RESUMO
Fusobacterium nucleatum (F. nucleatum) is a Gram-negative anaerobic bacterium that plays a key role in the development of oral inflammation, such as periodontitis and gingivitis. In the last 10 years, F. nucleatum has been identified as a prevalent bacterium associated with colorectal adenocarcinoma and has also been linked to cancer progression, metastasis and poor disease outcome. While the role of F. nucleatum in colon carcinogenesis has been intensively studied, its role in gastric carcinogenesis is still poorly understood. Although Helicobacter pylori infection has historically been recognized as the strongest risk factor for the development of gastric cancer (GC), with recent advances in DNA sequencing technology, other members of the gastric microbial community, and F. nucleatum in particular, have received increasing attention. In this review, we summarize the existing knowledge on the involvement of F. nucleatum in gastric carcinogenesis and address the potential translational and clinical significance of F. nucleatum in GC.
Assuntos
Carcinogênese , Infecções por Fusobacterium , Fusobacterium nucleatum , Neoplasias Gástricas , Humanos , Neoplasias Gástricas/microbiologia , Neoplasias Gástricas/patologia , Fusobacterium nucleatum/patogenicidade , Infecções por Fusobacterium/microbiologia , Infecções por Fusobacterium/complicações , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/complicações , Helicobacter pylori/patogenicidade , Helicobacter pylori/genética , Fatores de Risco , Microbioma Gastrointestinal , Animais , Mucosa Gástrica/microbiologia , Mucosa Gástrica/patologia , Estômago/microbiologia , Estômago/patologia , Adenocarcinoma/microbiologia , Adenocarcinoma/patologiaRESUMO
A bibliometric analysis of studies dedicated to autoimmune gastritis (AIG) recently published demonstrated a noteworthy surge in publications over the last three years. This can be explained by numerous publications from different regions of the world reporting the results of several studies that stimulated reassessment of our view of AIG as a precancerous condition. Follow-up studies and retrospective analyses showed that the risk of gastric cancer (GC) in AIG patients is much lower than expected if the patients ever being infected with Helicobacter pylori (H. pylori) were excluded. The low prevalence of precancerous lesions, such as the incomplete type of intestinal metaplasia, may explain the low risk of GC in AIG patients because the spasmolytic polypeptide-expressing metaplasia commonly observed in AIG does not involve clonal reprogramming of the gastric gland and can be considered as an adaptive change rather than a true precancerous lesion. However, changes in gastric secretion due to the progression of gastric atrophy during the course of AIG cause changes in the gastric mic-robiome, stimulating the growth of bacterial species such as streptococci, which may promote the development of precancerous lesions and GC. Thus, Streptococcus anginosus exhibited a robust proinflammatory response and induced the gastritis-atrophy-metaplasia-dysplasia sequence in mice, reproducing the well-established process for carcinogenesis associated with H. pylori. Prospective studies in H. pylori-naïve patients evaluating gastric microbiome changes during the long-term course of AIG might provide an explanation for the enigmatic increase in GC incidence in the last decades in younger cohorts, which has been reported in economically developed countries.
Assuntos
Doenças Autoimunes , Bibliometria , Mucosa Gástrica , Gastrite , Infecções por Helicobacter , Helicobacter pylori , Lesões Pré-Cancerosas , Neoplasias Gástricas , Neoplasias Gástricas/imunologia , Neoplasias Gástricas/patologia , Neoplasias Gástricas/microbiologia , Neoplasias Gástricas/epidemiologia , Humanos , Gastrite/imunologia , Gastrite/microbiologia , Gastrite/epidemiologia , Gastrite/patologia , Infecções por Helicobacter/epidemiologia , Infecções por Helicobacter/imunologia , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/patologia , Helicobacter pylori/isolamento & purificação , Helicobacter pylori/imunologia , Helicobacter pylori/patogenicidade , Lesões Pré-Cancerosas/imunologia , Lesões Pré-Cancerosas/microbiologia , Lesões Pré-Cancerosas/patologia , Lesões Pré-Cancerosas/epidemiologia , Animais , Doenças Autoimunes/imunologia , Doenças Autoimunes/epidemiologia , Mucosa Gástrica/patologia , Mucosa Gástrica/imunologia , Mucosa Gástrica/microbiologia , Metaplasia , Fatores de Risco , Estômago/patologia , Estômago/imunologia , Estômago/microbiologia , Microbioma Gastrointestinal/imunologia , CamundongosRESUMO
OBJECTIVE: To determine the presence of microplastics in the stomach, and the relationship between pathological changes in stomach tissue and microplastics. STUDY DESIGN: An analytical study. Place and Duration of the Study: Department of Internal Medicine, Sorgun State Hospital, Yozgat, Turkiye, from December 2022 to November 2023. METHODOLOGY: Fasting gastric fluid sampling and endoscopic sampling including mucosal and submucosal layers from the antrum were performed. The pH values of the gastric fluids were recorded. Samples were analysed gradually by adding iron solution, hydrogen peroxide, and sodium chloride (NaCl) in a beaker at 75 degrees for 30 minutes. Biopsy materials obtained from antrum were examined histopathologically and reported according to the Sydney classification. The relationship between gastric biopsy results and the presence of microplastic was evaluated using Chi-square test. The significance level was taken as p <0.005. RESULTS: The study included 61 individuals. The presence of microplastics was detected in 17 (27.86%) gastric fluid samples obtained from the individuals. A significant correlation was found between increased activity and inflammation in antrum biopsy and the presence of microplastic (χ2 = 8.55 p = 0.014; χ2 = 25.75, p = 0.001). The relationship between atrophy, metaplasia, and Helicobacter pylori in gastric tissue and the presence of microplastic was statistically insignificant (p >0.05). CONCLUSION: Microplastics were detected in gastric fasting fluid. These materials can cause histopathologic changes and inflammation in the gastric antrum. KEY WORDS: H. pylori, Intestinal metaplasia, Inflammation, Microplastic, Plastic, Sydney classification.
Assuntos
Jejum , Microplásticos , Humanos , Feminino , Masculino , Adulto , Pessoa de Meia-Idade , Microplásticos/análise , Suco Gástrico/química , Mucosa Gástrica/patologia , Biópsia , Estômago/patologia , Helicobacter pylori/isolamento & purificação , Antro Pilórico/patologia , Metaplasia/patologia , Turquia , IdosoRESUMO
OBJECTIVE: The relationship between lymphocyte-associated inflammatory indices and portal vein thrombosis (PVT) following splenectomy combined with esophagogastric devascularization (SED) is currently unclear. This study aims to investigate the association between these inflammatory indices and PVT, and to develop a nomogram based on these indices to predict the risk of PVT after SED, providing an early warning tool for clinical practice. METHODS: We conducted a retrospective analysis of clinical data from 131 cirrhotic patients who underwent SED at Lanzhou University's Second Hospital between January 2014 and January 2024. Independent risk factors for PVT were identified through univariate and multivariate logistic regression analyses, and the best variables were selected using the Akaike Information Criterion (AIC) to construct the nomogram. The model's predictive performance was assessed through receiver operating characteristic (ROC), calibration, decision, and clinical impact curves, with bootstrap resampling used for internal validation. RESULTS: The final model incorporated five variables: splenic vein diameter (SVD), D-Dimer, platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), and red cell distribution width-to-lymphocyte ratio (RLR), achieving an area under the curve (AUC) of 0.807, demonstrating high predictive accuracy. Calibration and decision curves demonstrated good calibration and significant clinical benefits. The model exhibited good stability through internal validation. CONCLUSION: The nomogram model based on lymphocyte-associated inflammatory indices effectively predicts the risk of portal vein thrombosis after SED, demonstrating high accuracy and clinical utility. Further validation in larger, multicenter studies is needed.
Assuntos
Linfócitos , Nomogramas , Veia Porta , Esplenectomia , Trombose Venosa , Humanos , Esplenectomia/efeitos adversos , Veia Porta/patologia , Masculino , Feminino , Estudos Retrospectivos , Pessoa de Meia-Idade , Trombose Venosa/etiologia , Fatores de Risco , Complicações Pós-Operatórias/etiologia , Adulto , Produtos de Degradação da Fibrina e do Fibrinogênio/análise , Produtos de Degradação da Fibrina e do Fibrinogênio/metabolismo , Cirrose Hepática/complicações , Cirrose Hepática/cirurgia , Contagem de Linfócitos , Curva ROC , Esôfago/cirurgia , Inflamação/etiologia , Inflamação/sangue , Veia Esplênica , Estômago/irrigação sanguínea , Estômago/patologia , Estômago/cirurgia , Contagem de PlaquetasRESUMO
This study elucidated the unique pathological features of tissue healing by magnamosis and revealed the changes in landmark molecule expression levels related to collagen synthesis and tissue hypoxia. Forty-eight male Sprague-Dawley rats were divided into the magnamosis and suture anastomosis groups, and gastrojejunal anastomosis surgery was performed. Rats were dissected at 6, 24, and 48 h and 5, 6, 8, 10, and 12 days postoperatively. Hematoxylin, eosin, and Masson's trichrome staining were used to evaluate granulation tissue proliferation and collagen synthesis density at the anastomosis site. Immunohistochemistry was used to measure TGF-ß1 and HIF-1α expression levels. Magnamosis significantly shortened the operation time, resulting in weaker postoperative abdominal adhesions (P < 0.0001). Histopathological results showed a significantly lower granulation area in the magnamosis group than in the suture anastomosis group (P = 0.0388), with no significant difference in the density of collagen synthesis (P = 0.3631). Immunohistochemistry results indicated that the magnamosis group had significantly lower proportions of TGF-ß1-positive cells at 24 (P = 0.0052) and 48 h (P = 0.0385) postoperatively and HIF-1α-positive cells at 24 (P = 0.0402) and 48 h postoperatively (P = 0.0005). In a rat model of gastrojejunal anastomosis, magnamosis leads to improved tissue healing at the gastrojejunal anastomosis, associated with downregulated expression levels of TGF-ß1 and HIF-1α.
Assuntos
Anastomose Cirúrgica , Subunidade alfa do Fator 1 Induzível por Hipóxia , Ratos Sprague-Dawley , Fator de Crescimento Transformador beta1 , Cicatrização , Animais , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Masculino , Ratos , Jejuno/cirurgia , Jejuno/metabolismo , Regulação para Baixo , Colágeno/metabolismo , Estômago/cirurgia , Estômago/patologiaAssuntos
Inteligência Artificial , Aprendizado Profundo , Mucosa Gástrica , Humanos , Mucosa Gástrica/patologia , Algoritmos , Biópsia/métodos , Estômago/patologia , Neoplasias Gástricas/patologia , Neoplasias Gástricas/diagnóstico , Consenso , Bases de Dados Factuais , Controle de Qualidade , Processamento de Imagem Assistida por Computador/métodosRESUMO
The mammalian gastrointestinal tract hosts a significant microbial symbiont community, an intriguing feature of this complex organ system. This study aimed to investigate the anti-inflammatory, antioxidant, and protective effects of caffeic acid phenethyl ester (CAPE) against Enterococcus faecalis infection in the stomach at a dose of 106 CFU in Swiss mice. A total of 30 mice were randomly assigned to three groups of ten mice each. Group I was the negative control, Group II was infected orally with E. faecalis for 18 days, and Group III was infected with E. faecalis and treated with CAPE orally at a daily dose of 4 mg/kg for 18 days. We assessed the antioxidant activities of stomach homogenate and the immunohistochemical expressions of the transcription factor nuclear factor kappa B (NF-κB) and proliferating cell nuclear antigen (PCNA). Histopathological examination was performed on the stomachs of all mice. Group II had decreased levels of antioxidant activity and positive expressions of NF-κB and PCNA. Histological observations revealed an increase in mucosal and glandular thickness compared with Group I. Group III, treated with CAPE, showed a significant increase in antioxidant activities and a significant decrease in NF-κB and PCNA immunoreactivities compared with Group II. In addition, Group III showed restoration of the normal thickness of the non-glandular and glandular parts of the stomach. Our results revealed that E. faecalis infection has damaging effects on the stomach and proved that CAPE has promising protective, anti-inflammatory, and antioxidant effects against E. faecalis. Further studies may investigate the potential therapeutic effects of CAPE against E. faecalis infection.
Assuntos
Antioxidantes , Ácidos Cafeicos , Enterococcus faecalis , NF-kappa B , Álcool Feniletílico , Animais , Ácidos Cafeicos/farmacologia , Ácidos Cafeicos/uso terapêutico , Álcool Feniletílico/análogos & derivados , Álcool Feniletílico/farmacologia , Álcool Feniletílico/uso terapêutico , NF-kappa B/metabolismo , Enterococcus faecalis/efeitos dos fármacos , Camundongos , Antioxidantes/farmacologia , Infecções por Bactérias Gram-Positivas/tratamento farmacológico , Estômago/patologia , Estômago/efeitos dos fármacos , Estômago/microbiologia , Masculino , Antígeno Nuclear de Célula em Proliferação/metabolismo , Mucosa Gástrica/efeitos dos fármacos , Mucosa Gástrica/patologia , Mucosa Gástrica/microbiologia , Mucosa Gástrica/metabolismoRESUMO
Helicobacter pylori infection predisposes carriers to a high risk of developing gastric cancer. The cell-of-origin of antral gastric cancer is the Lgr5+ stem cell. Here, we show that infection of antrum-derived gastric organoid cells with H. pylori increases the expression of the stem cell marker Lgr5 as determined by immunofluorescence microscopy, qRT-PCR, and Western blotting, both when cells are grown and infected as monolayers and when cells are exposed to H. pylori in 3D structures. H. pylori exposure increases stemness properties as determined by spheroid formation assay. Lgr5 expression and the acquisition of stemness depend on a functional type IV secretion system (T4SS) and at least partly on the T4SS effector CagA. The pharmacological inhibition or genetic ablation of NF-κB reverses the increase in Lgr5 and spheroid formation. Constitutively active Wnt/ß-catenin signaling because of Apc inactivation exacerbates H. pylori-induced Lgr5 expression and stemness, both of which persist even after eradication of the infection. The combined data indicate that H. pylori has stemness-inducing properties that depend on its ability to activate NF-κB signaling.
Assuntos
Infecções por Helicobacter , Helicobacter pylori , NF-kappa B , Receptores Acoplados a Proteínas G , Neoplasias Gástricas , Via de Sinalização Wnt , Animais , Camundongos , Antígenos de Bactérias/metabolismo , Antígenos de Bactérias/genética , Proteínas de Bactérias/metabolismo , Proteínas de Bactérias/genética , Mucosa Gástrica/metabolismo , Mucosa Gástrica/microbiologia , Infecções por Helicobacter/metabolismo , Infecções por Helicobacter/microbiologia , Células-Tronco Neoplásicas/metabolismo , Células-Tronco Neoplásicas/microbiologia , NF-kappa B/metabolismo , Organoides/metabolismo , Organoides/microbiologia , Receptores Acoplados a Proteínas G/metabolismo , Receptores Acoplados a Proteínas G/genética , Células-Tronco/metabolismo , Estômago/microbiologia , Estômago/patologia , Neoplasias Gástricas/microbiologia , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/genética , Neoplasias Gástricas/patologia , Sistemas de Secreção Tipo IV/metabolismo , Sistemas de Secreção Tipo IV/genética , Via de Sinalização Wnt/genéticaRESUMO
BACKGROUND: Metamizole is banned in some countries because of its toxicity, although it is widely used in some European countries. In addition, there is limited information on its safety profile, and it is still debated whether it is toxic to the heart, lungs, liver, kidneys, and stomach. AIMS: Our study investigated the effects of metamizole on the heart, lung, liver, kidney, and stomach tissues of rats. METHODS: Eighteen rats were divided into three groups, wassix healthy (HG), 500 mg/kg metamizole (MT-500), and 1000 mg/kg metamizole (MT-1000). Metamizole was administered orally twice daily for 14 days. Meanwhile, the HG group received pure water orally. Biochemical, histopathologic, and macroscopic examinations were performed on blood samples and tissues. RESULTS: Malondialdehyde (MDA), total glutathione (tGSH), superoxide dismutase (SOD), and catalase (CAT) in the lung and gastric tissues of MT-500 and MT-1000 groups were almost the same as those of the HG (p > 0.05). However, MDA levels in the heart and liver tissues of MT-500 and MT-1000 groups were higher (p < 0.05) compared to the HG, while tGSH levels and SOD, and CAT activities were lower (p < 0.05). MDA levels of MT-500 and MT-1000 groups in the kidney tissue increased the most (p < 0.001), and tGSH levels and SOD and CAT activities decreased the most (p < 0.001) compared to HG. Metamizole did not cause oxidative damage in the lung and gastric tissue. While metamizole did not change troponin levels, it significantly increased alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), and creatinine levels compared to HG. Histopathologically, mild damage was detected in heart tissue, moderate damage in liver tissue, and severe damage in renal tissue. However, no histopathologic damage was found in any groups' lung and gastric tissues. CONCLUSION: Metamizole should be used under strict control in patients with cardiac and liver diseases and it would be more appropriate not to use it in patients with renal disease.
Assuntos
Anti-Inflamatórios não Esteroides , Dipirona , Coração , Rim , Fígado , Pulmão , Estômago , Animais , Dipirona/toxicidade , Rim/efeitos dos fármacos , Rim/patologia , Rim/metabolismo , Fígado/efeitos dos fármacos , Fígado/patologia , Fígado/metabolismo , Pulmão/efeitos dos fármacos , Pulmão/patologia , Pulmão/metabolismo , Anti-Inflamatórios não Esteroides/toxicidade , Masculino , Ratos , Coração/efeitos dos fármacos , Estômago/efeitos dos fármacos , Estômago/patologia , Malondialdeído/metabolismo , Superóxido Dismutase/metabolismo , Glutationa/metabolismo , Catalase/metabolismo , Miocárdio/patologia , Miocárdio/metabolismoRESUMO
BACKGROUND Gastric bezoars are a relatively rare condition. We aim to summarize the clinical characteristics and endoscopic features of patients with gastric bezoars, and analyze the treatment process. MATERIAL AND METHODS The medical records of 44 patients with gastric bezoars treated at Henan Provincial People's Hospital from September 2017 to December 2023 were retrospectively reviewed. RESULTS Among the 44 patients, there were 20 males and 24 females. The average age was 55.36±15.17 years. Abdominal pain was the primary symptom in patients with gastric bezoars. Single gastric bezoars were more common than multiple ones, accounting for 86.4% of all cases. Endoscopic examination revealed ulcers in 36 (81.8%) patients, mainly at the gastric angle and antrum. Single ulcers were more common than multiple ulcers, with most ulcer diameters being less than 2 cm. The occurrence of ulcers was not significantly related to patient age or the size of the bezoars. Endoscopic examination confirmed complete clearance of gastric bezoars in 30 patients. In the 26 patients treated successfully under endoscopy, the number of endoscopic treatments ranged from 1 to 4, with an average of 1.27 interventions per patient. The interval for the second endoscopic re-examination ranged from 2 to 6 days, with an average of 3.87±1.22 days. CONCLUSIONS The most common type of gastric bezoar is phytobezoars. There is a close association between ulcer formation and gastric bezoars. Endoscopic therapy combined with oral treatment can effectively treat gastric bezoars. Most patients require only 1 endoscopic treatment to be successful. The appropriate interval for a follow-up endoscopy after the first endoscopic treatment is around 4 days.
Assuntos
Bezoares , Estômago , Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Estudos Retrospectivos , Adulto , Estômago/patologia , Idoso , Dor Abdominal , ChinaRESUMO
BACKGROUND: Dual-layer spectral-detector computed tomography (DLCT) may have the potential to evaluate gastric wall thickening. PURPOSE: To evaluate the efficacy of DLCT quantitative parameters in differentiating between benign and malignant thickening of the gastric wall. MATERIAL AND METHODS: A total of 58 patients with "gastric wall thickening" who underwent multi-phase abdominal enhanced DLCT scans were included in this study. Of these patients, 33 were malignant and 25 were benign. Parameters such as iodine concentration (IC), effective atomic number (Zeff), and attenuation of the lesions were measured during the arterial phase (AP) and venous phase (VP). Binary logistic regression was employed to calculate the combined prediction probabilities. The accuracy of the DLCT parameters was assessed using receiver operating characteristic (ROC) curves. RESULTS: The values of IC, nIC, Zeff, normalized Zeff, and attenuation in the AP and VP were significantly higher (all P < 0.05) in the malignant group compared to the benign group. The ROC curves revealed that the IC, Zeff, and attenuation in the VP exhibited high diagnostic performance, with area under the ROC curve (AUC) values of 0.864, 0.862, and 0.840, respectively. The new combination of these three factors and gastric wall thickness had an AUC of 0.884, and the sensitivity and specificity were determined to be 81.8% and 92.0%, respectively. CONCLUSION: Spectral CT parameters, particularly the combination of gastric wall thickness, attenuation, IC, and Zeff in VP, have value in distinguishing between benign and malignant gastric wall thickening.
Assuntos
Neoplasias Gástricas , Tomografia Computadorizada por Raios X , Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Neoplasias Gástricas/diagnóstico por imagem , Neoplasias Gástricas/patologia , Diagnóstico Diferencial , Tomografia Computadorizada por Raios X/métodos , Idoso , Adulto , Sensibilidade e Especificidade , Estômago/diagnóstico por imagem , Estômago/patologia , Meios de Contraste , Estudos Retrospectivos , Idoso de 80 Anos ou mais , Reprodutibilidade dos TestesRESUMO
Impaired E-cadherin (Cdh1) functions are closely associated with cellular dedifferentiation, infiltrative tumor growth and metastasis, particularly in gastric cancer. The class-I carcinogen Helicobacter pylori (H. pylori) colonizes gastric epithelial cells and induces Cdh1 shedding, which is primarily mediated by the secreted bacterial protease high temperature requirement A (HtrA). In this study, we used human primary epithelial cell lines derived from gastroids and mucosoids from different healthy donors to investigate HtrA-mediated Cdh1 cleavage and the subsequent impact on bacterial pathogenesis in a non-neoplastic context. We found a severe impairment of Cdh1 functions by HtrA-induced ectodomain cleavage in 2D primary cells and mucosoids. Since mucosoids exhibit an intact apico-basal polarity, we investigated bacterial transmigration across the monolayer, which was partially depolarized by HtrA, as indicated by microscopy, the analyses of the transepithelial electrical resistance (TEER) and colony forming unit (cfu) assays. Finally, we investigated CagA injection and observed efficient CagA translocation and tyrosine phosphorylation in 2D primary cells and, to a lesser extent, similar effects in mucosoids. In summary, HtrA is a crucially important factor promoting the multistep pathogenesis of H. pylori in non-transformed primary gastric epithelial cells and organoid-based epithelial models.
Assuntos
Proteínas de Bactérias , Caderinas , Células Epiteliais , Mucosa Gástrica , Helicobacter pylori , Organoides , Humanos , Caderinas/metabolismo , Organoides/metabolismo , Células Epiteliais/metabolismo , Células Epiteliais/microbiologia , Mucosa Gástrica/metabolismo , Mucosa Gástrica/microbiologia , Mucosa Gástrica/patologia , Proteínas de Bactérias/metabolismo , Proteínas de Bactérias/genética , Antígenos de Bactérias/metabolismo , Infecções por Helicobacter/metabolismo , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/patologia , Antígenos CD/metabolismo , Estômago/microbiologia , Estômago/patologia , Linhagem Celular , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia , Neoplasias Gástricas/microbiologia , Serina ProteasesRESUMO
BACKGROUND: Gastric cancer (GC) is the most common malignant tumor and ranks third for cancer-related deaths among the worldwide. The disease poses a serious public health problem in China, ranking fifth for incidence and third for mortality. Knowledge of the invasive depth of the tumor is vital to treatment decisions. AIM: To evaluate the diagnostic performance of double contrast-enhanced ultrasonography (DCEUS) for preoperative T staging in patients with GC by comparing with multi-detector computed tomography (MDCT). METHODS: This single prospective study enrolled patients with GC confirmed by preoperative gastroscopy from July 2021 to March 2023. Patients underwent DCEUS, including ultrasonography (US) and intravenous contrast-enhanced ultrasonography (CEUS), and MDCT examinations for the assessment of preoperative T staging. Features of GC were identified on DCEUS and criteria developed to evaluate T staging according to the 8th edition of AJCC cancer staging manual. The diagnostic performance of DCEUS was evaluated by comparing it with that of MDCT and surgical-pathological findings were considered as the gold standard. RESULTS: A total of 229 patients with GC (80 T1, 33 T2, 59 T3 and 57 T4) were included. Overall accuracies were 86.9% for DCEUS and 61.1% for MDCT (P < 0.001). DCEUS was superior to MDCT for T1 (92.5% vs 70.0%, P < 0.001), T2 (72.7% vs 51.5%, P = 0.041), T3 (86.4% vs 45.8%, P < 0.001) and T4 (87.7% vs 70.2%, P = 0.022) staging of GC. CONCLUSION: DCEUS improved the diagnostic accuracy of preoperative T staging in patients with GC compared with MDCT, and constitutes a promising imaging modality for preoperative evaluation of GC to aid individualized treatment decision-making.
Assuntos
Meios de Contraste , Tomografia Computadorizada Multidetectores , Estadiamento de Neoplasias , Neoplasias Gástricas , Ultrassonografia , Humanos , Neoplasias Gástricas/diagnóstico por imagem , Neoplasias Gástricas/patologia , Neoplasias Gástricas/cirurgia , Pessoa de Meia-Idade , Masculino , Feminino , Meios de Contraste/administração & dosagem , Estudos Prospectivos , Idoso , Ultrassonografia/métodos , Ultrassonografia/estatística & dados numéricos , Tomografia Computadorizada Multidetectores/métodos , Adulto , China/epidemiologia , Gastroscopia/métodos , Estômago/diagnóstico por imagem , Estômago/patologia , Estômago/cirurgia , Idoso de 80 Anos ou maisRESUMO
We evaluate the value of oral contrast-enhanced gastric ultrasonography (OCUS) by comparing it with conventional gastroscopy in diagnosing and staging benign peptic ulcer. From July 2018 to December 2020, 44 patients with gastroscopy-confirmed benign peptic ulcers (a total of 45 ulcers were detected), who also received OCUS, were retrospectively reviewed. Each patient's ultrasound images were compared with gastroscopy and pathology findings. The characteristics of ultrasonic images of different stages of ulcer were analysed. A total of 43 ulcers were detected by OCUS in 44 patients with benign peptic ulcers. There were no false positive results among the OCUS exams, but two ulcers were misdiagnosed. OCUS for benign peptic ulcer staging also shows acceptable clinical practice results. OCUS is useful for detecting and staging benign peptic ulcer, and may be considered an alternative method for conventional gastroscopy. OCUS is especially useful in the follow-up of BPU treatment, but futher study is needed to improve the diagnostic accuracy of benign and malignant ulcers.
Assuntos
Meios de Contraste , Úlcera Péptica , Ultrassonografia , Humanos , Masculino , Feminino , Ultrassonografia/métodos , Pessoa de Meia-Idade , Úlcera Péptica/diagnóstico por imagem , Úlcera Péptica/patologia , Idoso , Adulto , Estudos Retrospectivos , Gastroscopia/métodos , Estômago/diagnóstico por imagem , Estômago/patologia , Idoso de 80 Anos ou mais , Úlcera Gástrica/diagnóstico por imagem , Úlcera Gástrica/patologiaRESUMO
Sarcina ventriculi is a bacterium with a specific histological morphology and infection can present with symptoms such as abdominal pain, nausea, vomiting and occasionally fatal complications. Delayed gastric emptying is regarded as the most significant risk factor for infection. Its pathogenicity is currently unknown and treatment options are inconsistent. Here we report a case of gastric bezoars secondary to a mixed infection of Sarcina ventriculi and G + bacilli, which is diagnosed by a pathological biopsy.
Assuntos
Bezoares , Sarcina , Humanos , Sarcina/isolamento & purificação , Coinfecção/microbiologia , Masculino , Estômago/microbiologia , Estômago/patologia , Feminino , Pessoa de Meia-IdadeRESUMO
Helicobacter pylori is a common resident in the stomach of at least half of the world's population and recent evidence suggest its emergence in other organs such as the pancreas. In this organ, the presence of H. pylori DNA has been reported in cats, although the functional implications remain unknown. In this work, we determined distinct features related to the H. pylori manifestation in pancreas in a rodent model, in order to analyse its functional and structural effect. Gerbils inoculated with H. pylori exhibited the presence of this bacterium, as revealed by the expression of some virulence factors, as CagA and OMPs in stomach and pancreas, and confirmed by urease activity, bacterial culture, PCR and immunofluorescence assays. Non-apparent morphological changes were observed in pancreatic tissue of infected animals; however, delocalization of intercellular junction proteins (claudin-1, claudin-4, occludin, ZO-1, E-cadherin, ß-catenin, desmoglein-2 and desmoplakin I/II) and rearrangement of the actin-cytoskeleton were exhibited. This structural damage was consistent with alterations in the distribution of insulin and glucagon, and a systemic inflammation, event demonstrated by elevated IL-8 levels. Overall, these findings indicate that H. pylori can reach the pancreas, possibly affecting its function and contributing to the development of pancreatic diseases.
Assuntos
Gerbillinae , Infecções por Helicobacter , Helicobacter pylori , Junções Intercelulares , Pâncreas , Animais , Helicobacter pylori/patogenicidade , Helicobacter pylori/genética , Infecções por Helicobacter/microbiologia , Pâncreas/microbiologia , Pâncreas/patologia , Junções Intercelulares/microbiologia , Proteínas de Bactérias/metabolismo , Proteínas de Bactérias/genética , Antígenos de Bactérias/metabolismo , Antígenos de Bactérias/genética , Fatores de Virulência/metabolismo , Fatores de Virulência/genética , Estômago/microbiologia , Estômago/patologia , Modelos Animais de Doenças , Masculino , Proteínas da Membrana Bacteriana Externa/metabolismo , Proteínas da Membrana Bacteriana Externa/genéticaRESUMO
BACKGROUND & AIMS: Restricted gastric motor functions contribute to aging-associated undernutrition, sarcopenia, and frailty. We previously identified a decline in interstitial cells of Cajal (ICC; gastrointestinal pacemaker and neuromodulator cells) and their stem cells (ICC-SC) as a key factor of gastric aging. Altered functionality of the histone methyltransferase enhancer of zeste homolog 2 (EZH2) is central to organismal aging. Here, we investigated the role of EZH2 in the aging-related loss of ICC/ICC-SC. METHODS: klotho mice, a model of accelerated aging, were treated with the most clinically advanced EZH2 inhibitor, EPZ6438 (tazemetostat; 160 mg/kg intraperitoneally twice a day for 3 weeks). Gastric ICC were analyzed by Western blotting and immunohistochemistry. ICC and ICC-SC were quantified by flow cytometry. Gastric slow wave activity was assessed by intracellular electrophysiology. Ezh2 was deactivated in ICC by treating KitcreERT2/+;Ezh2fl/fl mice with tamoxifen. TRP53, a key mediator of aging-related ICC loss, was induced with nutlin 3a in gastric muscle organotypic cultures and an ICC-SC line. RESULTS: In klotho mice, EPZ6438 treatment mitigated the decline in the ICC growth factor KIT ligand/stem cell factor and gastric ICC. EPZ6438 also improved gastric slow wave activity and mitigated the reduced food intake and impaired body weight gain characteristic of this strain. Conditional genomic deletion of Ezh2 in Kit-expressing cells also prevented ICC loss. In organotypic cultures and ICC-SC, EZH2 inhibition prevented the aging-like effects of TRP53 stabilization on ICC/ICC-SC. CONCLUSIONS: Inhibition of EZH2 with EPZ6438 mitigates aging-related ICC/ICC-SC loss and gastric motor dysfunction, improving slow wave activity and food intake in klotho mice.
Assuntos
Envelhecimento , Proteína Potenciadora do Homólogo 2 de Zeste , Células Intersticiais de Cajal , Piridonas , Animais , Proteína Potenciadora do Homólogo 2 de Zeste/metabolismo , Proteína Potenciadora do Homólogo 2 de Zeste/antagonistas & inibidores , Células Intersticiais de Cajal/metabolismo , Células Intersticiais de Cajal/efeitos dos fármacos , Camundongos , Piridonas/farmacologia , Estômago/patologia , Estômago/efeitos dos fármacos , Morfolinas/farmacologia , Proteínas Klotho/metabolismo , Proteína Supressora de Tumor p53/metabolismo , Masculino , Glucuronidase/metabolismo , Benzodiazepinas/farmacologia , Mucosa Gástrica/patologia , Mucosa Gástrica/metabolismo , Mucosa Gástrica/efeitos dos fármacos , Mucosa Gástrica/citologia , Benzamidas , Compostos de BifeniloRESUMO
Reports of Helicobacter pylori (Hp)-naïve gastric neoplasm (HpNGN) cases have been rapidly increasing due to the recent increase in the Hp-naïve population in Japan. Most HpNGNs exhibit the gastric immunophenotype and a low malignant potential regardless of histological type. Especially, foveolar-type gastric adenoma (FGA) and intestinal-type gastric dysplasia (IGD) rarely progress to invasive carcinoma. FGA is a foveolar epithelial neoplasm that occurs in the fundic gland (oxyntic gland) mucosa and is classified as the flat type or raspberry type (FGA-RA). The flat type is a large, whitish flatly elevated lesion while FGA-RA is a small reddish polyp. Genomically, the flat type is characterized by APC and KRAS gene mutations and FGA-RA by a common single nucleotide variant in the KLF4 gene. This KLF4 single-nucleotide variant reportedly induces gastric foveolar epithelial tumorigenesis and activates both cell proliferation and apoptosis, leading to its slow-growing nature. IGD consists of an intestinalized epithelial dysplasia that develops in the pyloric gland mucosa, characterized as a superficial depressed lesion surrounded by raised mucosa showing a gastritis-like appearance. Immunohistochemically, it exhibits an intestinal or gastrointestinal phenotype and, frequently, p53 overexpression. Thus, IGD shows unique characteristics in HpNGNs and a potential multistep tumorigenic process.
Assuntos
Adenoma , Mucosa Gástrica , Helicobacter pylori , Fator 4 Semelhante a Kruppel , Neoplasias Gástricas , Humanos , Neoplasias Gástricas/patologia , Neoplasias Gástricas/microbiologia , Adenoma/patologia , Adenoma/microbiologia , Mucosa Gástrica/patologia , Mucosa Gástrica/microbiologia , Helicobacter pylori/isolamento & purificação , Infecções por Helicobacter/patologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/microbiologia , Lesões Pré-Cancerosas/patologia , Lesões Pré-Cancerosas/microbiologia , Proteínas Proto-Oncogênicas p21(ras)/genética , Mutação , Estômago/patologia , Estômago/microbiologiaRESUMO
Helicobacter pylori is a microaerophilic Gram-negative bacterium that resides in the human stomach and is classified as a class I carcinogen for gastric cancer. Numerous studies have demonstrated that H. pylori infection plays a role in regulating the function of host cells, thereby contributing to the malignant transformation of these cells. However, H. pylori infection is a chronic process, and short-term cellular experiments may not provide a comprehensive understanding of the in vivo situation, especially when considering the lower oxygen levels in the human stomach. In this study, we aimed to investigate the mechanisms underlying gastric cell dysfunction after prolonged exposure to H. pylori under hypoxic conditions. We conducted a co-culture experiment using the gastric cell line GES-1 and H. pylori for 30 generations under intermittent hypoxic conditions. By closely monitoring cell proliferation, migration, invasion, autophagy, and apoptosis, we revealed that sustained H. pylori stimulation under hypoxic conditions significantly influences the function of GES-1 cells. This stimulation induces epithelial-mesenchymal transition and contributes to the propensity for malignant transformation of gastric cells. To confirm the in vitro results, we conducted an experiment involving Mongolian gerbils infected with H. pylori for 85 weeks. All the results strongly suggest that the Nod1 receptor signaling pathway plays a crucial role in H. pylori-related apoptosis and autophagy. In summary, continuous stimulation by H. pylori affects the functioning of gastric cells through the Nod1 receptor signaling pathway, increasing the likelihood of cell carcinogenesis. The presence of hypoxic conditions further exacerbates this process.IMPORTANCEDeciphering the collaborative effects of Helicobacter pylori infection on gastric epithelial cell function is key to unraveling the development mechanisms of gastric cancer. Prior research has solely examined the outcomes of short-term H. pylori stimulation on gastric epithelial cells under aerobic conditions, neglecting the bacterium's nature as a microaerophilic organism that leads to cancer following prolonged stomach colonization. This study mimics a more genuine in vivo infection scenario by repeatedly exposing gastric epithelial cells to H. pylori under hypoxic conditions for up to 30 generations. The results show that chronic exposure to H. pylori in hypoxia substantially increases cell migration, invasion, and epithelial-mesenchymal transition, while suppressing autophagy and apoptosis. This highlights the significance of hypoxic conditions in intensifying the carcinogenic impact of H. pylori infection. By accurately replicating the in vivo gastric environment, this study enhances our comprehension of H. pylori's pathogenic mechanisms in gastric cancer.
Assuntos
Transformação Celular Neoplásica , Células Epiteliais , Transição Epitelial-Mesenquimal , Mucosa Gástrica , Gerbillinae , Infecções por Helicobacter , Helicobacter pylori , Neoplasias Gástricas , Helicobacter pylori/patogenicidade , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/patologia , Animais , Neoplasias Gástricas/microbiologia , Neoplasias Gástricas/patologia , Humanos , Células Epiteliais/microbiologia , Mucosa Gástrica/microbiologia , Mucosa Gástrica/patologia , Hipóxia/microbiologia , Linhagem Celular , Proliferação de Células , Apoptose , Movimento Celular , Autofagia , Estômago/microbiologia , Estômago/patologiaRESUMO
A 35-year-old female patient with hypothyroidism and Ehler-Danlos syndrome presents with fatigue, abdominal distension, and dyspnea. What is your diagnosis?