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ABSTRACT: Background: The prevalence of gastric polyps is unknown in Hungary. Aim: The aim of the authors was to assess the prevalence of polypoid lesions of the stomach in the endoscopic centre of the 2nd Department of Medicine, Semmelweis University. Methods: Results of upper gastrointestinal endoscopies carried out between March 2010 and June 2011 were analysed. Results: 193 cases with polyps were diagnosed in 4174 endoscopies (4.62%). Hyperplastic polyps, fundic gland polyps and malignant lesion were detected in 33.67%, 31.09% and 2.07% of the cases, respectively. Proton pump inhibitor use was more frequent among patients diagnosed with fundus gland polyps (p = 0.007), while hyperplastic polyps were diagnosed more frequently in patients with chronic gastritis (p = 0.032). Conclusions: The frequency of gastric polyps was higher than expected from data published in the literature. Long-term proton pump-inhibitor use and chronic gastritis were associated with fundus gland and hyperplastic polyps, respectively. Orv. Hetil., 2013, 154, 770-774.
Orvosi Hetilap 05/2013; 154(20):770-4.
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ABSTRACT: The etiology and pathogenesis of collagenous colitis (CC) is poorly understood and probably multifactorial; many potential pathophysiological mechanisms have been described, although none have been conclusively proved. Circumstantial evidence suggests that CC appears as an autoimmune response to a luminal or epithelial antigen of unknown origin. Infections and certain drugs (e.g. NSAID, lansoprazole) may act as triggers for an immune-mediated process. CC is characterized clinically by chronic watery, nonbloody diarrhea with normal endoscopic appearance and without radiological abnormalities, but specific microscopic changes in the colon. Histopathology is featured by the presence of a thickened subepithelial collagen band adjacent to the basal membrane. Up to 40% of patients with CC have associated diseases of autoimmune or inflammatory origin, such as thyroid disease, coeliac disease, rheumatoid arthritis, diabetes mellitus, Sjögren's syndrome, CREST syndrome, scleroderma, pernicious anemia, and sarcoidosis. Prurigo nodularis is a chronic condition characterized by intensely pruritic, lichenified, or excoriated papules and nodules of unknown etiology. It is assumed to represent a cutaneous reaction pattern to repeated scrubbing or scratching caused by pruritus. We report a case of CC and prurigo nodularis. To our knowledge, this association has not been reported earlier.
European journal of gastroenterology & hepatology 05/2009; 21(8):946-51. · 1.66 Impact Factor
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Orsolya Galamb,
Balázs Gyõrffy,
Ferenc Sipos,
Elek Dinya,
Tibor Krenács, Lajos Berczi,
Dominika Szõke,
Sándor Spisák,
Norbert Solymosi,
Anna Mária Németh,
Márk Juhász,
Béla Molnár,
Zsolt Tulassay
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ABSTRACT: Chronic Helicobacter pylori infection affects approximately half of the world, leads to chronic gastritis and peptic ulceration, and is linked to gastric carcinoma. Our aims were to compare the gene expression profile (GEP) of H. pylori-positive and H. pylori-negative gastric erosions and adjacent mucosa to explain the possible role and response to H. pylori infection and to get erosion-related mRNA expression patterns.
Total RNA was extracted, amplified, and biotinylated from gastric biopsies of patients with H. pylori-positive and H. pylori-negative antrum erosions (ER) (8/8) and adjacent macroscopically normal mucosae (8/8). The GEP was evaluated using HGU133plus2.0 microarrays. Two independent normalizations (MAS5.0, RMA), PAM feature selection, hierarchical cluster analysis, and discriminant analysis were done. The expression of 14 genes was also measured by real-time-polymerase chain reaction. VCAM-1 and CXCL13 immunohistochemistry (IHC) was done.
In H. pylori infection, significant overexpression of MHC class II antigen-presenting genes, interleukin-7 receptor, ubiquitin-D, CXCR4, lactoferrin immune response-related genes, CXCL-2 and -13, CCL18 chemokine ligand, and VCAM-1 genes were established. In erosive gastritis, increased proliferation (MET) and transport (UCP2, SCFD1, KPNA4) were found, while genes associated with adhesion (SIGLEC11), transcription regulation (ESRRG), and electron and ion transport (ACADM, CLIC6) were down-regulated. Discriminant analysis successfully classified all samples into four groups (HP+ER-, HP+ER+, HP-ER+, HP-ER-) using a reduced gene set (20). Significant overexpression of VCAM-1 and CXC13 protein was detected by IHC in HP+ samples (p < .05).
Whole genomic microarray analysis yielded new H. pylori infection and erosion-related gene expression changes. Discriminative genes can be used in mRNA-based diagnostic classification of gastric biopsies.
Helicobacter 05/2008; 13(2):112-26. · 3.15 Impact Factor
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ABSTRACT: Mesenteric panniculitis can develop in every patient after abdominal surgery. The clinical and pathological signs are usually vague, so different therapeutic approaches are recommended at various stages of the disease. While some authors suggest that these stages are different manifestations of the the same disease, others claim that the various stages represent the progression of a single entity. We report a case of a 65 year-old male patient with mesenteric panniculitis and fibrosis, which developed after laparoscopic sigmoid resection first, and required a Hartmann's procedure finally. The disease developed once again after the elective reconstruction of the colon. This time surgical intervention was not possible and he was treated conservatively with intravenous steroids, antibiotics, parenteral nutrition and continuous nasogastric tube. The patient gradually recovered in three weeks time. We report this successful treatment, and review the relevant literature.
Magyar Sebészet (Hungarian Journal of Surgery) 05/2008; 61(2):84-7.
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ABSTRACT: The risk of development of colorectal carcinoma is elevated in chronic, long-standing ulcerative colitis (UC). The changes in regenerative and immortalizing pathways caused by the inflammatory process, and that have been proved to be carcinogenic in other human tissues, have not been fully and uniformly described. We assayed the expression alterations of regenerative signal receptors and cell-aging inhibitory systems within colonic crypts by considering the histological activity of the disease.
I-type insulin-like growth factor receptor (IGF1R), hepatocyte growth factor receptor (HGFR), telomerase reverse transcriptase (TERT) and telomerase associated protein (TP-1) expression were evaluated immunohistochemically on biopsy specimens from 11 mild, 11 moderate and 12 severe active inflammation of UC cases and from 10 normal colonic tissue cases. Independent colonic biopsies from 5 healthy and 7 severe UC cases were used for TaqMan real-time RT-PCR validation.
In mild inflammation, all observed parameters showed significantly elevated epithelial protein expression (IGF1R: 22.3 +/- 9.46%; HGFR: 35.3 +/- 22.8%; TERT/TP-1: 2.1 +/- 1.87%/2 +/- 1.32%) compared to normal (p < 0.005). In moderately active inflammation, only IGF1R expression was significantly higher (50.2 +/- 8.6%) compared to normal and mild inflammation (p < 0.005). In severe inflammation, all parameters showed decreased epithelial expression; IGF1R showed decreased mRNA expression, while HGFR was overexpressed and TERT showed a decreased tendency.
The epithelial expression of IGF1R, HGFR and TERT/TP-1 is elevated in mildly active UC. This phenomenon may allow the epithelial cells that collected genetic defects during severe inflammatory episodes pathologically to survive and proliferate.
Scandinavian Journal of Gastroenterology 03/2008; 43(3):289-98. · 2.02 Impact Factor
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ABSTRACT: It has been proposed that matrix metalloproteinases (MMPs) play a role in tumor invasion. We determined protein expression of matrix metalloproteinase-9 (MMP-9) in colorectal cancer (CRC), corresponding normal mucosa and colorectal adenomas. For confirmation of immunohistochemical results MMP-9 TaqMan RT-PCR analysis was performed. Expression of MMP-9 was determined on paraffin embedded biopsy sections by immunohistochemistry in 31 CRC patients (from cancer tissue and corresponding normal mucosa) and in 30 patients with adenoma (nine adenomas with high grade of dysplasia). MMP-9 immunostaining was determined semi-quantitatively. For Taqman RT-PCR analyses normal mucosa (n = 5), adenoma without (n = 6) and with high grade dysplasia (n = 7) and CRC (n = 10) were investigated. Statistical analysis with ANOVA, LSD test and correlation analysis were performed. P value of <0.05 was considered significant. The MMP-9 expression in CRC was significantly higher compared to adenomas or the normal mucosa (P = 0.001). Significantly higher expression of MMP-9 has been observed in adenomas with high grade dysplasia compared to other adenomas or normal colon (P < 0.001). Diffuse strong MMP-9 expression was present in tumor as well as in stromal cells. In adenoma samples, dysplastic epithelial cells showed moderate intensive cytoplasmic MMP-9 expression, with a clear-cut differentiation between dysplastic and non-dysplastic areas. Staining intensity correlated with the grade of CRC. We demonstrate a significantly higher expression of MMP-9 in adenoma with high grade dysplasia-CRC sequence as compared to normal tissue. The over-expression of MMP-9 strongly suggests its association with colorectal carcinogenesis.
Pathology & Oncology Research 01/2008; 14(1):31-7. · 1.37 Impact Factor
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ABSTRACT: Automated virtual microscopy of specimens from gastrointestinal biopsies is based on cytometric parameters of digitized histological sections. To our knowledge, cytometric parameters of gastritis and of adenocarcinoma have yet to be fully characterized. Our objective was to classify gastritis and adenocarcinoma based on cytometric parameters. We hypothesized that automated virtual microscopy using this novel classification can reliably diagnose gastritis and adenocarcinoma.
Routinely processed hematoxylin-and-eosin-stained histological sections from specimens that showed normal mucosa (14 cases), gastritis (35 cases), and adenocarcinoma (30 cases) diagnosed by conventional optical microscopy were scanned and digitized at high resolution. Thirty-eight cytometric parameters based on density and morphometry were applied to glands and superficial epithelium. Twelve cytometric parameters based on cytologic detail were applied to individual cells.
Statistically significant differences in cytometric parameters for normal mucosa, gastritis, and adenocarcinoma were found. The most discriminatory parameter was the ratio of the total number of cells to the number of interstitial cells. These differences correctly classified adenocarcinoma at 100% accuracy and overall correctness was 86%.
We describe a novel method of analyzing gastric mucosal histology based on cytometric parameters. Automated virtual microscopy can be used to classify gastric mucosa as normal, gastritis, or adenocarcinoma with reasonable accuracy. Further research is necessary to determine whether automated virtual microscopy can subclassify gastric mucosal histology in greater detail.
Cytometry Part B Clinical Cytometry 12/2006; 70(6):423-31. · 2.53 Impact Factor
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ABSTRACT: Transforming growth factor beta1 (TGF beta1) has antiproliferative and/or apoptotic effect on lymphoid cells. In certain lymphomas exogenous TGF beta1 is able to induce apoptosis, however many lymphoid malignancies are resistant to the endogenous TGF beta1 production. We studied the expression and the activity of TGF beta1 signalling components in B cell lymphoma cell lines (e.g. HT 58 cells) and in isolated human peripheral mononuclear cells (PBMCs) from healthy individual's and B-CLL patient's blood. We found that all signal transducer Smads (Smad2,-3; Smad4) and at least one of the inhibitory Smads (Smad6,-7) were expressed in non-treated lymphoma cells, but the inhibitory Smads did not in normal/control PBMCs. However, after TGF beta1 treatment Smad6 disappeared, while the expression of Smad7 increased in HT 58 cells. The activity of Smad signals was proved by phosphorylation of Smad2, nuclear translocation of Smad2/3, and the increased expression of Smad-dependent gene, TIEG in TGF beta1 treated lymphoma cells. These results showed that Smad signaling is available in certain different human lymphoma cells, however ISmads expression could inhibit the signal transmission. This findings indicates that the lost sensitivity of lymphoma cells toward a physiological regulatory factor could be reversed.
Cytokine 07/2005; 30(5):228-35. · 3.02 Impact Factor
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ABSTRACT: Epithelial cell turnover related differences between ulcerative colitis, Crohn's colitis, and aspecific colitis are not known yet.
Totally 345 formalin-fixed, paraffin-embedded biopsy specimens from 33 ulcerative colitis, 26 Crohn's colitis, 30 aspecific colitis, and 10 healthy patients were observed with the TdT-mediated dUTP nick end labeling method and proliferating cell nuclear antigen-, p53-, and epithelial growth factor receptor immunohistochemistry. Because of epithelial growth factor receptor positivity of subepithelial cells epithelial growth factor receptor and CD45, CD68, or CD83 double fluorescence immunohistochemistry were performed on 16 freshly frozen samples from 8 severely active ulcerative colitis and 8 severely active Crohn's colitis patients to describe lamina propria's mononuclear cells, respectively.
The epithelial growth factor receptor expression was significantly lower in each inflammatory group compared with normal (P < 0.005) and decreased significantly in mild ulcerative colitis compared with mild Crohn's colitis or aspecific colitis (P < 0.005). Numerous epithelial growth factor receptor and CD45 double-positive submucosal mononuclear cells were observed in moderate-severe inflammations. The p53-expression was significantly higher in each inflammatory group compared with normal (P < 0.05). Significant differences were found between mildly, moderately, and severely inflamed samples in ulcerative colitis (P < 0.05) compared with Crohn's colitis or aspecific colitis. Apoptotic/proliferative rates increased significantly in line with the inflammatory process (P < 0.0001/0.05), but the TdT-mediated dUTP nick end labeling and proliferating cell nuclear antigen-labeling characteristics did not show disease type specificity.
Based on our results, the alterations of epithelial growth factor receptor and p53 expression show ulcerative colitis specificity, whereas the rate of epithelial apoptosis and proliferation are determined by the histologic activity of the inflammation. The increased epithelial growth factor receptor expression by the lamina propria's mononuclear cells in inflammation may suggest its role as an autoantigen.
Diseases of the Colon & Rectum 05/2005; 48(4):775-86. · 3.13 Impact Factor
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ABSTRACT: A 39-year-old man was admitted to our Medical Department, because of regular abdominal cramps. At physical examination a palpable mass was detected in the ileocoecal region with tenderness. Examinations proved ileocoecal intussusception. Emergency operation was performed. At histology the cause of small-bowel invagination was Burkitt-lymphoma. After the complex haematological examination chemotherapy was started. Six month after surgery the patient is symptomless.
Magyar Sebészet (Hungarian Journal of Surgery) 09/2003; 56(3-4):116-9.
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ABSTRACT: Henoch-Schoenlein syndrome in an adult patient, localised only to the gastrointestinal system is very rare. A 50 year old male was treated in our Intensive Department because of acute respiratory distress syndrome (ARDS) and renal failure. After temporary improvement massive gastrointestinal bleeding developed with shock. Blood was found in the descending duodenum without evident pathology at endoscopy. Angiogram showed bleeding at the hepatic flexure of the colon, which was successfully treated by a coil and bleeding was also present in the terminal part of the small intestine. The catheter was left in situ and the bleeding part of the bowel was painted intraoperatively, so we could resect the stained part of the intestine. Because of rebleeding, bowel resection was performed an other two occasions in the same way. The histology of the bowel showed Henoch-Schoenlein syndrome in each specimen. Our patient was totally non-responsive to treatment, which is usually successful in this disease. After the resections the bleeding stopped temporarily, but as the underlying disease was unmanageable the patient died but we have not found any surgical complication at autopsy. We think that this method in the surgical treatment of massive intestinal bleeding is very useful and effective.
Magyar Sebészet (Hungarian Journal of Surgery) 05/2002; 55(2):93-6.
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ABSTRACT: A new flow cytometric method was developed to detect apoptotic cells with fragmented DNA and to determine cell cycle distribution of viable cells, in the same sample, by propidium iodide staining. Apoptosis, in HT58 human B lymphoma cells, was induced by etoposide and/or by staurosporine. Using appropriate alkaline solutions (between 1-10 mN NaOH in 150 mM saline) followed by neutralization with buffer solution, the fragmented DNA can be extracted quantitatively from ethanol fixed cells. Further, good resolution of the cell cycle distribution can be obtained in unimpaired cells without RNase treatment. Furthermore, unlike the widely used hypotonic-detergent extraction of unfixed cells, the suggested extraction method can prevent drug-induced disintegration of dead cells when karyorrhexis occurs.
Pathology & Oncology Research 02/1996; 2(1-2):78-83. · 1.37 Impact Factor
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ABSTRACT: Although Helicobacter pylori (HP) is frequently associated with chronic active gastritis and peptic ulcers, its exact pathogenic role or the pathomechanism is still unclear. Here, we describe a striking, statistically significant increase of eosinophils in HP infected gastric mucosa compared to HP negative gastritis with similar activity. In both cases, the mean number of the mast cells in the mucosa was comparable, although the individual values showed wide distribution. The source and role of eosinophilia in HP infected mucosa, the potential link between the degree of eosinophilia and the clinical progression, as well as between eosinophils and mast cells require further study.
Pathology & Oncology Research 01/1996; 2(4):229-236. · 1.37 Impact Factor
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ABSTRACT: Kutató munkánk során a terveknek megfelelően vizsgáltuk a daganatsejtek aktív sejthalálát szabályozó jelátviteli utak működését. Vastagbélrák sejtekben kimutattuk, hogy a TRAIL halálligand által kiváltott apoptózis szabályozásában elsősorban az IAP (Inhibitor of Apoptózis) fehérjék, elsősorban a XIAP játszik szerepet. A XIAP gátlása közvetlenül siRNA-vel, vagy a SMAC/DIABLO mitokondriumból történő felszabadulását indukáló hatóanyagokkal illetve SMAC/DIABLO oligopeptidekkel fokozhatja a vastagbélráksejtek TRAIL érzékenységét. A rhabdomyoszarkómák esetében kimutattuk, hogy proteasoma gátlók a DR5 halálreceptor expressziójának és aggregációjának növelésével és a Bcl-2 expressziójának gátlásával fokozzák a TRAIL hatékonyságát. Tüdőrákokban kimutattuk, hogy az EGFR (Epidermális Növekedési Faktor Receptor) gátlókra rezisztens tüdődaganatok esetében a TRAIL kezelés hatékony lehet a jövőben. A mellékpajzsmirigy daganatok esetében a kutatási terv eredeti hipotézisével összhangban azt találtuk, hogy a transzformáció során a pro-apoptotikus gének (pl. TRAIL) expressziója emelkedik, azonban ezt az antiapoptotikus (pl. IAP) gének expressziója kompenzálhatja. Nemzetközi kollaborációban kimutattuk, hogy a FAS halálreceptor expressziójának szabályozásában szerepe lehet egy specifikus CpG sziget hypermetilációjának hólyagrákokban. Kutatásaink tehát számos lehetséges terápiás célpontot azonosítottak a halálreceptorok jelátviteli mechanizmusában. | During our research project we have studied several aspects of the signal transduction pathways regulating the active cell death in tumor cells. In colon cancer, we identified the IAP family of proteins (Inhibitor of Apoptosis Proteins), in particular XIAP as the main regulator of TRAIL sensitivity. Silencing of XIAP expression or indirect inhibition by the drug induced release of the SMAC/DIABLO peptide from the mitochondria or by SMAC/DIABLO mimetic oligopeptide restored TRAIL sensitivity. In rhabdomyosarcomas, we found the upregulation and increased aggregation of DR5 death receptor and downregulation of Bcl-2 as the main mechanism of synergism between TRAIL and proteasome inhibitors. In lung cancer cells we found that cells resistant to EGFR (Epidermal Growth Factor Receptor) inhibitors are often sensitive to TRAIL. In the malignancies of the parathyroid gland we found an upregulation of proapoptotic proteins (E.g. TRAIL) which is compensated by the upregulation of anti-apoptotic proteins (e.g. IAP). In international cooperation we found a single CpG site of which hypermethylation can regulate the expression of FAS death receptor in bladder cancer. This research project has identified several potential anti-cancer therapeutic targets in the signal transduction pathways of death receptors.
