Atrophic Gastritis Type Research Articles

Iron and Vitamin B12 Deficiency in Patients with Autoimmune Gastritis and Helicobacter pylori Gastritis: Results from a Prospective Multicenter Study.

Iron and vitamin B12 deficiencies are common in patients with atrophic gastritis, but there are limited data on the prevalence of these deficiencies in different types of atrophic gastritis. This multicenter, prospective study assessed micronutrient concentrations in histologically confirmed autoimmune gastritis (AIG, n = 45), Helicobacter pylori-related non-autoimmune gastritis (NAIG, n = 109), and control patients (n = 201). A multivariate analysis was performed to determine factors influencing those deficiencies. The median vitamin B12 concentration was significantly lower in AIG (367.5 pg/mL, Q1, Q3: 235.5, 524.5) than in NAIG (445.0 pg/mL, Q1, Q3: 355.0, 565.0, p = 0.001) and control patients (391.0 pg/mL, Q1, Q3: 323.5, 488.7, p = 0.001). Vitamin B12 deficiency was found in 13.3%, 1.5%, and 2.8% of AIG, NAIG, and control patients, respectively. Similarly, the median ferritin concentration was significantly lower in AIG (39.5 ng/mL, Q1, Q3: 15.4, 98.3 ng/mL) than in NAIG (80.5 ng/mL, Q1, Q3: 43.6, 133.9, p = 0.04) and control patients (66.5 ng/mL, Q1, Q3: 33.4, 119.8, p = 0.007). Iron deficiency and iron deficiency adjusted to CRP were present in 28.9% and 33.3% of AIG, 12.8% and 16.5% of NAIG, and 12.9% and 18.4% of controls, respectively. Multivariate analysis demonstrated that AIG patients had a higher risk of developing vitamin B12 deficiency (OR: 11.52 [2.85-57.64, p = 0.001]) and iron deficiency (OR: 2.92 [1.32-6.30, p = 0.007]) compared to control patients. Factors like age, sex, and H. pylori status did not affect the occurrence of vitamin B12 or iron deficiency. Iron and vitamin B12 deficiencies are more commonly observed in patients with AIG than in those with NAIG or control patients. Therefore, it is essential to screen for both iron and vitamin B12 deficiencies in AIG patients and include the treatment of micronutrient deficiencies in the management of atrophic gastritis patients.

Updated Kimura-Takemoto classification of atrophic gastritis.

BACKGROUNDThe Updated Sydney system for visual evaluation of gastric mucosal atrophy via endoscopic observation is subject to sampling error and interobserver variability. The Kimura-Takemoto classification system was developed to overcome these limitations. AIMTo compare the morphological classification of atrophic gastritis between the Kimura-Takemoto system and the Updated Sydney system.METHODSA total of 169 patients with atrophic gastritis were selected according to diagnosis by the visual endoscopic Kimura-Takemoto method. Following the Updated Kimura-Takemoto classification system, one antrum biopsy and five gastric corpus biopsies were taken according to the visual stages of the Kimura-Takemoto system. The Updated Kimura-Takemoto classification system was then applied to each and showed 165 to have histological mucosal atrophy; the remaining 4 patients had no histological evidence of atrophy in any biopsy. The Updated Kimura-Takemoto classification was verified as a reference morphological method and applied for the diagnosis of atrophic gastritis. Adding one more biopsy from the antrum to the six biopsies according to the Updated Kimura-Takemoto classification, constitutes the updated combined Kimura-Takemoto classification and Sydney system. RESULTSThe sensitivity for degree of mucosal atrophy assessed by the Updated Sydney system was 25% for mild, 36% for moderate, and 42% for severe, when compared with the Updated Kimura-Takemoto classification of atrophic gastritis for morphological diagnosis. Four types of multifocal atrophic gastritis were identified: sequential uniform (type 1; in 28%), sequential non-uniform (type 2; in 7%), diffuse uniform (type 3; in 23%), diffuse non-uniform (type 4; in 24%), and "alternating atrophic – non-atrophic" (type 5; in 18%). The pattern of the spread of atrophy, sequentially from the antrum to the cardiac segment of the stomach, which was described by the Updated Kimura-Takemoto system, was histologically confirmed in 82% of cases evaluated.CONCLUSIONThe Updated Sydney system is significantly inferior to the Updated Kimura-Takemoto classification for morphological verification of atrophic gastritis.

Serum pepsinogen levels and OLGA/OLGIM staging in the assessment of atrophic gastritis types

BackgroundWe assessed the validity of using serum pepsinogen tests (sPGTs) to differentiate autoimmune atrophic gastritis (AAG) from environmental atrophic gastritis (EAG). We also investigated the correlation and prognostic value between...

Chronic Atrophic Gastritis: A Review.

Chronic atrophic gastritis is a generally asymptomatic condition of great importance because it develops into gastric cancer in a number of patients. It is described as an atrophy of the gastric mucosa. There are two types of atrophic gastritis: a gastric body predominant type in patients with infection of Helicobacter pylori, and an autoimmune type, limited to the gastric body and fundus. The autoimmune type is quite rare and affects people of all ethnicities. Globally, H. pylori infection is very common and is considered a class I carcinogen due to the large number of patients who subsequently develop gastric cancer. The pathogenesis of the autoimmune type involves an antibody-mediated loss of parietal cells resulting in achlorhydria and an antibody-mediated loss of intrinsic factor that causes pernicious anemia. The diagnosis of H. pylori infection is based on endoscopy and culture of the organisms. Patients with atrophic gastritis as well as H. pylori infection should be treated with antibiotics to eradicate the organism. Patients with the autoimmune type need to be evaluated for anemia, and if present, treated with vitamin B12.

Histidine decarboxylase and urinary methylimidazoleacetic acid in gastric neuroendocrine cells and tumours.

To study histidine decarboxylase (HDC) expression in normal and neoplastic gastric neuroendocrine cells in relationship to the main histamine metabolite. Control tissues from fundus (n = 3) and corpus (n = 3) mucosa of six patients undergoing operations for gastric adenocarcinoma, biopsy and/or gastric surgical specimens from 64 patients with primary gastric neuroendocrine tumours (GNETs), as well as metastases from 22 of these patients, were investigated using conventional immunohistochemistry and double immunofluorescence with commercial antibodies vs vesicular monoamine transporter 2 (VMAT-2), HDC and ghrelin. The urinary excretion of the main histamine metabolite methylimidazoleacetic acid (U-MeImAA) was determined using high-performance liquid chromatography in 27 of the 64 patients. In the gastric mucosa of the control tissues, co-localization studies identified neuroendocrine cells that showed immunoreactivity only to VMAT-2 and others with reactivity only to HDC. A third cell population co-expressed both antigens. There was no co-expression of HDC and ghrelin. Similar results were obtained in the foci of neuroendocrine cell hyperplasia associated with chronic atrophic gastritis type A and also in the tumours. The relative incidence of the three aforementioned markers varied in the tumours that were examined using conventional immunohistochemistry. All of these GNETs revealed both VMAT-2 and HDC immunoreactivity, and their metastases showed an immunohistochemical pattern and frequency similar to that of their primary tumours. In four patients, increased U-MeImAA excretion was detected, but only two of the patients exhibited related endocrine symptoms. Human enterochromaffin-like cells appear to partially co-express VMAT-2 and HDC. Co-expression of VMAT-2 and HDC might be required for increased histamine production in patients with GNETs.

Gastrectomy with isoperistaltic jejunal parallel pouch in a 15-year-old adolescent boy with gastric adenocarcinoma and autosomal recessive agammaglobulinemia

A 15-year-old adolescent boy with autosomal recessive agammaglobulinemia underwent endoscopy because of unexplained growth failure and malnutrition. Esophagogastroduodenoscopy revealed antropyloric stenosis, and a biopsy showed an invasive gastric adenocarcinoma. Chronic atrophic corpus gastritis type A and Helicobacter pylori were also identified. Abdominal magnetic resonance imaging confirmed the stenosis resulting from a semicircular intramural tumor without obvious local or distant metastatic spread. Gastrectomy with an extended lymphadenectomy was performed. Esophagoduodenal continuity was restored by an interposed jejunal parallel pouch developed from the first jejunal loop. Oral feeding was supplemented by parenteral nutrition via a Broviac catheter, and the patient is well 4 months later. Several cases of gastric cancer have been reported in children with hereditary agammaglobulinemia. Thus, endoscopy is mandatory in such patients with gastrointestinal symptoms to identify and treat tumors before metastasis occurs. Total gastrectomy, extended lymphadenectomy, and reconstruction using a jejunal reservoir with maintenance of duodenal continuity should be considered.

Vitamin B12Deficiency and Depression in the Elderly

Vitamin B₁₂Deficiency and Depression in the Elderly

Precursor Lesions in Patients With Multiple Endocrine Neoplasia Type 1--Associated Duodenal Gastrinomas

The identification of precursor lesions has a great impact on the understanding of tumorigenesis. Precursor lesions of endocrine tumors are known to occur in the setting of the MEN1 syndrome. The aim of this study was to test the hypothesis that MEN1-associated duodenal gastrinomas originate from diffuse preneoplastic gastrin cell changes. Precursor lesions may precede the development of duodenal gastrinomas because, in contrast to sporadic gastrinomas, these tumors are usually multiple. The distribution of endocrine cells in the nontumorous duodenal tissue was analyzed qualitatively and quantitatively for 25 patients operated on for a duodenal gastrinoma. MEN1 status was assessed clinically and by polymerase chain reaction-based mutational analysis. Fourteen of 25 patients with gastrinoma had proliferative, hyperplastic lesions consisting of gastrin cells in the nontumorous duodenal mucosa, similar to the gastric enterochromaffin-like cell lesions observed in chronic atrophic gastritis. All patients with Zollinger-Ellison syndrome with proven MEN1 had such proliferative gastrin cell lesions, and all patients with Zollinger-Ellison syndrome without precursor lesions were MEN1 negative. Duodenal gastrinomas in MEN1, but not sporadic duodenal gastrinomas, are associated with proliferative gastrin cell changes within the nontumorous mucosa. It is likely that these lesions precede the development of MEN1-associated duodenal gastrinomas.

Biomarkers in Various Types of Atrophic Gastritis and Their Diagnostic Usefulness

Atrophic gastritis has been shown to involve either the oxyntic gland area, resulting in hypergastrinemia and hypopepsinogenemia I, the antral gland area, causing hypogastrinemia without change in serum pepsinogen I (diffuse antral gastritis; DAG), or the entire gastric mucosa (multifocal atrophic gastritis; MAG), resulting in both hypogastrinemia and hypopepsinogenemia I; and rare atrophic gastritis limited to the oxyntic gland area, with antibodies against oxyntic cells and/or intrinsic factor (autoimmune metaplastic atrophic gastritis; AMAG). This study was performed on 126 patients with various forms of gastritis and on 126 age- and gender-matched controls, who were subjected to endoscopy with biopsy, H. pylori testing (13C-UBT, serology), assays for serum gastrin and pepsinogen I, and testing for basal and pentagastrin-induced gastric acid secretion. The following groups of patients were examined: group I (N = 22), with AMAG; group II (N = 53), with DAG; group III (N = 51), with MAG; and group IV (N = 126), age- and gender-matched controls without gastritis. The following changes were found. In group I very high serum gastrin and very low pepsinogen I were observed, and all patients were achlorhydric and H. pylori negative. In group II, with low serum gastrin and normal pepsinogenemia and gastric chlorhydria, all patients were H. pylori positive. In group III, with lower serum gastrin and lower pepsinogen I levels and reduced chlorhydria, all patients were also H. pylori positive. And all group IV controls, with normal serum gastrin and pepsinogen I and normal gastric acid secretion without antral or fundic gastritis, were H. pylori negative. We conclude that measurements of serum gastrin and pepsinogen I and gastric acid secretion as well as testing for H. pylori infection may be useful in noninvasive diagnosis of various types of atrophic gastritis and in identification of patients with premalignant gastritis and a high risk of gastric cancerogenesis.

Tumores neuroendocrinos gástricos: presentación clínica, endoscópica y alternativas de tratamiento

Gastric neuroendocrine tumors correspond to less than 1% of all gastric tumors. These tumors can be of three types. Seventy five percent are type I and are associated to chronic atrophic gastritis type A (CAG-A). Half of them are associated with pernicious anemia. Type II tumors are associated with Zollinger Ellison syndrome and type I multiple endocrine neoplasia. Type III are sporadic tumors.To report the clinical, endoscopical features and response to the treatment of gastric neuroendocrine tumors.A retrospective study of eleven patients (seven male, aged 38 to 72 years old) with a pathological diagnosis of gastric neuroendocrine tumor. Their clinical presentation, associated diseases, treatment and follow up were reviewed.Epigastric pain was present in eight patients, weight loss in three, epigastric pain and weight loss in one and post prandial abdominal pain in two. At endoscopy, multiple polyps in the fundus were observed in six, verrucose gastritis in one, polyps in the antrum in one, two subcardial polyps in 1, a fundus ulcer in one and a Bormann III type lesion in one. Chronic atrophic gastritis was diagnosed in seven patients and pernicious anemia in five. Serum gastrin levels were determined in 4 patients and were high in all. Four subjects were treated with endoscopic polipectomy only. A partial or total gastrectomy was done in seven patients. No complications or mortality occurred during the follow up.Abdominal pain is a common presentation of patients with gastric neuroendocrine neoplasia. Polyps predominantly in the fundus are the most common endoscopic finding. Surgical treatment or endoscopical polypectomy, depending of the extension of the disease, yield satisfactory results.

Benign gastric carcinoid tumor with hypergastrinemia followed up for 12 years.

Gastric carcinoid tumors associated with chronic atrophic gastritis type A have been reported to show good prognosis, because invasion and metastasis are rare. We report a case of gastric carcinoid tumor associated with hypergastrinemia that showed no malignant changes for 12 years. A 15-year-old man with abdominal discomfort underwent endoscopic examination. A polypoid lesion was detected on the atrophic mucosa of the fundus, and was diagnosed as a carcinoid tumor. Serological examination revealed a high level of anti-parietal-cell antibody, suggesting that the patient had chronic atrophic gastritis type A. The tumor was treated by endoscopic mucosal resection. Follow-up examinations were performed for 12 years, but showed no recurrence. This case confirms that gastric carcinoid tumors associated with chronic atrophic gastritis type A may have a good prognosis.

Multimodality treatment for gastric carcinoid tumor with liver metastases

Carcinoid tumors are the most common neuroendocrine tumors in the gastrointestinal tract, and between 10% and 30% of these tumors are gastric in origin. Three types of gastric carcinoid tumors are recognized: type I, associated with chronic atrophic gastritis type A; type II, associated with multiple endocrine neoplasia; and type III, sporadic and the most malignant. We present a patient with an aggressive, sporadic-type gastric carcinoid that metastasized to the liver. Her symptomatic treatment included the somatostatin analog octreotide. Octreotide scintigraphy demonstrated that this tumor avidly bound the peptide. The patient’s gastric carcinoid (assessed by endoscopy and endoscopic ultrasound) regressed and she underwent hepatic artery embolization for her liver metastases. After initial partial CT resolution the tumor grew, compressing the inferior vena cava. The patient underwent orthotopic liver transplant with excellent recovery, although she was subsequently found to have two small lung metastases. She has responded well to adjuvant Indium-111 octreotide receptor targeted therapy. This case highlights the therapeutic options for metastatic neuroendocrine tumors, including liver transplantation and adjuvant receptor targeted therapy.

Helicobacter pylori infection accelerates human gastric mucosal cell proliferation.

Helicobacter pylori causes chronic atrophic gastritis and intestinal type gastric cancer arises against a background of atrophic gastritis. Increased proliferation of epithelial cells is an important indicator of increased risk for gastric adenocarcinoma. We investigated gastric mucosal cell proliferation in H. pylori-associated gastritis and the effect of eradication therapy on this proliferation in 45 patients endoscopically diagnosed (31 with persistent eradication and 14 in whom H. pylori) recurred. H. pylori status was determined by culture and histology in biopsied specimens from the gastric antrum and corpus. Eradication of the infection was defined as reversal to negative on both tests. In vitro Ki-67 immunostaining of endoscopic biopsy specimens was used to measure mucosal cell proliferation in H. pylori-associated gastritis before and after therapy. The proliferative zone was defined as the distance of Ki-67-positive gastric epithelial cells between the highest and the lowest cells. In patients in whom H. pylori was eradicated, cell proliferation in both the antral and corpus mucosa had decreased 4 weeks after completion of the eradication therapy (P < 0.01, P < 0.001), and 6 months later, it had markedly decreased (P < 0.05, P < 0.05) and returned to normal. In patients in whom H. pylori recurred, only antral epithelial cell proliferation was reduced 4 weeks after eradication therapy, but when H. pylori recurred, determined by culture and histology, cell proliferation level was the same as that before eradication. These results suggest that H. pylori infection accelerates cell proliferation in gastric mucosa and may play a causal role in the chain of events leading to gastric carcinoma.

Clinical Management of Gastric Carcinoid Tumors

Four types of gastric carcinoids have been identified: (1) multiple small body-fundus carcinoids associated with chronic atrophic gastritis type A (A-CAG); (2) sporadic solitary lesions without specific pathogenetic background (non-A-CAG); (3) carcinoidosis associated with Zollinger-Ellison/MEN 1 syndrome, and (4) rare tumors, e.g. gastrin cell tumors, neuroendocrine carcinomas and mixed endocrine-exocrine tumors. In a retrospective study of 15 patients with gastric carcinoids (11 A-CAG, 3 non-A-CAG and 1 gastrin cell tumor) over a 10-year period, the histopathological and clinical features were assessed. The A-CAG-type carcinoids were clinically silent with lymph node metastases in 2/11 cases but no hepatic metastases. The non-A-CAG-type carcinoids were malignant with disseminated disease, hormonal symptoms and increased urinary excretion of the main histamine metabolite, MeImAA. Five patients with A-CAG tumors were subjected to antrectomy to remove hypergastrinemia, which is thought to be of pathogenetic importance for these tumors. During the observation period (1.5-8 years) 1 patient developed recurrent tumors, while the other 4 showed persistent argyrophil cell hyperplasia. A prospective treatment protocol of these tumors is suggested with endoscopic removal of less numerous, small lesions as first-step therapy, followed by antrectomy at recurrence. Larger lesions should be excised in combination with antrectomy. Gastrectomy is reserved for the rare cases of invasive tumors with lymph node metastases. As evident from the outcome of patients with non-A-CAG tumors radical surgery should be performed whenever practicable.

Morphometry of gastric endocrine cells in hypergastrinemic patients treated with the somatostatin analogue octreotide

The aim of the study was to evaluate whether treatment with 200 μg/d of the somatostatin analogue octreotide (SMS 201–995) for three months can influence the trophic action exerted by hypergastrinemia on endocrine cells of the oxyntic mucosa, a condition potentially leading to hyperplasia and carcinoid tumors. Endocrine cells were morphometrically investigated in Grimelius silver stained sections of endoscopic biopsies of oxyntic mucosa collected from 13 hypergastrinemic patients with Zollinger-Ellison syndrome (ZES) ( n = 5), antral G cell hyperfunction (AGCH) ( n = 4) and atrophic gastritis type A (AG-A) ( n = 4) before and after 3 months treatment and 3 months after drug discontinuance. The treatment induced a reduction of the volume density ( P<0.015), profile cross sectional area ( P<0.05) and number of cell profiles per unit area ( P<0.015) of argyrophil cells. A rebound of all these parameters was observed 3 months after drug withdrawal with values usually exceeding those at the entry, except in cases of AG-A. The patients' plasma gastrin concentrations presented similar variations showing a significant relation with all morphometric parameters of argyrophil cells. Also, the cell content in α subunit of human chorionic gonadotropin was related to the plasma gastrin levels, a finding confirming the close gastrin dependence of the expression of this protein by oxyntic endocrine cells. No significant changes were observed in mucosal somatostatin D cells. These results indicate that variations in circulating gastrin levels are the most likely factor responsible for the hypotrophic effect of octreotide on oxyntic argyrophil cells (mostly corresponding to the ECL cells) of hypergastrinemic patients.

Primary Sj�gren's syndrome from the viewpoint of an internal physician

The characteristics of primary Sjögren's syndrome are described on the basis of the follow-up of 65 patients with extraglandular symptoms at the onset and during the disease. The mean age of the patients at onset was 41.8 years and at the time of definite diagnosis was 45.8 years. Articular (32 cases), lacrimal (30 cases) and salivary (30 cases) manifestations were the most frequent initial symptoms. In only 22 of the 65 patients could Sjögren's syndrome be diagnosed at the onset. In most cases, the articular symptoms observed observed in 56 patients during the course corresponded to true polyarthritis, as verified by joint scintigraphy. Most frequently the wrists and ankles were affected. Chronic atrophic gastritis was found in 35 patients. In the young patients (13 cases), both the antrum and the corpus were affected more frequently than in the controls. In middle-aged patients (21 cases), atrophy of the antrum, and in the elderly (10 cases) atrophy of the corpus was more frequent than in the controls. All three types of chronic atrophic gastritis occurred in the disease. The decreased gastric acid secretion was characteristic of types A and AB gastritis, but the hypergastrinaemia only of type A. It was verified that chronic duodenitis and jejunitis occur in the disease. The pancreatic lesions were mild. Renal involvement was detected in 15 patients, vascular symptoms in 22 and lower-airway changes in 21. The variety of the different symptoms proved that primary Sjögren's syndrome can involve many organs.

Types of atrophic gastritis in patients with primary Sjogren's syndrome.

Histological examination of the gastric mucosa was performed in 44 patients with primary Sjögren's syndrome with extraglandular symptoms (mean age 51.9, range 22-76). Biopsy specimens were taken from each of three separate regions: the antrum, the corpus, and the transitional zone between the antrum and the corpus. The incidence of chronic atrophic gastritis was considerably higher in patients with Sjögren's syndrome than in the controls. In the young patients with Sjögren's syndrome atrophic lesions were more common both in the antrum and in the corpus than in the control group. In middle aged patients, however, only the antrum, and in the elderly only the corpus, was much more commonly affected than in the controls. All three types of chronic atrophic gastritis occurred in patients with Sjögren's syndrome. Decreased gastric acid secretion was associated mainly with atrophic gastritis of types A and AB, whereas hypergastrinaemia occurred almost exclusively in gastritis of type A.

Gastric carcinoids and their precursor lesions. A histologic and immunohistochemical study of 23 cases

A histologic and immunohistochemical study was carried out in 23 unselected nonantral gastric carcinoids and their precursor lesions classified according to Solcia et al. None of the patients showed Zollinger-Ellison syndrome. Two variants of carcinoids showing distinctive pathologic and pathogenetic characteristics were identified on the basis of presence or absence of associated chronic atrophic gastritis type A (A-CAG). Chronic atrophic gastritis type A was found in 19 cases showing either single or multiple neoplasms, tumor extension limited to the mucosa or submucosa, consistent endocrine cell precursor changes in extratumoral mucosa, and consistent hypergastrinemia and/or G cell hyperplasia. Associated precursor lesions were only hyperplastic in all but two cases with single carcinoids whereas they were also dysplastic in all but one case with multiple carcinoids. The four tumors arising in nonatrophic mucosa were all single, more aggressive, and not associated with extratumoral endocrine cell proliferations or with signs of gastrin hypersecretion. Tumor cells were diffusely immunoreactive for chromogranin A and synaptophysin but usually negative for chromogranin B or HISL-19. Scattered serotonin cells were found in ten carcinoids. They were more frequent in infiltrating than in intramucosal tumors as were the less represented pancreatic polypeptide cells whereas the reverse was found for alpha-subunit-containing cells. These results are of relevance for tumor pathogenesis and may provide the rationale for a less aggressive therapeutic approach in the patients.

Serum Pepsinogen I and Serum Gastrin in the Screening of Atrophic Pangastritis with High Risk of Gastric Cancer

Serum pepsinogen I (S-PGI) and serum gastrin (S-gastrin) were examined in the screening of three types of atrophic gastritis with inherent high risk of gastric cancer: in 102 cases with severe atrophic corpus gastritis (SACG), in 5 cases with severe atrophic antrum gastritis (SAAG), and in 15 cases with severe atrophic pangastritis (SAPG) (atrophy both in corpus and in antrum) found among 916 subjects from three family series (265 from gastric cancer families, 425 from randomly selected control families and 226 from pernicious anaemia families). There is no way to screen directly atrophic gastritis restricted to the antral mucosa. In pangastritis atrophy of antral glands causes a failure of the hypergastrinemic reaction of achlorhydria. The combination of S-PGI less than 25 micrograms/l + S-gastrin less than 200 pmol/l detected 80.0% of our cases with SAPG, and only 17 subjects of 794 (2.1%) were false positives i.e. who had not advanced atrophic gastritis. The risk of gastric cancer may be significantly higher in SAPG than in SACG. The estimated prevalence of SAPG was 3% in random-family members over 60 years. The combination of S-PGI and S-gastrin is recommended when the cost/benefit ratio in the screening program of gastric cancer is considered and people from a general population are selected for endoscopic studies.

Atrophic gastritis and gastric carcinoid tumours.

During recent decades an increasing number of case reports have pointed at a relation between atrophic gastritis type A and gastric carcinoid. This relation has now been quantitatively documented in endoscopic screening studies. Among patients with pernicious anaemia the prevalence of gastric carcinoid was 2-9%. Many of these carcinoids, however, remain subclinical. The majority are broadbased polypoid tumours. Most are situated in the gastric body or fundus. Of 95 patients with atrophic gastritis and gastric carcinoid reported in the literature, 60 (63%) had multicentric tumours and 13 (14%) lymph node and/or hepatic metastases. Microscopically, the tumours, which are frequently of the enterochromaffin-like cell type, show various structural differentiations, glandular differentiation indicating malignant potential. Purely intramucosal carcinoids have been described. The precurser lesion to such "early carcinoids", as well as to infiltrating carcinoids, is probably hyperplasia of endocrine cells in the atrophic fundic mucosa. Such hyperplasias, whether nodular or diffuse, are quantitatively related to hypergastrinaemia, which is a typical feature of antrum sparing (type A) atrophic gastritis. Most tumours can be treated endoscopically, although antrectomy with abolition of hypergastrinemia may be the definitive treatment. It seems that the risk of developing gastric carcinoid 'per se' does not justify regular gastric screening in patients with type A atrophic gastritis. However, as these patients also run an increased risk of developing several benign diseases, gastric adenocarcinoma, and probably also pancreatic malignancy, regular survey in selected cases is indicated.