慢性萎缩性胃炎的症状与临床治疗

性萎缩性胃炎是消化系统的常见顽固难治的疾病,是慢性胃炎中的一种,呈局限性或广泛性的胃粘膜固有腺萎缩,常伴有不同类型的胃黏膜上皮和腺体的化生.胃黏膜细胞增殖和凋亡失衡是其中的核心问题,其诊断主要依据胃镜检查和胃粘膜活组织检查.慢性萎缩性胃炎已经被公认为癌前疾病,但临床上尚缺乏特效的治疗方法.资料显示对慢性萎缩性胃炎尽早诊断和治疗对预防胃癌的发生有重要的意义.本文旨在探讨慢性萎缩性胃炎的症状和临床治疗经验.     

体表胃电频谱分析对胃十二指肠疾病的诊断价值

体表胃电频谱分析对胃十二指肠疾病的诊断价值徐瑞萍，梁守德（兰州军区总医院消化科）为探讨胃电图对胃十二指肠疾病的诊断价值及对胃蠕动功能检查的意义，我们对２８５例经胃镜检查确诊的患者进行了胃电图检查，其中慢性浅表性胃炎１０７例，慢性萎缩性胃炎９３例，消化...     

慢性萎缩性胃炎中医药治疗现状

慢性萎缩性胃炎是指胃粘膜已发生萎缩性改变的慢性胃炎，常伴有肠上皮化生。近年来诸多中医药学者进行了不同层面的研究和探讨，各有特色。对慢性萎缩性胃炎的诊断与治疗都有长足的进步与发展，且已取得了初步疗效。本文着重讨论慢性萎缩性胃炎的诊断与中医药治疗等问题，结合复习国内诸多学者研究之佳作，作以简要综述。以飨读者。     

鼠抗人胃癌单克隆抗体血清学检查在胃癌普查中的意义

为了防治胃癌,对58204人进行胃癌普查。本组报告经初级筛选后的4810人。采用放射免疫学技术,使用鼠抗人胃癌单克隆抗体(MG-单抗),检查血清中的胃癌相应抗原(MG-Ags),对阳性者中的340例,作胃镜检查。在胃癌普查中,采用MC-单抗检测血清中MG-Ags的出现,浓度高低,持续时间,即可在分子水平上了解癌变过程,而确定出易患人群,并可采取措施,阻断癌变的发展,达到一级预防的目的。本组慢性浅表性胃炎、慢性萎缩性胃炎及疾病     

柴胡疏肝散在中药内科的临床运用研究

目的：通过实例研究探索柴胡疏肝散治疗慢性萎缩性胃炎的疗效和中药内科中的临床应用。方法本次研究选定慢性萎缩性胃炎患者100例,应用数理法则随机分为观察组和对照组,各50例患者,对照组应用吗丁啉和维酶素进行治疗,观察组采用柴胡疏肝散进行治疗,观察两组的治疗效果。结果观察组应用柴胡疏肝散进行治疗的方法明显优于对照组的方法。结论中医内科中,应用柴胡疏肝散治疗慢性萎缩性胃炎具有很好的效果,具有一定的推广使用价值。     

PGⅠ、PGⅡ、G 17和Hp IgG抗体筛查慢性萎缩性胃炎和胃癌的价值

分析胃蛋白酶Ⅰ（PGⅠ）、胃蛋白酶Ⅱ（PGⅡ）、胃泌素 17（G 17）和幽门螺杆菌（Hp IgG）抗体筛查对慢性萎缩性胃炎和胃癌的诊断价值。方法：以2014年5月至2015年5月胃部不适来我院就诊的90例患者为研究对象,根据病理诊断结果分为正常对照组（包括慢性非萎缩性胃炎）、慢性萎缩性胃炎组和胃癌组,每组各30例,比较三组患者PGⅠ、PGⅡ、G 17水平及Hp IgG抗体阳性检出率。结果：胃癌组患者的PGⅠ、PGⅡ水平低于对照组和慢性萎缩性胃炎组,且慢性萎缩性胃炎组患者上述指标低于对照组;胃癌组G 17水平高于慢性萎缩性胃炎组和对照组,而慢性萎缩性胃炎组和对照组无明显差异;三组间Hp IgG抗体阳性率有明显差别,胃癌组显著高于对照组和慢性萎缩性胃炎组;Hp感染患者的PGⅠ和PGⅡ水平低于未感染Hp者,而G 17水平高于未感染Hp者;胃癌患者的PGⅠ、PGⅡ水平与年龄、病理分期和转移显著负相关,与分化程度显著正相关,而G 17水平及Hp IgG抗体阳性率与年龄、病理分期和转移显著正相关,而与分化程度显著负相关。结论： PGⅠ、PGⅡ和Hp IgG抗体筛查对慢性萎缩性胃炎和胃癌均有很好的诊断价值,而对胃癌的诊断价值更好,G17对胃癌的诊断价值远远好于慢性萎缩性胃炎;且PGⅠ、PGⅡ、G17水平及Hp IgG抗体阳性检出率与胃癌患者的临床病理特征密切相关。     

胃癌患者血清β2—mRIA的临床意义

本文报告我院68例胃病患者(其中良性胃病48例,胃癌20例)胃镜检查同时辅以血清β_2-m测定,评价其对胃癌的临床意义。 材料和方法 一、临床资料:68例(男38,女30),均为因胃部疾患而作纤维胃镜检查明确诊断的患者。年龄19～68岁,平均41岁。经胃镜检查确诊的胃部良性疾病共48例(慢性浅表性胃炎24例,慢性萎缩性胃炎11例,胃溃疡6例,十二指肠球部溃疡4例,残胃炎3例)。胃     

血清胃蛋白酶原对慢性萎缩性胃炎的诊断价值

近年来的研究表明,慢性萎缩性胃炎是重要的癌前病变,与胃癌的发生密切相关,80％以上的胃癌伴有萎缩性胃炎。胃粘膜的萎缩可由多种因素引起,常伴有肠上皮化生和异型增生,胃体粘膜释放的因子胃蛋白酶原（PGⅠ、PGⅡ）减少。本研究通过定量测定正常人与患者血清PGⅠ、PGⅡ水平并计算其比值PGⅠ／PGⅡ来评价能否对慢性萎缩性胃炎进行初步筛查。     

观察中医活血化瘀法联合西药治疗慢性萎缩性胃炎的效果

目的：探究中医活血化瘀与西药联合在慢性萎缩性胃炎治疗的效果。方法选取本院2012年3月~2014年3月收治的慢性萎缩性胃炎患者60例，随机分成对照组和研究组各30例，对照组单纯使用西药实施治疗，研究组使用活血化瘀中药联合西药实施治疗，对比两组治疗的效果。结果研究组患者的有效率为93.33%，明显高于对照组的76.67%，研究组的不良反应情况明显少于对照组，差异明显，具有统计学意义(<0.05)。结论采用中医活血化瘀联合西药治疗慢性萎缩性胃炎具有显著的效果，能减少患者的不良反应发生率，值得临床推广。     

70例慢性萎缩性胃炎临床分析

目的：探讨慢性萎缩性胃炎的临床特点及治疗方法。方法选取我院自2010年1月~2013年1月收治的70例慢性萎缩性胃炎患者进行分析研究,随机分为两组,每组35例,对照组患者采用常规西药治疗,观察组患者采用中药进行治疗,分析比较两组患者临床治疗效果。结果观察组患者治疗总有效率达到94.29%,对照组患者治疗总有效率为65.71%,观察组患者临床治疗效果明显优于对照组,<0.05,具有统计学意义。结论采用中药进行慢性萎缩性胃炎的治疗,可以有效改善患者临床症状,减轻患者痛苦,提高治疗效果,安全、有效。     

7033例纤维胃镜活检的病理分析

我们从1977～1987年10年间进行纤维胃镜粘膜活检7033例,其中正常粘膜288例,占4.09%;浅表性胃炎4487例,占63.79%;萎缩性胃炎357例,占5.07%;肥厚性胃炎3例(0.04%),各部位息肉56例(0.79%);慢性溃疡232例(3.29%);肿瘤1091例(15.55%),其中胃癌780例,占11.09%;食管癌302例,占4.29%;其他慢性炎症519例(7.37%)。正常粘膜检出率偏高萎缩性胃炎检出率偏低。浅表性胃炎最终可发展为萎缩性胃炎,而萎缩性胃炎部分可引起肠型胃癌的发生,三者之间的病变有一定的关系。提高纤维胃镜的活检诊断水平必须从取材、制片、阅片等每个环节做起,病理诊断必须结合纤维胃镜肉眼所见及临床资料。     

Histologic and morphometric study of chronic gastritis in alcoholic patients.

The effect of chronic alcohol ingestion on the gastric mucosa was determined in 96 patients in whom gastroscopy was performed because of upper gastrointestinal symptoms. Seventy-two patients were classified as alcoholics and 24 patients as nonalcoholics. In all cases biopsy specimens were taken from the fundus and antrum. The diagnoses of chronic superficial and atrophic gastritis were based on conventional histologic criteria and a morphometric technique utilizing quantitation of the chronic inflammatory cells in the lamina propria. Alcoholic patients were found to have a higher incidence of chronic gastritis of the antrum than nonalcoholics (p less than 0.001). Fundic involvement was also more common, probably accounting for the decreased gastric acid output described in chronic alcoholic patients. Finally, gastritis was more severe in the alcoholics; below 45 years of age chronic atrophic gastritis was seen only in alcoholics. We conclude that chronic gastritis develops more frequently in alcoholic patients and evolves into chronic atrophic gastritis at an earlier age than in nonalcoholic subjects.     

胃癌单抗检测活检粘膜组织833例结果分析

应用胃癌单抗ID1-2对833例内窥镜活检组织进行了免疫学荧光检查,胃癌阳性检出率为81.6％:胃溃疡为32.7％;肠化生性蒌缩性胃炎为40.0％;食管和结肠腺癌分别为60.0％和62.5％,与单纯性萎缩性胃炎和浅表性胃炎的阳性检出率相比有非常显著的差异(P<0.01)。表明ID1-2单抗可用于检测活检粘膜组织中的癌细胞以及具有癌细胞相关抗原的癌前病变组织,如果与内窥镜及常规病理学检查联合应用,将可进一步提高早癌的阳性检出率。     

胃蛋白酶原联合放大染色内镜在早期胃癌诊断中的应用

目的：探讨乳胶增强免疫比浊法测定血清胃蛋白酶原（PG）Ⅰ、PGⅡ以及PGⅠ/PGⅡ比值在胃癌筛查中的价值,以及联合人工智能电子染色内镜（FICE）在早期胃癌中的诊断价值。方法：全部患者行胃蛋白酶原普查,如发现异常,即行普通胃镜检查,普通胃镜下发现可疑病变者（如溃疡、胃癌、息肉等）再以人工智能电子染色内镜＋靶向活检,最后明确病变。正常对照组85例。根据组织病理学及胃镜检查结果,将受检者分为5组,即慢性萎缩性胃炎组105例、慢性胃炎伴瘤变组33例、胃良性溃疡组53例、早期胃癌组48例、进展期胃癌组90例。确定胃良性病变的PGⅠ及PGⅡ、PGⅠ/PGⅡ比值参考值范围,并与正常对照组相比较。比较慢性胃炎与胃癌,早期胃癌与进展期胃癌,胃癌术前术后PGⅠ及PGⅡ、PGⅠ/PGⅡ的变化。结果：胃良性溃疡组患者血清PGⅠ及PGⅡ比对照组升高,PGⅠ/PGⅡ比值降低（P〈0.05）。慢性胃炎组比对照组PGⅠ下降,PGⅡ升高,PGⅠ/PGⅡ比值降低。胃癌患者血清PGⅠ及PGⅠ/PGⅡ比值较慢性胃炎组均显著降低（P〈0.05）,其中早期胃癌与进展期胃癌组相比PGⅠ及PGⅠ/PGⅡ比值均无显著差异（P〉0.05）。胃癌患者手术后PGⅠ及PGⅡ值均降低,PGⅠ/PGⅡ比值升高（P〈0.05）。血清PGⅠ、PGⅡ检测结合FICE放大胃镜技术对早期胃癌早诊率达80%。结论：乳胶增强免疫比浊法测定血清PG可作为大规模人群胃癌的普查手段,无创,便于推广;胃蛋白酶原联合放大染色内镜可提高早期胃癌诊断率。     

不同胃黏膜病变患者的血清胃蛋白酶原变化

目的：探讨胃溃疡、十二指肠球部溃疡、非萎缩性胃炎、萎缩性胃炎、胃癌患者胃蛋白酶原(pepsinogen,PG)Ⅰ、PGⅡ水平和PGⅠ/PGⅡ比值变化。方法：选择2015年1月至2015年10月因消化道症状行胃镜检查的门诊及住院患者共133例,根据胃镜检查及组织病理学结果,将受检者分为5组。非萎缩性胃炎组42例、萎缩性胃炎组33例、胃溃疡组20例、十二指肠球部溃疡组23例、胃癌组15例、比较各组血清PGⅠ、PGⅡ水平。结果：与非萎缩性胃炎组相比,胃溃疡、十二指肠球部溃疡患者PGI明显升高(P<0.05),胃溃疡PGII明显升高(P<0.05),萎缩性胃炎组、胃癌组血清PGⅠ及PGⅠ/PGⅡ水平降低(P<0.05)。结论：血清PGⅠ、PGⅡ水平以及PGⅠ/PGⅡ比值对提高消化性溃疡、胃癌前病变及胃癌的诊断有重要的临床价值。     

胃蛋白酶原Ⅰ、Ⅱ测定在胃癌早期诊断中的研究

研究血清胃蛋白酶原Ⅰ、Ⅱ含量变化与胃癌发生的关系,探讨血清胃蛋白酶原Ⅰ、Ⅱ作为胃癌早期诊断标志物的可行性.应用化学发光法测定非萎缩性胃炎、慢性萎缩性胃炎、胃癌患者的血清胃蛋白酶原Ⅰ、Ⅱ的含量并计算其比值的变化.结果显示:与非萎缩性胃炎组相比,萎缩性胃炎和胃癌组血清胃蛋白酶原Ⅰ水平下降,差异均有统计学意义(P<0.05)...     

Absence of pepsinogen A3 gene expression in the gastric mucosa of patients with gastric cancer.

AIMS--To investigate the expression of pepsinogen A3 (Pg3) encoding genes in the gastric mucosa of normal controls and subjects with atrophic gastritis and gastric cancer. METHODS--One hundred and fifty nine patients underwent upper gastrointestinal endoscopy with sampling of gastric biopsy specimens and serum. Pg3 isoproteins were determined by electrophoresis in serum and gastric mucosal biopsy specimens. Pg3 encoding genes were assessed by PCR in DNA obtained from peripheral blood. RESULTS--One hundred and one subjects (82 normal histology/chronic gastritis, 17 atrophic gastritis, two gastric cancer) showed a pepsinogen phenotype with presence of Pg3 and a corresponding pepsinogen genotype with presence of Pg3 encoding genes. Fifty eight subjects showed a phenotype lacking Pg3. In 39 of them (23 normal histology/chronic gastritis, 11 atrophic gastritis, five gastric cancer), a corresponding genotype without Pg3 encoding genes was found. However, in the remaining 19 subjects (4 normal histology/chronic gastritis, nine atrophic gastritis, six gastric cancer); Pg3 encoding genes were demonstrable in the absence of Pg3 production. CONCLUSIONS--Unexpressed Pg3 encoding genes can be shown in many cases of atrophic gastritis and gastric cancer, but rarely in healthy controls and subjects with superficial gastritis. The correlation of atrophic gastritis and gastric cancer with a pepsinogen phenotype lacking Pg3 can be explained by loss of expression of Pg3 encoding genes throughout the complete gastric mucosa. The mechanism of such loss and the importance as a marker for premalignant degeneration have to be elucidated.     

Serum pepsinogen and Helicobacter pylori infection—a Japanese population study

The decreased ratio of serum pepsinogen (PG) I and II has good correlation with the presence of atrophic gastritis. A total of 1,540 residents aged 30-89?years were enrolled into this study to investigate which serum PG level of residents with Helicobacter pylori infection would represent an adjunct to the diagnosis and progression of atrophic gastritis. All participants received esophagogastroduodenoscopy. Serum antibody to H. pylori (anti-H. pylori) was measured by an enzyme-linked immunosorbent assay (ELISA). Serological atrophic gastritis was defined as serum PG I isozyme level ≤70?ng/ml and a PG I/II ratio of ≤3.0. Of the 1,540 participants, 923 (59.9%) were positive for anti-H. pylori. Serological atrophic gastritis was found significantly more often in anti-H. pylori-positive participants (40.8%) than in anti-H. pylori-negative participants (7.9%) (p?≤?0.0001). The endoscopic findings of anti-H. pylori-positive participants with serological atrophic gastritis were significantly more frequent by 4.06 times for atrophic gastritis (p?≤?0.0001) than anti-H. pylori-negative participants without serological atrophic gastritis. Eight anti-H. pylori-positive participants were diagnosed with gastric cancer, but no cancer was found in anti-H. pylori-negative participants without serological atrophic gastritis. Serum PG testing is clinically useful for the prediction of gastric lesions in H. pylori-infected persons.     

Clinical, endoscopic and histologic aspects of chronic Helicobacter pylori gastritis in Côte d'Ivoire: study of 102 patients

BACKGROUND: Helicobacter pylori (H. pylori) is the most frequent aetiological factor of chronic gastritis (CG). The relationship between H. pylori gastritis, gastro-duodenal ulcer and some gastric cancers (adenocarcinoma, gastric MALT lymphoma) has now been proven. AIM: Describe clinical, endoscopical and histological aspects of H. pylori gastritis in C?te d'Ivoire. METHODS: Retrospective analysis of 1960 gastroscopy reports carry out between January 1994 and December 1995. Analysis of clinical and gastric histological results in 137 patients. FINDINGS: Among 137 patients with gastric biopsy, 102 had H. pylori gastritis (68 men, 38 women, mean age: 39.3 years) and 35 had chemical gastritis. Epigastric pain was the most frequent symptom. The mucosa was frequently erythematous or exsudative at endoscopy. Histological anomalies were located in the antrum, the fundus or generalised, respectively in 33.3%, 25.5% and 41.2% of cases. Mild atrophic CG was more frequent in various locations. Gastritis activity was present in 81.4%, intestinal metaplasia in 18.6% and follicular lymphoid hyperplasia in 36.3% of cases. CONCLUSION: Clinical and endoscopical aspects of H. pylori gastritis did not present any particularities. Fundic gastritis without antral localisation was not unusual. This situation could be the result of antibiotic and gastric acid secretion inhibitor treatments.