Eradication of Helicobacter pylori inorder to eliminate or exterminate chances of Gastric Cancer:INTRODUCTION: Subsequently in 1983 after the detection ofHelicobacter pylori the underlying association among the causative agent andgastritis and gastric carcinoma has been increasingly interpreted. 1.
International agency of research particularly incancer under world health organization already has categorized helicobacterpylori as a definite carcinogen in the year 1994 2. Consequently,in numerous countries many clinical studies were carried out to judge whether eliminationof H pylori could play any significant role in preventing the gastric carcinoma.Conversely, due to less sufficient data the conclusions couldn’t be drawn toprove that h.pylori is the causative agent and its incident seem low.
A randomized study in japan was conducted inthe year 2008, that was actually multicenter discovered that eradication of Hpylori has consequently reduced the occurrence to up to two third of tributarygastric cancer after early gastric analysis of endoscopic mucosal resection. Signifyingthe effectiveness of H pylori eradication for occurrence of gastric cancers. Nonetheless,this study also exposed that eradication of h pylori did not totally abolishgastric cancer risk. Hence, in order to completely eliminate the risk fordeveloping gastric cancer subsequently later than eradication of h pylori, theperiodic surveillance would be recommended periodically.On the other hand, several otherfactors must also be brought under consideration in evaluating whether gastriccancer can be prevented by completely treating the infection or the riskfactors for its occurrences can be reduced only. Moreover, H pylori infectionhas been anticipated to provide some benefits, such as decreasing the risks ofchildhood asthma obesity, even though there are no considerable data to supportthese benefits of H pylori infections.As per studies up till now h pylorihas been considered as the major cause of gastric cancers but does not howeverproofs it as sufficient for h pylori-associated gastric cancer Analogous in theory to human papilloma virushepatitis B and C viruses .in precise words this infection is one of the causefor development of gastric cancers but helicobacter pylori is not the onlyreason or is sufficient enough to cause gastric carcinogenesis, several otherrisk factors are also involved .
Conversely, H pylori is not the only reason ofgastric cancer 5 to 3 percent of the contribution is from the other leastcommon factors involved such as ofgastric adenocarcinomas and embrace infection with Epstein-Barr virus,autoimmune gastritis, genetic abnormalities in the host and possibly proximalcancers related to esophageal adenocarcinoma. Consequently adenocarcinomachances will always be there or would not entirely vanish in absence ofhelicobacter pylori infection. Helicobacter pylori- associated Gastric Cancer Epithelial lining atrophy of the gastric canalis the primary factor to carcinoma it may lead to diminished gastric acidsecretion which directly affects the microbes in the gastrointestinal tract andworsening the condition. The consequence of each specific infection is not predictable,as is the degree of advancement of the gastric epithelial mucosal destructionbut still the aggravation in the situation is stopped by the removal of bacteria.
Cancer risk can becompletely eradicated if h pylori is treated before the worsening of theatrophic destruction of the mucosal epithelium. eradication of h pylori caneither stop or reversed or partially reverse the consequences of worsening ofthe carcinomas merely depending upon the extent of atrophic changes that have .thequestion arises that why does the risk of gastric carcinoma progression prevails even if there is a completeeradication of h pylori done in such cases the secondary reasons responsible forthe issue can be managed like endoscopic surveillance programs that are costeffective too besides being useful in preventing deaths from gastric carcinoma. MECHANISM OF H PYLORI’S GASTRIC ATROPHY:The significance of H pylorieradication to avert gastric carcinogenesis strongly relies upon the patient’sdegree of severity of cancer at the time of eradicating h pylori.It has been noticed that themetachronous gastric cancer risk lies in a range of 1 to 4 % per Anum in thosepatients who have already been treated successfully against early gastric tumorthrough endoscopic removal but h pylori infection left untreated.Further study in this area has revealedthat the part of helicobacter pylori in progressing carcinogenesis is actuallythrough the production of inflammation both as acute or chronic that causesgenetical instability in the formation of the epithelial membrane of gastric tract.
Besides this one more contributing factor is actually the interaction betweenpylori and the other microbiomes of the gut, other endogenous may also beinvolved in producing carcinogenic products.PEOPLE AT RISK:There is a particular population whois affected more often contributing factors are diet and other environmentalfactors as well as the food preservation techniques may also contribute to theoccurrence of h pylori accompanying mucosal injury and cancer risk. GENETIC INFLUENCE:Moreover, H pylori infection can causegenetical instability simply by breaking up the DNA double helix and alteringthe micro RNA expressions. One of the most causative virulent strains like CagA-positive has even greater potential of causinggastric carcinoma.
H PYLORI STRAINS IMPACT:Prominently, no specific virulent strainof H pylori has been isolated in fact all the virulent and non-virulent strainshave happened to be equally potent in causing carcinomas. However the whencompared between the most virulent and the least virulent strains thedifference between the risks of gastric cancer turned out to be less than 3folds The variance in gastric cancer risk amongstthe most and the least-virulent strains is perhaps lesser than three folds, encouragingthe endorsement that all the Helicobacter pylori infections better be eliminated,regardless of virulence features in short., CLINICAL RESEARCH FINDINGS: H pylori eradication abolishes the harmfultriggers and stimulates perseverance of inflammation. Nonetheless, perseveranceof inflammation is an extremely harmonized process controlled by anti inflammatorydrugs, containing lipoxins and resolving acting as a lipid mediators.
This highlightsthe issue if the h pylori induced inflammation has been resolved so