Chronic active and atrophic gastritis as significant contributing factor to the development of gastric cystica profunda.

Gastric cystica profunda (GCP) is an uncommon but underestimated gastric lesion. Its precancerous potential determines its significance. In addition to previous mucosa injury due to operations, biopsy or polypectomy, chronic active and atrophic gastritis may also lead to the development of GCPs. By carefully examining the stomach and taking biopsy samples from the susceptible regions, the stage of atrophy can be determined. Chronic atrophic gastritis is a risk factor for cancer evolvement and it can also contribute to GCPs formation. GCPs frequently occur close to early gastric cancers (EGCs) or EGC can arise from the cystic glands. Endoscopic resection is an effective and minimally invasive treatment in GCP.

Chronic atrophic gastritis and risk of incident upper gastrointestinal cancers: a systematic review and meta-analysis.

BACKGROUND: Previous literature has explored the relationship between chronic atrophic gastritis (CAG) and isolated cancers within the upper gastrointestinal cancers; However, an integrative synthesis across the totality of upper gastrointestinal cancers was conspicuously absent. The research objective was to assess the relationship between CAG and the risk of incident upper gastrointestinal cancers, specifically including gastric cancer, oesophageal cancer, and oesophagogastric junction cancer. METHODS: Rigorous systematic searches were conducted across three major databases, namely PubMed, Embase and Web of Science, encompassing the timeline from database inception until August 10, 2023. We extracted the necessary odds ratio (OR) and their corresponding 95% confidence interval (CI) for subsequent meta-analysis. Statistical analyses were conducted using Stata 17.0 software. RESULTS: This meta-analysis included a total of 23 articles encompassing 5858 patients diagnosed with upper gastrointestinal cancers. CAG resulted in a statistically significant 4.12-fold elevated risk of incident gastric cancer (OR = 4.12, 95% CI 3.20-5.30). Likewise, CAG was linked to a 2.08-fold increased risk of incident oesophageal cancer (OR = 2.08, 95%CI 1.60-2.72). Intriguingly, a specific correlation was found between CAG and the risk of incident oesophageal squamous cell carcinoma (OR = 2.29, 95%CI 1.77-2.95), while no significant association was detected for oesophageal adenocarcinoma (OR = 0.62, 95%CI 0.17-2.26). Moreover, CAG was correlated with a 2.77-fold heightened risk of oesophagogastric junction cancer (OR = 2.77, 95%CI 2.21-3.46). Notably, for the same type of upper gastrointestinal cancer, it was observed that diagnosing CAG through histological methods was linked to a 33-77% higher risk of developing cancer compared to diagnosing CAG through serological methods. CONCLUSION: This meta-analysis indicated a two- to fourfold increased risk of gastric cancer, oesophageal cancer, and oesophagogastric junction cancer in patients with CAG. Importantly, for the same upper gastrointestinal cancer, the risk of incident cancer was higher when CAG was diagnosed histologically compared to serological diagnosis. Further rigorous study designs are required to explore the impact of CAG diagnosed through both diagnostic methods on the risk of upper gastrointestinal cancers.

Clinicopathologic and endoscopic characteristics of ten patients with gastric hamartomatous inverted polyp: a single center case series.

BACKGROUND: Gastric hamartomatous inverted polyps (GHIPs) are not well characterized and remain diagnostically challenging due to rarity. Therefore, this study aims to investigate the clinicopathologic and endoscopic characteristics of patients with GHIP. METHODS: We retrospectively reviewed clinicopathologic and endoscopic features of ten patients with GHIP who were admitted to Beijing Friendship Hospital from March 2013 to July 2022. All patients were treated successfully by endoscopic resection. RESULTS: GHIPs were usually asymptomatic and found incidentally during gastroscopic examination. They may be sessile or pedunculated, with diffuse or local surface redness or erosion. On endoscopic ultrasonography, the sessile submucosal tumor-type GHIP demonstrated a heterogeneous lesion with cystic areas in the third layer of the gastric wall. Histologically, GHIPs were characterized by a submucosal inverted proliferation of cystically dilated hyperplastic gastric glands accompanied by a branching proliferation of smooth muscle bundles. Inflammatory cells infiltration was observed in the stroma, whereas only one patient was complicated with glandular low-grade dysplasia. Assessment of the surrounding mucosa demonstrated that six patients (60%) had atrophic gastritis or Helicobacter pylori-associated gastritis, and four patients (40%) had non-specific gastritis. Endoscopic resection was safe and effective. CONCLUSIONS: GHIPs often arise from the background of abnormal mucosa, such as atrophic or H.pylori-associated gastritis. We make the hypothesis that acquired inflammation might lead to the development of GHIPs. We recommend to make a full assessment of the background mucosa and H. pylori infection status for evaluation of underlying gastric mucosal abnormalities, which may be the preneoplastic condition of the stomach.

Gastric neuroendocrine neoplasms.

Gastric neuroendocrine neoplasms (gNENs) display peculiar site-specific features among all NENs. Their incidence and prevalence have been rising in the past few decades. gNENs comprise gastric neuroendocrine carcinomas (gNECs) and gastric neuroendocrine tumours (gNETs), the latter further classified into three types. Type I anatype II gNETs are gastrin-dependent and develop in chronic atrophic gastritis and as part of Zollinger-Ellison syndrome within a multiple endocrine neoplasia type 1 syndrome (MEN1), respectively. Type III or sporadic gNETs develop in the absence of hypergastrinaemia and in the context of a near-normal or inflamed gastric mucosa. gNECs can also develop in the context of variable atrophic, relatively normal or inflamed gastric mucosa. Each gNEN type has different clinical characteristics and requires a different multidisciplinary approach in expert dedicated centres. Type I gNETs are managed mainly by endoscopy or surgery, whereas the treatment of type II gNETs largely depends on the management of the concomitant MEN1. Type III gNETs may require both locoregional approaches and systemic treatments; NECs are often metastatic and therefore require systemic treatment. Specific data regarding the systemic treatment of gNENs are lacking and are derived from the treatment of intestinal NETs and NECs. An enhanced understanding of molecular and clinical pathophysiology is needed to improve the management and outcomes of patients' gNETs.

Creating a Framework for Treating Autoimmune Gastritis-The Case for Replacing Lost Acid.

Autoimmune gastritis (AIG) is characterized by the destruction of gastric parietal cells, resulting in hypochlorhydria and eventual achlorhydria, as oxyntic glands in the corpus are destroyed and become atrophic. The permanent loss of gastric acid has many impacts-both theoretical and documented. The most concerning of these are hypergastrinemia and increased N-nitroso compounds, both of which increase the risk of gastric cancers. While known deficiencies of B12 and iron are often replaced in AIG, acid is not. Moreover, patients with AIG are often prescribed acid suppression for a stomach that is decidedly no longer acidic, worsening the sequelae of gastric atrophy. Betaine hydrochloride (BHCL) is a short-acting acidifying agent, available over the counter in capsule form. Mealtime acid supplementation has an historic basis and could ameliorate many AIG-related gastrointestinal symptoms. Theoretically, acidification could also reduce the potential for hypergastrinemia and the production of N-nitroso compounds, consequently reducing the risk of gastric cancers. Supplemental vitamin C may also help in preventing gastric N-nitroso formation, regardless of the gastric pH. This narrative review describes the functions of gastric acid in gastrointestinal and immune health, documents the effects of hypochlorhydria in AIG, and proposes potential options for safely re-establishing the acid milieu of the stomach for patients with AIG.

Helicobacter Pylori and Gastric Cancer: An Update in the Literature.

Of the chronic bacterial infections that affect humans, Helicobacter pylori (H. pylori) infection is one of the most common. It inhabits the stomachs of half of the adult human population. In Puerto Rico, a US territory, it has an overall prevalence of 33%, similar to the prevalence reported in the population of the US as a whole. Helicobacter pylori infection is responsible for mucosal inflammation that may lead to chronic gastritis, most peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. The International Agency for Research on Cancer identified H. pylori as a definite carcinogen in 1994, the only bacterium to be given such a classification. Its oncogenic effect has been postulated to be caused by different mechanisms, including bacterial characteristics and host factors. Epidemiologic studies have shown that gastric cancer risk differs among regions. One of the top 10 causes of cancer death in Puerto Rico is gastric cancer. Although the eradication of H. pylori has well-known benefits, there are some concerns when considering mass screening and treatment of infected patients. These include the fact that such eradication could provoke an increase in antibiotic resistance rates, the disturbance of the gut microbiota, an increase in body weight, and the aggravation of existing gastroesophageal reflux symptoms. Gastric cancer is a major health concern, and we should understand the role of H. pylori eradication in its prevention. This article is geared to summarize current knowledge and controversies.

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

INTRODUCTION: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Gastric intestinal metaplasia and gastric cancer prevention: Watchful waiting.

Gastric intestinal metaplasia (GIM), a common histologic finding, is associated with increased risk of gastric cancer, and GIM associated with Helicobacter pylori infection is classified as an environmental metaplastic atrophic gastritis. Patients may be asymptomatic or present with various dyspeptic symptoms. Autoimmune metaplastic atrophic gastritis is a less common but important cause of chronic gastritis. The Correa cascade describes the evolution of precancerous mucosal changes that lead to development of GIM, with differentiation of 2 histologic types of GIM (complete and incomplete) and the consequences of each type. The risk of progression to malignancy is higher with incomplete GIM. It is also higher for those who immigrate from regions with a high incidence of H pylori infection to areas where the incidence is low. Guidelines regarding endoscopic management of GIM vary by geographic region.

Nutrición enteral por yeyunostomía como causa de perforación y necrosis intestinal / Enteral feeding via jejunostomy as a cause of intestinal perforation and necrosis

Introducción: la yeyunostomía de alimentación es una excelente manera de nutrir por vía enteral a pacientes que no pueden tolerar dieta oral con una tasa de complicaciones baja. Se utiliza comúnmente una sonda de Foley, tubo de Ryle, de Kerh o catéter con aguja (Jejuno-Cath®). Caso clínico: presentamos el caso de un paciente varón de 80 años que presentó una perforación intestinal como consecuencia de la nutrición a través de un yeyunocath en el postoperatorio de una gastrectomía subtotal con reconstrucción en Y de Roux, y de otro paciente varón de 53 años con perforación gástrica y múltiples complicaciones postoperatorias, entre ellas, necrosis de un segmento de intestino delgado por impactación de nutrición enteral. Discusión: revisamos la literatura existente sobre esta rara complicación (AU)

Jejunostomy for enteral feeding is excellent for patients who cannot manage oral intake, with a low complication rate. A Foley catheter, Ryle tube, Kerh tube or needle-catheter (Jejuno-Cath®) are commonly used. It is a safe procedure but it can lead to severe complications. We present two cases: firstly, an 80 year old male who was admitted to the Emergency Room with a bowel perforation secondary to Jejuno-Cath® for enteral feeding after a subtotal gastrectomy with Roux-en-Y reconstruction; and secondly, a 53 year old male who was admitted to the Emergency Room due to gastric perforation developing multiple complications, including bowel necrosis and enteral feeding impaction. We have reviewed the recent literature with regard to this rare complication (AU)

Mujer de 42 años con pancitopenia / A 42 year-old woman with pancytopenia

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Analysis of alarming signals for the progression of atrophic gastritis to dysplasia / Análisis de las señales de alarma en la progresión de la gastritis atrófica a displasia

Background and aims: atrophic gastritis (AG) and dysplasia are precancerous lesions, with which early surveillance of disease progression is particularly important for patients. The present study aimed to explore potential alarming signals for atrophic gastritis progression towards dysplasia. Methods: clinical data for patients with AG in the Digestive Endoscopy Center of Guangzhou Nanfang Hospital between 2001 and 2011 were retrospectively reviewed. Survival analysis, dichotomous logistic regression analysis and rank correlation analysis were carried out. Results: in 234 patients with atrophic gastritis, after follow up of 0.5, 1, 2, 5 and 10 years, the occurrence rates of dysplasia were respectively 2.3, 4.4, 9.6, 19.3, and 42.4%. Patients with AG combined with antral ulcer or gastric angle ulcer, had a higher risk for dysplasia than patients with simple AG (OR = 2.427, 95%Cl 1.069 ~ 5.511, p = 0.034; OR = 2.961, 95%Cl 1.336 ~ 6.564, p = 0.008). The constituent ratios of moderate to severe dysplasia were respectively 8.6, 2.7 and 1.2% (p = 0.000) in three patient groups: AG combined with antral ulcer/gastric angle ulcer (n = 255), antral ulcer/gastric angle ulcer alone (n = 1,389), and AG alone (n = 3,106). The Spearman correlation coefficients between a) Hp infection; and b) atrophy, intestinal metaplasia and dysplasia were -0.114 (p = 0.078), -0.169 (p = 0.009) and 0.064 (p > 0.05), respectively. Conclusions: long follow-up interval and gastric ulcer may be alarming signals for the progression of AG to dysplasia. But in patients with atrophy, intestinal metaplasia or dysplasia, Hp infection may not be a risk factor for these lesions aggravated, further studies are required to confirm it(AU)

Enfermedad tiroidea autoinmunitaria: posibilidad de asociación a gastritis autoinmunitaria / Autoimmune thyroid disease: Autoimmune gastritis association's possibility

Introducción: Se ha descrito una elevada prevalencia de anticuerpos anticélula parietal gástrica (ACPG) en niños con enfermedad tiroidea autoinmunitaria (ETAI). El objetivo de este trabajo fue determinar la prevalencia de marcadores de gastritis autoinmunitaria en niños con ETAI. Sujetos y métodos: Se incluyó a 26 pacientes con ETAI. Se realizaron hemograma, valores plasmáticos de vitamina B12, ácido fólico, gastrina y ACPG. Se estudió también la comorbilidad de otras enfermedades autoinmunitarias. Resultados: Los valores de tiroxina libre y tirotropina fueron normales con tratamiento hormonal sustitutivo. Los valores de hemoglobina, volumen corpuscular medio, hemoglobina corpuscular media, vitamina B12, ácido fólico y gastrina estaban en rango de normalidad en todos los niños. Se detectaron 6 casos de diabetes mellitus de tipo 1 (DM1) y 2 de ellos también tenían enfermedad celíaca (EC). Se halló ACPG en una niña hipertiroidea de 14 años sin comorbilidad autoinmune. Conclusiones: La ETAI se asocia a otras enfermedades de similar etiología, principalmente DM1 y EC. La presencia de ACPG es un marcador precoz y sensible de gastritis autoinmunitaria (AU)

Introduction: A high prevalence of parietal cell antibodies (PCA) has been reported in children with autoimmune thyroid disease (AITD). The aim of this study was to determine the prevalence of autoimmune gastritis markers among children diagnosed as AITD. Patients and methods: We studied 26 patients with AITD. Basal samples were taken to determine: hemogram, vitamin B12 and folic acid plasmatic levels, gastrin plasmatic levels, and PCA’s determination. Other autoimmune disease comorbility were also studied. Results: Free T4 and TSH values were normal, with hormonal substitutive treatment. Hb, MCV, HCM, vitamine B12, folic acid and gastrin were in normal range for all 26 patients. We reported 6 cases diabetes mellitus type 1 and 2 of celiac disease. A single patient was PCA positive. It was a 14-year-old hyperthyroid girl without any other autoimmune disease. Conclusions: AITD in childhood and adolescence is associated with other autoimmune diseases, specially DM1 and CD. PCA becomes an early and sensitive marker to detect autoinmune gastritis (AU)

Pernicious anaemia in triplets. A case report an literature review

Pernicious anemia is the most common cause of vitamin B12 deficiency in adults. This entity is associated with chronic atrophic gastritis. We report a case of pernicious anaemia in triplets. We also report a fourth case of cobalamin deficiency with antibodies against intrinsic factor and anti parietal cell antigen negative antibodies in a sibling. The present article reviews the pediatric presentation of pernicious anemia and highlights the possible existence of familial aggregation. Furthermore, the need for systematic familial screening and the usefulness of an endoscopic follow-up program in patients with pernicious anemia are evaluated

La anemia perniciosa es la causa más frecuente de déficit de vitamina B12 en adultos. Esta entidad se ha asociado con la gastritis crónica atrófica. En este trabajo se describe la existencia de anemia perniciosa en 3 hermanas trillizas. Asimismo, también se describe un cuarto caso de déficit de cobalamina con anticuerpos antifactor intrínseco y negatividad para anticuerpos anticélula parietal gástrica en una her-mana no trilliza. En este trabajo se revisa la presentación pediátrica de la anemia perniciosa, así como la posible existencia de una agregación familiar. Por otra parte, se ha evaluado la necesidad de realizar un estudio sistemático de los familiares y el beneficio de establecer un protocolo de se-guimiento endoscópico de los pacientes con anemia perniciosa

Prevention of gastric cancer: a challenging but feasible task

Despite its declining incidence gastric cancer still ranks as the second most common malignancy of the digestive tract, accounting for 10% of cancer deaths worldwide. At the time of the diagnosis less than 15% of the patients are in the stage of early cancer, the only stage in which a definite cure of gastric cancer is possible. Therefore the challenges are either early detection or even better prevention of gastric cancer. H. pylori has become recognized as the major risk factor for gastric adenocarcinoma. Epidemiological, biological, histomorphologic, molecular-genetic, epidemiological evidence and more recently few clinical trails have shown that H. pylori eradication has the potential to prevent the development of gastric cancer. Currently, H. pylori eradication is an indication for the prevention of gastric cancer in patients and groups of individuals with strongly increased risk, but further investigations are still required before an implementation of a general and global policy to eradicate H. pylori for the prevention of gastric cancer can be instituted. At present time, the main challenge remains to find out at what point mucosal abnormalities are no longer reversible and gastric cancer development cannot be prevented despite H. pylori eradication.(AU)

A pesar de la disminución en su incidencia, aún hoy el cáncer gástrico se presenta como la segunda causa más común de muerte por enfermedad maligna del tubo digestivo, siendo responsable del 10% de las muertes por cáncer a nivel mundial. Al momento del diagnóstico menos del 15% de los pacientes se encuentran en la etapa de cáncer gástrico temprano, el único estadío en el cual es posible su curación. Por lo tanto, el desafío está en la detección temprana o aún mejor, en la prevención del cáncer gástrico. H. pylori ha sido reconocido como el factor de riesgo más importante para el desarrollo del adenocarcinoma de estómago. Evidencia epidemiológica, biológica, histológica, molecular y más recientemente algunos estudios clínicos han demostrado que la erradicación del H. pylori tiene el potencial de prevenir el desarrollo de lesiones premalignas y del cáncer gástrico. Actualmente la erradicación del H. pylori está indicada para la prevención del cáncer gástrico en pacientes y grupos de individuos con alto riesgo, pero futuras investigaciones son aún necesarias antes de que sea establecida una política global para la erradicación del H. pylori en la prevención del cáncer gástrico. Actualmente el mayor desafío radica en encontrar en qué punto los cambios en la mucosa gástrica se tornan irreversibles, siendo el cáncer gástrico no prevenible a pesar de la erradicación del H. pylori.(AU)

Prevention of gastric cancer: a challenging but feasible task / Prevención del cáncer gástrico: una tarea difícil pero factible

Despite its declining incidence gastric cancer still ranks as the second most common malignancy of the digestive tract, accounting for 10% of cancer deaths worldwide. At the time of the diagnosis less than 15% of the patients are in the stage of early cancer, the only stage in which a definite cure of gastric cancer is possible. Therefore the challenges are either early detection or even better prevention of gastric cancer. H. pylori has become recognized as the major risk factor for gastric adenocarcinoma. Epidemiological, biological, histomorphologic, molecular-genetic, epidemiological evidence and more recently few clinical trails have shown that H. pylori eradication has the potential to prevent the development of gastric cancer. Currently, H. pylori eradication is an indication for the prevention of gastric cancer in patients and groups of individuals with strongly increased risk, but further investigations are still required before an implementation of a general and global policy to eradicate H. pylori for the prevention of gastric cancer can be instituted. At present time, the main challenge remains to find out at what point mucosal abnormalities are no longer reversible and gastric cancer development cannot be prevented despite H. pylori eradication.

A pesar de la disminución en su incidencia, aún hoy el cáncer gástrico se presenta como la segunda causa más común de muerte por enfermedad maligna del tubo digestivo, siendo responsable del 10% de las muertes por cáncer a nivel mundial. Al momento del diagnóstico menos del 15% de los pacientes se encuentran en la etapa de cáncer gástrico temprano, el único estadío en el cual es posible su curación. Por lo tanto, el desafío está en la detección temprana o aún mejor, en la prevención del cáncer gástrico. H. pylori ha sido reconocido como el factor de riesgo más importante para el desarrollo del adenocarcinoma de estómago. Evidencia epidemiológica, biológica, histológica, molecular y más recientemente algunos estudios clínicos han demostrado que la erradicación del H. pylori tiene el potencial de prevenir el desarrollo de lesiones premalignas y del cáncer gástrico. Actualmente la erradicación del H. pylori está indicada para la prevención del cáncer gástrico en pacientes y grupos de individuos con alto riesgo, pero futuras investigaciones son aún necesarias antes de que sea establecida una política global para la erradicación del H. pylori en la prevención del cáncer gástrico. Actualmente el mayor desafío radica en encontrar en qué punto los cambios en la mucosa gástrica se tornan irreversibles, siendo el cáncer gástrico no prevenible a pesar de la erradicación del H. pylori.

Pólipo fibroide inflamatorio gastrointestinal. Características clínicas y seguimiento de una serie de 26 pacientes / Gastrointestinal inflammatory fibroid polyps. Clinical characteristics and follow-up in a series of 26 patients

INTRODUCCIÓN: El pólipo fibroide inflamatorio (PFI) es una lesión protuberante que se localiza cerca de la muscularis mucosae y está constituida por una proliferación de células fusiformes y fibras conjuntivas alrededor de los capilares y un infiltrado inflamatorio variable. Se considera una reacción inflamatoria reparadora mal controlada. El objetivo de este trabajo ha sido estudiar las características clínicas, anatomo-patológicas y de seguimiento de una serie de pacientes con PFI.PACIENTES Y MÉTODO: Se han estudiado 26 PFI (25 pacientes:16 mujeres y 9 varones) recogidos entre los años 1985 y2001 en un registro específico de 3 centros de la ciudad de Girona. Las variables analizadas fueron la edad, el sexo y la presentación clínica, la localización y el tamaño del PFI, las características de la mucosa y las enfermedades asociadas, así como información del seguimiento. Se realizaron las pruebas estadísticas habituales. RESULTADOS: El PFI fue antral en 16 casos, ileal en 7, yeyunalen 2 y colónico en el restante. Su tamaño condicionó su carácter sintomático (35 ± 13,6 mm) o asintomático (8,4 ±6,3 mm). Los pólipos gástricos fueron significativamente más pequeños que los intestinales. Los pólipos sintomáticos(5 de 16 gástricos y 9 de 10 intestinales) predominaron en mujeres y en edades significativamente inferiores que los asintomáticos (59,2 frente a 74,1 años). La mayoría delos PFI gástricos se asociaron a gastritis crónica atrófica, mientras que sólo un PFI ileal lo hizo a divertículo de Meckel. El seguimiento medio fue de 60,6 meses y, salvo en un caso de resección incompleta, no se constató recidiva del PFI. CONCLUSIÓN: El PFI es una entidad heterogénea según la edad de presentación, el sexo de los pacientes, su tamaño y la localización en el tubo digestivo. Tras la resección, el PFI no recidiva. La asociación de los PFI gástricos a gastritis crónica atrófica podría apuntar a un efecto modulador de la mucosa sobre el crecimiento del PFI

INTRODUCTION: Inflammatory fibroid polyp (IFP) is a protuberant lesion, located near the muscularis mucosae and composed of a proliferation of fusiform cells and conjunctive fiberssurrounding capillaries and a variable inflammatoryin filtrate. It is believed to be a poorly controlled inflammatory repair response. Our aim was to study the clinical, pathological and follow up characteristics of a series of patients with IFP.PATIENTS AND METHOD: We studied 26 IFPs from 25 patients(16 women and 9 men) registered between 1985 and 2001 ina specific register of 3 centers in the city of Gerona (Spain).The variables analyzed were age, sex and clinical presentation, IFP localization and size, mucosal characteristics and associated disease, as well as follow-up information. Routine statistical analyses were performed. RESULTS: IFPs were antral in 16 patients, ileal in 7, jejunal in 2and colonic in the remaining patient. Size determined whether they were symptomatic (35 ± 13.6 mm) or asymptomatic (8.4 ±6.3 mm). Gastric polyps were significantly smaller than intestinal polyps. Symptomatic polyps (5 out of 16 gastric polyps and9 out of 10 intestinal polyps) predominated in women and occurred at a significantly lower age than asymptomatic polyps(59.2 versus 74.1 years). Most gastric IFPs were associated with chronic atrophic gastritis while only one ileal polyp was associated with Meckel’s diverticulum. The mean length of follow up was 60.6 months and, except in one patient who underwent in complete resection, no recurrences of IFP were observed. CONCLUSION: IFP is a heterogeneous entity, depending on age at presentation, sex, size and location in the digestive tract. IFP does not recur after resection. The association of gastric IFP and chronic atrophic gastritis could suggest a modulatory effect of the mucosa on IFP growth