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Helicobacter pylori and urinary system stones: endoluminal damage as sub-hypothesis to support the current stone
Ayhan Verit1, Numan Dogu Güner1
1Fatih Sultan Mehmet Research & Training Hospital, Dept. of Urology, Istanbul, Turkey.
Abstract:
Helicobacter pylori (H. pylori) is a atypical gram-negative bacteria preferring gastric mucosa which also have bizarre multisystem effects extended to some malignancies, hematologic and vascular disorders through some not well defined pathophysiologic pathways. Our pioneer data was pointing that the urinary system stone existence was seemed to be high in the group of H. pylori+cases. While the explanation of the reason of the coincidence of renal-gall bladder stones, it was previously suggested that there may be a shift mechanism of intestinal microbial flora, from Oxalobacter formigenes that may reduce the risk of renal stone by consuming intestinal oxalate, to H. pylori which is known to induce gallstone by unknown mechanism. This hypothesis is an indirect one and highly controversial for the effect of H. pylori in the renal stone formation because intestinal absorption of oxalate is not significant when it is compared with the endogen oxalate. The present preliminary unique data in connection with our hypothesis claimed that a possible relation between H. pylori and renal stones. We think that this detrimental effect is due to the possible systemic influence such as vascular and/or endoluminal sickness due to the H. pylori other than directs bacteriologic colonization. There is strong evidence that H. pylori have some role in the atherosclerotic procedure. The vascular theory of Randall plaque formation at renal papilla and subsequent calcium oxalate stone development that suggests microvascular injury of renal papilla in an atherosclerotic-like fashion results in calcification near vessel walls that eventually erodes as a calculus format into the urinary system. Briefly, theories of stone and atherosclerosis seemed to be overlap and H. pylori is one of the factor of both processes. In addition to our hypothesis, we claimed that H. pylori might have same detrimental effect on endoluminal surfaces of urinary and genital systems and resulting in some special pathologies as Hunner's ulcers in interstitial cystitis and even posttesticular infertility. The accumulating knowledge about extragastric sequelae of H. pylori may open new aspects on therapeutic and the prevention strategies of urolithiasis and even this progress may reach to chronic pelvic pain syndromes and idiopathic infertility.
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