结节型十二指肠炎的内镜表现及其临床病理学特征

目的 探讨结节型十二指肠炎内镜下表现与其组织学特征的关系及其发病机制。方法 观察内镜下136例结节型十二指肠炎的表现，对其活检标本均行H-E染色，观察病理改变，Giemsa染色及快速尿素酶试验诊断幽门螺杆菌感染，十二指肠黏膜兼作AB／PAS染色，观察十二指肠胃上皮化生。结果 136例结节型十二指肠炎内镜下表现为直径0．2～1．0cm大小不等的结节，伴有不同程度的充血、水肿，其中伴糜烂21例，出血点及（或）瘀斑30例。检出率占同期15820例内镜检查的0．9％，十二指肠炎的3．8％。病理诊断为十二指肠炎107例，其中慢性十二指肠炎53例，表现为间质内可见慢性炎性细胞浸润，肠绒毛缩短或萎缩、变平．肠腺不同程度减少；活动性十二指肠炎54例，除慢性炎性细胞外，黏膜层及固有层内还有不同程度的中性粒细胞浸润，伴Brunner腺增生51例，胃型上皮化生59例。136例中检出胃黏膜异位增生7例以及血吸虫虫卵所致的炎性病变4例，107例结节型十二指肠炎中，幽门螺杆阳性（Hp^＋）者为45．8％（49／107）。其中，53例慢性十二指肠炎患者中HP^＋者为32．1％（17／53），54例活动性十二指肠炎中Hp^＋检出率为59．3％（32／54），后者的Hp^＋检出率显著高于前者（P〈0．01）。结论 结节型十二指肠炎是一类特殊的非特异性十二指肠炎，内镜下表现与组织学改变存在不一致性。其发生可能与Hp感染及胃上皮化生、Brunner腺增生有关。     

Duodenitis in stomach diseases--a quantitative histologic study

The coincidence of gastric diseases and chronic duodenitis has been investigated on biopsies and preparations of stomach and duodenum by a quantitative histologic method. The histologic classification of duodenitis was made according to Whitehead et al. 9 of 40 patients with a chronic atrophic gastritis had a duodenitis grade 1. 10 of 40 patients with a chronic gastric ulcer had a duodenitis grade 1 and one patient grade 2. 14 of 40 patients with a gastric cancer had a duodenitis grade 1. By statistical investigations it has been found out that patients with an ulcer or cancer do not have duodenitis more often than patients with gastritis. A possible duodenitis concerning the investigated gastric diseases is mainly due to the chronic gastritis that also could be proved by all patients suffering from ulcer or cancer.     

Mucosal cell proliferation in duodenal ulcer and duodenitis.

Mucosal cell proliferation in the first part of the duodenum was studied in 24 patients using a tissue culture technique in which endoscopic biopsies were subjected to autoradiography after exposure to tritiated thymidine. Eight patients had a normal duodenum, eight had duodenal ulcer, and eight had symptomatic chronic non-specific duodenitis. The mean crypt labelling index (LI) in normal duodenum was 8.8 0.4% (SEM). Increased labelling indices of 15.6 +/- 1.7% were found near the edge of duodenal ulcers and 17.8 1.8% in duodenitis. Treatment with cimetidine reduced both the severity of duodenitis and the mean crypt LI. The LI of histologically normal duodenal mucosa distal to ulcer of duodenitis was similar to that of the control subjects' mucosa. The increased mucosal cell proliferation seen in severe duodenitis, either alone or associated with duodenal ulceration, suggested that erosions and ulcers arose when the crypts passed into 'high output failure' and were unable to compensate for further epithelial cell loss. There was no evidence in out study for a generalised failure of mucosal cell proliferation in duodenal ulcer or duodenitis.     

Nodular duodenitis in chronic maintenance hemodialysis patients

A retrospective study of 138 cases of chronic hemodialysis between 1977 and 1982 were reviewed for endoscopic, radiographic, and histologic characteristics of duodenitis. Forty patients underwent upper gastrointestinal barium x-rays; 13 were found to have multiple duodenal bulb nodules and three of these patients had very prominent duodenal bulb folds. There were 42 patients on whom upper panendoscopy was performed, and multiple duodenal nodules were seen in 15 patients and thickened folds in three patients. There were five patients in whom nodules were seen only on endoscopy. The size of the nodules varied between 3 and 8 mm in diameter and mucosal folds between 4 and 8 mm. Duodenal mucosal hyperplasia with chronic inflammatory cell infiltrate was found on biopsy of the nodules in 12 cases, while three cases with nodules revealed blunted villous structure with chronic inflammatory cells.     

A Study of the Correlation between Endoscopic and Histological Diagnoses in Gastroduodenitis

Serial histological specimens from 14 patients with the endoscopic diagnosis of erosive gastritis and/or duodenitis were examined for correlation between endoscopic and histological findings. All patients were symptomatic outpatients without history of alcoholism or usage of aspirin or nonsteroidal antiinflammatory drugs. After the initial diagnosis, the patients underwent follow-up endoscopy until healing of erosions at 1, 4, and 8 wk. Pairs of biopsies from the gastric fundus, body, and antrum, and the duodenum were obtained at each endoscopy. Agreement between histological and endoscopic findings occurred in only 56% of the 161 sites studied. The best correlation occurred in the duodenum when there was endoscopic disease (89%) and was worst in the stomach at all sites regardless of endoscopic findings (46%). A normal histology in the face of abnormal endoscopic changes was seen in only 16% of all biopsies. Histological inflammation occurred in 27% of all biopsies with a normal endoscopic appearance and in 55% of the normal endoscopic areas in the stomach. Histological appearances at each biopsy site remained constant in individual patients throughout the study. The specific histological findings, such as activity and severity, did not correlate with the endoscopic severity of inflammation or with any specific endoscopic appearances, such as erosions, petechiae, or nodules. In conclusion, the histological and endoscopic findings in the stomach from patients with symptomatic erosive gastroduodenitis correlate poorly while good correlation occurs in the duodenum.     

The clinical relevance of endoscopic and histologic inflammation of gastroduodenal mucosa in dyspepsia of unknown origin

Two hundred and ten patients were defined as having dyspepsia of unknown origin. At endoscopy 11% had body gastritis, 46% antral gastritis, and 19% bulbitis (two thirds combined with antral gastritis). Histologically, 22% had chronic corpus gastritis (79% superficial, 21% atrophic), which was combined with chronic antral gastritis in 84%, 33% had chronic antral gastritis (82% superficial, 18% atrophic); and 14% had duodenitis, which was combined with antral gastritis in 65%. Polymorphonuclear leukocytes were found in specimens from the body mucosa in 6%, from the antral mucosa in 13%, and from the duodenal cap in 4%. The endoscopic findings correlated significantly with the histologic findings in the duodenal bulb (kappa = 0.33) but not in the stomach. The frequency of endoscopic antral gastritis and the frequency of histologic chronic body and antral gastritis increased with age. Endoscopic bulbitis and histologic duodenitis and gastric metaplasia were commoner in men than in women. Peak acid output was higher in patients with than in those without endoscopic bulbitis and higher in smokers than in non-smokers when the significant sex differences in peak acid output were taken into account. Gastric metaplasia of the bulb was predominantly correlated to higher peak acid output and to some extent also to sex and smoking. Episodic pain was correlated to histologic duodenitis. Other dyspeptic symptoms and the intragastric bile acid concentration were not associated with any endoscopic or histologic findings. Of the 210 patients, 172 were reexamined after a double-blind 6-week treatment period with cimetidine, antacid, or placebo. The symptomatic outcome of these treatments was not associated with any significant change in endoscopic or histologic findings.     

Do scattered white spots in the duodenum mark a specific gastrointestinal pathology?

OBJECTIVE: To discover whether scattered white spots (SWS) in the duodenum are related to a specific kind of disease. We also scrutinized other upper endoscopic findings which might be associated with SWS. METHODS: Among the patients who were admitted for upper gastrointestinal system endoscopy, those having the endoscopic appearance of SWS in duodenum were enrolled in this study. In total 107 patients [70 women, 37 men, mean age: 51.6 ± 16.88 years (range: 17–82 years)] were included. At least three duodenal biopsies were taken from each patient and histopathological examinations were done by experienced pathologists. RESULTS: The histopathological examination revealed that 39 (36.4%) patients had intestinal lymphangiectasia (IL), 15 (14%) patients had giardiasis (G) and 30 (28.1%) patients had chronic non‐specific duodenitis (CD). Two patients with IL were also found to have G. Twenty patients had both IL and CD. One had both G and CD. G was the least common etiology for SWS in the duodenum. The most common reasons for SWS in the duodenum in this study group were IL and CD, in order of decreasing frequency. There was no significant relationship with the other upper endoscopic findings in all these patients. CONCLUSION: Histopathological examinations should be provided for each patient with SWS in the duodenum to assess the etiology.     

十二指肠结节性病变病理分型及诊断17例

目的:确定十二指肠结节性病变组织病理学特征及分型.方法:统计分析经内镜下被确诊为十二指肠结节性病变患者的资料.对其年龄、性别、类型、症状、最后诊断、相关疾病和组织病理学特点等记录进行回顾性研究.同时亦分析患者血红蛋白、平均细胞体积、血清铁蛋白、白蛋白、免疫球蛋白、腹腔自身抗体、贾第虫和粪便OVA寄生虫,ELISA分析贾第虫的特异性抗原水平.结果:筛选出17例经内镜确诊为十二指肠结节性病变的患者.诊断时平均年龄为28.1岁(17-56岁),男9例,女8例.十二指肠结节性病变中,腹痛(47%)是最常见的临床症状,胃窦结节(41%)是最常见的内镜表现.十二指肠结节性病变的组织病理学评估显示,所有患者均有慢性炎症,嗜酸性粒细胞在隐窝间和上皮内增殖占70.5%,47%的患者存在绒毛萎缩.通过组织学检查和/或特定的蓝氏贾第鞭毛虫粪便抗原阳性实验显示有6例患者感染贾第虫.患者的临床诊断显示某些特征,如腹泻、贾第虫病、分泌型IgA缺乏症和幽门螺杆菌(Helicobacter pylori,H.pylori)胃炎,并且他们中的一些与其他的有相关性.结论:十二指肠结节性病变其黏膜有明显淋巴细胞和/或嗜酸性粒细胞浸润,建议应对造成这一显著炎症反应的微生物学和免疫学病因进行进一步研究.     

Glomerulosclerosis in Type 2 (non0insulin-dependent) diabetes mellitus: relationship to glycaemia in the University Group Diabetes Program (UGDP)

Summary Kidney tissue of acceptable quality was available from autopsies of 55 patients who had been followed prospectively for 3 to 15 years as participants in the University Group Diabetes Program, a study of vascular disease in Type 2 (non-insulin-dependent) diabetic patients. Slides were prepared for light microscopic reading by uniform histologic techniques, and then were randomly intermixed and coded with tissues identically prepared from matched nondiabetic subjects (morphologic controls). After independent review by three morphologists, the results were tabulated and assigned to one of four diagnostic groups: 1) typical diabetic nodular glomerulosclerosis; 2) mesangial changes suggestive of diabetes (diffuse lesion); 3) non-diabetic renal disease; 4) normal for age. Of the diabetic cases 31% (17 of 55) were found to show nodular glomerulosclerosis, and another 47% (26 of 55) showed suggestive changes; none of the morphologic control slides was read as showing nodular glomerulosclerosis, but some were judged to show suggestive mesangial (diffuse) changes. Although only 4 of the 17 diabetic patients with nodules had died of uraemia, many had hypertension, which may have contributed to their deaths from vascular disease. The patients with nodular glomerular changes also showed, on the average, the highest blood glucose levels during life. Type 2 diabetes in later life appears to be associated with a high risk for typical tissue changes of diabetic kidney damage, which may contribute significantly to morbidity and mortality and may be present before azotaemia and qualitative proteinuria have been recognized.     

Duodenitis: a reliable radiologic diagnosis?

The authors performed a retrospective study of 50 patients with endoscopically diagnosed duodenitis who had undergone double-contrast upper gastrointestinal (GI) examinations. Duodenitis was diagnosed on the original radiographic reports in six of 37 patients (16%) with mild-to-moderate duodenitis, five of 13 patients (38%) with severe duodenitis, and 11 of 50 patients (22%) with all grades of duodenitis on endoscopy. Subsequent analysis of the films revealed one or more radiologic signs of duodenitis (including folds more than 4 mm in thickness, mucosal nodularity, bulbar deformity, and erosions) in 18 of 37 patients (49%) with mild-to-moderate duodenitis, eight of 13 patients (62%) with severe duodenitis, and 26 of 50 patients (52%) with all grades of duodenitis on endoscopy. In a separate part of the study, the authors identified another 20 patients with radiographically diagnosed duodenitis who had undergone endoscopic examinations. Nine of those 20 patients (45%) had duodenitis on endoscopy. Subsequent analysis of the films revealed one or more signs of duodenitis in 17 patients from this group. Nine of the latter patients (53%) had duodenitis on endoscopy. Using established radiologic criteria for duodenitis, our rate of false-positive and false-negative radiologic diagnoses still was about 50%. Thus, the double-contrast upper GI examination is a relatively unreliable technique for diagnosing duodenitis.     

Recurrent cavitary nodules secondary to Hodgkin's disease

A patient with nodular sclerosing Hodgkin's disease had at least three episodes of lung involvement consisting of an infiltrate on one occasion and multiple cavitating nodules on the other two. The cytologic and histologic studies of the lung specimens disclosed the presence of Reed-Sternberg cells on each occasion without any evidence for infection. This represents the first time in which recurrent cavitating nodules have been reported with Hodgkin's disease.     

Erosive duodenitis after eradication therapy for Helicobacter pylori]

We studied the characteristics of erosive duodenitis after eradication therapy for Helicobacter pylori (Hp). Fifty-nine patients with Hp-positive peptic ulcer disease were treated with a combination of amoxicillin, clarithromycin, lansoprazol, and polaprezinc Subsequently, erosive duodenitis developed in 18 (43.2%) of 44 patients in whom Hp was eradicated successfully. There were no significant differences in demographic characteristics between the patients in whom duodenitis developed and those whom it did not, except that the incidence of duodenal ulcer before treatment was highte in the former group than in the latter. Erosions were located not only in the anterior wall of the first portion of the duodenum but also in the posterior wall or the second portion. Our results suggest that the development erosive duodenitis after Hp eradication therapy is a favorable, rather than an unfavorable, event, because erosive duodenitis appeared only in the patients with in whom Hp was successfully eradicated, moreover, the patients with duodenitis had no complaints and had a good prognosis without follow-up treatment.     

Treatment of duodenitis with cimetidine: a clinical, endoscopic, and histologic study

We studied the effectiveness of cimetidine in the treatment of endoscopically diagnosed duodenitis. Sixty-nine patients with the solitary endoscopic finding of duodenitis (6% of 1,200 patients who underwent fiberoptic endoscopy of the upper gastrointestinal tract in our unit over 3 years) were studied retrospectively: a good clinical response was apparent in 45 of 69 patients treated with cimetidine (65%), and a fair response in another four (6%). In a controlled, randomized prospective study, we evaluated the effectiveness of cimetidine in duodenitis. Statistically significant improvement for the clinical and endoscopic scores was found in 10 patients treated with cimetidine (p less than 0.01). Improvement in the histologic score did not reach statistical significance. No such improvement was demonstrated in seven placebo-treated patients. We believe that duodenitis is a "peptic syndrome," has a good response to cimetidine treatment, and behaves much like duodenal ulcer disease.     

Duodenal epithelial thymidine uptake in patients with duodenal ulcer or endoscopic duodenitis

To evaluate the relationship between duodenal ulcer disease and duodenitis, duodenal epithelial cell renewal was measured in mucosal biopsies by the incorporation of [³H]thymidine. When 14 patients with duodenal ulcer were compared to 13 control subjects or 7 with endoscopic duodenitis alone, the crypt size was the same in all groups. Similar to other inflammatory processes of the gastrointestinal tract, patients with endoscopic duodenitis showed increased proliferative indices including a greater number of cells incorporating [³H]thymidine. In contrast, the proliferative indices from the duodenal mucosa of patients with duodenal ulcers did not differ from a control group. In a group of 6 patients with both endoscopic duodenitis and duodenal ulcer, the [³H]thymidine incorporation was intermediate between control subjects or patients with duodenal ulcer alone and those with endoscopic duodenitis alone. When subjects were divided according to the histologic appearance of the duodenal mucosa, those having chronic duodenitis demonstrated enhanced [³H]thymidine incorporation in comparison to a control group or patients with chronic active duodenitis (polymorphonuclear leukocytes present). Although there are many possible explanations of these findings, one may speculate that duodenal ulceration does not stimulate duodenal epithelial proliferation. This project was supported by the Yale Digestive Cancer Research Fund. Dr. Gorelick was supported by a Research Fellowship Award from the National Foundation for Ileitis and Colitis during a portion of this study and is currently a recipient of a Clinical Investigator Award (KO8-AM-00659) from the National Institute of Arthritis, Metabolism and Digestive Diseases.     

Endoscopic and histopathological study on the duodenum of Strongyloides stercoralis hyperinfection

AIM： To investigate endoscopic and histopathological findings in the duodenum of patients with Strongyloides stercoralis （S. stercoralis） hyperinfection. METHODS： Over a period of 23 years （1984-2006）, we investigated 25 patients with S. stercoralis hyperinfection who had had an esophagogastroduodenoscopy before undergoing treatment for strongyloidiasis. The clinical and endoscopic findings were analyzed retrospectively. RESULTS： Twenty-four （96%） of the patients investigated were under immunocompromised condition which was mainly due to a human T lymphotropic virus type 1 （HTLV-1） infection. The abnormal endoscopic findings, mainly edematous mucosa, white villi and erythematous mucosa, were observed in 23 （92%） patients. The degree of duodenitis including villous atrophy/destruction and inflammatory cell infiltration corresponded to the severity of the endoscopic findings. The histopathologic yield for identifying larvae was 71.4% by duodenal biopsy. The endoscopic findings of duodenitis were more severe in patients whose biopsies were positive for larvae than those whose biopsies were negative （Endoscopic severity score： 4.86 ± 2.47 vs 2.71 ±1.38, P 〈 0.05）. CONCLUSION： Our study clearly demonstrates that, in addition to stool analysis, endoscopic observation and biopsies are very important. We also emphasize that S. stercoralis and HTLV-1 infections should be ruled out before immunosuppressive therapy is administered in endemic regions.     

十二指肠炎的内镜和组织学研究

目的 探讨十二指肠炎内镜和组织学诊断。 方法 内镜下正常(n=26)与炎症(n=44)患者进行组织学形态定量研究。 结果 内镜下轻度充血、红斑不足以诊断十二肠炎,需病理组织学证实。固有层炎性细胞密度,特别是园细胞密度是诊断的依据。胃上皮化生有助诊断,绒毛高度、宽度和肠腺深度对诊断无价值。 结论 固有层炎性细胞密度是诊断十二指肠炎的依据。     

Duodenal mucosal architecture in non-specific and ulcer-associated duodenitis.

This study was done to determine the severity and extent of abnormalities of duodenal mucosal architecture in non-specific (non-ulcerative) and ulcer-associated duodenitis. The effect of successful treatment with cimetidine on these changes has also been assessed. A method of microdissection and measurement of villus height, crypt depth, and mitotic figure count per crypt was applied to endoscopic biopsies from the duodenum. Five groups of patients were studied: untreated ulcer-associated duodenitis, untreated non-specific duodenitis, healed ulcer-associated and non-specific duodenitis after cimetidine treatment, and controls. Significant reduction in villus height, increase in crypt length, and increase in mitotic figure count per crypt were all found in both ulcer-associated and severe non-specific duodenitis as compared with controls. These changes were localised to visually inflamed areas and regressed after healing of these lesions with cimetidine. This is the first quantitative comparison of the architectural features between diseased states in the duodenum and control in the same study. Identical morphological changes in the form of crypt hyperplasia and villus atrophy were demonstrated in areas of non-specific and ulcer-associated duodenitis. No evidence could be found from this study that non-specific duodenitis constitutes a different disease from ulcer-associated duodenitis.     

Gastroduodenal mucosa in uraemia: endoscopic and histological correlation and prevalence of helicobacter-like organisms.

This study aimed to determine the prevalence of endoscopic and histological gastroduodenitis as well as helicobacter-like organisms in patients with end stage renal failure undergoing maintenance dialysis treatment. A total of 322 out of 422 patients in our dialysis programme underwent endoscopy and gastroduodenal biopsy specimens were taken from 260. Endoscopic gastroduodenitis occurred in 158 (49%). Histological gastritis occurred in the gastric body or antrum in 134 patients (52%) and duodenitis in 52 (21%). There was no correlation between endoscopic and histological gastritis in contrast to a significant correlation for duodenitis. Helicobacter-like organisms occurred in the body or antrum in 81 (31%). Their presence was associated with gastritis--in particular acute and acute on chronic gastritis rather than chronic gastritis. Patients with gastritis were significantly older than those without (p less than 0.001) and had lower basal and peak acid outputs.     

Campylobacter pylori-related gastrointestinal disease in children

Over a one-year period, 95 children and adolescents presenting with epigastric pain and/or vomiting, and without associated risk factors for development of peptic disease, underwent endoscopic antral biopsies for pathologic diagnosis and to detect presence of Campylobacterss. pylori (C. pylori). Additional biopsies of the esophagus, stomach, and duodenum were obtained for histologic evaluation. C. pylori was identified in 16 patients (16.8%), all of whom had evidence of acute and/or chronic gastritis. Significant discriminating factors between C. pylori-positive and -negative subjects included age at presentation (positive vs negative=14.6 vs 9.9 years, P<0.01, biopsy-confirmed gastritis (100% vs 30.4%, P<0.001), and diagnosis of duodenitis alone (0% vs 46.8%, P<0.001). Risk for bacterial colonization was significantly higher in the presence of endoscopic gastritis (P<0.001). Among C. pylori-positive patients, none responded to standard antiulcer therapy (H₂-receptor antagonists, antacids). Symptomatic and histologic remission was achieved utilizing combined therapy with bismuth subsalicylate and antibiotics. Seven of 79 C. pylori-negative patients with biopsyproven gastritis who responded poorly to antisecretory therapy had the organism identified in follow-up antral biopsies; these patients improved clinically following treatment for C. pylori. These data suggest that C. pylori is a significant factor in the etiology of upper gastrointestinal tract inflammatory disease in pediatrics, and presence of the organism should be evaluated, particularly in children with evidence of acute and/or chronic gastritis.     

Necrotizing sarcoid granulomatosis.

Twelve cases of necrotizing sarcoid granulomatosis are presented as a retrospective study. The population of patients consisted of ten women and two men, with an average age of 50 years. Nine patients initially had a variety of pulmonary and nonpulmonary complaints, while three were asymptomatic. Chest roentgenograms demonstrated bilateral nodules in seven patients, solitary nodules in four, and a miliary pattern progressing to nodules in one. Enlarged hilar nodes were found in six. Histologically, all biopsies showed a combination of individual granulomas, confluent masses of granulomas which formed the nodular masses seen on the roentgenograms, a variable amount of necrosis of tissue and hyalinization, and a granulomatous vasculitis. Follow-up periods ranged from four months to 11 years. Eleven patients are alive and asymptomatic. The sole death occurred in a patient treated with an immunosuppressive agent (cyclophosphamide). We conclude that the clinical behavior of necrotizing sarcoid granulomatosis is not similar to that of the other angiocentric granulomatoses and that most patients with this disease can be left untreated or be treated with steroids alone. We suggest the possibility that necrotizing sarcoid granulomatosis may be the histologic counterpart of so-called nodular sarcoid.