patients, reflux was abolished; 90% of the patients had a Visick grade of 1 or 2. CONCLUSIONS: Vagotomy and antrectomy combined with duodenal bile diversion abolish acid and duodenal reflux into the distal esophagus in patients with BE, which is accompanied by a regression of BE from intestinal to cardiac or fundic mucosa in about 60% of patients. This regression is time dependent and varies directly with the length of BE. The potential for an antineoplastic effect, especially in young patients with long segment BE, suggests that this operation may become an attractive option as a definitive surgical treatment. Patients with short segment BE submitted to this procedure behave similar to patients submitted to Nissen fundoplication, and therefore in these patients, we do not advocate this complex operation.

Adolescent↗
PubMed1980

Early physiologic squamous metaplasia of the cervix: light and electron microscopic observations.

A light and electron microscopic study was undertaken of the early phases of cervical squamous metaplasia. A study of areas of columnar epithelium with one row of subcolumnar cells revealed a spectrum of squamous differentiation ranging from cytologically undifferentiation to more characteristically basal type squamous cells. With increasing differentiation, squamous characteristics, such as tonofibrils and desmosomes, became qualitatively and quantitatively more evident in the cells. Ultrastructural examination also revealed cells in the subepithelial stroma with prominent basal lamina and hemidesmosome-like structures along the periphery. From a light and electron microscopic viewpoint, the most likely origin for the subcolumnar progenitor cells appears to be the subepithelial stromal cells. The resemblance of these subepithelial stromal cells to the subcolumnar cells in very early stages of metaplasia is often striking.

Adult↗
PubMed2003

Pathogenesis of mucous cell metaplasia in a murine asthma model.

Increased mucus production in asthma is an important cause of airflow obstruction during severe exacerbations. To better understand the changes in airway epithelium that lead to increased mucus production, ovalbumin-sensitized and -challenged mice were used. The phenotype of the epithelium was dramatically altered, resulting in increased numbers of mucous cells, predominantly in the proximal airways. However, the total numbers of epithelial cells per unit area of basement membrane did not change. A 75% decrease in Clara cells and a 25% decrease in ciliated cells were completely compensated for by an increase in mucous cells. Consequently, by day 22, 70% of the total epithelial cell population in the proximal airways was mucous cells. Electron microscopy illustrated that Clara cells were undergoing metaplasia to mucous cells. Conversely, epithelial proliferation, detected with 5-chloro-2-deoxyuridine immunohistochemistry, was most marked in the distal airways. Using ethidium homodimer cell labeling to evaluate necrosis and terminal dUTP nick-end labeling immunohistochemistry to evaluate apoptosis, this proliferation was accompanied by negligible cell death. In conclusion, epithelial cell death did not appear to be the stimulus driving epithelial proliferation and the increase in mucous cell numbers was primarily a result of Clara cell metaplasia.

Animals↗
PubMed2000

Chromosomal imbalances in Barrett's adenocarcinoma and the metaplasia-dysplasia-carcinoma sequence.

To characterize cytogenetic alterations found in Barrett's adenocarcinoma (BA) and, more importantly, its premalignant stages, we studied chromosomal imbalances in various lesions in the histologically proposed metaplasia-dysplasia-carcinoma sequence using comparative genomic hybridization (CGH). Using 30 esophageal adenocarcinoma resection specimens, we were able to study 30 areas of Barrett's adenocarcinoma and 8 lymph node metastases (LN). In addition, we investigated 25 premalignant lesions adjacent to BA derived from a subset of 14 resection specimens including 11 areas of high grade dysplasia (HGD), 8 areas of low grade dysplasia (LGD), and 6 areas of intestinal metaplasia (IM), which were laser-microdissected and studied with CGH. To validate the CGH findings, fluorescence in situ hybridization analysis on 13 BA with probes specific for HER-2/neu and 20q13.2 were performed. The chromosomal alterations most often identified in BA were: gains on 8q (80%), 20q (60%), 2p, 7p and 10q (47% each), 6p (37%), 15q (33%) and 17q (30%). Losses were observed predominantly on the Y-chromosome (76%), 4q (50%), 5q and 9p (43% each), 18q (40%), 7q (33%) and 14q (30%). High-level amplifications were observed on 8q23-qter, 8p12-pter, 7p11-p14, 7q21-31, 17q11-q23. Recurrent chromosomal changes were also identified in metaplastic (gains on 8q, 6p, 10q, losses on 13q, Y, 9p) and dysplastic epithelium (gains on 8q, 20q, 2p, 10q, 15q, losses on Y, 5q, 9p, 13q, 18q). Novel amplified chromosomal regions on chromosomes 2p and 10q were detected in both Barrett's adenocarcinoma and premalignant lesions. An increase of the average number of detected chromosomal imbalances from IM (7.0 +/- 1.7), to LGD (10.8 +/- 2.2), HGD (13.4 +/- 1.1), BA (13.3 +/- 1.4), and LN (22 +/- 1.2) was seen. Although the detection of common chromosomal alterations in premalignant lesions and adjacent carcinomas suggest a process of clonal expansion, the occurrence of several chromosomal changes in an apparently random order relative to one another is striking evidence that clonal evolution is more complex than would be predicted by linear models. This is probably a reflection of the existence of many divergent neoplastic subpopulations and highlights one of the main problems associated with surveillance of Barrett's patients, namely sampling error.

Adenocarcinoma↗
PubMed1999

Helicobacter pylori-induced chronic active gastritis, intestinal metaplasia, and gastric ulcer in Mongolian gerbils.

The establishment of persisting Helicobacter pylori infection in laboratory animals has been difficult, but in 1996 Hirayama reported the development of a successful Mongolian gerbil model. The present study was undertaken with two aims: to better characterize the normal histological structure and histochemical properties of the gastric mucosa of the Mongolian gerbil; and to evaluate the progression of the histopathological features of H. pylori-induced gastritis in this animal model for one year after the experimental infection. Seventy-five Mongolian gerbils were used. Mongolian gerbils were sacrificed at 2, 4, 8, 12, 26, 38, and 52 weeks after H. pylori inoculation. Sections prepared from stomachs immediately fixed in Carnoy's solution were stained with hematoxylin and eosin and Alcian blue at pH 2.5/periodic acid-Schiff, a dual staining consisting of the galactose oxidase-cold thionin Schiff reaction and paradoxical Concanavalin A staining, and with immunostaining for H. pylori and BrdU. H. pylori infection induced in the Mongolian gerbil a chronic active gastritis, in which a marked mucosal infiltration of neutrophils on a background of chronic inflammation became detectable 4 weeks after inoculation and continued up to 52 weeks. Intestinal metaplasia and gastric ulcers appeared after 26 weeks in some of the animals, whereas others developed multiple hyperplastic polyps. The Mongolian gerbil represents a novel and useful model for the study of H. pylori-induced chronic active gastritis and may lend itself to the investigation of the epithelial alterations that lead to intestinal metaplasia and gastric neoplasia.

Animals↗
PubMed1999

Molecular evolution of the metaplasia-dysplasia-adenocarcinoma sequence in the esophagus.

The incidence of adenocarcinoma of the esophagus has been increasing in developing countries over the last three decades and probably reflects a genuine increase in the incidence of its recognized precursor lesion, Barrett's metaplasia. Despite advances in multimodality therapy, the prognosis for invasive esophageal adenocarcinoma is poor. An improved understanding of the molecular biology of this disease may allow improved diagnosis, therapy, and prognosis. We focus on recent developments in the molecular and cell biology of Barrett's metaplasia, a heterogeneous lesion affecting the transitional zone of the gastro-esophageal junction whose associated molecular alterations may vary both in nature and temporally. Early premalignant clones produce biological and genetic heterogeneity as seen by multiple p53 mutations, p16 mutations, aneuploidy, and abnormal methylation resulting in stepwise changes in differentiation, proliferation, and apoptosis, allowing disease progression under selective pressure. Abnormalities in expression of growth factors of the epidermal growth factor family and cell adhesion molecules, especially cadherin/catenin complexes, may occur early in invasion. Exploitation of these molecular events may lead to a more appropriate diagnosis and understanding of these lesions in the future.

Adenocarcinoma↗
PubMed1999

Accelerated atherosclerosis and premature calcified cartilaginous metaplasia in the aorta of diabetic male Apo E knockout mice can be prevented by chronic treatment with 17 beta-estradiol.

Epidemiological data indicate that estrogens significantly reduce the risk of morbidity and mortality due to cardiovascular diseases in postmenopausal women. Although numerous animal studies demonstrated inhibition of early atheromatous lesion formation by estrogen treatment in several species, information about the potential benefits of estrogens on complex, advanced atherosclerotic lesions is still lacking. The present study was designed to test whether chronic treatment with 17 beta-estradiol affects hyperglycemia-induced premature advanced lesion formation in 40-week-old male apolipoprotein E-deficient (Apo E-KO) mice. In order to accelerate advanced lesion formation, we treated male Apo E-KO mice with streptozotocin (STZ) at the age of 6 weeks. Two weeks later the STZ-treated mice received a slow release pellet containing either 17 beta-estradiol or placebo. STZ treatment caused sustained hyperglycemia without changes in serum total cholesterol or triglyceride levels compared to citrate control mice. STZ-treated Apo E-KO mice developed significantly more lesions in some (but not all) parts of the aorta and its main branches, and caused premature calcified cartilaginous metaplasia in the lesions of the proximal aorta. Chronic treatment with 17 beta-estradiol lead to a significant decrease in blood glucose and triglyceride levels, reduced the lesion area in all vascular segments studied and prevented cartilaginous metaplasia in STZ-treated Apo E-KO mice. The results of this study show that STZ treatment leads to significant acceleration of atherosclerotic lesion formation and premature occurrence of calcified cartilaginous areas in Apo E-KO mice, which could be effectively prevented by chronic estrogen treatment.

Animals↗
PubMed1981

Colonic adenomatous polyp with focal squamous metaplasia.

A case of adenomatous polyp of the colon with focal squamous metaplasia is reported. Squamous metaplasia has been described in both neoplastic and non-neoplastic conditions of the colon. However, it has not previously been documented to occur in adenomatous polyp. The histogenesis, possible predisposing factors, and clinical significance of the lesion are discussed.

Adenoma↗
PubMed1999

Lymphoid proliferations and lymphomas associated with gastric metaplasia, dysplasia, and carcinoma.

Gastric carcinomas are invariably accompanied by lymphoid proliferations. We studied their features in 22 resected gastric carcinomas in which the lymphoid proliferations ranged from reactive lymphoid follicles to mucosa-associated lymphoid tissue (MALT) lymphomas. In most cases, the collections of lymphocytes were abundant, which is remarkable considering the lack of lymphoid tissue in the normal stomach. They were not haphazardly located but in direct contact with the metaplastic, dysplastic, and neoplastic epithelial cells, in positions suggestive of defense barriers. They consisted of newly formed lymphoid follicles with reactive germinal centers sometimes high up in the superficial mucosa, collections of plasma cells beneath the surface epithelium, and large aggregates of B cells above and below the muscularis mucosae as well as abundant T cells. The latter, both CD4+ and CD8+, were seen within metaplastic epithelial cells as well as within carcinomatous glands that were partially destroyed, resembling apparent neoplastic lympho-epithelial lesions (LEL). In three cases, the B cells infiltrating the gastric muscular layers represented MALT-lymphomas adjacent to gastric carcinomas, as confirmed by polymerase chain reaction (PCR) analysis in two cases. In a case of lymphoepithelioma-like carcinoma, the excessive lymphoid cells were predominantly of T-CD8+ type. In this case, EBV identified by EBV-encoded RNA and latent membrane protein was present in large amounts. Helicobacter pylori was seen in only six cases in areas of chronic gastritis that were distant from carcinoma. H. pylori was not present in the areas of metaplasia, dysplasia, or carcinoma. It appears that the lymphoid proliferations accompanying these gastric changes do not arise in response to the pathogenic agent H. pylori, which caused the persistent infection leading to them yet is no longer present, but rather in response to the existence of the abnormal epithelial cells. Thus the lymphoid proliferations consistently associated with gastric metaplasia, dysplasia, and neoplasia may be regarded as immune reactions to the long-term cellular changes triggered by the initial chronic gastritis. On rare occasions, the exaggerated lymphoid proliferations may reach the end of the spectrum, resulting in MALT lymphomas coexistent with gastric carcinomas.

Aged↗
PubMed1999

LOH at the sites of the DCC, APC, and TP53 tumor suppressor genes occurs in Barrett's metaplasia and dysplasia adjacent to adenocarcinoma of the esophagus.

Barrett's esophagus carries a 30- to 100-fold increased risk of adenocarcinoma, which is thought to develop via a metaplasia-dysplasia-carcinoma progression. A common genetic abnormality detected in Barrett's adenocarcinoma is loss of heterozygosity (LOH) at the sites of known or putative tumor suppressor genes, of which there are at least 9 associated with esophageal adenocarcinoma. The aim of this study was to identify at which histological stage of carcinogenesis LOH at these sites occur. Microdissection of multiple paraffin-embedded tissue blocks from 17 esophagogastrectomy specimens of adenocarcinoma arising in Barrett's esophagus yielded areas of metaplasia, low-, intermediate- and high-grade dysplasia, and carcinoma. LOH analysis of microdissected tissues was performed using a double polymerase chain reaction technique with 11 microsatellite primers shown previously to have LOH in at least 30% of esophageal adenocarcinomas. Identical LOH was detected in premalignant and malignant tissues in 4 of 17 patients, and was located at 5q21-q22 (D5S346 primer), 17p11.1-p12 (TCF2 primer), 17p13.1 (TP53 primer), 18q21.1 (detected in colon cancer tumor suppressor gene [DCC] primer), and 18q23-qter (D18S70 primer). These results suggest that LOH at the sites of the DCC, adenomatous polyposis coli (APC), and TP53 tumor suppressor genes occur before the development of adenocarcinoma in Barrett's esophagus, and so merit further study as potential biomarkers of neoplastic progression in patients with Barrett's esophagus undergoing endoscopic and histological surveillance.

Adenocarcinoma↗
PubMed2000

Ureteral obstruction after kidney transplantation secondary to bone metaplasia.

We report a case of ureteral obstruction after kidney transplantation caused by localized bone metaplasia in the donor ureter. Surgical treatment consisted of removal of the involved ureteral segment, which was located 3 cm above the bladder and creation of a spatulated end-to-end anastomosis. Although bone metaplasia has been observed in the ureteral wall of some animal species secondary to experimental ischemia and microtrauma, it is exceedingly rare in humans and has never before been documented after kidney transplantation.

Adult↗
PubMed2002

Squamous metaplasia of the canaliculi associated with 5-fluorouracil: a clinicopathologic case report.

OBJECTIVE: To illustrate a newly recognized histopathologic change in a patient with canalicular obstruction after weekly administration of 5-fluorouracil for colon cancer. DESIGN: Interventional case report. METHODS: A full-thickness section of canaliculus was obtained during surgical repair. MAIN OUTCOME MEASURE: Histopathologic changes in the specimen. RESULTS: The prominent histologic feature of the canalicular specimen was severe squamous metaplasia with narrowing of the lumen. CONCLUSION: Canalicular obstruction may follow systemic use of 5-fluorouracil due to squamous metaplasia.

Aged↗
PubMed1985

Staging of conjunctival squamous metaplasia by impression cytology.

We modified the conventional impression cytology technique for conjunctival study by designing a 24-well Teflon sample holder, using cellulose acetate paper cut in an asymmetrical shape, and introducing Gill's modified Papanicolaou stain. Using this modified technique, we studied 35 normal subjects and 67 patients with various ocular surface disorders, 42 of whom were later found to have squamous metaplasia. Six different cytological stages were defined based on changes of goblet cell density, nucleus, and cytoplasm, encompassing three major steps: (1) loss of goblet cells, (2) increase of cellular stratification or enlargement of superficial cells, and (3) keratinization. This staging system allowed us to correlate pathological changes with clinical findings, and to investigate the action mechanism of squamous metaplasia of conjunctival epithelium. This modified impression cytology technique may help increase understanding of various ocular surface disorders.

Adolescent↗