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Helicobacter pylori and urinary system stones: Endoluminal damage as sub-hypothesis to support the current stone theory

机译:幽门螺杆菌和泌尿系统结石:腔内损伤为亚假说,支持当前的结石理论

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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. (C) 2014 Elsevier Ltd. All rights reserved.
机译:幽门螺杆菌(H. pylori)是一种典型的革兰氏阴性细菌,偏爱胃粘膜,它还具有奇异的多系统作用,并通过一些未明确定义的病理生理学途径扩展到某些恶性肿瘤,血液学和血管疾病。我们的先驱数据指出,幽门螺杆菌+病例组中泌尿系统结石的存在似乎很高。虽然解释了肾-胆囊结石重合的原因,但以前曾暗示可能存在肠道微生物菌群的转移机制,从富氧草酸杆菌可通过摄入草酸草酸盐降低肾结石的风险,向H幽门螺杆菌,已知通过未知机制诱发胆结石。该假说是一种间接假说,对幽门螺杆菌在肾结石形成中的作用存在争议,因为与草酸内源酶相比,草酸在肠道中的吸收并不明显。目前与我们的假设有关的初步独特数据声称幽门螺杆菌与肾结石之间可能存在联系。我们认为这种有害作用是由于幽门螺杆菌引起的可能的全身性影响,例如血管和/或腔内疾病,而不是直接细菌定殖。有强有力的证据表明幽门螺杆菌在动脉粥样硬化过程中有一定作用。肾乳头上的兰德尔斑块形成以及随后的草酸钙结石形成的血管理论表明,肾动脉乳头的微血管损伤以动脉粥样硬化的方式出现,导致血管壁附近钙化,最终以牙结石的形式侵蚀进入泌尿系统。简而言之,结石和动脉粥样硬化的理论似乎是重叠的,幽门螺杆菌是这两个过程的因素之一。除了我们的假设外,我们还声称幽门螺杆菌可能对泌尿和生殖系统的腔内表面具有相同的有害作用,并导致一些特殊的病理,如间质性膀胱炎甚至是睾丸后不育的汉纳溃疡。有关幽门螺杆菌胃外后遗症的知识积累可能会为尿石症的治疗和预防策略打开新的领域,甚至这一进展可能会导致慢性盆腔疼痛综合征和特发性不育。 (C)2014 Elsevier Ltd.保留所有权利。

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