M Sartori, S Andorno, E Avogadro, M Ballarè, G La Terra, F Leone, V Quaglia, G Fortina, M Aglietta
The prevalence of different genotypes of Hepatitis C virus may vary between geographic areas and it is possible that various genotypes have different pathogenic characteristics. Therefore, 90 consecutive Italian patients anti-Hepatitis C Virus positive with a broad spectrum of chronic liver disease, have been analysed to observe prevalence of various genotypes of Hepatitis C Virus. Genotyping was performed by polymerase chain reaction with a set of nested biotinylated primers, located in 5'UTR region. Genotype 1b and genotype 2a were the most commonly encountered (respectively, 50% and 37%) whereas other genotypes were rare. The unexpected high prevalence of genotype 2a allowed direct comparison of clinical characteristics and response to therapy between patients with genotype 2a and those with 1b. Genotype 1b was more prevalent than 2a in patients over 60 years (29 vs 12) and in those with more severe liver disease (34 vs 16). In a univariate analysis, genotype 2a was associated with less severe liver disease (p = 0.02) and younger age (p = 0.018), in comparison with genotype 1b. Patients with genotype 2a responded to interferon alpha therapy better than those with 1b (p = 0.007). In a multivariate analysis, only younger age was associated with genotype 2a. Genotype 2a (in comparison with 1b) and absence of cirrhosis were independent predictors of response to interferon alpha. In conclusion, genotype 2a is playing an emerging role in younger Italian patients and seems more sensitive than 1b to interferon alpha therapy.
不同基因型丙型肝炎病毒的流行率可能因地理区域而异,不同基因型可能具有不同的致病特征。因此,我们分析了90例连续的意大利丙型肝炎病毒抗体阳性的广谱慢性肝病患者,观察了不同基因型丙型肝炎病毒的流行情况。基因分型采用聚合酶链反应,在5'UTR区嵌套一套生物素化引物。基因型1b和基因型2a是最常见的(分别为50%和37%),而其他基因型则罕见。基因型2a出乎意料的高患病率使得基因型2a和基因型1b患者的临床特征和对治疗的反应可以直接比较。基因型1b在60岁以上患者(29 vs 12)和肝病较严重患者(34 vs 16)中比2a更普遍。在单变量分析中,与基因型1b相比,基因型2a与较轻的肝脏疾病(p = 0.02)和较年轻的年龄(p = 0.018)相关。基因型2a患者对α干扰素治疗的反应优于基因型1b患者(p = 0.007)。在多变量分析中,只有较年轻的年龄与基因型2a相关。基因型2a(与1b相比)和无肝硬化是干扰素应答的独立预测因子。总之,基因型2a在年轻的意大利患者中发挥着越来越重要的作用,似乎比1b对干扰素治疗更敏感。
{"title":"High prevalence of hepatitis C virus (HCV) genotype 2 in Italian patients with chronic liver disease.","authors":"M Sartori, S Andorno, E Avogadro, M Ballarè, G La Terra, F Leone, V Quaglia, G Fortina, M Aglietta","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The prevalence of different genotypes of Hepatitis C virus may vary between geographic areas and it is possible that various genotypes have different pathogenic characteristics. Therefore, 90 consecutive Italian patients anti-Hepatitis C Virus positive with a broad spectrum of chronic liver disease, have been analysed to observe prevalence of various genotypes of Hepatitis C Virus. Genotyping was performed by polymerase chain reaction with a set of nested biotinylated primers, located in 5'UTR region. Genotype 1b and genotype 2a were the most commonly encountered (respectively, 50% and 37%) whereas other genotypes were rare. The unexpected high prevalence of genotype 2a allowed direct comparison of clinical characteristics and response to therapy between patients with genotype 2a and those with 1b. Genotype 1b was more prevalent than 2a in patients over 60 years (29 vs 12) and in those with more severe liver disease (34 vs 16). In a univariate analysis, genotype 2a was associated with less severe liver disease (p = 0.02) and younger age (p = 0.018), in comparison with genotype 1b. Patients with genotype 2a responded to interferon alpha therapy better than those with 1b (p = 0.007). In a multivariate analysis, only younger age was associated with genotype 2a. Genotype 2a (in comparison with 1b) and absence of cirrhosis were independent predictors of response to interferon alpha. In conclusion, genotype 2a is playing an emerging role in younger Italian patients and seems more sensitive than 1b to interferon alpha therapy.</p>","PeriodicalId":22546,"journal":{"name":"The Italian journal of gastroenterology","volume":"28 8","pages":"452-6"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19990272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R L Riepl, F Fiedler, C Kowalski, J Teufel, P Lehnert
Bile salts are intraduodenal stimulants of basal pancreatic secretion. This study aims to show whether the three main bile salts of human bile differ in their action on pancreatic secretion, and whether they enhance or inhibit each other after combined use. Furthermore, the effect on gastroenteropancreatic peptide release is evaluated. Twelve subjects were provided with a gastroduodenal double-lumen tube. Equimolar doses (0.6 mmol) of taurocholate (322 mg), taurodeoxycholate (313 mg), and a combination of both stimuli were given intraduodenally. Another 12 subjects received taurochenodeoxycholate (313 mg) instead of taurocholate. Volume, bicarbonate, trypsin, and lipase were determined in duodenal aspirates. Cholecystokinin, pancreatic polypeptide, and somatostatin were measured radioimmunologically in plasma samples. All bile salts and combinations exerted a significant hydrokinetic and ecbolic effect. The hydrokinetic response of the combined stimuli was significantly higher as compared with taurocholate and taurochenodeoxycholate, respectively. As far as concerns the ecbolic response, the difference was significant only for trypsin output as compared with taurochenodeoxycholate. Plasma cholecystokinin rose significantly only after the combined stimuli. Pancreatic polypeptide and somatostatin increased significantly after all stimuli, except pancreatic polypeptide after taurocholate. Combined use enhances the hydrokinetic and ecbolic effects of single bile salts. Cholecystokinin may, hereby, be involved as a mediator of the ecbolic effect. Pancreatic polypeptide release indicates cholinergic mechanisms as further mediators. As demonstrated by somatostatin release, counter-regulatory mechanisms are also triggered by intraduodenal bile salts.
{"title":"Exocrine pancreatic secretion and plasma levels of cholecystokinin, pancreatic polypeptide, and somatostatin after single and combined intraduodenal application of different bile salts in man.","authors":"R L Riepl, F Fiedler, C Kowalski, J Teufel, P Lehnert","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Bile salts are intraduodenal stimulants of basal pancreatic secretion. This study aims to show whether the three main bile salts of human bile differ in their action on pancreatic secretion, and whether they enhance or inhibit each other after combined use. Furthermore, the effect on gastroenteropancreatic peptide release is evaluated. Twelve subjects were provided with a gastroduodenal double-lumen tube. Equimolar doses (0.6 mmol) of taurocholate (322 mg), taurodeoxycholate (313 mg), and a combination of both stimuli were given intraduodenally. Another 12 subjects received taurochenodeoxycholate (313 mg) instead of taurocholate. Volume, bicarbonate, trypsin, and lipase were determined in duodenal aspirates. Cholecystokinin, pancreatic polypeptide, and somatostatin were measured radioimmunologically in plasma samples. All bile salts and combinations exerted a significant hydrokinetic and ecbolic effect. The hydrokinetic response of the combined stimuli was significantly higher as compared with taurocholate and taurochenodeoxycholate, respectively. As far as concerns the ecbolic response, the difference was significant only for trypsin output as compared with taurochenodeoxycholate. Plasma cholecystokinin rose significantly only after the combined stimuli. Pancreatic polypeptide and somatostatin increased significantly after all stimuli, except pancreatic polypeptide after taurocholate. Combined use enhances the hydrokinetic and ecbolic effects of single bile salts. Cholecystokinin may, hereby, be involved as a mediator of the ecbolic effect. Pancreatic polypeptide release indicates cholinergic mechanisms as further mediators. As demonstrated by somatostatin release, counter-regulatory mechanisms are also triggered by intraduodenal bile salts.</p>","PeriodicalId":22546,"journal":{"name":"The Italian journal of gastroenterology","volume":"28 8","pages":"421-9"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19990268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
G Maggi, R Bottelli, D Gola, G Perricone, M Posca, C Zavaglia, G Ideo
Total serum cholesterol levels have been studied in 100 patients with histological diagnoses of chronic hepatitis B and 100 wit chronic Hepatitis C, all without cirrhosis, and two age- and sex-matched control groups (B and C). Mean serum cholesterol levels of the groups were compared also in relation to sex, liver function, duration of the disease, alcohol intake, mass index, liver enzymes, presence of liver steatosis and severity of the liver disease on the basis of the histological activity index. The percentages of patients with serum cholesterol level < 150 mg/dl and > 240 mg/dl were also calculated. The mean serum cholesterol level was significantly lower in hepatitis C: 176 md/dl vs 194 mg/dl of hepatitis B (p = 0.004) and 198 of control C (p = 0.000). Twenty eight hepatitis C patients had serum cholesterol < 150 mg/dl vs 10 with hepatitis B (p = 0.001). In multivariate regression analysis, only the type of virus infection was independent related to serum cholesterol level (p = 0.0063).
{"title":"Serum cholesterol and chronic hepatitis C.","authors":"G Maggi, R Bottelli, D Gola, G Perricone, M Posca, C Zavaglia, G Ideo","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Total serum cholesterol levels have been studied in 100 patients with histological diagnoses of chronic hepatitis B and 100 wit chronic Hepatitis C, all without cirrhosis, and two age- and sex-matched control groups (B and C). Mean serum cholesterol levels of the groups were compared also in relation to sex, liver function, duration of the disease, alcohol intake, mass index, liver enzymes, presence of liver steatosis and severity of the liver disease on the basis of the histological activity index. The percentages of patients with serum cholesterol level < 150 mg/dl and > 240 mg/dl were also calculated. The mean serum cholesterol level was significantly lower in hepatitis C: 176 md/dl vs 194 mg/dl of hepatitis B (p = 0.004) and 198 of control C (p = 0.000). Twenty eight hepatitis C patients had serum cholesterol < 150 mg/dl vs 10 with hepatitis B (p = 0.001). In multivariate regression analysis, only the type of virus infection was independent related to serum cholesterol level (p = 0.0063).</p>","PeriodicalId":22546,"journal":{"name":"The Italian journal of gastroenterology","volume":"28 8","pages":"436-40"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19990269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fedotozine was rested in colonic strips removed during surgery from patients suffering from different diseases of the colon; the effects were compared to those of morphine and of the selective opiate agonist U-69593. Fedotozine did not affect the spontaneous motility of human colonic strips, unless very high concentrations were used. Fedotozine (10(-6)-3 x 10(-4) M) induced a concentration-dependent reduction of the excitatory effect induced by field stimulation, an effect which was partially mimicked by compound U-69593 and by morphine but not inhibited by naloxone. The cumulative dose-response curve to exogenous acetylcholine was inhibited by fedotozine (3 x 10(-4) M), whereas morphine had no effect up to 3 x 10(-4) M. In colonic strips incubated with [3H]-choline, fedotozine (10(-5)-10(-4) M) induced an erratic decrease of acetylcholine-release induced by electric stimulation. In our experimental model, the inhibitory effect of fedotozine does not seem to be related to opioid receptor activation.
{"title":"Effect of fedotozine on human distal colon.","authors":"M Adami, G Bertaccini, L Roncoroni, F Cobianchi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Fedotozine was rested in colonic strips removed during surgery from patients suffering from different diseases of the colon; the effects were compared to those of morphine and of the selective opiate agonist U-69593. Fedotozine did not affect the spontaneous motility of human colonic strips, unless very high concentrations were used. Fedotozine (10(-6)-3 x 10(-4) M) induced a concentration-dependent reduction of the excitatory effect induced by field stimulation, an effect which was partially mimicked by compound U-69593 and by morphine but not inhibited by naloxone. The cumulative dose-response curve to exogenous acetylcholine was inhibited by fedotozine (3 x 10(-4) M), whereas morphine had no effect up to 3 x 10(-4) M. In colonic strips incubated with [3H]-choline, fedotozine (10(-5)-10(-4) M) induced an erratic decrease of acetylcholine-release induced by electric stimulation. In our experimental model, the inhibitory effect of fedotozine does not seem to be related to opioid receptor activation.</p>","PeriodicalId":22546,"journal":{"name":"The Italian journal of gastroenterology","volume":"28 8","pages":"441-6"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19990270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
F Luzza, M Maletta, M Imeneo, G Monteleone, R Marasco, L Biancone, F Pallone
Aim of this study is to provide indirect evidence that human colonic mucosa harbour Helicobacter pylori. The antibody response of IgG and IgA class against Helicobacter pylori was examined in autologous homogenate of gastric and rectal endoscopic biopsies from 26 patients and in rectal samples of a further 36. All had a documented (histology and/or serology) Helicobacter pylori status. Helicobacter pylori specific IgG and IgA were measured by an in-house ELISA. In Helicobacter pylori positive patients having both gastric and rectal homogenate, mean level of Helicobacter pylori IgG and IgA was higher in gastric than in rectal samples (0.810 +/- 0.668 optical density vs 0.329 +/- 0.509 optical density for IgG, p = 0.007 and 0.660 +/- 0.477 vs 0.116 +/- 0.229 for IgA, p < 0.001, respectively). In each patient, level of the two isotypes was clearly higher in gastric than in autologous rectal sample. In the overall study population, mean level of Helicobacter pylori IgG in rectal homogenate was not significantly (p = 0.16) different between Helicobacter pylori positive (48/62, 77%, 0.243 +/- 0.388 optical density) and negative (14/62, 23%; 0.095 +/- 0.088) patients. In same material, levels of Helicobacter pylori IgA were very low and undetectable either in Helicobacter pylori positive or negative patients. Although Helicobacter pylori IgG are detectable in rectal homogenates of Helicobacter pylori positive patients, present data suggest that these antibodies may not be local in origin but rather reflect circulating response. These observations do not support the view that large bowel mucosa is colonised by Helicobacter pylori.
{"title":"Evidence against colonic mucosa colonisation by Helicobacter pylori. Lack of a specific antibody response in homogenates of rectal endoscopic biopsies.","authors":"F Luzza, M Maletta, M Imeneo, G Monteleone, R Marasco, L Biancone, F Pallone","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Aim of this study is to provide indirect evidence that human colonic mucosa harbour Helicobacter pylori. The antibody response of IgG and IgA class against Helicobacter pylori was examined in autologous homogenate of gastric and rectal endoscopic biopsies from 26 patients and in rectal samples of a further 36. All had a documented (histology and/or serology) Helicobacter pylori status. Helicobacter pylori specific IgG and IgA were measured by an in-house ELISA. In Helicobacter pylori positive patients having both gastric and rectal homogenate, mean level of Helicobacter pylori IgG and IgA was higher in gastric than in rectal samples (0.810 +/- 0.668 optical density vs 0.329 +/- 0.509 optical density for IgG, p = 0.007 and 0.660 +/- 0.477 vs 0.116 +/- 0.229 for IgA, p < 0.001, respectively). In each patient, level of the two isotypes was clearly higher in gastric than in autologous rectal sample. In the overall study population, mean level of Helicobacter pylori IgG in rectal homogenate was not significantly (p = 0.16) different between Helicobacter pylori positive (48/62, 77%, 0.243 +/- 0.388 optical density) and negative (14/62, 23%; 0.095 +/- 0.088) patients. In same material, levels of Helicobacter pylori IgA were very low and undetectable either in Helicobacter pylori positive or negative patients. Although Helicobacter pylori IgG are detectable in rectal homogenates of Helicobacter pylori positive patients, present data suggest that these antibodies may not be local in origin but rather reflect circulating response. These observations do not support the view that large bowel mucosa is colonised by Helicobacter pylori.</p>","PeriodicalId":22546,"journal":{"name":"The Italian journal of gastroenterology","volume":"28 8","pages":"447-51"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19990271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Y Yasunaga, Y Shinomura, S Kanayama, Y Miyazaki, J J Bonilla Palacios, Y Matsuzawa
It has been shown that serum pepsinogen I levels are correlated with maximal acid outputs and can be used as an indicator for parietal cell mass. In this study, the effect of Helicobacter pylori infection on the relationship between serum pepsinogen I levels and maximal acid outputs was investigated in 27 patients with Helicobacter pylori associated enlarged fold gastritis. Before treatment, serum pepsinogen I levels and maximal acid outputs were not significantly correlated. After eradication of Helicobacter pylori, a significant positive correlation was found between serum pepsinogen I levels and maximal acid outputs with a significant increase in pepsinogen I levels and a significant increase in maximal acid outputs. These results indicate that Helicobacter pylori infection distorts the relationship between serum pepsinogen I levels and maximal acid outputs by elevating the former and lowering the latter, and that serum pepsinogen I level after eradication of Helicobacter pylori may reflect parietal cell mass in patients with Helicobacter pylori associated enlarged fold gastritis.
{"title":"Serum pepsinogen I levels and acid secretion in Helicobacter pylori associated enlarged fold gastritis.","authors":"Y Yasunaga, Y Shinomura, S Kanayama, Y Miyazaki, J J Bonilla Palacios, Y Matsuzawa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>It has been shown that serum pepsinogen I levels are correlated with maximal acid outputs and can be used as an indicator for parietal cell mass. In this study, the effect of Helicobacter pylori infection on the relationship between serum pepsinogen I levels and maximal acid outputs was investigated in 27 patients with Helicobacter pylori associated enlarged fold gastritis. Before treatment, serum pepsinogen I levels and maximal acid outputs were not significantly correlated. After eradication of Helicobacter pylori, a significant positive correlation was found between serum pepsinogen I levels and maximal acid outputs with a significant increase in pepsinogen I levels and a significant increase in maximal acid outputs. These results indicate that Helicobacter pylori infection distorts the relationship between serum pepsinogen I levels and maximal acid outputs by elevating the former and lowering the latter, and that serum pepsinogen I level after eradication of Helicobacter pylori may reflect parietal cell mass in patients with Helicobacter pylori associated enlarged fold gastritis.</p>","PeriodicalId":22546,"journal":{"name":"The Italian journal of gastroenterology","volume":"28 8","pages":"457-61"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19990178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hepatitis G virus in liver disease: cause or case?","authors":"G Raimondo, M Pernice, G Longo","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":22546,"journal":{"name":"The Italian journal of gastroenterology","volume":"28 8","pages":"470-3"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19990182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A Archimandritis, C Spiliadis, M Tzivras, B Vamvakousis, P Davaris, Z Manika, N Scandalis
This is a retrospective endoscopic study on the incidence of gastric epithelial polyps (adenomas, hyperplastic, inflammatory) in 12,974 consecutive symptomatic Greek adults submitted to endoscopy during a 4-year period, in two endoscopy units. A total of 258 polyps were found in 157 patients (1.2%), 80 males and 77 females (age: 22-87 years); 67.5% of these patients were older than 60 years. Two hundred and two (202) polyps were totally removed. In 43 patients (27%), more than one polyp was found. Polyps were mainly hyperplastic (75.6%). Adenomas were found in 6.6%, and only in patients older than 50 years. Hyperplastic and inflammatory polyps were equally distributed in males and females. A male predominance was observed in adenomas (2:1). Most of the polyps were in the antrum (43.8%) and were hyperplastic (75.2%). Of 501 previously operated patients (gastrectomy or gastrojejunostomy), 26 (5.2%) had polyps. No adenomas were seen in the anastomosis area. Most of the polyps (61.9%) were smaller than 0.5 cm; 13.3% were greater than 1 cm. No coincidence of polyps with gastric cancer was observed.
这是一项回顾性的内镜研究,在4年的时间里,在两个内镜单元中,对12974名连续有症状的希腊成年人进行了胃上皮性息肉(腺瘤、增生、炎症)的发生率进行了研究。157例(1.2%)息肉258例,其中男性80例,女性77例(年龄22 ~ 87岁);67.5%的患者年龄在60岁以上。202个息肉被完全切除。43例(27%)患者发现不止一个息肉。息肉以增生性为主(75.6%)。腺瘤发生率为6.6%,且仅发生在50岁以上的患者中。增生性息肉和炎性息肉在男女中分布均匀。男性在腺瘤中占优势(2:1)。息肉以上颌窦息肉为主(43.8%),增生性息肉占75.2%。501例既往手术患者(胃切除术或胃空肠吻合术)中,26例(5.2%)有息肉。吻合区未见腺瘤。大多数息肉小于0.5 cm (61.9%);13.3%大于1 cm。息肉与胃癌没有重合。
{"title":"Gastric epithelial polyps: a retrospective endoscopic study of 12974 symptomatic patients.","authors":"A Archimandritis, C Spiliadis, M Tzivras, B Vamvakousis, P Davaris, Z Manika, N Scandalis","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This is a retrospective endoscopic study on the incidence of gastric epithelial polyps (adenomas, hyperplastic, inflammatory) in 12,974 consecutive symptomatic Greek adults submitted to endoscopy during a 4-year period, in two endoscopy units. A total of 258 polyps were found in 157 patients (1.2%), 80 males and 77 females (age: 22-87 years); 67.5% of these patients were older than 60 years. Two hundred and two (202) polyps were totally removed. In 43 patients (27%), more than one polyp was found. Polyps were mainly hyperplastic (75.6%). Adenomas were found in 6.6%, and only in patients older than 50 years. Hyperplastic and inflammatory polyps were equally distributed in males and females. A male predominance was observed in adenomas (2:1). Most of the polyps were in the antrum (43.8%) and were hyperplastic (75.2%). Of 501 previously operated patients (gastrectomy or gastrojejunostomy), 26 (5.2%) had polyps. No adenomas were seen in the anastomosis area. Most of the polyps (61.9%) were smaller than 0.5 cm; 13.3% were greater than 1 cm. No coincidence of polyps with gastric cancer was observed.</p>","PeriodicalId":22546,"journal":{"name":"The Italian journal of gastroenterology","volume":"28 7","pages":"387-90"},"PeriodicalIF":0.0,"publicationDate":"1996-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19901933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
There is limited information about the natural history of hepatitis C in problematic patients and this may affect development of treatment strategies. In patients with persistently normal serum transaminases, infection is often a benign condition which does not require therapy. By contrast, treatment with antiviral drugs is advisable for recipients of renal or liver grafts who may have shortened life expectancies as a consequence of hepatitis C. However, interferon alpha, which is the only available anti-hepatitis C treatment, has limited efficacy in immuno-compromised patients and it may accelerate graft rejection in some. Patients coinfected with the human immuno-deficiency virus (HIV-1) are another group for which treatment is uncertain, mainly because of the short survival times due to HIV-1. Thus, the current policy is not to treat HIV-1/HCV coinfected patients. Symptomatic patients with serum cryoglobulins may respond to interferon therapy, but symptoms recur in virtually all these patients after withdrawal of treatment.
{"title":"Treatment of \"problematic\" hepatitis C patients.","authors":"M Colombo","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>There is limited information about the natural history of hepatitis C in problematic patients and this may affect development of treatment strategies. In patients with persistently normal serum transaminases, infection is often a benign condition which does not require therapy. By contrast, treatment with antiviral drugs is advisable for recipients of renal or liver grafts who may have shortened life expectancies as a consequence of hepatitis C. However, interferon alpha, which is the only available anti-hepatitis C treatment, has limited efficacy in immuno-compromised patients and it may accelerate graft rejection in some. Patients coinfected with the human immuno-deficiency virus (HIV-1) are another group for which treatment is uncertain, mainly because of the short survival times due to HIV-1. Thus, the current policy is not to treat HIV-1/HCV coinfected patients. Symptomatic patients with serum cryoglobulins may respond to interferon therapy, but symptoms recur in virtually all these patients after withdrawal of treatment.</p>","PeriodicalId":22546,"journal":{"name":"The Italian journal of gastroenterology","volume":"28 7","pages":"393-5"},"PeriodicalIF":0.0,"publicationDate":"1996-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19901935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"International meeting on inflammatory bowel disease. Trigger factors and trends in therapy. Capri, Italy, September 19-21, 1996. Abstracts.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":22546,"journal":{"name":"The Italian journal of gastroenterology","volume":"28 Suppl 1 ","pages":"1-40"},"PeriodicalIF":0.0,"publicationDate":"1996-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19916874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}