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Extradigestive manifestations of Helicobacter pylori gastric infection
  1. A Gasbarrinia,
  2. F Franceschia,
  3. A Armuzzib,
  4. V Ojettib,
  5. M Candellib,
  6. E Sanz Torreb,
  7. A De Lorenzoc,
  8. M Antib,
  9. S Pretolanib,
  10. G Gasbarrinib
  1. aDepartment of Medical Pathology, Catholic University of Rome, Rome, Italy, bDepartment of Internal Medicine, Catholic University of Rome, Rome, Italy, cDepartment of Neuroscience, Tor Vergata University, Rome, Italy
  1. Dr A Gasbarrini, Istituto di Patologia Medica, Gemelli Hospital, Catholic University, Largo Gemelli 8–00168 Roma, Italy.

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Summary

In the past year, several studies have been carried out on the association between Helicobacter pyloriinfection and a miscellany of extradigestive diseases, such as cardiovascular, immunological, and various other pathologies. In particular, a higher prevalence of H pyloriinfection in patients affected by ischaemic heart disease has been described and there is growing evidence for an association betweenH pylori and some autoimmune diseases. Moreover, recent studies have shown that various helicobacter species have been detected in human bile; if confirmed, this finding could revise the diagnostic and therapeutic approach to diseases of the biliary tract.

It has long been known that some infectious agents which affect specific areas of the body may also have systemic sequelae. A typical example of this phenomenon is infection by β haemolytic streptococcus group A, a frequent determinant of acute or chronic tonsillitis, which can also lead to rheumatic fever, cardiac inflammation, glomerulonephritis, and neurological involvement.1 It has been shown that the extrapharyngeal manifestations of the infection are caused by cross mimicry between bacterial and host antigens.1

H pylori is one of the most frequent causes of gastrointestinal infections worldwide; it is known that the immunological response elicited by the bacterium is an important determinant of gastric mucosal damage.2 In particular, the production of large amounts of various proinflammatory substances, such as cytokines, eicosanoids, and proteins of the acute phase follows gastric colonisation by H pylori (fig1).2 It has also been shown that there is cross mimicry between some bacterial and host antigens which may be responsible, at least in part, for the mucosal damage during the infection.3 On the basis of these observations, some authors have also investigated the role of H pylori as a pathogenic determinant of some extragastroduodenal idiopathic diseases, such as cardiovascular, …

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