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The gastrointestinal system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Sharon J. White, Francis A. Carey
Acute inflammation of the gastric mucosa has long been associated with chemical injury, particularly by alcohol and non-steroidal anti-inflammatory drugs (NSAIDs). More recently, another form of acute gastritis occurring in the early stages of H. pylori infection has been described. Acute gastritis may be subclinical, or present with abdominal pain, vomiting, and/or haemorrhage. Macroscopically, the mucosa is oedematous and congested, and may show superficial mucosal erosion (the site of blood loss). Histologically, there is capillary congestion and leakage of blood cells into the lamina propria. In erosive gastritis the superficial epithelium is lost. This picture of haemorrhagic, erosive gastritis is typical of chemical injury. H. pylori acute gastritis is characterized by a more prominent neutrophil response. Occasionally other more virulent organisms (particularly streptococci) may cause a severe, usually fatal, purulent gastritis.
Stomach and duodenum
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
Erosive gastritis has a variety of causes, especially NSAIDs. Fortunately, most such bleeding settles spontaneously, but when it does not it can be a major problem to treat. In general terms, although there is a diffuse erosive gastritis, there is one (or more) specific lesion that has a significant-sized vessel within it. This should be dealt with appropriately, preferably endoscopically, but sometimes surgery is necessary.
Stomach and duodenum
Published in Michael Gaunt, Tjun Tang, Stewart Walsh, General Surgery Outpatient Decisions, 2018
There are four main types of gastritis. Type A is an autoimmune condition. Circulating parietal cell antibodies cause pernicious anaemia with achlorhydria and absent intrinsic factor. The antrum is spared, so serum gastrin levels are high due to alkaline conditions. There is significant increased risk of development of carcinoma, usually of the diffuse type.Type B begins distally in the pyloric region due to H. pylori infection. Gastrin levels are normal. It is always present in duodenal ulceration.Lymphocytic gastritis involves infiltration of the gastric epithelium by T lymphocytes. OGD shows nodularity, erosions and enlarged mucosal folds.Erosive gastritis is caused by NSAIDs and alcohol.Other causes include reflux, stress, granulomatous (TB, Crohn’s) gastritis, cystica polyposa, AIDS gastritis, eosinophilic gastritis, Ménétrier’s disease, suppurative gastritis, and emphysematous gastritis.
Immune thrombocytopenic purpura secondary to Helicobacter pylori
Published in Baylor University Medical Center Proceedings, 2022
Lintu Ramachandran, Luqman Baloch, Taha Mohamed Djirdeh, Yadwinder Sidhu, Nicole Gentile, Mario Affinati
Initial laboratory results showed a platelet count of <3000/µL, leukocyte count of 14,500/µL, and hemoglobin of 11.3 g/dL, with a mean corpuscular volume of 82.8 fL. Lactate dehydrogenase, haptoglobin, iron, and ferritin were normal. An ADAMTS13 level was normal at 6 units/mL. The patient was diagnosed with ITP, given 10 mg of oral dexamethasone, and started on a pantoprazole drip for concern of an acute upper gastrointestinal bleed. His repeat platelet count improved to 7000/µL in 4 hours. Thereafter, he developed another episode of hematemesis with 500 mL of bright red blood. He was taken urgently for upper endoscopy, which demonstrated diffuse erosive gastritis (Figure 1). His bleeding resolved without further episodes of hematemesis. The pantoprazole drip was continued due to the severity of his thrombocytopenia, along with treatment of his ITP, which included intravenous immunoglobulin, with a 1 g/kg one-time dose and daily 40 mg dexamethasone orally for 4 days.
Successful early introduction of mepolizumab for peripheral neuropathy with a peripheral circulatory disorder in a patient with myeloperoxidase anti-neutrophil cytoplasmic antibody-negative eosinophilic granulomatosis with polyangiitis
Published in Modern Rheumatology Case Reports, 2021
Masahiro Nishihara, Marina Hamaguchi, Natsumi Ikumi, Atsuma Nishiwaki, Kaita Sugiyama, Yosuke Nagasawa, Hiroshi Tsuzuki, Shoei Yoshizawa, Yutaka Tanikawa, Shinya Asatani, Hitomi Kobayashi, Masami Takei, Noboru Kitamura
Laboratory findings were as follows: white blood cell count was 16200/μL (neutrophils, 64%; eosinophils, 27%; basophils, 0%; monocytes, 1%; and leukocytes, 8%), haemoglobin level of 15.5 g/dL, and platelet count of 35.3 × 104/μL. Liver function tests were normal: blood urea nitrogen level of 4.6 mg/dL, creatinine level of 0.51 mg/dL, total protein count of 8.1 g/dL, albumin level of 4.4 g/dL, C-reactive protein level of 0.80 mg/dL, anti-nuclear antibody negative, 50% haemolytic complement activity of 42.5 U/mL, proteinase 3-ANCA < 1.0 U/mL, MPO-ANCA < 1.0 U/mL, soluble interleukin 2 receptors 1810 U/mL, serum immunoglobulin G (IgG) level of 1415 mg/dL, IgA 118 mg/dL, IgM 169 mg/dL, and IgE 702 mg/dL. Urine protein and occult blood test results were negative. Bone marrow aspiration did not reveal eosinophilic leukaemia. Contrast-enhanced abdominal computed tomography (CT) revealed thickness and edoema on the wall of the small intestine without any ascites. A head CT scan revealed thickening of the nasal mucosa and accumulation of mucus in both maxillary sinuses. The nasal mucosa revealed marked eosinophilic infiltration of the blood vessels in the subcutaneous tissue (Figure 1). T2-weighted short-tau inversion recovery imaging revealed patchy high-intensity areas in muscles. The SPP of the dorsal right foot was reduced to 28 mm Hg, indicating severe peripheral ischaemia. Esophagogastroduodenoscopy revealed erosive gastritis. Colonoscopy revealed multiple erosions from the sigmoid colon to the rectum (Figure 2). The pathological examination revealed mild eosinophilic infiltration.
Role of vacuolating cytotoxin A in Helicobacter pylori infection and its impact on gastric pathogenesis
Published in Expert Review of Anti-infective Therapy, 2020
Shamshul Ansari, Yoshio Yamaoka
The alteration of several cellular proteins has been linked with the development and progression of cancer. Cortactin (cortical actin-binding protein), a filamentous actin-binding protein, is an activator of actin-related protein complexes (ARP)2/3 and important molecular link between signal transduction pathways and the cytoskeleton [109110111112114–113]. In cancer tissue samples, the expression of the cortactin gene is abnormally high and is associated with cancer cell metastasis [114115116–117]. In an in-vitro study, AGS gastric epithelial cells that expressed cortactin and were treated with VacA showed a significant increase in the percentage of apoptotic cells and expression of the proapoptotic protein Bax, whereas a decrease in the expression of the antiapoptotic protein Bcl-2 was observed, suggesting the role of VacA in association with cortactin for gastric pathogenicity [118]. Similarly, the role of connexin 43 (Cx43), a member of the human Cx family, is responsible for VacA-induced cell death and gastric pathogenicity [119,120]. The Cx-family proteins are membrane proteins that form channels at gap junctions to regulate development and homeostasis via intercellular communication, cell-cell channel formation, and exchange of signaling molecules [121122–123]. A recent in-vitro study demonstrated the role of Cx43 in VacA-induced AZ-521 cell death via a Rac1/ERK-dependent pathway in H. pylori-infected gastric mucosa [124]. Elevated Cx43 level in H. pylori-infected gastric tissue is observed, which is associated with erosive gastritis.