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ABSTRACT: Helicobacter pylori infection is associated with variable clinical outcomes, including gastroduodenal diseases, and genetic factors may be relevant in this process.
We investigated the effects of an interleukin 8 (IL-8) gene polymorphism on the risk of gastroduodenal diseases, the degree of H pylori induced gastritis, and IL-8 gene transcription.
The study was performed in 244 healthy control subjects and 690 H pylori positive patients with non-cardia gastric cancer, gastric ulcer, duodenal ulcer, or gastritis.
We identified the IL-8 -251 A/T polymorphism by direct sequence analysis, and measured the gastritis score and serum pepsinogen (PG). The transcriptional promoter activity of the IL-8 gene was assessed by luciferase assay.
IL-8 -251A was associated with a higher risk of gastric cancer and gastric ulcer. Patients carrying IL-8 -251A showed an increased risk of gastric cancer (odds ratios (OR) 2.01 (95% confidence interval (CI) 1.38-2.92)) and gastric ulcer (OR 2.07 (95% CI 1.37-3.12)). Compared with patients younger than 49 years, atrophy and metaplasia scores in the antrum were significantly higher and the PG I/II ratio significantly lower in -251A carriers than in T/T carriers. In the in vitro assay, IL-8 -251A showed enhanced promoter activity in response to IL-1beta or tumour necrosis factor alpha.
The IL-8 -251A allele may be associated with progression of gastric atrophy in patients with H pylori infection, and may increase the risk of gastric cancer and gastric ulcer in Japanese people.
Gut 04/2005; 54(3):330-5. · 10.11 Impact Factor
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ABSTRACT: In Japan, where the incidence of gastric cancer is high, Helicobacter pylori infection could affect gastric acid secretion differently from that in Western countries. The aim of this study was to investigate the relationship between H. pylori infection, acid secretion, aging, and gender in normal Japanese subjects.
The study comprised 193 Japanese subjects who had undergone routine endoscopy. Gastrin-stimulated acid output was performed during the routine endoscopic examination using the endoscopic method of gastric acid secretory testing (EGT: endoscopic gastrin test), which has been reported previously. H. pylori status was determined by histology, rapid urease test, and serology.
Mean EGT values were 3.9 +/- 1.5 mEq/10 min in H. pylori-negative men, 1.6 +/- 2.5 in H. pylori-positive men, 2.2 +/- 0.9 in H. pylori-negative women, and 1.5 +/- 1.2 in H. pylori-positive women. Although acid secretion was lower in H. pylori-positive subjects compared with H. pylori-negative subjects in both men and women, the decrease was more marked in men with H. pylori infection. Multiple linear regression analysis showed that aging is positively associated with gastric acid secretion in the H. pylori-negative subjects, whereas a negative association was found between them in the H. pylori-positive subjects.
In Japanese subjects, aging affects gastric acid secretion differently depending on the status of H. pylori infection. H. pylori infection showed a stronger inhibitory effect on the acid secretion in men than in women. This gender-related difference in the susceptibility of acid secretion to H. pylori infection may explain the higher rates of gastric cancer in men in Japan.
Scandinavian Journal of Gastroenterology 08/2004; 39(8):709-16. · 2.02 Impact Factor
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ABSTRACT: Although profound hypochlorhydria is considered to be an important risk factor for development of gastric cancer, long-term effect of Helicobacter pylori eradication on its reversibility remains uncertain.
To clarify the change in acid secretion after eradication in a long-term follow-up over 5 years in patients with profound hypochlorhydria.
Twenty-three H. pylori-positive patients with hypochlorhydria (<0.6 mmol/10 min) were enrolled prospectively. Assessment of gastrin-stimulated acid output and histologic evaluation of biopsy specimens were performed prior to, and 1, 7 months after eradication. Subsequently, gastric acid secretion was assessed for long-term period over 5 years after eradication in 12 patients.
Gastric acid secretion was reversed to normal range in nine of 23 patients (39%) at 7 months after eradication. In the long-term follow-up, gradual and significant recovery in gastric acid secretion was observed up to 2 years post-therapy. However, there was no additional increase during the last 3 years of 5-year follow-up period, leaving the acid secretory levels subnormal in the majority of the patients.
This long-term follow-up study suggests that the pathologic process has already progressed to an irreversible stage in the majority of H. pylori-positive patients with marked body atrophy and profound hypochlorhydria.
Alimentary Pharmacology & Therapeutics 07/2004; 19(11):1181-8. · 3.77 Impact Factor
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T Sano,
G Hirasawa,
J Takeyama,
A D Darnel,
T Suzuki,
T Moriya,
K Kato, H Sekine,
S Ohara,
T Shimosegawa,
J Nakamura,
M Yoshihama,
N Harada,
H Sasano
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ABSTRACT: The 17 beta-hydroxysteroid dehydrogenases (17 beta HSDs) play an important role in the regulation of intracellular levels of biologically active sex steroid hormones in various human tissues. To date, eight distinctive 17 beta HSD enzymes have been cloned and characterized in humans. Among these isoenzymes, 17 beta HSD type 2 (17 beta HSD2) catalyses the conversion of testosterone into androstenedione and/or oestradiol into oestrone in various tissues, and it has thus been suggested to be involved in the biological inactivation of these sex steroids. The human gastrointestinal tract and liver are considered as the principle sites of inactivation and metabolism of various forms of orally administered sex steroids. We therefore examined 17 beta HSD2 expression and activity in human adult non-pathological gastrointestinal tract in order to clarify further the biological significance of this enzyme. A total of 80 specimens (40 from males and 40 from females) of normal oesophageal, stomach, duodenal, ileal, colonic and rectal tissues were examined for immunohistochemistry. Altogether, 17 tissue specimens were used for enzyme assay, and eight for RNA analysis. 17 beta HSD2 activity was detected in the stomach, duodenum, ileum, colon and rectum. 17 beta HSD2 mRNA was most abundant in the small intestine. 17 beta HSD2 immunoreactivity was localized almost exclusively to the absorptive epithelium, which may be involved in the inactivation of excessive endogenous and exogenous active sex steroids. Results from the present study thus suggest that the human gastrointestinal tract is an important sex steroid metabolizing organ in humans.
Clinical Science 12/2001; 101(5):485-91. · 4.61 Impact Factor
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ABSTRACT: Helicobacter pylori infection is less prevalent and atrophic gastritis is less extensive in patients with reflux oesophagitis than those without it, but few studies have examined this relationship directly.
We investigated the relationship between H pylori infection, acid secretion, and reflux oesophagitis in Japanese subjects.
A total of 105 patients with erosive reflux oesophagitis were compared with 105 sex and age matched patients without reflux oesophagitis.
The diagnosis of H pylori infection was made by histological examination of gastric mucosal biopsy specimens, rapid urease test, and detection of serum IgG antibodies. Acid secretion was assessed by the endoscopic gastrin test.
H pylori infection was present in 36 patients with erosive reflux oesophagitis (34.3%) and in 80 control subjects (76.2%) (odds ratio 0.163, 95% confidence interval 0.09-0.29). Overall acid secretion was significantly greater in patients with reflux oesophagitis. Among H pylori positive patients, acid secretion was greater in patients with reflux oesophagitis than those without oesophagitis.
In Japan, erosive reflux oesophagitis occurs most often in the absence of H pylori infection and gastric hyposecretion. Even in the presence of H pylori infection, reflux oesophagitis is more likely to develop in patients without gastric hyposecretion. H pylori infection may inhibit reflux oesophagitis by inducing hypoacidity.
Gut 10/2001; 49(3):330-4. · 10.11 Impact Factor
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ABSTRACT: The role of acid secretion in reflux oesophagitis which may develop after H. pylori eradication is not well known.
To investigate the participation of altered gastric acid secretion and the presence of hiatal hernia in the development of reflux oesophagitis after eradication therapy for H. pylori.
A total of 105 patients with H. pylori infection, but without reflux oesophagitis at the time of eradication therapy, were followed prospectively for 7 months after the clearance of this microorganism. Gastric acid secretion was assessed by endoscopic gastrin test, and the presence of hiatal hernia by endoscopy.
Reflux oesophagitis developed in 11 out of 105 (10.5%) patients when examined at 7 months after the eradication therapy. The incidence was correlated significantly with the increase in gastric acid secretion after the eradication of H. pylori, and was significantly higher in the patients with hiatal hernia (20%) than in those without it (0%).
Increased acid secretion after H. pylori eradication is an important risk factor of reflux oesophagitis, especially in patients with hiatal hernia.
Alimentary Pharmacology & Therapeutics 07/2001; 15(6):813-20. · 3.77 Impact Factor
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T Kikuchi,
K Kato,
S Ohara, H Sekine,
T Arikawa,
T Suzuki,
K Noguchi,
M Saito,
Y Saito,
H Nagura,
T Toyota,
T Shimosegawa
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ABSTRACT: Helicobacter pylori (HP)-infected gastric mucosa displays a conspicuous infiltration of mononuclear cells as well as neutrophils. RANTES is a potent chemoattractant peptide for memory T lymphocytes and eosinophils. RANTES protein concentration and the numbers of RANTES-, CD45RO-, and major basic protein (MBP)-positive cells were therefore evaluated in the gastric mucosa from 51 patients with HP-positive chronic gastritis before and after HP eradication and from 22 HP-negative healthy volunteers. RANTES protein concentration was significantly elevated in HP-positive cases and remained high after HP eradication. The numbers of RANTES-, CD45RO-, and MBP-positive cells were significantly increased in HP-positive cases and were well correlated with RANTES protein levels. All tended to decrease after HP eradication, but did not reach the level of HP-negative cases, even at 24 months after HP eradication. It was concluded that persistent expression and secretion of RANTES were closely related to residual infiltration of memory T lymphocytes and eosinophils, for a prolonged period after HP eradication. This seems to be an important mechanism of prolonged gastric mucosal immune response against HP infection, even after HP eradication, and of persistent mucosal damage and atrophy.
The Journal of Pathology 11/2000; 192(2):243-50. · 6.32 Impact Factor
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ABSTRACT: It remains controversial whether or not Helicobacter pylori infection causes altered gastric acid secretion. A novel test for evaluating gastric acid secretion (endoscopic gastrin test; EGT) has recently been developed.
To investigate by EGT the effects of H pylori eradication on the state of gastric acid secretion in patients with peptic ulcer.
Twenty six patients with duodenal ulcer and 33 with gastric ulcer, for all of whom H pylori infection had been documented, were studied by EGT, histological examination of gastric mucosa, and measurement of plasma gastrin levels before and one and seven months after H pylori eradication.
In patients with duodenal ulcer, the mean EGT value before H pylori eradication was higher than that in H pylori negative controls, but it had decreased significantly seven months after the treatment. In contrast, the mean EGT value of patients with gastric ulcer before H pylori eradication was lower than that in H pylori negative controls, but it had increased one month after the treatment; this was followed by a slight decrease at seven months. In both groups, mean EGT values seven months after the treatment were not significantly different from the mean control value.
The reduced acid secretion in gastric ulcer patients and gastric acid hypersecretion in duodenal ulcer patients were both normalised after the clearance of H pylori.
Gut 02/2000; 46(1):20-6. · 10.11 Impact Factor
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ABSTRACT: Although it is widely accepted that Helicobacter pylori (H. pylori) infection is an important cause of atrophic gastritis, few studies have examined the relationship between H. pylori-induced atrophic gastritis and the occurrence of reflux esophagitis. The present study was aimed to examine the relationship between H. pylori infection, atrophic gastritis, and reflux esophagitis in Japan.
A total of 175 patients with reflux esophagitis were compared with sex- and age-matched 175 control subjects. Diagnosis of H. pylori infection was made by gastric mucosal biopsy, rapid urease test, and serum IgG antibodies. Severity of atrophic gastritis was assessed by histology and serum pepsinogen I/II ratio.
H. pylori infection was found in 59 (33.7%) patients with reflux esophagitis, whereas it was found in 126 (72.0%) control subjects. The grade of atrophic gastritis was significantly lower in the former than in the latter. Among the H. pylori-positive patients, atrophic gastritis was milder in the patients with reflux esophagitis than in the patients without it.
These findings suggest that most cases of reflux esophagitis in Japan occur in the absence of H. pylori infection and atrophic gastritis, and it may also tend to occur in patients with milder gastritis even in the presence of H. pylori infection. Therefore, H. pylori infection may be an inhibitory factor of reflux esophagitis through inducing atrophic gastritis and concomitant hypoacidity.
The American Journal of Gastroenterology 01/2000; 94(12):3468-72. · 7.28 Impact Factor
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T Kikuchi,
K Kato,
S Ohara, H Sekine,
T Arikawa,
T Suzuki,
Y Konno,
K Noguchi,
M Saito,
Y Saito,
T Simosegawa,
T Toyota
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ABSTRACT: We attempted to evaluate the relationship between the expression of IL-8 and RANTES and the dynamics of their target cells in human gastric mucosa of H. pylori associated gastritis, including their changes after H. pylori eradication. We performed the measurement of the mucosal level of IL-8 and RANTES protein by ELISA and immunohistochemistry. The neutrophil infiltration into the gastric mucosa was identified by the histological examination based on the Updated Sydney system and the measurement of MPO activity. The memory T lymphocyte and eosinophil were indicated by immunohistochemistry of CD45RO that is one of surface markers indicating memory T lymphocytes and MBP that is contained in the granules of eosinophils. H. pylori positive gastric mucosa demonstrated a remarkable increase in neutrophils. CD45RO positive cells and eosinophils, compared to H. pylori negative gastric mucosa. Gastric mucosal level of IL-8 and RANTES protein and MPO activity was significantly higher in H. pylori positive cases than that in H. pylori negative controls after H. pylori eradication, both of the level of IL-8 protein and MPO activity reduced at the same levels as negative controls. However, RANTES expression, CD45RO positive T lymphocytes and eosinophils remained in H. pylori eradicated gastric mucosa at the significantly high level, compared with H. pylori negative cases. Therefore, it seems possible that IL-8 might enhance the inflammation by facilitating the neutrophil infiltration into H. pylori infected gastric mucosa and that RANTES might play an important role in the specific immune response against H. pylori and the maintenance of the immune memory after H. pylori eradication.
Nippon Shokakibyo Gakkai zasshi The Japanese journal of gastro-enterology 09/1999; 96(8):933-40.
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K Kato,
H Sasano,
S Ohara, H Sekine,
S Mochizuki,
T Mune,
K Yasuda,
H Nagura,
T Shimosegawa,
T Toyota,
Z Krozowski
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ABSTRACT: The role of mineralocorticoids in human gastrointestinal tract is well established. In the stomach, aldosterone is thought to regulate electrolyte transport associated with gastric acid secretion. In mineralocorticoid target organs, the action of the glucocorticoid inactivating enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) facilitates aldosterone binding to a nonselective mineralocorticoid receptor (MR) in the face of high levels of circulating glucocorticoids. In the present study, we examined 25 specimens of human stomach for the presence of MR and 11beta-HSD2 using a [3H]aldosterone binding assay, Northern blot analysis, RT-PCR, and immunohistochemistry. Specific [3H]aldosterone binding sites were detected in gastric fundic mucosa, but not in the antrum. In fundic mucosa the Kd was 0.72+/-0.05 nmol/L (mean +/- SE), and Bmax was 6.0+/-1.4 fmol per milligram of protein. Northern blot analysis demonstrated a faint band for MR mRNA at 6.0 kb, although message for 11beta-HSD2 was undetectable. However, RT-PCR demonstrated specific PCR products for both MR and 11beta-HSD2. Immunohistochemistry demonstrated the colocalization of MR and 11beta-HSD2 only in parietal cells. MR-positive cells were further characterized by electron microscopy, confirming the identity of parietal cells. This study shows that parietal cells contain both MR and 11beta-HSD2, suggesting that the human stomach is a novel target organ for mineralocorticoids. Aldosterone may, therefore, regulate biological functions of parietal cells including gastric acid secretion.
Journal of Clinical Endocrinology & Metabolism 08/1999; 84(7):2568-73. · 6.50 Impact Factor
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ABSTRACT: Three hundred thirty-three patient (116 gastric ulcer, 119 duodenal ulcer, 98 gastritis) who were successfully eradicated were enrolled in the study of H. pylori recurrence rate. H. pylori status was determined by histology, rapid urease test, 13C-urea breath test. The mean of the follow-up period was 13.3 months (2-56 months), and 15 patients showed negative to positive conversion of H. pylori. The recurrence rate was 4.4% for one year and 8.3% for two years using Kaplan-Meier analysis. Second eradication therapy after initial failure is another concern. Nineteen patients were assigned to receive an 1-week new triple therapy (clarithromycin, metronidazole and PPI), in whom a 2-week course of dual therapy (amoxicillin plus PPI) failed (group1). Another 15 patients in whom the 1-week new triple therapy failed were switched to the 2-week course of dual therapy plus ecabet sodium (group2). H. pylori was eradicated in 84.2% (16/19) of patients in group1 and 86.7% (13/15) in group2.
Nippon rinsho. Japanese journal of clinical medicine 02/1999; 57(1):116-20.
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ABSTRACT: The aims of this study were to investigate whether the changes in gastric acid secretion after H. pylori eradication might influence the development of acute duodenitis (AD) and reflux esophagitis (RE). Stimulated acid output was assessed by EGT (mEq/10 min), which is the new endoscopic method of gastric secretory testing described previously. Changes in the EGT values before and after eradication were divided into 4 groups; decreased group, no change group, increased group, markedly increased group. Results estimated by EGT demonstrated that AD and RE development after eradication significantly correlated with the increase of acid secretion. In conclusion, the increase of acid secretion was thought to be one of the most important risk factors of both AD and RE developed after H. pylori eradication.
Nippon rinsho. Japanese journal of clinical medicine 02/1999; 57(1):196-200.
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ABSTRACT: To date, the effect of Helicobacter pylori on acid secretion remains controversial. To evaluate changes in the gastric acid secretory response before and after H. pylori eradication in a large number of patients, we devised a new endoscopic method of gastric acid secretory testing, the endoscopic gastrin test (EGT).
In EGT, endoscopy was begun 15 min after intramuscular injection of 4 microg/kg tetragastrin. Gastric fluid secreted between 20 and 30 min after gastrin injection was aspirated and collected during endoscopic examination. The amount of acid in the sample collected over this 10-min period was estimated by titration and expressed in H+ mEq/10 min. Fifteen subjects underwent a conventional secretory test using a nasogastric tube (conventional method) and EGT on different days to assess the correlation between results obtained with the two methods. In 10 of these subjects, EGT was repeated under the same conditions to assess its reproducibility.
EGT values correlated very well with peak acid output determined by the conventional method (n = 15, r = 0.92) and had high reproducibility (n = 10, CV = 5.6). We noted that EGT takes just a little longer to perform than a routine endoscopic examination, and the influence of an endoscope in the stomach on acid secretion was not present.
The EGT should be very useful as a rapid, simple substitute for conventional secretory testing when repeated gastric secretory tests are required, especially in investigating the effect of H. pylori on acid secretion in a larger population.
The American Journal of Gastroenterology 12/1998; 93(11):2113-8. · 7.28 Impact Factor
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T Koike,
S Ohara, H Sekine,
K Iijima,
S Moriyama,
K Katoh,
K Honda,
M Kitagawa,
Y Konno,
K Noguchi,
S Asaki,
T Toyota
Nippon Shokakibyo Gakkai zasshi The Japanese journal of gastro-enterology 05/1998; 95(4):317-20.
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ABSTRACT: 13C-urea breath test (UBT), available for diagnosis of Helicobacter pylori (HP) in the stomach, measures the 13CO in the breath in which 13C urea is resolved in the stomach by urease derived from HP. Accordingly UBT is useful for a test of HP infection. This study is aimed at clarifying the relationship between the UBT and gastric histological findings. For this study we selected 63 patients with HP infection who showed both positive UBT and positive histological diagnosis. Briefly in the UBT procedure, the patients were given 13C-urea (100 mg dissolved 100 ml water) in a fasting state and kept in the left decubitus position for 5 minutes, and then the patients were asked to expire into testing bags before and 20 minutes after administration of the urea. Biopsy specimens were taken endscopically from the gastric antrum and the body. The specimens of all patients showed positive CLO test. HP organisms, inflammation, activity, and atrophy of the gastric specimens, were expressed in score from 0 to 3 according to the Update Sydney system. The UBT values were high correlated with the increase of HP organisms. The UBT was 11.8, 26.3, and 37/1000 in the groups with the scores of 0.1, and 2 in the number of HP organisms from the gastric body, respectively. The UBT was 19.2, 22.2, 36.1, 26.7/1000 in the groups with scores of 0, 1, 2, and 3 for the specimens from the antrum, respectively. The results show that there is a positive correlation between the UBT values and HP organisms. As a result, the UBT correlated with the activity score. Grade of gastric mucosal atrophy was expressed histologically in scores of 0,1,2, and 3. The UBT was 29.4, 19.1, 17.5, and 9.3/1000 in the groups with scores 0,1,2, and 3 in the grades of gastric atrophy from the gastric body, respectively. There was a negative correlation between the UBT values and the grade of gastric atrophy. We conclude that the UBT values which indicate the number of HP organisms can be used not only for diagnosis of HP infection but also the quantitative index of HP load.
Nippon Shokakibyo Gakkai zasshi The Japanese journal of gastro-enterology 02/1998; 95(1):18-25.
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ABSTRACT: In this study, we investigate simple breath test for detection of Helicobacter pylori (HP) infection using 13C-urea. Thirty-nine patients (30 were HP positive, 9 were HP negative) were given three different doses (50, 100 and 150 mg) of 13C-urea at fasting, and keep sitting after mouth washing with water. Breath samples were taken before and 10, 20, 30, 45, and 60 minutes after urea administration. More than 100mg of 13C-urea was necessary for correct diagnosis of HP infection, because 2 HP positive cases were not detected by 50mg 13C-urea administration. In cases with patchy distribution of HP in the stomach, it may be necessary to change the posture to distribute urea within the whole stomach. In most of HP positive cases, peak delta 13CO2 were obtained within 30 minutes, but one HP negative case showed high delta 13CO2 at 10 minutes, which was probably caused by urease activity in the mouth. So it is appropriate to take breath sample at 20 minutes after urea administration. In this study, cut-off value for a positive test can be setted between 4 to 7 delta/1000, it is necessary to investigate much more cases to set exact cut-off value.
Nippon Shokakibyo Gakkai zasshi The Japanese journal of gastro-enterology 09/1996; 93(8):530-6.
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S Ohara, H Sekine,
K Iijima,
S Moriyama,
Y Nakayama,
T Kinpara,
K Kato,
S Asaki,
T Katakura,
T Ikeda,
T Toyota
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ABSTRACT: This study is aimed at a role of Helicobacter pylori (HP) infection in reflux esophagitis of the elderly. 46 patients with reflux esophagitis aged at older than 60 years are selected for this study with informed consent. 43 patients without reflux esophagitis, peptic ulcer, and gastric cancer are used as a control group. In reflux esophagitis, gastric mucosal atrophy is judged as closed type of endoscopic findings in all cases. In control, 27 of 43 patients were judged as open type. Serum pepsinogen I, II ratio is 4.73 +/- 1.28 which is higher significantly than 3.39 +/- 1.69 in control. Serological positive rate of HP antibody is 39.1% in reflux esophagitis. This rate is significantly lower than 62.7% in control. In conclusion, low frequency of chronic HP infection protects gastric mucosa from atrophy, and keeps secretion of gastric acid, resulting in reflux esophagitis of the elderly accompanied with various abnormal esophago-gastric functions.
Nippon Shokakibyo Gakkai zasshi The Japanese journal of gastro-enterology 05/1996; 93(4):235-9.
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ABSTRACT: Ki67 expression, S-phase fraction, p53 immunoreactivity and DNA content were examined in morphologically normal mucosa and squamous dysplasia of both cancerous and non-cancerous human oesophagi in order to understand possible early events in the development of esophageal squamous cell carcinoma. 103 different foci from cancerous esophagi including 17 non-pathological epithelium, 10 mild, 17 moderate and 15 severe dysplasia, 14 intraepithelial carcinomas and 30 invasive squamous cell carcinomas were examined. Also studied were 57 biopsy specimens from cancer-free individuals, including 12 normal epithelia, 15 oesophagitis, and 16 mild, 11 moderate and 3 severe dysplasia. Areas of squamous dysplasia from both cancer-free and cancerous oesophagi were morphologically indistinguishable and both demonstrated increased cellular proliferation compared to normal or non-pathological epithelia. However, squamous dysplasia in cancerous oesophagi demonstrated significantly larger ki67 labelling indices and smaller S-phase fractions than dysplasia in cancer-free patients. Squamous dysplasia in cancerous and non-cancerous oesophagi demonstrated an non-diploid DNA histogram in 67.9% and 43.3% respectively. However, dysplasia from cancer-free individuals demonstrated a non-diploid pattern with one or more peaks (Type I non-diploid histogram) and that from oesophageal cancer patients predominantly exhibited non-diploid histograms without any distinctive peaks (Type II non-diploid histogram). Significant differences in the frequency of p53 positive foci were observed between dysplasia of cancer-free (23.3%) and cancerous (56.8%) oesophagi. IN cancerous oesophagi, dysplasia associated with Type II non-diploid histograms had a significantly larger number of p53-positive foci than those with diploid histograms or Type I non-diploid histograms. These results indicated that the biological features of squamous dysplasia were different between cancerous and non-cancerous human oesophagi despite indistinguishable morphological features. In addition, the combination of p53 immuno-histochemistry and DNA ploidy analysis may contribute to identify possible high-risk squamous dysplasia of the oesophagus.
Anticancer research 16(1):201-8. · 1.73 Impact Factor
