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The stomach is a marvel of chemistry.  The main acid which is produced, hydrochloric acid, could easily dissolve a hole through the stomach were it not for a complicated series of protective measures in the form of mucous secretion, bicarbonate neutralization, and a unique epithelial barrier.  The finding of  Helicobacter pylori as the cause of some stomach ulcers owes much of its noteriety to pathologists. 

There is some controvery regarding terminology of common inflammatory conditions of the stomach. In general, gastritis is used for inflammatory conditions. Gastropathy is reserved for conditions with evidence of injury to the endothelium or epithelium, but without inflammatory cells.

General Anatomy and Histology

Adenoma of the Stomach
Autoimmune Gastritis
Cancer of the Stomach
Collagenous Gastritis
Fundic Gland Polyp
Helicobacter Pylori Gastritis/Peptic Ulcer Disease
Hyperplastic Gastropathies (Zollinger-Ellison Syndrome)
Hyperplastic Polyps
Lymphocytic Gastritis
Lymphoma of the Stomach
Peptic Ulcer Disease
Pyloric Stenosis


Gross Appearance and Clinical Variants  
Histopathological Features and Variants  
Special Stains/
Electron Microscopy
Differential Diagnosis  
Commonly Used Terms  
Internet Links  


Autopsy findings following gastric bypass surgery for morbid obesity.

Melinek J, Livingston E, Cortina G, Fishbein MC.

Departments of Pathology and Laboratory Medicine (Drs Melinek, Cortina, and Fishbein) and General Surgery (Dr Livingston), UCLA School of Medicine, Los Angeles, Calif.

Arch Pathol Lab Med 2002 Sep;126(9):1091-5 Abstract quote

Background.-Roux-en-Y gastric bypass, currently the most frequently performed surgical procedure for morbid obesity, has a low but significant mortality rate. There are limited data documenting the findings at necropsy in patients who have died following this procedure.

Objective.-To determine cause of death and pathologic processes present in obese subjects dying after gastric bypass surgery.

Patients.-We studied 10 patients who underwent autopsy following gastric bypass surgery for morbid obesity between the years 1994 and 2000.

Results.-There were 6 men and 4 women. The mean age of the patients was 48 years (range, 28-62 years). The mean preoperative weight was 162 kg (range, 112-245 kg), and the mean body mass index was 54 kg/m(2) (range, 39-76 kg/m(2)), similar to all patients undergoing gastric bypass at our institution during the same period. Five deaths were directly attributable to technical complications. Five deaths were attributed to underlying comorbid conditions. One patient died of cirrhosis and one of pulmonary hemorrhage. Three patients died from pulmonary embolism. However, 8 of 10 patients had microscopic evidence of pulmonary emboli, despite prophylaxis for deep vein thrombosis. Most patients had some degree of steatohepatitis and hepatic fibrosis (80% and 70%, respectively). There were no deaths from primary cardiac events.

Conclusions.-In patients who die after Roux-en-Y gastric bypass, half die due to technical complications, whereas the other half die of complications of their obesity. Clinically, only 20% of patients were suspected to have pulmonary emboli, yet at autopsy, 80% of patients had pulmonary emboli. In morbidly obese patients undergoing Roux-en-Y gastric bypass, there is an unexpectedly high rate of clinically silent pulmonary emboli contributing to morbidity and mortality.


Acute cellular rejection grading scheme for human gastric allografts.

Garcia M, Delacruz V, Ortiz R, Bagni A, Weppler D, Kato T, Tzakis A, Ruiz P.

Hum Pathol 2004;35:343-349 Abstract quote

The control of acute cellular rejection (ACR) in multivisceral transplantation improves long-term survival, but monitoring this process can be challenging because different allografts can display varying forms and degrees of rejection. Criteria for ACR of small bowel and liver have been established, but a systematic analysis for ACR in stomach is lacking.

For this reason we have developed a comprehensive grading scheme for the evaluation of gastric allograft rejection. The grading scheme was designed to individually grade a variety of changes in the surface epithelium, lamina propria, and glandular structures. The individual values are cumulated, and the final score determines assignment of the rejection grade. The ACR grades range from no evidence of acute cellular rejection to severe rejection.

We performed a retrospective study based on 70 gastric allograft biopsies from 20 patients who received multivisceral transplantation from 1995 to 2001. We found that the scoring system showed no significant interobserver variability and allowed for an accurate designation of the ACR grade to the gastric allografts. We found with this grading system that neither clinical symptoms nor gastric endoscopic findings could serve as specific indicators of gastric ACR. Our results also showed that there were differences in the occurrence and intensity of acute rejection between the stomach and other transplanted organs, suggesting that ACR can occur independently among different allografts of the same host.

In conclusion, we find that this scheme for grading ACR in gastric transplants is objective and reproducible. This grading system will likely allow for improved correlation between gastric ACR grade and clinical symptoms, as well as improve interobserver uniformity within and between institutions.
Gastric Siderosis: Patterns and Significance.

Marginean EC, Bennick M, Cyczk J, Robert ME, Jain D.

*Department of Anatomic Pathology, Program in Gastrointestinal Pathology daggerDepartment of Internal Medicine, Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT.

Am J Surg Pathol. 2006 Apr;30(4):514-520. Abstract quote  

Recently, we encountered 2 cases of diffuse iron deposition in gastric antral and fundic glandular epithelium, which in 1 patient eventually led to the diagnosis of hemochromatosis.

Gastric mucosal siderosis (GS) has previously been described in hemochromatosis patients, alcoholics, and in association with iron medications. However, the prevalence of various patterns of iron deposition in the gastric mucosa and their clinical significance have not been studied in detail. The 2 index cases mentioned above and 500 additional consecutive gastric biopsies examined over a period of 8 months at our institution were stained for iron by the Prussian blue method. In addition, all patients with genetic hemochromatosis diagnosed by liver biopsy in our department between 1998 and 2003 who also had gastric biopsies were identified from the surgical pathology files and included in the study (n=3). The location of iron deposition {stromal cells (endothelium, fibroblasts, macrophages), glandular epithelium, or extracellular} was recorded and subjectively graded as 1+ to 3+ according to the severity of deposition within the mucosa. Relevant histologic changes (inflammation, presence of H. pylori, ulceration) and clinical features were reviewed.

Three patterns of GS were identified: A) "nonspecific GS" with predominant iron deposition in the stromal cells including macrophages, and focally in epithelium; B) "iron-pill gastritis" with often mild gastritis and reactive gastropathy type changes, and mostly extracellular deposition with focal stromal cells and epithelial deposition; and C) predominant deposition in antral and fundic glandular epithelium. Of the 500 cases studied, a total of 18 (3.6%) cases were found to have GS. Of these 18 cases, 11 (2.2%) showed pattern A, 4 (0.8%) showed pattern B, and 3 (0.6%) showed pattern C. The GS in patterns A and B was always focal or patchy (1+ to 2+), whereas in pattern C it was generally diffuse and strong (2+ to 3+). A history of oral iron medication was present in 2 (n=11, 0.4%) patients with pattern A, in all patients with pattern B (n=4, 100%), and in none of patients with pattern C (n=3, 0%). Varying degrees of mucosal inflammation were noted in patients with pattern A cases, and 2 had evidence of active Helicobacter pylori infection. Of the 3 cases with known hemochromatosis, only one gastric biopsy showed pattern C GS (1+).

In conclusion, gastric mucosal siderosis is relatively uncommon (3%) but is important to look for as it may lead to a diagnosis of hemochromatosis in some cases.

Three patterns are recognized: A) a "nonspecific" stromal cell predominant pattern, which may be associated with gastric inflammation, possibly prior mucosal hemorrhages or iron medications; B) extracellular coarse clumps of crystalline iron deposition associated with oral iron medications, mild gastritis, and reactive gastropathy type changes ("Iron-pill gastritis"); and C) gastric glandular siderosis, which may be associated with systemic iron overload/hemochromatosis.
Granulomatous Gastritis: A Clinicopathologic Analysis of 18 Biopsy Cases.

Maeng L, Lee A, Choi K,
Kang CS, Kim KM.

Departments of *Pathology
and daggerInternal Medicine, College of Medicine, The Catholic University of Korea, Bupyung-gu, Inchon, Korea.
Am J Surg Pathol. 2004 Jul;28(7):941-945. Abstract quote  

Granulomas in gastric biopsy specimens are extremely rare, and in Western countries, more than half are associated with Crohn's disease.

To evaluate the incidence and their etiology in a gastric carcinoma (and Helicobater pylori infection)-prevalent area, gastric mucosal biopsies were reviewed and their clinicopathologic findings were analyzed. The clinicopathologic diagnoses of the 18 patients with granulomatous gastritis were as follows: chronic gastritis with (n = 14) and without (n = 1) H. pylori infection; gastric adenocarcinomas (n = 2); and Crohn's disease (n = 1). Almost all cases of granulomatous gastritis in this study showed small erosions or ulcers on the endoscopic examinations.

H. pylori were found to be one of the most common causes of granulomatous gastritis after excluding all other causes for the granulomas in this study. The granulomas were more frequently found in the antrum, superficially located, and were related to damage within a pit in which the H. pylori were commonly observed.

These findings suggest that H. pylori can be causal in the pathogenesis of granulomatous gastritis.

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Weedon D. Weedon's Skin Pathology Second Edition. Churchill Livingstone. 2002
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Weiss SW and Goldblum JR. Enzinger and Weiss's Soft Tissue Tumors. Fourth Edition. Mosby 2001.

Commonly Used Terms

Intestinal Metaplasia-A change in the mucosa from the normal gastric mucosa to a type resembling that seen in the intestines.  

Basic Principles of Disease
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Diagnostic Process
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Surgical Pathology Report
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Special Stains
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Last Updated April 28, 2006

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