Body Mucosa Research Articles

Sa1867 Evidence of Two Aetiologies of Gastroesophageal Junctional Cancers Based on Gastric Parietal Cell Density

Introduction Serum pepsinogen I:II ratio, a surrogate marker of atrophic gastritis, suggests that some adenocarcinomas at the gastroesophageal junction (GOJ) develop on a background of atrophic gastritis, similar to non-cardia gastric cancer, while others arise on a backgrounds of healthy, non-atrophic gastric mucosa similar to oesophageal adenocarcinoma. In this current study, we have directly the background gastric body mucosa in patients with junctional adenocarcinomas compared to oesophageal adenocarcinomas and non-cardia gastric cancers. Methods 127 gastrectomy and oesophagectomy specimens for adenocarcinoma were identified for which clear topographic description allowed assignment to oesophageal, junctional (including cardia) and gastric non-cardia locations. In these gastric body mucosa specimens, well clear of the tumour margin, parietal cells were immunostained using anti- H + /K + ATPase. Parietal cell density was counted in 3 to 5 well-oriented fields (1 mm 2 each) and expressed as mean parietal cell number per 1 mm 2 area. Total mucosal thickness, glandular thickness, intestinal metaplasia, inflammation indicated by polymorphonuclear (PMN) and mononuclear (MN) cells and reactive atypia (RA) were also scored. Non-parametric statistics were used to compare distributions. Results Ten (8%) cases lacked well-orientated blocks of body mucosa. The remaining 117 patients included 34 oesophageal, 52 GOJ and 31 non-cardia gastric adenocarcinomas. Median (IQR) parietal cell densities were 836 (173), 602 (389) and 411 (334) per mm 2 in gastric mucosa of oesophageal, GOJ and gastric cancers, respectively (all differences P 2 , 85% of oesophageal adenocarcinomas had a higher and 84% of non-cardia gastric cancers had a lower values. With the same cut-off, 50% of GOJ adenocarcinomas were gastric and remaining was oesophageal in origin. Glandular mucosa was thicker in patients with GOJ cancer compared to gastric (0.735 vs. 0.600, p = 0.005) and thinner than oesophageal cancer (0.735 vs. 0.900, p Conclusion This study provides direct evidence for marked differences in the gastric mucosal phenotype in the patients with oesophageal versus gastric non-cardia cancer, with the former being healthy and uninflamed, but the latter atrophic and inflamed. The background gastric mucosa of GOJ cancer supported them being two distinct aetiologies, one group resembling oesophageal adenocarcinoma and other gastric non-cardia cancer. Disclosure of Interest None Declared.

Sa1868 Is Endoscopic Submucosal Dissection Safe for Papillary Adenocarcinoma of Stomach?

Background & Aim: Serum pepsinogen I:II ratio, a surrogate marker of atrophic gastritis, suggests that some adenocarcinomas at the gastroesophageal junction (GOJ) develop on a background of atrophic gastritis, similar to non-cardia gastric cancer, while others arise on a background of healthy, non-atrophic gastric mucosa similar to oesophageal adenocarcinoma. In this current study, we have directly examined the background gastric body mucosa in patients with junctional adenocarcinomas compared to oesophageal adenocarcinomas and non-cardia gastric cancers. Methods: 127 gastrectomy and oesophagectomy specimens for adenocarcinoma were identified for which clear topographic description allowed assignment to oesophageal, junctional (including cardia) and gastric non-cardia locations. In these gastric body mucosa specimens, well clear of the tumour margin, parietal cells were immunostained using antiH+/K+ ATPase. Parietal cell density was counted in 3 to 5 well-oriented fields (1 square mm each) and expressed as mean parietal cell number per 1 square mm area. Inflammation indicated by polymorphonuclear (PMN) and mononuclear (MN) cells were also scored. Non-parametric statistics were used to compare distributions. Results: Ten (8%) cases lacked well-orientated blocks of body mucosa. The remaining 117 patients included 34 oesophageal, 52 GOJ and 31 non-cardia gastric adenocarcinomas. Median (IQR) parietal cell densities were 836 (173), 602 (389) and 411 (334) per square mm in gastric mucosa of oesophageal, GOJ and non-cardia gastric cancers, respectively (all differences P <0.001) (Figure). Using a parietal cell density of 630/square mm, 85% of oesophageal adenocarcinomas had higher and 84% of non-cardia gastric cancers had lower values. In contrast, 50% of the GOJ adenocarcinomas had values greater than and 50% less than this parietal cell density of 630 square mm. Frequency distribution curves of gastric mucosal parietal cell density indicated monophasic patterns for both oesophageal adenocarcinomas and noncardia gastric adenocarcinomas but a biphasic distribution for junctional adenocarcinomas. The chronic inflammatory cell infiltrate [median, (IQR)] was significantly greater in the gastric body mucosa of the non-cardia gastric adenocarcinomas [3(2)] than the oesophageal adenocarcinomas [0(1)]. The junctional adenocarcinoma again had an intermediate score [1(21)], all p values were <0.01. Conclusion: This study provides direct evidence for marked differences in the gastric mucosal phenotype in patients with oesophageal versus gastric non-cardia cancer, with the former being healthy and uninflamed, but the latter atrophic and inflamed. The background gastric mucosa of GOJ cancer supports them being of two distinct aetiologies, one group resembling oesophageal adenocarcinoma and the other gastric non-cardia cancer.

271 Cathelicidin Inhibits Colitis Associated Colon Cancer Development by Inhibition of Epithelial-Mesenchymal Transition and Cancer Associated Fibroblasts

Oxyntic atrophy and intestinal metaplasia are considered critical precursors for the development of gastric adenocarcinoma. Autoimmune atrophic gastritis (AAG) is characterized by immune-mediated destruction of gastric parietal cells, chronic inflammation, atrophic gastritis, and pernicious anemia. While AAG is associated with increased risk of carcinoids, the risk for adenocarcinoma in the absence of H. pylori infection is controversial. Here, we investigated the differences between AAG and chronic atrophic gastritis (CAG) with intestinal metaplasia (IM). Methods: Tissue from 6 patients with CAG were obtained at the time of resection for gastric adenocarcinomna and all patients showed IM. 20 AAG patients were diagnosed by upper endoscopy, oxyntic atrophy, and the presence of anti-parietal cell antibodies. 20/20 AAG patients were negative for H. pylori. 19/20 AAG patient showed marked elevations in both serum gastrin and serum chromogranin. In the body mucosa, we evaluated the presence of spasmolytic-polypeptide expressing metaplasia (SPEM) with TFF2 staining, IM with MUC2, macrophages with CD68, neutrophils with myeloperoxidase (MPO) and proliferative cells with Ki67. Results: 20/20 AAG patients showed profound parietal cell loss with SPEM and 15 demonstrated IM (75%). AAG patients had significantly fewer MPO positive neutrophils (6.4/1000 cells) compared to CAG patients (21.9/1000 cells) (p<0.01). The gastric biopsies from AAG patients also showed significantly fewer CD68 positive macrophages (10.1/1000 cells) compared to CAG patients (17.4/1000 cells, p= 0.01). Ki67 positive cells were markedly decreased in AAG patients (0.2/1000 cells) compared to CAG patients (14.5/1000 cells) (p<0.01). Conclusions: The metaplasia observed in AAG patients exhibited a low proliferative rate compared with the metaplasia samples from CAG patients. This lower proliferative rate was associated with smaller macrophage and neutrophil numbers in AAG patients compared to those in CAG patients. The lower proliferative rate in metaplasia and reduced macrophage and neutrophil infiltrates may explain in part the lower tendency of metaplasia in H. pylori-negative AAG patients to evolve into gastric adenocarcinoma compared with individuals with CAG.

Therapeutic Efficacy of Stable Analogues of Vasoactive Intestinal Peptide against Pathogens

Vasoactive intestinal peptide (VIP) is an anti-inflammatory neuropeptide recently identified as a potential antimicrobial peptide. To overcome the metabolic limitations of VIP, we modified the native peptide sequence and generated two stable synthetic analogues (VIP51 and VIP51(6-30)) with better antimicrobial profiles. Herein we investigate the effects of both VIP analogues on cell viability, membrane integrity, and ultrastructure of various bacterial strains and Leishmania species. We found that the two VIP derivatives kill various non-pathogenic and pathogenic Gram-positive and Gram-negative bacteria as well as the parasite Leishmania major through a mechanism that depends on the interaction with certain components of the microbial surface, the formation of pores, and the disruption of the surface membrane. The cytotoxicity of the VIP derivatives is specific for pathogens, because they do not affect the viability of mammalian cells. Docking simulations indicate that the chemical changes made in the analogues are critical to increase their antimicrobial activities. Consequently, we found that the native VIP is less potent as an antibacterial and fails as a leishmanicidal. Noteworthy from a therapeutic point of view is that treatment with both derivatives increases the survival and reduces bacterial load and inflammation in mice with polymicrobial sepsis. Moreover, treatment with VIP51(6-30) is very effective at reducing lesion size and parasite burden in a model of cutaneous leishmaniasis. These results indicate that the VIP analogues emerge as attractive alternatives for treating drug-resistant infectious diseases and provide key insights into a rational design of novel agents against these pathogens.

Treatment of Lymphocytic Gastritis with Cyclosporine in a Cat

A 7-year-old spayed female domestic shorthair cat was referred for chronic intermittent vomiting. The frequency of vomiting increased recently, and the cat showed anorexia at presentation. There were no remarkable abnormalities on the blood analyses and diagnostic imaging. However, the endoscopic examination revealed focal erosions of the gastric body mucosa, and subsequent multiple biopsies were obtained. Histopathologic examination indicated mild to moderate lymphocytic gastritis. The vomiting was completely disappeared 7 days after the administration with prednisolone (PDS). However, because of side effects caused by the long-term PDS administration, cyclosporine was added on the prescription with tapered dose of PDS. The dog’s condition improved with continued cyclosporine treatment, and no further vomiting and anorexia episodes have been noted. This case describes the successful management with administration of cyclosporine in feline lymphocytic gastritis.

Cell lineage distribution atlas of the human stomach reveals heterogeneous gland populations in the gastric antrum

ObjectiveThe glands of the stomach body and antral mucosa contain a complex compendium of cell lineages. In lower mammals, the distribution of oxyntic glands and antral glands define the anatomical...

Nasal mucosa ulceration and septal perforation as initial presentation of a patient with probable Behcet's disease

Behcet's disease is a vasculitis that affects multiple systems in the body, classically oral and genital mucosa. Nasal mucosa involvement is a rare manifestation of the disease, reported in only a handful of patients. We present an HLA-B51 positive, suspected Behcet's patient with predominantly nasal manifestations including epistaxis, nasal mucosa ulceration and septal perforation. Her nasal symptoms have improved since being started on a daily regimen of colchicine. We believe this case supports the wide clinical heterogeneity of the disorder, and serves as a reminder to consider Behcet's disease when a patient presents with an atypical head and neck manifestation.

Amyotropic lateral sclerosis as a para-neoplastic manifestation of gastric adenocarcinoma - A rare case report

Motor neuron diseases(MND) have been reported as a rare paraneoplastic syndrome (PNS) of a systemic neoplasm.Amyotropic Lateral Sclerosis as a paraneoplastic manifestation of gastric carcinoma is even rarer. We present a patient with amyotrophic lateral sclerosis (ALS) in association with adenocarcinoma of stomach. A 48year old man presented with a four months history of progressive dysphagia, spastic dysarthria and marked fasciculation in his atrophic tongue. Gag reflexes were diminished bilaterally. There was significant atrophy in thenar and hypothenar areas of both hands and dorsum of both feet.Electromyography result was compatible with diffuse motor neuronopathy with active denervation.MRI brain showed classical findings of ALS. Upper GI endoscopic study showed ulcerated mucosa in body of stomach. Histological biopsy of stomach confirmed the presence of adenocarcinoma. The importance of considering a paraneoplastic syndrome in a patient with presentation of ALS is that it can lead to searching for underlying neoplasm before its apparent signs and symptoms develop and a scope to initiate treatment for primary carcinoma. Again treating the underlying neoplasm may halt or even resolve the neurologic signs and symptoms.

Confocal microscopy for healthy and pathological nail

Nail diseases are often annoying for the patient and diagnostically challenging for dermatologists. New imaging techniques are of high interest in the diagnosis of nail disorders to reduce the number of nail biopsies. Confocal microscopy is a high-resolution emerging imaging technique that can be used to explore the entire body surface, including skin, mucosa, hair and nails. A systematic review of the literature concerning the use of confocal microscopy for the study of either healthy or pathological nail has been performed to evaluate the current use of this technique and possible future applications. Confocal microscopy is particularly suitable for nails because it allows a non-invasive in vivo examination of this sensitive body area, and nail plate transparency permits to image up to the nail bed with an easy identification of corneocytes. Confocal microscopy can play a role in the diagnosis of onychomycosis and melanonichia, and in the study of drug penetration through the nail plate. It could be used in the future as a non-invasive procedure for the investigation of different nail diseases, such as psoriasis and lichen planus. Further application could be the intra-operative ex vivo examination of nail specimens to outline tumour margins to assist surgery.

An Unusual Case of Helicobacter pylori Negative Gastric MALToma Presenting as Nodular Gastritis

Introduction: MALT lymphomas or MALToma, make up 8% of all B-cell lymphomas. MALTomas can affect many tissues but the gastrointestinal tract is the commonest site affected by the disease of which gastric MALTomas are the most common. Case Report: We present a 50-year-old female who presented with a sharp epigastric pain of 4/10 in intensity after eating, not related to any particular food, lasting for an hour, associated with nausea and bloating, of 6 months' duration. No history of weight loss, fever, chills, fatigue, or anorexia was given. An upper GI series was performed which showed nodular gastritis. Esophagogastroduodenoscopy (EGD) showed nodular mucosa in body and antrum of stomach. Multiple biopsies were taken from them and histopathology showed lymphoplasmacytic infiltrate withn the lamina propria. Giemsa stain was negative for Helicobacter pylori. Immunohistochemistry showed marginal B cell lymphoma - mucosal associated lymphoid tissue with CD 20 positivity. She was given clarithromycin, amoxicillin and lanzoprazole for 4 weeks and a repeat endoscopy was performed twice with same endoscopy findings and pathology. After this, she was referred to an oncologist for further management.Figure: Nodular gastritis.Discussion: Usually, gastric MALT lymphoma or MALTomas present with vague symptoms like abdominal pain, early satiety, nausea, vomiting, anorexia. Most commonly found in middle third of the stomach with ulceration being the most common finding on EGD. The main method of diagnosis is EGD with histopathology. H. pylori infection plays a pathogenic role and is seen in 90% of cases. Treatment for gastric maltoma patients should be chosen individually depending on the clinical stage of disease. Radiotherapy, chemotherapy, and/or surgery can be considered after unsuccessful eradication treatment as in our patient. Conclusion: As the presenting symptoms and EGD findings in MALToma are nonspecific, high degree of suspicion and confirmation with prompt biopsy is needed for early detection and improved prognosis.

Hypoproteinemia in childhood: What should you look for?

Introduction: Menetrier’s disease (MD) is a fundus and body gastritis frequently associated with hypoalbuminemia secondary to protein loss through the gastricmucosa. Clinical findings include vomiting, diarrhoea, abdominal pain, anorexia and peripheral oedema inmost cases. In one third of cases Cytomegalovirus (CMV) it is demonstrated having a central role in the pathogenesis and in childhood MD is usually a benign and self-limiting condition, lasting for a few weeks. Patients and methods: We present a 2 yrs old girl with important protein-loss admitted to our Unit; we describe diagnosis and management discussing the causative role of CMV in MD. Results: Two yrs-old girl with a few days history of diarrhoea, cough and fever especially during the night, important peripheral and periorbital oedemas presented at our Unit. Serological tests revealed anemia, iron deficiency, WBC elevated, hyponatremia, hypocalcemia, low level of thyroid hormones, hypoproteinemia, hypoalbuminemia and she was treated by human albumin. Antigliadin, antiendomysial and anti-tissue transglutaminase antibodies were negative. Urinary protein loss was excluded and her liver synthetic function was normal. Abdominal ultrasonography was negative for abdominal ascitic fluid. Nephrological cause was excluded and gastrointestinal causes were studied. Upper gastrointestinal endoscopy was performed and it showed mild multinodular duodenitis and a widely bleeding mucosa with large areas of erosions in the gastric body and fundus. Histologic examination confirmed a profound chronic active hypertrophic gastritis with intense regenerative epithelial hyperplasia. Tissue culture for Helicobacter Pylori and intranuclear CMV inclusion bodies were negative. Duodenal biopsy revealed normal mucosa and villous that excluded coeliac syndrome. An infectious cause is hypothised and serological tests for virus, bacteria and parasites revealed positive serum IgM antibodies against CMV; CMV DNAwas detected in blood through polymerase chain reaction (PCR). During her stay in hospital, shewas treatedwith PPI and another human albuminwas not necessary because of the improvement of her clinical condition. Next upper endoscopy after 20 days showed healing of duodenitis and an erythematous mucosa in the gastric body and fundus without erosions. She continued therapy with PPI and at clinical follow-up 4weeks later shewas free of symptomswith satisfactory weight gain and her haemoglobin, serum electrolytes and serum protein levels were normal, including IgA levels that exclude any Ig deficit. Conclusions: One of the major causes of MD in children is the CMV infection that should be suspected in every childwhopresents with protein-losing gastropathy. Upper endoscopy with histological examination and PCR level should be performed. Usually only supportive care is required, according to literature that describes MD in children as a transient and self-limiting condition. PO26

Greater resistance of the rabbit antropyloric region to experimental acute gastric ischemia

INTRODUCTION: Gastric ischemia represents an important medical challenge in pathology and surgical practice. OBJECTIVE: The purpose of this study was to assess the effects of acute gastric ischemia on different regions of the stomach. METHOD: Rabbit stomachs were subjected to devascularization of the greater and lesser curvatures for 3, 6 and 12 hours. After these periods, the stomachs were removed for macro and microscopic analysis. RESULTS: Hemorrhagic necrosis was more marked in the gastric fundus and body. In contrast, the antropylorus remained preserved in 100% of the rabbits after 3 hours of ischemia (group I), and in 80% of the rabbits after 6 and 12 hours of ischemia (groups II and III). Necrosis of the gastric body and fundus mucosa were observed in all animals after 6 and 12 hours of ischemia. CONCLUSION: We concluded that this experimental model of acute gastric ischemia was effective in producing hemorrhagic necrosis of the gastric fundus and body in rabbits even within a short period of time. Furthermore, the antropyloric region was preserved in most animals.

Iron Deficiency Anemia Due to Lymphocytic Gastritis With Helicobacter pylori Infection in Childhood

Lymphocytic gastritis (LG) is a chronic inflammatory process of poorly understood pathogenesis. We report the case of a 12-year-old premenstrual girl with refractory iron deficiency anemia in which the oral iron absorption challenge suggested iron malabsorption. Laboratory studies ruled out celiac disease and autoimmune gastritis, and carbon-13 urea breath test for Helicobacter pylori was also negative. Upper endoscopy with gastric body and antral mucosa biopsies revealed a LG with focal intestinal metaplasia and H. pylori infection. H. pylori eradication was undertaken with success and 3 months later her hematologic parameters normalized. Histologic reevaluation showed disappearance of LG. This case shows that investigation of malabsorption disease in the presence of refractory iron deficiency anemia can lead to the diagnosis of important gastric diseases, even in the absence of gastrointestinal symptoms. This nonceliac child was diagnosed with a severe histopathologic pattern of LG, with potential risk of malignant transformation, which was completely reverted with adequate H. pylori eradication treatment.

4. Eosinophils in autoimmune atrophic gastritis – typically numerous and a potentially helpful diagnostic feature

<h3>Background</h3> Autoimmune atrophic gastritis (AAG) is an autoimmune condition characterised by loss of gastric parietal cells and subsequent replacement by metaplastic intestinal, gastric or pancreatic acinar epithelium. A lymphocyte rich inflammatory infiltrate localised to the parietal cell bearing gastric body and fundic mucosa and sparing the gastric antrum is typical. We have noted eosinophils to be a prominent component of the inflammatory process, and recently experimental evidence has suggested activation of the Th17 effector cell mechanism to be responsible. <h3>Aims</h3> To investigate eosinophils in AAG and their usefulness as a diagnostic adjunct. <h3>Methods</h3> Gastric body/fundic biopsies were collected in a consecutive prospective manner of AAG (<i>n</i>=52; diagnosed on basis of body only inflammation and suggestive history and/or antiparietal cell/ anti intrinsic factor antibodies and <i>H. pylori</i> immunohistochemical stain negative); <i>H. pylori</i> gastritis (HPG; <i>n</i>=49; immunohistochem-ical stain ± urease positive); multifocal atrophic gastritis (MAG; <i>n</i>=16; <i>H. pylori</i> immunohistochemical stain negative and atrophy of gastric antrum) and normal controls (NC; <i>n</i>=50; endoscopy and biopsy normal). Eosinophils were countered as the maximum in 1 HPF (field diameter 0.4mm) and maximum total in any 3 HPF. <h3>Results</h3> Maximum mean eosinophil numbers counts were as follows: 1 HPF, AAG 44; HPG 9; MAG 19; normal controls 3; 3 HPF, AAG 104; HPG 23; MAG 43, NC 6. There was a significant difference between the counts in AAG and those in NC, HPG and MAG (all <i>p</i> < 0.05). In 7 AAG cases (13.5%) eosinophil counts were ≤11 (the maximum count in NC). Eosinophils were common in both evolving and established disease as evidenced by the extent of metaplasia in biopsies. <h3>Conclusions</h3> A prominent increase in eosinophils is frequently identified in AAG and is greater than other conditions that comprise the histological differential diagnosis. This may serve as an additional diagnostic marker in histologically equivocal gastric body biopsies or where supportive clinical history is not available.

A case of endoscopic ultrasound diagnosis of gastric amyloidosis

A 37-year-old female presented to our hospital with the complaint of abdominal distension for one month. A gastroscopy examination showed extensive chyme retention and varying erosion and ulceration of the gastric body. The pathology showed moderate chronic inflammation and erosion of the gastric body mucosa, with accompanying Helicobacter pylori infection. She accepted treatment for one month. The patient then accepted to undergo endoscopic ultrasonography, which showed that normal structure of the gastric body intumescence was discernible. The pathology showed chronic mild-moderate inflammation of the gastric body mucosa associated with interstitial amyloidosis, with accompanying Helicobacter pylori infection. She accepted treatment for the eradication of Helicobacter pylori, and the original ulcer healed.

Citrate synthase, sarcoplasmic reticular calcium ATPase, and choline acetyltransferase activities of specific pelvic floor muscles of the rabbit

There is a clear relationship between the pelvic floor muscles and urinary systems, which relates to urgency, frequency, incontinence, pelvic pain, and bowel complaints. The specific mechanisms which relate these two systems are not clear. Improved understanding of the relation between the pelvic floor muscles and bladder function is clinically relevant in establishing effective treatments to such problems as incontinence, secondary to birth. The following tissues were collected from normal adult female rabbits: pubococcygeus (Pc) and ischiocavernosus/bulbospongiosus (Ic/Bs) pelvic floor muscles. Bladder body muscle and mucosa, bladder base muscle and mucosa, and leg skeletal muscle were also collected. The following enzymatic assays were performed on each tissue: citrate synthase (CS), sarcoplasmic-endoplasmic reticular ATPase (SERCA), and choline acetyltransferase (ChAT). CS and SERCA activities were significantly higher in the Pc compared with the Ic/Bs pelvic floor muscles, whereas the ChAT activity of the Ic/Bs was higher than that of the Pc muscle. Based on our results, the Pc muscle is expected to have a significantly greater capacity to contract and a higher metabolic activity than those of the Ic/Bs muscles. We believe that an understanding of the biochemical activities of these three biomarker enzymes in normal pelvic floor muscles is essential in evaluating the effects of specific experimental dysfunctions created in pelvic floor muscle activity.

Erythema Multiforme in a Patient with Recurrent Non-Hodgkins Lymphoma/Chronic Lymphocytic Leukemia

Erythema multiforme major (EMM) is a hypersensitivity reaction usually secondary to medications, viruses or other infections. Its presentation is fairly typical with a symmetrical distribution of vesicles, bullae or targeted lesions on the upper body, arms, legs, palms, feet and oral mucosa. The authors present a delineated case of EMM in association with chronic lymphocytic leukemia (CLL) and non-Hodgkin’s lymphoma (NHL) with a very unusual clinical presentation evolving overtime into a unique, almost dermatomal distribution. Typical therapies were not initially helpful and intravenous immunoglobulin antibody had to be administered.

Differential Expression of Ghrelin mRNA According to Anatomical Portions of Human Stomach

The detailed ghrelin distribution on mRNA level in different anatomical portions of adult stomach and its association with plasma ghrelin levels are not yet well established. We investigated the ghrelin mRNA and peptide expression in different anatomical portions of stomach in human adults. Stomach tissue samples were obtained from 16 patients with gastric cancer who underwent total gastrectomy. The normal stomach tissues were taken from the upper (gastric fundus and upper body), middle (gastric middle and lower body) and lower (gastric antrum and pylorus) portions of stomach, respectively. The expression of ghrelin mRNA and peptide in stomach tissue samples were measured using RT-PCR and immunohistochemistry. The ghrelin/actin ratio was 0.78 (range 0-3.38; n=16) at the upper portion, 0.20 (range 0-1.28; n=16) at the middle portion and 0.07 (range 0-0.67; n=16) at the lower portion of the stomach (p=0.001). Ghrelin-positive cells were seen in all parts of the gastric mucosa and were most numerous in the glandular compartment compared to foveolar compartment. Gastric body or fundic mucosa showed ghrelin-positive cells most abundantly as compared to other portions of the gastric mucosa (p<0.001). Ghrelin mRNA expression and immunoreactivity is highest at the upper portion of the human stomach.

IL-10, TNF-α and IFN-γ levels in serum and stomach mucosa of Helicobacter pylori-infected patients.

H. pylori is a human pathogen that colonizes the epithelium of the stomach. The host immune response may influence the disease process, where cytokines play important roles in the development of disease. In this study, the concentrations of selected cytokines in the gastric antrum and stomach body mucosa and also in the serum were evaluated. Eighty patients according to their rapid urease test were divided into two groups: H. pylori positive (n=39) and H. pylori-negative (n=41). The concentrations of cytokines in biopsies and serum were determined by ELISA method. The mean TNF-α and IFN-γ levels in the infected group were significantly higher than that of uninfected patients. In contrast, IL-10 level in most patients was undetectable. The mean antral of stomach TNF-α and IFN-γ levels were significantly higher than that of the stomach body. IFN-γ serum level showed positive correlation with antrum and stomach body levels, whereas no correlation was found in TNF-α in different samples. Higher levels of TNF-α and IFN-γ in antral indicate that the colonization of bacteria in the antrum may be higher than stomach body (culture results from two sites support this statement). Increased serum level of IFN-γ indicates the activation of circulating-T cells against infection. Induced H. pylori-related TNF-α is concentrated is gastric mucosa and this pathogen does not cause any significant change in the serum level of this cytokine. Therefore H. pylori by inducing certain inflammatory cytokines but not IL-10 may contribute the process of disease development.

IL-10, TNF-α and IFN-γ levels in serum and stomach mucosa of Helicobacter pylori-infected patients.

H. pylori is a human pathogen that colonizes the epithelium of the stomach. The host immune response may influence the disease process, where cytokines play important roles in the development of disease. In this study, the concentrations of selected cytokines in the gastric antrum and stomach body mucosa and also in the serum were evaluated. Eighty patients according to their rapid urease test were divided into two groups: H. pylori positive (n=39) and H. pylori-negative (n=41). The concentrations of cytokines in biopsies and serum were determined by ELISA method. The mean TNF-α and IFN-γ levels in the infected group were significantly higher than that of uninfected patients. In contrast, IL-10 level in most patients was undetectable. The mean antral of stomach TNF-α and IFN-γ levels were significantly higher than that of the stomach body. IFN-γ serum level showed positive correlation with antrum and stomach body levels, whereas no correlation was found in TNF-α in different samples. Higher levels of TNF-α and IFN-γ in antral indicate that the colonization of bacteria in the antrum may be higher than stomach body (culture results from two sites support this statement). Increased serum level of IFN-γ indicates the activation of circulating-T cells against infection. Induced H. pylori-related TNF-α is concentrated is gastric mucosa and this pathogen does not cause any significant change in the serum level of this cytokine. Therefore H. pylori by inducing certain inflammatory cytokines but not IL-10 may contribute the process of disease development.