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| Itt írjon a(z) Helicobacter_stomach-ról/ről | . ''<<TableOfContents>>'' = 1. Abstract = = 2. Introduction = = 3. Helicobacter pylori = == 3.1 Definition, characteristic of helicobacter pylori == == 3.2 physiological background == == 3.3 pathophysiology and gastric pathology == Helicobacter.pylori is presumed to be transmitted through the oral or fecal route, and for humans, it has a very high infection rate within the family. In the stomach of individuals infected with H.pylori, H.pylori produces urease, decomposes the urea component of the stomach and reduces the acidity of the surrounding area. H.pylori migrates in the stomach using flagella, and adheres to the gastric epithelial cells through adhesion factors such as BabA. H.pylori does not always cause acute non-specific digestive symptoms, however, it is reported that H.pylori leads to chronic gastrointestinal diseases around 10-20% of the case. The complex interaction between virulence factors such as CagA and VacA, which were secreted by Helicobacter. pylori, preservation of the mucous membrane of the body, and other environmental factors are implicated in causing H. pylori-borne diseases. The immune response of the body activates for H. pylori infection, but it is known to accelerate damage to the gastric mucosa rather than removing the source of infection(virulence factors). Helicobacter. pylori causes antrum-predominant gastritis, promotes gastrin secretion, inhibits somatostatin secretion, and leads duodenal ulcer. It is also reported that H. pylori inhibits gastric acid secretion, causes pangastritis or corpus predominant gastritis, and leads gastric ulcer and gastric cancer. Helicobacter. Pylori is known as the main factor to cause intestinal type gastric cancer through the sequential process of atrophic gastritis, intestinal meta-plasia and dysplasia. It is reported that H. pylori was the main factor of gastric cancers in 71-95% cases, but conversely, not all H. pylori-infected patients got gastric cancer (less than 1% of H. pylori-infected patients had gastric cancer). It is estimated that cancer occurs due to multifactorial etiology such as genetic factors, diet, and the characteristics of the bacteria themselves. Primary gastric displacement zone B-cell lymphoma accounts for 1-7% of malignant tumors in the stomach, but is known to be the most common type, accounting for 50-60% of all gastrointestinal lymphomas. Up to 98% of gastric B-cell lymphomas and 30% of H. pylori infections produce lymphoid follicles through the inflammatory reaction of the mucous membrane, which is presumed to be a precursor to marginal B-cell lymphoma. In about 60% of patients complaining of symptoms of functional dyspepsia are diagnosed as functional dyspepsia, it shows a prevalence rate of 11-14% and no organic diseases are found through endoscopy and/or radiological examination, etc. However, the diseases such as Postprandial discomfort, bloating, epigastric pain, heartburn, etc. occur chronically and recurrently. Research says that 40 to 70% of functional indigestion is caused by H. pylori infection, and chronic gastric inflammation by H. pylori infection was suggested as a mechanism of the functional dyspepsia occurrence. Inflammatory reaction activated by chronic infection causes abnormalities in gastrointestinal motility and awareness due to hyper hormones and changes in gastric acid secretion. == 3.4 clinical presentation == === 3.4.1 symptoms === As aforesaid, Helicobacter bacteria is presumed to be transmitted through oral-oral and fecal-oral routes. However, it is speculated and not clearly confirmed, and vector transmission can occur. In a specific area, waterborne sources of infection may be important to Helicobacter bacteria infection. Helicobacters have the potential to infect animals as well as humans. Helicobacter species have been identified in dog saliva and tartar, and possibly have oral-to-oral transmission. It supports the concerns about oral-to-oral transmission between dog-to-dog or dog-to-human. H. pylori is rarely isolated in cats (rather than dogs). Although, the possibility of animal infection is a reasonable concern. In the human body, H. pylori infection has been associated with an increased risk of peptic ulcer disease and gastric cancer. H. canis, H. felis, H. heilmannii infections are believed to be acquired in dogs and cats, and have been reported along with associated bacteremia, peptic ulcer disease, and gastritis. Anthropozoonosis (human-animal transmission) can occur in cats. Several types of Helicobacter have been found in dogs and cats. In dogs, H. felis, H. bizzozeronii, H. salomonis, H. bilis, H. heilmannii, and Flexispira rappini were observed. For cats, H. felis, H. pametensis, H. pylori, H. heilmannii. About 41%-100% of healthy cats and 57%-100% of vomiting cats have Helicobacter-like organisms. Gastritis caused by Helicobacter bacteria varies in severity and is often lymphoplasmacytic. Whether gastric erosion and ulcers occur in infected dogs or cats is still under discussion.It is still unknown whether human pathophysiological mechanisms, namely the production of ammonia by bacterial urease and other secretions that damage epithelial cells and induce gastric acid secretion occur in dogs and cats. Helicobacter species are not critically pathogenic in all dogs and cats. Helicobacter is often found accidentally in histological examination of a gastric biopsy. The diagnosis of Helicobacter infection is difficult to confirm by gastric biopsy, and the pathogenic importance of dogs and cats is controversial. If possible, an underlying diagnosis should be sought in animals with gastrointestinal symptoms or ulcers. Helicobacter organisms can be identified even in healthy animals. Most common symptoms may include chronic vomiting, intermittent loss of appetite, and acute gastritis with marked vomiting and loss of appetite (with gastric palsy) with a small probability. These cases are reported to be more common in hospitalized dogs and in dogs who have recently been exposed to the stool of other dogs in kennels, salons or veterinary clinics. === 3.4.2 diagnostics === === 3.4.3 treatments === === 3.4.4 virulence factors === = 4. Conclusion = = 5. References = McColl KE. Clinical practice. Helicobacter pylori infection. N Engl J Med 2010;362:1597-1604. ,Yim JY, Kim N, Choi SH, et al. Seroprevalence of Helico- bacter pylori in South Korea. Helicobacter 2007;12:333-340. .Lim SH, Kwon JW, Kim N, et al. Prevalence and risk factors of Helicobacter pylori infection in Korea: nationwide multi- center study over 13 years. BMC Gastroenterol 2013;13:104. Lee JY, Kim N. Future trends of Helicobacter pylori erad- ication therapy in Korea. Korean J Gastroenterol 2014;63:158-170. Lee JH, Lee YC, Jeon SW, Kim JW, Lee SW; Korean College of Helicobacter and Upper Gastrointestinal Research; Korean Association of Gastroenterology. Guidelines of pre- vention and treatment for NSAID-related peptic ulcers. Korean J Gastroenterol 2009;54:309-317. W Prachasilpchai, et al.: Diagnosis of Helicobacter spp. infection in canine stomach. J Vet Sci. 8:139 2007 17519566 C Recordati, et al.: Spatial distribution of Helicobacter spp. in the gastrointestinal tract of dogs. Helicobacter . 14:180 2009 19702848 R Sapierzyniski, et al.: The diagnosis of gastritis and Helicobacter -like organisms infection in endoscopic biopsies of the canine gastric mucosa. Pol J Vet Sci. 9:17 2006 16573271 Shantha A, Taslima T L, Jazmin G, Irina V P, Ellen J B, Victor E B (2014): Effect of Helicobacter pylori on gastric epithelial cells 20(36): 12767–12780 Breno B, Filipe S, Aline S, Vinicious A, Maria S, Pedro M, Mariana S, Fabricio M (2019) Pathogenesis and clinical management of Helicobacter pylori gastric infection. 25(37): 5578–5589 ---- CategoryCategory |
1. Abstract
2. Introduction
3. Helicobacter pylori
3.1 Definition, characteristic of helicobacter pylori
3.2 physiological background
3.3 pathophysiology and gastric pathology
Helicobacter.pylori is presumed to be transmitted through the oral or fecal route, and for humans, it has a very high infection rate within the family. In the stomach of individuals infected with H.pylori, H.pylori produces urease, decomposes the urea component of the stomach and reduces the acidity of the surrounding area. H.pylori migrates in the stomach using flagella, and adheres to the gastric epithelial cells through adhesion factors such as BabA. H.pylori does not always cause acute non-specific digestive symptoms, however, it is reported that H.pylori leads to chronic gastrointestinal diseases around 10-20% of the case.
The complex interaction between virulence factors such as CagA and VacA, which were secreted by Helicobacter. pylori, preservation of the mucous membrane of the body, and other environmental factors are implicated in causing H. pylori-borne diseases. The immune response of the body activates for H. pylori infection, but it is known to accelerate damage to the gastric mucosa rather than removing the source of infection(virulence factors). Helicobacter. pylori causes antrum-predominant gastritis, promotes gastrin secretion, inhibits somatostatin secretion, and leads duodenal ulcer. It is also reported that H. pylori inhibits gastric acid secretion, causes pangastritis or corpus predominant gastritis, and leads gastric ulcer and gastric cancer.
Helicobacter. Pylori is known as the main factor to cause intestinal type gastric cancer through the sequential process of atrophic gastritis, intestinal meta-plasia and dysplasia. It is reported that H. pylori was the main factor of gastric cancers in 71-95% cases, but conversely, not all H. pylori-infected patients got gastric cancer (less than 1% of H. pylori-infected patients had gastric cancer). It is estimated that cancer occurs due to multifactorial etiology such as genetic factors, diet, and the characteristics of the bacteria themselves.
Primary gastric displacement zone B-cell lymphoma accounts for 1-7% of malignant tumors in the stomach, but is known to be the most common type, accounting for 50-60% of all gastrointestinal lymphomas. Up to 98% of gastric B-cell lymphomas and 30% of H. pylori infections produce lymphoid follicles through the inflammatory reaction of the mucous membrane, which is presumed to be a precursor to marginal B-cell lymphoma.
In about 60% of patients complaining of symptoms of functional dyspepsia are diagnosed as functional dyspepsia, it shows a prevalence rate of 11-14% and no organic diseases are found through endoscopy and/or radiological examination, etc. However, the diseases such as Postprandial discomfort, bloating, epigastric pain, heartburn, etc. occur chronically and recurrently.
Research says that 40 to 70% of functional indigestion is caused by H. pylori infection, and chronic gastric inflammation by H. pylori infection was suggested as a mechanism of the functional dyspepsia occurrence. Inflammatory reaction activated by chronic infection causes abnormalities in gastrointestinal motility and awareness due to hyper hormones and changes in gastric acid secretion.
3.4 clinical presentation
3.4.1 symptoms
As aforesaid, Helicobacter bacteria is presumed to be transmitted through oral-oral and fecal-oral routes. However, it is speculated and not clearly confirmed, and vector transmission can occur. In a specific area, waterborne sources of infection may be important to Helicobacter bacteria infection. Helicobacters have the potential to infect animals as well as humans.
Helicobacter species have been identified in dog saliva and tartar, and possibly have oral-to-oral transmission. It supports the concerns about oral-to-oral transmission between dog-to-dog or dog-to-human. H. pylori is rarely isolated in cats (rather than dogs). Although, the possibility of animal infection is a reasonable concern. In the human body, H. pylori infection has been associated with an increased risk of peptic ulcer disease and gastric cancer. H. canis, H. felis, H. heilmannii infections are believed to be acquired in dogs and cats, and have been reported along with associated bacteremia, peptic ulcer disease, and gastritis. Anthropozoonosis (human-animal transmission) can occur in cats.
Several types of Helicobacter have been found in dogs and cats. In dogs, H. felis, H. bizzozeronii, H. salomonis, H. bilis, H. heilmannii, and Flexispira rappini were observed. For cats, H. felis, H. pametensis, H. pylori, H. heilmannii. About 41%-100% of healthy cats and 57%-100% of vomiting cats have Helicobacter-like organisms. Gastritis caused by Helicobacter bacteria varies in severity and is often lymphoplasmacytic. Whether gastric erosion and ulcers occur in infected dogs or cats is still under discussion.It is still unknown whether human pathophysiological mechanisms, namely the production of ammonia by bacterial urease and other secretions that damage epithelial cells and induce gastric acid secretion occur in dogs and cats.
Helicobacter species are not critically pathogenic in all dogs and cats. Helicobacter is often found accidentally in histological examination of a gastric biopsy. The diagnosis of Helicobacter infection is difficult to confirm by gastric biopsy, and the pathogenic importance of dogs and cats is controversial. If possible, an underlying diagnosis should be sought in animals with gastrointestinal symptoms or ulcers.
Helicobacter organisms can be identified even in healthy animals. Most common symptoms may include chronic vomiting, intermittent loss of appetite, and acute gastritis with marked vomiting and loss of appetite (with gastric palsy) with a small probability. These cases are reported to be more common in hospitalized dogs and in dogs who have recently been exposed to the stool of other dogs in kennels, salons or veterinary clinics.
3.4.2 diagnostics
3.4.3 treatments
3.4.4 virulence factors
4. Conclusion
5. References
McColl KE. Clinical practice. Helicobacter pylori infection. N Engl J Med 2010;362:1597-1604.
,Yim JY, Kim N, Choi SH, et al. Seroprevalence of Helico- bacter pylori in South Korea. Helicobacter 2007;12:333-340.
.Lim SH, Kwon JW, Kim N, et al. Prevalence and risk factors of Helicobacter pylori infection in Korea: nationwide multi- center study over 13 years. BMC Gastroenterol 2013;13:104.
Lee JY, Kim N. Future trends of Helicobacter pylori erad- ication therapy in Korea. Korean J Gastroenterol 2014;63:158-170.
Lee JH, Lee YC, Jeon SW, Kim JW, Lee SW; Korean College of Helicobacter and Upper Gastrointestinal Research; Korean Association of Gastroenterology. Guidelines of pre- vention and treatment for NSAID-related peptic ulcers. Korean J Gastroenterol 2009;54:309-317.
W Prachasilpchai, et al.: Diagnosis of Helicobacter spp. infection in canine stomach. J Vet Sci. 8:139 2007 17519566
C Recordati, et al.: Spatial distribution of Helicobacter spp. in the gastrointestinal tract of dogs. Helicobacter . 14:180 2009 19702848
R Sapierzyniski, et al.: The diagnosis of gastritis and Helicobacter -like organisms infection in endoscopic biopsies of the canine gastric mucosa. Pol J Vet Sci. 9:17 2006 16573271
Shantha A, Taslima T L, Jazmin G, Irina V P, Ellen J B, Victor E B (2014): Effect of Helicobacter pylori on gastric epithelial cells 20(36): 12767–12780
Breno B, Filipe S, Aline S, Vinicious A, Maria S, Pedro M, Mariana S, Fabricio M (2019) Pathogenesis and clinical management of Helicobacter pylori gastric infection. 25(37): 5578–5589