十二指肠球部溃疡伴发早期胃癌一例

患者,女性,36岁。反复上腹部不适伴黑便7～8年。该患者7～8年前在当地医院做胃镜检查确诊为十二指肠球部溃疡,不规则给予制酸剂治疗。病情多次反复,1月前患者再次出现黑便,伴乏力、纳差、消瘦。来院就诊查血常规示血红蛋白62g/l,胃镜检查发现十二指肠球部前壁一0.4cm×0.5cm的凹陷,表面覆盖黄苔,周围黏膜充血,胃窦小弯近胃角处黏膜粗糙,糜烂,中央稍有凹陷。胃镜诊断:(1)十二指肠球部溃疡(A2期);(2)糜烂性胃炎。病理报告为胃窦部低分化腺癌,住院行胃癌根治术+毕II式手术,手术后病理诊断:胃窦黏膜内癌(早期胃癌IIc型),随访8月健康状况良好。…     

十二指肠球部溃疡与胃癌共存18例分析

我院检出十二指肠球部溃疡与胃癌共存１８例，现对其临床、内镜和病理资料，结合文献分析其预后差的原因，并探讨改善预后与避免漏误诊的措施。一、一般资料：１９７８年～１９９６年６月，我院胃镜检查总人数１２９２４例。共检出球溃２７８３例、胃溃疡９１１例、胃癌３...     

中西医结合治疗十二指肠球部溃疡40例

笔者自１９９３年２月～１９９８年２月间采用中西医结合治疗十二指肠球部溃疡４０例,取得满意疗效,现报告如下。１　资料与方法１．１　临床资料：８０例病例均有十二指肠球部溃疡的典型症状和体征,均经纤维胃镜或上消化道Ｘ线钡餐检查证实有溃疡活动、龛影。将８０例病例随机分为中西医结合组４０例,对照组４０例。中西医结合组中男３２例,女８例;年龄１７～６０岁。对照组男３０例,女１０例;年龄２０～５２岁。两组病例病程均为１～５年。１．２　治疗方法：对照组服西米替丁０．２ｇ,每日３次,睡前加服０．４ｇ,同时口服胃舒…     

十二指肠球部溃疡与ABO血型相关性探讨

目的从幽门螺杆菌（H.pylori）感染角度，探讨ABO血型鉴定与十二指肠球部溃疡（DU）相关性。方法收集2000—2005年本院120例Du患者资料，与本院门诊300例健康对照组比较血型分布的差别。利用快速尿素酶及C^13呼吸试验确定Du组不同血型者Hp感染并进行比较。结果Du组O型血占58．3％，明显高于O型血在正常人群中分布（30．0％），差异有统计学意义（P〈0．05）。结论O型血者是Du患者的高危人群，临床上应重视O型血患者Hp感染情况，及时诊疗。     

奥美拉唑治疗十二指肠球部溃疡的疗效观察

十二指肠球部溃疡是指发生在十二指肠球部的慢性溃疡,主要是胃酸、胃蛋白酶侵袭球部粘膜,前者攻击力超过后者防御力所致。一般十二指肠球部溃疡好发于中青年,而胃溃疡则发病年龄较迟,多发于中壮年。临床上十二指肠球部溃疡明显多于胃溃疡,两者之比约为3：1,均以男性居多。奥美拉唑是一种新型质子泵抑制剂,广泛应用于临床。现将2006年7月～2007年4月新疆维吾尔自治区第一济困医院应用奥美拉唑治疗十二指肠球部溃疡的结果分析如下。     

金不换冲剂治疗十二指肠球部溃疡63例疗效观察

应用自制金不换冲剂治疗十二指球部溃疡６３例，并与西药泰胃美作同期对照，治愈率分别为７１．４％和７２．７％，总有效率分别为９０．４８％和９５．４６％，经卡方检验，Ｐ＞０．０５．两组疗效无显著差异。金不换冲剂对各型十二指肠溃疡均有效，无毒副作用，使用方便．药源广，价格低廉，故在临床上有推广应用价值。     

胃癌及十二指肠球部溃疡患者胃肠激素含量的研究

我们应用放射免疫法对正常人、胃癌（ＧＣ）及十二指肠球部溃疡（ＤＵ）患者的血浆、胃液及粘膜（十二指肠降部、幽门前区、溃疡和癌变处）中的生长抑素（ＳＳ）、胃动素（ＭＴＬ）、胃泌素（ＧＡＳ）同时进行检测，进一步观察三者在胃癌和十二指肠球部溃疡发生和发展的关...     

洛赛克治疗十二指肠球部溃疡并出血疗效观察

目的探讨洛赛克治疗十二指肠球部溃疡并出血的疗效。方法将经胃镜确诊为十二指肠球部溃疡并出血的60例患者，随机分为治疗组和对照组。治疗组30例，给予洛赛克40mg，静脉滴注，2次／d，连用5天；对照组30例，给予雷尼替丁100mg，静脉滴注，2次／d，连用5天；比较这两种抑酸剂对十二指肠球部溃疡并出血的疗效。结果治疗组总有效率为96．7％，对照组总有效率为70．O％，两组总有效率比较差异有显著性（P〈0．05）。结论洛赛克治疗十二指肠球部溃疡并出血有很高的止血率，无明显副作用，是治疗十二指肠球部溃疡并出血的一种安全、有效的药物，值得临床推广使用。     

Diet and duodenal ulcer

BACKGROUND: Despite the fact that the main cause of duodenal ulcer incidence and recurrence is the Helicobacter pylori bacterium, more than 80% of Helicobacter pylori-infected people never develop an ulcer. Diet may be one of the most important environmental factors contributing to duodenal ulcer. AIMS: To explore the role of diet in causation, treatment and prevention of duodenal ulcer recurrence. METHODS: All research papers published in English from 1966 to October 1999 present in Medline, involving human subjects, and having duodenal ulcer as outcome, entered the review. RESULTS AND CONCLUSIONS: Soluble fibre from fruit and vegetables seem to be protective against duodenal ulcer and refined sugars a risk factor. The role of fibre in the treatment and prevention of recurrence of duodenal ulcer is uncertain, as is that of essential fatty acids. However, none of the epidemiological studies on the relationship between diet and duodenal ulcer disease controlled for Helicobacter pylori.     

Monthly variation in frequency of active duodenal ulcer and maximal acid output

The frequency of duodenal ulcer has been reported to vary seasonally. It is not known whether gastric acid secretion of patients with this condition has similar seasonal variation. During 1981–85, 1864 patients (mean age 38.0 years, s.d. = 24.2, males comprising 67.1%) with newly diagnosed active duodenal ulcer were documented endoscopically. Of these 626 patients (mean age 38.5 years, s.d. = 15.0, males comprising 71.4%) agreed to have their basal acid output (BAO) and pentagastrin-stimulated maximal acid output (MAO) measured. Time series analysis using the frequency domain approach identified that the monthly frequencies of duodenal ulcer over the 5-year period occurred in cycles of 12 months. Multiple comparison using Duncan's procedure identified the occurrence of a significant peak in November and December. MAO varied significantly ( P < 0.04) with season with two peaks, one occurring in February and another in July. Month-adjusted MAO was significantly higher ( P < 0.001) in male than in female patients. BAO showed no significant variation by month. It is concluded that active duodenal ulceration and MAO manifest significant variation by month, but their peaks do not coincide, indicating that acidity is unlikely to be a major factor responsible for the frequency of duodenal ulcer peaking in winter. These results also suggest that it is advisable to adjust for seasonal variation when MAO is compared among groups of duodenal ulcer patients.     

Prevalence of Helicobacter pylori infection in duodenal ulcer and gastro‐duodenal ulcer diseases in Taiwan

Background and Aim: The prevalence of Helicobacter pylori‐negative duodenal ulcer (DU) is increasing in Western countries but is rare in Japan. We aimed to examine the prevalence of H. pylori infection and the characteristics in DU and gastro‐duodenal ulcer (GDU) diseases in Taiwan. Study: All patients with an endoscopic diagnosis of DU or GDU from September 2003 to May 2004 at Taipei Veterans General Hospital were included. Rapid urease test was done for all patients, while urea breath test was carried out on those with negative rapid urease tests. A patient was considered infected if either test was positive. Results: The prevalence of H. pylori was 88.7% (555/626) in DU and 90.5% (95/105) in GDU patients. There was no difference in sex and prevalence of H. pylori between the two groups but age was higher in the GDU patients (60.1 ± 15.5 vs. 55.4 ± 15.5, P = 0.005). Of H. pylori‐negative DU patients, 28.2% (20/71) reported using non‐steroidal anti‐inflammatory drugs (NSAIDs)/aspirin, which were used by all 10 H. pylori‐negative GDU patients (100%) (P < 0.001). There was no difference in sex and age between H. pylori‐positive and negative DU patients. The prevalence rate of H. pylori in DU was not statistically different among outpatients, inpatients, and physical check‐up subjects (86.8% vs. 93.3% vs. 90.7%, P = 0.163). Conclusion: The prevalence of H. pylori infection in DU appears to be decreasing in Taiwan. Thus, eradication therapy without confirming the presence of H. pylori in DU patients cannot be recommended. NSAIDs/aspirin is the major risk factor for H. pylori‐negative DU patients, especially those with co‐morbid gastric ulcer.     

Giant duodenal ulcer

Patients with giant duodenal ulcer (>2 cm) have more ulcer complications (ie, bleeding) than patients with duodenal ulcer in the standard range (0.5–1.5 cm). To evaluate possible differences between patients with giant duodenal ulcer and those with duodenal ulcer in the standard range, we determined basal acid outputs by nasogastric suction, percentage of patients with daily nonsteroidal antiinflammatory drug (NSAID) use, and percentage of ulcer complications in 184 patients with endoscopically documented active duodenal ulcer. Seventeen patients had giant duodenal ulcer, and 167 patients had duodenal ulcer in the standard range. The mean basal acid outputs for the 17 patients with giant duodenal ulcer was 7.9 meq/hr (range 0.0–27.8 meq/hr) and for the 167 patients with duodenal ulcer in the standard range was 9.0 meq/hr (range 0.0–49.1 meq/hr), which were not significantly different. There was a significant difference in the percentages of ulcer complications between the 17 patients with giant duodenal ulcer and the 167 patients with duodenal ulcer in the standard range: 65% compared to 25% (P=0.001), and in the percentages of patients with regular daily NSAID use, during the one month preceding the upper gastrointestinal endoscopy: 53% compared to 8% (P=0.00001). However, a significant association between NSAID use and duodenal ulcer complication was not apparent. These results suggest that the development of giant duodenal ulcer and the significant increase in complications associated with giant duodenal ulcer are not attributable to increased basal acid output, however, they may be attributable to increased NSAID use.     

Increased dopamine receptor binding in duodenal mucosa of duodenal ulcer patients

High-affinity and saturable membrane-bound dopamine binding sites have been characterized in rat and human gastrointestinal tissues. Although their role in experimental ulcerogenesis has been suggested, dopamine receptor activity in peptic ulcer disease has not been investigated. Radioligand binding studies were performed with mucosal tissue homogenates obtained from the antrum and duodenum of six male healthy volunteers and six male duodenal ulcer patients. The binding assay was performed in triplicate with a crude membrane fraction using [³H] dopamine as a ligand at a final concentration of 1 nM at 22 °C in the dark. Nonspecific binding (which usually comprised about 30% of total binding) was determined in the presence of a 100-fold excess of unlabeled dopamine. A significant (P<0.05) increase of [³H]dopamine binding was found in duodenal mucosa of duodenal ulcer patients. [³H]Dopamine binding in stomach (antrum) of normal and duodenal ulcer patients did not differ significantly. These findings provide preliminary evidence for a role of dopamine receptors in duodenal ulcer and suggest that biochemical abnormalities of gut dopamine function may be operative in the pathogenesis of peptic ulcer disease.     

Hypersomatostatinaemia in duodenal ulcer

Abstract A sensitive and specific radioimmunoassay of serum somatostatin has been developed that overcomes the problems encountered in earlier assays of peptide disintegration and the need for prior plasma extraction, which is known to result in artifactual loss of somatostatin. In 37 normal controls, a significant positive correlation between fasting serum gastrin and somatostatin concentrations, and a significant negative correlation between pentagastrin-stimulated maximal acid output and fasting serum somatostatin levels were observed. In the majority of 134 patients with active duodenal ulcer in whom the fasting serum somatostatin levels were normal, these relationships were absent. In the remaining 25% in whom the fasting serum somatostatin levels were abnormally raised, these relationships were retained. Following a mixed meal, circulating somatostatin levels remained unchanged in controls and patients as a group. These results suggest that: (i) in the normal state, fasting levels of circulating gastrin and somatostatin are closely related, and that acid secretion may paradoxically exert an inhibitory effect on fasting somatostatin levels; (ii) hypersomatostatinaemia identifies a subgroup of patients with duodenal ulcer in whom these relationships are retained; and (iii) somatostatin may not have a significant hormonal role in the postprandial state in man.     

Effect of Helicobacter pylori eradicated therapy on water gastric emptying in patients with active duodenal ulcer

BACKGROUND AND AIMS: It remains debatable if duodenal ulcer (DU) or Helicobacter pylori infection has a definite impact on human gastric emptying (GE). We explored the nature of water GE in active DU patients before and after ulcer healing and the influence of H. pylori eradication on GE. METHODS: A home made applied potential tomography (APT) was used to measure liquid GE. Twelve electrodes were placed in a circular array around the upper abdomen of studied subjects. After drinking 500 mL of ion-free water, paired electrodes injected electrical current and the remaining 10 electrodes recorded signals, one-by-one in a rotating order. Based on tomographical calculation, the serial changes of averaged signals from altered resistivities were constructed to display GE. Initially, 64 H. pylori infected active DU patients were enrolled. After APT measurement, one-week triple therapy (omeprazole, amoxicillin and clarithromycin) was dispensed. Patients were asked back to determine ulcer/H. pylori status and GE on a scheduled date 3 months later. Finally, 58 patients finished the trial with valid and readable GE data obtained. RESULTS: The ulcer healing and H. pylori eradicated rates were 91.4% and 82.8%, respectively. In general, liquid GE was prolonged in all DU patients at follow up. Of 48 eradicated patients, 35.4% manifested either enhanced or delayed GE before treatment, whereas only five (10.4%) had abnormal GE after treatment (P < 0.0001). In contrast, this characteristically normalized GE was not found in non-eradicated patients. CONCLUSIONS: Water GE of active DU patients ranges from enhanced to delayed, while an effective H. pylori triple therapy is useful not only for healing ulcers, but also for restoring abnormal GE.     

Duodenal mucosal histology and histochemistry in active, treated and healed duodenal ulcer: Correlation with duodenal prostaglandin E2 production

We investigated whether impaired duodenal mucosal prostaglandin E₂ (PGE₂) production previously observed in duodenal ulcer (DU) was a primary pathophysiological abnormality or secondary to mucosal architectural changes that accompany ulceration. One hundred patients were studied: at endoscopy, paired duodenal biopsies were taken in patients with normal endoscopies and from the ulcer edge or scar and background mucosa in active or healed DU. One of the pair of biopsies was used to estimate PGE₂ synthesis ability, the other was processed for histology and histochemistry. The following features graded: goblet cell numbers and staining with Periodic acid-Schiff reagent (PAS), epithelial staining with PAS, villous atrophy, columnar cell height, inflammatory cell infiltrate and micro-erosions and gastric metaplasia taken as a whole. Patients were found to have normal endoscopy (n= 31), active untreated DU (n= 20), active DU on treatment with either cimetidine or ranitidine (n= 13), healed DU on maintenance treatment (n= 27) and healed DU off treatment (n= 9). Active duodenal ulceration was found to be associated with decreased numbers of goblet cells, loss and blunting of villi, increased columnar cell height, increased epithelial cell PAS staining and with gastric metaplasia. After healing, only villous blunting remained. These changes were present, but less marked, at sites removed from the ulcer and were not apparent in the patient groups with healed ulcers. A strong correlation between overall gastric metaplasia and epithelial cell PAS staining and the reduced ability to synthesize PGE₂ (P < 0.001) was only apparent when biopsies from all patients were grouped together, but not within individual patient subgroups. There was no consistent correlation between PGE₂ generation and individual parameters of pathological change in the duodenum. We conclude that, although inflammatory and mucosal changes may contribute, the evidence suggests that the impaired PGE₂ generation in DU disease is, to a large extent, independent of histological and histochemical features.