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PubMed1998

Atrophic gastritis and intestinal metaplasia in Helicobacter pylori infection: the role of CagA status.

OBJECTIVE: Helicobacter pylori (H. pylori) is a major factor in determining the risk for development of gastric adenocarcinoma through the intermediate steps of atrophic gastritis and intestinal metaplasia. Because H. pylori infection is highly prevalent in asymptomatic populations and only a few people develop cancer, additional factors may influence the risk for development of cancer, once infection is established. Some factors may pertain to differences among bacterial strains. Because infection by H. pylori strains possessing cagA (cytotoxin-associated gene A), a gene encoding a high-molecular-weight immunodominant antigen (CagA), is associated with enhanced induction of gastritis, the aim of our study was to evaluate potential differences in the prevalence and intensity of atrophy and intestinal metaplasia between CagA-positive and CagA-negative H. pylori-infected patients. METHODS: Eighty H. pylori-infected patients among 120 consecutive dyspeptic patients referred for upper gastrointestinal endoscopy were studied. Six bioptic specimens were taken from the gastric antrum: five for histological examination, and one for urease test. The H. pylori status was determined by histology, CLO test, and serology (in a standardized ELISA) for serum IgG and IgA directed to H. pylori. The CagA status was determined by Western blotting to detect serum IgG antibodies to CagA. Gastritis was classified according to the Sydney System. A score from 0 to 3 was assigned to each of the following morphological variables: atrophy, intestinal metaplasia, and mononuclear and neutrophilic cell infiltration. The association between CagA status and histological features was assessed by means of the chi2 test for trend. RESULTS: Among the 80 H. pylori-infected patients 53 (66%) were CagA seropositive and 27 (34%) were CagA seronegative. The mean age of the two groups was similar. CagA-positive patients had significantly higher scores for atrophy (p = 0.006), intestinal metaplasia (p = 0.01), and mononuclear (p < 0.001) and polymorphonuclear (p = 0.002) cell infiltration than did CagA-negative patients. No differences in contrast, were found for H. pylori density. CONCLUSION: Infection with CagA-positive H. pylori strains is associated with an increased prevalence and intensity of antral atrophy and intestinal metaplasia, in addition to higher degrees of gastritis. Our results seem to suggest that the CagA status could be a helpful parameter to define a subgroup of H. pylori-infected patients at increased risk of developing gastric adenocarcinoma.

Adult↗
PubMed1999

Comparative study of intestinal metaplasia and mucin staining at the cardia and esophagogastric junction in 225 symptomatic patients presenting for diagnostic open-access gastroscopy.

OBJECTIVE: Adenocarcinoma around the esophagogastric junction (EGJ) is increasing in incidence, and is frequently associated with areas of macroscopic or microscopic intestinal metaplasia (IM). The aim of this study was to define the incidence and type of metaplastic changes in the cardia and at the EGJ in symptomatic patients in whom there was no endoscopic columnar segment. METHODS: Patients attending for open-access gastroscopy had three sets of endoscopic biopsies taken at 3-cm intervals, from cardia, EGJ, and distal esophagus. Hematoxylin and eosin, Alcian blue/PAS (AB/PAS), and high-iron diamine/Alcian blue (AB/HID) were used to define and characterize IM. RESULTS: Of 225 patients, eight (4%) had carcinoma, eight (4%) had conventional long-segment Barrett's esophagus, 15 (7%) showed endoscopic short-segment Barrett's change, with no endoscopic Barrett's in 194 (86.2%). Of the latter, 34 (17.5%) had IM at the EGJ, and nine (4.6%) had IM at the cardia on hematoxylin and eosin. Acid mucin stains were positive at the EGJ in 135 (69.6%) and at the cardia in 75 (38.7%). Metaplasia at the EGJ was associated with sulphomucins (p < 0.0001) and involved the surface glandular epithelium (p < 0.0001) more frequently than the cardia. Metaplasia was not related to reflux symptoms, hiatus hernia, or endoscopic esophageal inflammation. Ninety percent of those with IM detectable by hematoxylin and eosin were taking acid suppression, compared with 72.8% overall. CONCLUSIONS: Intestinal metaplasia is very common at the esophagogastric junction and gastric cardia, with marked differences in incidence and characteristics of mucin staining between the two sites. The relationship of intestinal metaplasia to the development of carcinoma is yet to be determined.

Adolescent↗
PubMed2003

Intestinal metaplasia at the gastroesophageal junction: Barrett's, bacteria, and biomarkers.

For patients found to have intestinal metaplasia at the gastroesophageal junction, technical problems can make it difficult to distinguish short-segment Barrett's esophagus from intestinal metaplasia of the gastric cardia. Whereas the risk of malignancy for the former condition seems to be higher than that for the latter, the distinction between these conditions can have practical clinical implications. Immunostaining for cytokeratins has been proposed as a means to distinguish intestinal metaplasia of esophageal and gastric origins. We review recent data on this issue, and conclude that immunostaining for cytokeratins has no clear advantages over other biomarkers that have been proposed for identifying Barrett's esophagus (e.g., mucin histochemistry, mAb Das-1 immunoreactivity). Presently, the importance of intestinal metaplasia at the gastroesophageal junction remains unclear, and the clinical utility of biomarkers in distinguishing short-segment Barrett's esophagus from intestinal metaplasia of the gastric cardia has not yet been established.

Bacteria↗
PubMed1977

The diagnostic significance of intestinal metaplasia in endoscopic gastric biopsies.

The incidences of intestinal metaplasia in two groups of benign endoscopic biopsies taken from stomachs with malignant and benign lesions respectively were compared. 315 single biopsies were taken from stomachs with proven carcinoma, but outside the carcinomatous area. They were compared to 786 single biopsies taken from stomachs with proven benign lesions. Each single biopsy was placed in one of three groups: intestinal metaplasia absent, or making up less or more than 50 per cent of the epithelium in the biopsy. The results showed that single biopsies with intestinal metaplasia regardless of the extension of the metaplasia in the biopsy were found more often in stomachs with carcinoma than in stomachs with benign lesions but without any significant difference. If more than half of the benign biopsies taken during an examination demonstrated extensive grades of intestinal metaplasia a sligtly significant difference in favour of carcinomas was found.

Biopsy↗
PubMed1991

Helicobacter-associated duodenitis and gastric metaplasia in duodenal ulcer patients.

Biopsy specimens were taken from the duodenal bulb and the distal duodenum in 45 duodenal ulcer patients before and after treatment with histamine-2 antagonists, prostaglandin analogues or antacids. After four weeks of treatment, the ulcer had healed in 31 patients. The treatment did not lead to a reduced frequency of helicobacter-associated duodenitis or gastric metaplasia of the duodenal epithelium. We found gastric metaplasia in 52.3% of all biopsy specimens from the duodenal bulb, chronic active duodenitis in 71.9% and helicobacter-like structures in 15.9%. The helicobacter organisms were found only in areas of gastric metaplasia, and an accompanying chronic active duodenitis was found in 94.1%. In the distal duodenum, we observed chronic active duodenitis in 15.0% of the specimens. Here the inflammation was not associated with gastric metaplasia or helicobacter-like structures. These observations support the hypothesis that Helicobacter pylori colonizes the duodenal mucosa only in areas of gastric metaplasia, and that such colonization may lead to an active duodenitis.

Antacids↗
PubMed1983

Bilateral and unilateral mesodermal corneal metaplasia.

We report on 2 infants, one with a bilateral and the other with a unilateral corneal metaplasia. The first case with bilateral corneal metaplasia showed shortening of both upper and lower lids with formation of symblephara. By ultrasonography the right eye presented with microphthalmos, aphakia, and persistent hyaloid, whereas the inner parts of the left eye appeared to be normal. The question remains to be answered whether this is an abortive cryptophthalmos leading to bilateral corneal metaplasia or a primary corneal metaplasia inhibiting the lid growth. No suggestions concerning the aetiology are made. The second case presented with a unilateral corneal metaplasia, normal eye lids, aphakia, and microphthalmos. This aberration was probably caused by an amniotic band, as it is associated with malformation of the nose on the same side. In case 2 the dermoid was excised and a lamellar corneal graft performed. The histology is reported.

Cornea↗
PubMed1993

Gastric metaplasia and Helicobacter pylori infection.

Duodenal and antral mucosal biopsy specimens were obtained from 139 patients with dyspeptic complaints to study the prevalence and extent of gastric metaplasia in the duodenal bulb in relation to Helicobacter pylori (H pylori) infection and duodenal ulcer disease. On logistic regression, the presence and extent of gastric metaplasia was not significantly associated with H pylori infection. The prevalence of gastric metaplasia, however, was found to be higher in patients with current or past evidence of duodenal ulcer disease in comparison with subjects with functional dyspepsia (p = 0.01). A follow up study on 22 patients before and at least one year after eradication of H pylori showed that the mean extent of gastric metaplasia did not change significantly after eradication and did not differ when compared with 21 patients with persisting infection. It is concluded that the unchanged gastric acid output after eradication of H pylori is a more important factor in the development of gastric metaplasia than the H pylori related inflammatory process.

Adult↗
PubMed2000

The pathogenesis of duodenal gastric metaplasia: the role of local goblet cell transformation.

BACKGROUND AND AIMS: Gastric metaplasia is frequently seen in biopsies of the duodenal cap, particularly when inflamed or ulcerated. In its initial manifestation small patches of gastric foveolar cells appear near the tip of a villus. These cells contain periodic acid-Schiff (PAS) positive neutral mucins in contrast with the alcian blue (AB) positive acidic mucins within duodenal goblet cells. Previous investigations have suggested that these PAS positive cells originate either in Brunner's gland ducts or at the base of duodenal crypts and migrate in distinct streams to the upper villus. To investigate the origin of gastric metaplasia in superficial patches, we used the PAS/AB stain to distinguish between neutral and acidic mucins and in addition specific antibodies to immunolocalise foveolar cell mucin MUC5AC, the foveolar cell secretory product, gastric trefoil factor (TFF1), the mature goblet cell mucin MUC2, and MUC2 core antigen. RESULTS: Cells in focal patches of gastric metaplasia contained secretory granules of both gastric and goblet cell phenotypes. MUC5AC and TFF1 were present as expected in gastric foveolar cells but in addition, MUC2 core antigen, normally present only in the Golgi of intestinal goblet cells, was expressed in secretory granules. Goblet cells in the vicinity of metaplastic patches also expressed both gastric and intestinal antigens. MUC5AC/MUC2 containing goblet cells were most common near the villus tip but were also seen at the base of crypts. Where crypts and Brunner's gland ducts merged they were always seen on the crypt side of the junction. Goblet cells were the only cells to express gastric antigens in these areas. In advanced metaplastic lesions, dual phenotype goblet cells were less evident and fewer cells expressed intestinal mucin antigens. CONCLUSIONS: We suggest that goblet cells that express both intestinal and gastric antigens may represent local precursors of gastric metaplasia undergoing a transition to foveolar-like cells of mixed phenotype at the site of early metaplastic patches. As metaplasia becomes more widespread, a more pure gastric phenotype emerges. This progression is likely to be controlled by local inflammatory signals.

Adolescent↗
PubMed2001

Cytokeratin immunoreactivity of intestinal metaplasia at normal oesophagogastric junction indicates its aetiology.

BACKGROUND AND AIMS: Cytokeratin (CK) 7 and 20 patterns are specific for long and short segments of Barrett's oesophagus but their use has not been assessed in intestinal metaplasia arising in macroscopically normal gastro-oesophageal junction (GOJ). PATIENTS AND METHODS: This study was carried out in a large prospective series of 254 patients who underwent upper endoscopy, had normal gastro-oesophageal anatomy, and who had biopsies of the antrum, fundus, cardia, GOJ, and lower oesophagus. Intestinal metaplasia of the GOJ was typed by histochemistry with high iron diamine-alcian blue staining and by immunohistochemistry using CK7 and CK20 antibodies. Results were correlated with clinical, endoscopic, and pathological data. RESULTS: Sixty (23.6%) of our patients presenting with a normal GOJ had intestinal metaplasia. The CK7/CK20 pattern identified two groups of patients: one highly correlated with Barrett's and the other with characteristics of Helicobacter pylori gastritis. The Barrett's type CK7/CK20 pattern was related to a high frequency of gastro-oesophageal reflux symptoms (p<0.02) and normal endoscopic appearance of the stomach (p<0.03). In contrast, the gastric type CK7/CK20 pattern was linked to atrophic (p<0.02) or erythematous (p<0.05) appearance of the stomach (p<0.03), high frequency of H pylori infection (p<0.04), antral inflammation (p<0.006) with atrophy (p<0.02), and intestinal metaplasia (p<0.02). CONCLUSION: In patients presenting with intestinal metaplasia in normal appearing GOJ, the cytokeratin pattern identifies two groups of patients, one with features identical to those of long segment Barrett's oesophagus and one with features seen in H pylori gastritis. These data may be used by clinicians and should result in improved endoscopic surveillance strategies targeted specifically at patients at increased risk of Barrett's oesophagus and thus cancer.

Adolescent↗
PubMed1987

Campylobacter pyloridis and acid induced gastric metaplasia in the pathogenesis of duodenitis.

Biopsy specimens of gastric and duodenal mucosa from 290 patients were examined histologically for metaplasia and Campylobacter pyloridis. Estimates of pH on samples of fasting gastric juice from 55 of the patients were performed, and mucosal biopsy specimens from 33 patients were also cultured for C pyloridis. Active duodenitis was seen in 34 duodenal biopsy specimens. Thirty (88%) of the patients with active duodenitis had both greater than 5% gastric metaplasia in the duodenal specimen and C pyloridis associated gastritis. These two factors coexisted in only 0.43% of patients with no duodenal inflammation. When C pyloridis were seen histologically in duodenal biopsy specimens they were confined to areas of gastric metaplasia and never occurred in the absence of a polymorph infiltrate. Of the 55 patients with measurements of gastric juice pH, gastric metaplasia was present in the duodenum in 20 of 42 with a pH of less than 2.5, and in 0 of 13 with a pH of greater than 2.5. These results suggest that acid induced gastric metaplasia in the duodenum and C pyloridis associated gastritis may be synergistic in the pathogenesis of duodenitis; the metaplastic gastric epithelium allows C pyloridis to colonise the duodenal mucosa, where it produces an acute inflammatory response.

Adolescent↗
PubMed1996

Immunohistochemical evaluation of keratin 20 expression in intestinal metaplasia types I to III.

AIMS: To investigate differences in expression of keratin 20, a cytoskeletal protein in gastrointestinal epithelial cells, in completely differentiated intestinal metaplasia (type I) and incomplete metaplasia (types II and III). METHODS: Gastric biopsy specimens from 66 patients with intestinal metaplasia were analysed immunohistochemically. Expression of keratin 20 was quantified as the percentage of immunoreactive cells on the tips, the upper, and deep foveolae. RESULTS: In all specimens keratin 20 was found on the tips and in the upper foveolae of intestinal metaplasia. Keratin 20 was not observed in the deep foveolae. No differences were seen between the antrum and the body. Expression patterns were comparable between types I and III. In type II, however, lower immunoreactivity was found. Both the differences between types I and II as well as between types II and III were significant (p < 0.05). CONCLUSIONS: Keratin 20 is expressed in metaplastic mucosa as a result of intestinal differentiation. Positive staining found exclusively in juxtaluminal cells occurs only in mature cells containing keratin 20. Lowered immunoreactivity in type II compared with types I and III indicates the different nature of type II intestinal metaplasia. Further studies are needed to shed light on the basic fundamental mechanism responsible for this.

Adult↗
PubMed1976

Squamous metaplasia of the tracheal epithelium in children.

Thirty-seven (1-6%) tracheas from 2170 children showed squamous metaplasia. (Cases with tracheo-oesophageal fistula and congenital heart disease were excluded). The metaplasia extended into the bronchi in 15 cases. Features of pulmonary retention were present in seven cases. Respiratory infection, probably viral, seemed to be the most significant causative factor in 20 children, including those with cystic fibrosis. Tracheal instrumentation was a possible factor in 11 cases but oxygen therapy alone did not seem important. The metaplasia was almost certainly congenital in one child and probably in two others but no stillborn infants showed metaplasia. In many children the metaplasia seemed to be due to a combination of factors.

Child↗
PubMed2004

Development of gastric carcinoma from intestinal metaplasia in Cdx2-transgenic mice.

In the progression of chronic gastritis, gastric mucosal cells deviate from the normal pathway of gastric differentiation to an intestinal phenotype. Many epidemiologic studies have found an association between the formation of intestinal metaplasia and the development of gastric carcinoma. However, there is no direct evidence that shows intestinal metaplasia is a precursor lesion of gastric carcinoma, to date. We periodically examined the intestinal metaplastic mucosa of Cdx2-transgenic mice we have previously generated. Gastric polyps developed from intestinal metaplastic mucosa in all stomachs of Cdx2-transgenic mice examined. These gastric polyps consisted of intestinal-type adenocarcinoma that invaded the submucosa and muscularis propria and occasionally spread into the subserosa. p53 and APC gene mutations were recognized in the adenocarcinomas. The participation of APC and p53 gene mutations in gastric carcinogenesis from the intestinal metaplasia was verified by the Cdx2-transgenic mice, carrying Apc(Min) mutation or p53 deficiency, that developed gastric polyps much earlier than Cdx2 alone. We successfully showed that long-term intestinal metaplasia induces invasive gastric carcinoma. These results indicate that intestinal metaplasia itself plays a significant role in the genesis and progression of gastric carcinoma.

Adenocarcinoma↗
PubMed2000

Inflammation and intestinal metaplasia of the gastric cardia: Helicobacter pylori, gastroesophageal reflux disease, or both.

The gastric cardia is a microscopic zone that is normally found in the most proximal portion of the stomach, although cardiac-type mucosa may arise in the distal esophagus as a metaplastic phenomenon secondary to gastroesophageal reflux disease (GERD). Inflammation of the native gastric cardia is strongly associated with Helicobacter pylori infection, although there may be a second form of 'carditis' in which metaplastic cardiac-type mucosa becomes inflamed secondary to GERD. Intestinal metaplasia of the cardia may be difficult to recognize because of the difficulty in accurately identifying the esophagogastric junction by endoscopy and the histologic similarities of intestinal metaplasia in the proximal stomach and distal esophagus. However, cytokeratin 7 and 20 immunoreactivity patterns appear to be useful in distinguishing between these forms of intestinal metaplasia. The preponderance of data suggests that intestinal metaplasia of the cardia is associated with H. pylori infection as opposed to GERD, and preliminary data suggest a lower risk of progression to dysplasia and adenocarcinoma when compared to intestinal metaplasia of the distal esophagus.

Cardia↗
PubMed1996

P53 in squamous metaplasia: a marker for risk of respiratory tract carcinoma.

Dysplasia in squamous metaplasia of the respiratory tract was believed to be a reversible premalignant lesion. Recently, presumably irreversible genetic alterations have been demonstrated in squamous metaplasia with dysplasia in lung-resection specimens. The genetic alterations were closely similar to those in adjacent bronchial carcinoma. There remains the question of which changes in squamous metaplastic lesions are premalignant, and which of these changes predict the occurrence of carcinoma of the respiratory tract. The purpose of this study was to determine the positive predictive value for respiratory-tract malignancy of the grade of dysplasia, p53 immunoreactivity, proliferative activity, and Bcl-2 in bronchial biopsy specimens exhibiting squamous metaplasia. Bronchial biopsies of 51 patients with squamous metaplasia diagnosed between 1982 and 1993 were used. Immunohistochemistry was done after microwave pretreatment of the biopsy specimens. Only unequivocally stained nuclei were counted. Normal bronchial epithelium obtained from autopsies was used as a control. In 31 patients, a synchronous or metachronous carcinoma was present (61%). Positive p53 immunoreactivity was found in 22 of the 51 patients (43%). The positive predictive values of p53 and of a high grade of dysplasia for carcinoma of the respiratory tract were 91% and 80%, respectively. Although the hyperproliferative state of squamous metaplastic lesions was clearly established, neither the percentage of MIB-1 labelling nor the mitotic index distinguished patient groups with and without carcinoma. No increased Bcl-2 immunostaining was found in squamous metaplasia. In conclusion, p53 immunoreactivity in squamous metaplastic lesions in bronchial biopsies is a marker of carcinoma of the respiratory tract.

Adenocarcinoma↗
PubMed1998

Fluticasone propionate attenuates ozone-induced rhinitis and mucous cell metaplasia in rat nasal airway epithelium.

Ozone (O3) is the principal oxidant pollutant in photochemical smog. Repeated exposures to O3 induces inflammation and mucous cell metaplasia in the nasal airways of laboratory animals. Our study was designed to determine the efficacy of a topical anti-inflammatory corticosteroid in preventing O3-induced rhinitis and mucous cell metaplasia in rat nasal epithelium. Male F344 rats were exposed to filtered air (0 ppm O3; air-controls) or 0.5 ppm O3, 8 h/day, for 3 or 5 days. Immediately before and after each exposure, rats received an intranasal instillation (50 microl/nasal passage) of a topical corticosteroid, fluticasone propionate (FP; 25 microg/nasal passage) or its vehicle only (0.01% ethanol in saline). Rats were killed 2 h after the third exposure (3-day exposure) or 3 days after the fifth exposure (5-day exposure) and nasal tissues were processed for light microscopy. Numeric densities of epithelial cells and neutrophils, and the amount of intraepithelial mucosubstances (IM) in the epithelium lining the maxilloturbinates were morphometrically determined. There were no significant differences in any measured parameter in air-exposed rats instilled with FP compared with air-exposed rats instilled with vehicle. Vehicle-treated rats exposed to ozone had neutrophilic rhinitis with 3.3- and 1.6-fold more intraepithelial neutrophils (3-day and 5-day exposure, respectively) and marked mucous cell metaplasia (5-day exposure only) with numerous mucous cells and approximately 60 times more IM in the nasal transitional epithelium compared with vehicle-treated air-controls. FP-treated rats exposed to ozone had minimal nasal inflammation (1.3-fold more intraepithelial neutrophils only after 3-day exposure) and minimal mucous cell metaplasia (5-fold more IM only after 5-day exposure) compared with vehicle-instilled, air-exposed rats. Results of this study indicate that FP-treatment is effective in attenuating not only O3-induced rhinitis (30-60% reduction) but also O3-induced mucous cell metaplasia (85% reduction) in rat nasal transitional epithelium. The cellular and molecular mechanisms involved in FP-induced attenuation of O3-induced nasal lesions remain to be determined.

Administration, Topical↗
PubMed2006

Epidermal growth factor receptor activation by epidermal growth factor mediates oxidant-induced goblet cell metaplasia in human airway epithelium.

Mucus overproduction in inflammatory and obstructive airway diseases is associated with goblet cell (GC) metaplasia in airways. Although the mechanisms involved in GC metaplasia and mucus hypersecretion are not completely understood, association with oxidative stress and epidermal growth factor receptor (EGFR) signaling has been reported. To explore the mechanisms involved in oxidative stress-induced GC metaplasia, cultures of differentiated normal human bronchial epithelial cells grown at the air-liquid interface were exposed to reactive oxygen species (ROS) generated by xanthine/xanthine oxidase. EGFR activation and signaling was assessed by measuring EGF and transforming growth factor-alpha release and EGFR and (44/42)MAPK phosphorylation. The GC population was evaluated by confocal microscopy. ROS-induced EGFR activation resulted in GC proliferation and increased MUC5AC gene and protein expression. Signaling was due to pro-EGF processing by tissue kallikrein (TK), which was activated by ROS-induced hyaluronan breakdown. It was inhibited by catalase, a TK inhibitor, and EGF-blocking antibodies. Exposure to recombinant TK mimicked the ROS effects, increasing the expression of MUC5AC and lactoperoxidase. In addition, ROS induced the antiapoptotic factor Bcl-2 in a TK-dependent fashion. In conclusion, ROS-induced GC metaplasia in normal human bronchial epithelial cells is associated with HA depolymerization and EGF processing by TK followed by EGFR signaling, suggesting that increases in TK activity could contribute to GC metaplasia and mucus hypersecretion in diseases such as asthma and chronic bronchitis. The data also suggest that increases in GC population could be sustained by the associated upregulation of Bcl-2 in airway epithelial cells.

Cell Differentiation↗
PubMed1986

Squamous metaplasia in the trachea: the tracheotomized rabbit as an experimental model and implications in recurrent papillomatosis.

Squamous metaplasia following tracheotomy has been well documented. Most studies have dealt primarily with changes at--or adjacent to--the cuff site and have failed to evaluate its effect in the distal trachea. We have used rabbits as experimental models for the induction of tracheal squamous metaplasia, using uncuffed tracheotomy tubes. Rabbits were routinely killed 24, 36, 48, 72, 120, and 168 hours posttracheotomy, and the entire larynx, trachea, and main-stem bronchi were step-sectioned for histologic examination. Patchy areas of squamous metaplasia were found in all rabbits with tracheotomy equal to or longer than 48 hours. The metaplasia appeared to increase with time of intubation. Induction of squamous metaplasia (following tracheotomy as a contributing factor to the spread of laryngeal papillomatosis) is discussed.

Animals↗