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Extra gastric & extra intestinal manifestations of h.pylori
- 1. Extra gastric & extra intestinal manifestations of H.pylori By Ahmed Mosaad EL-Eraky Assistant lecturer of Tropical Medicine Mansoura University
- 8. History of H. pylori • 1890’s: Spirochetes in animal stomachs • 1900’s: Spirochetes in human stomachs • 1954: No bacteria in gastric biopsies of 1000 patients • 1975: Gm-ve bacteria in 80% of GU’s (Pseudomonas) • 1983: Warren and Marshall characterize H. pylori • 2005 Nobel prize in 2005
- 9. EBM pyramid
- 10. Extragastric gastrointestinal manifestations EvidenceAssociationDisease Epidemiological&meta-analyses-IBD Epidemiological&cohort-Microscopic colitis Epidemiological&cohort-Celiac disease Meta-analysis-barrett's esophagus No cross reactivityNo ss associationPBC Cohort and prospective analysis+PSC Epidemiological and cohort+Gallstone disease cross-sectional & cohortLimited dataAIH majority+NAFLD cross-sectional & cohort+pancreatitis a meta-analysis, but two case-control studies found no association. +Pancreatic cancer Systematic review and meta-analysis+Colorectal cancer cross-sectional & meta-analyses+Liver cirrhosis& HCC
- 13. H.Pylori &NAFLD positive correlations between H. pylori and NAFLD have been reported in some clinical and ex-perimental studies, but other studies have presented con-tradictory data. Further analyses focusing on the effect of H. pylori eradication on histopathological changes in patients with biopsy-proven NAFLD are necessary
- 14. H.P&Viral Hepatitis,Cirrhosis,HCC In summary, although H. pylori genes are frequently detected in HCC samples, possible correlations between H. pylori and hepatocarcinogenesis seem to be doubtful. Further studies showing the direct contribution in vivo using infectious animal models or mice transgenic for H. pylori genes are necessary to confirm this relationship.
- 16. H.P&Viral Hepatitis,Cirrhosis,HCC In summary, although H. pylori genes are frequently detected in HCC samples, possible correlations between H. pylori and hepatocarcinogenesis seem to be doubtful. Further studies showing the direct contribution in vivo using infectious animal models or mice transgenic for H. pylori genes are necessary to confirm this relationship.
- 18. Hematological + • IDA • Vit B 12 deficiency • ITP +/No • autoimmune neutropenia • anti-phospholipid syndrome • plasma cell dyscrasias -
- 21. H.pylori&Anemia
- 22. H.pylori&ITP
- 26. H.pylori&ITP
- 27. Dermatological + • Rosacea +/No • Chronic urticaria • Psoriasis • HSP • Behcet’S disease • Alopecia areata • Lichen planus -
- 28. H.pylori&Rosacea • It is a chronic facial dermatitis that manifests as erythema and cutaneous lesions characterized by much dilated red superficial capillaries, called telangiectasia, and its etiology remains unknown. • Although the etiopathogenesis is not fully known, an element commonly found in patients with rosacea is the presence of gastrointestinal disorders. Several studies have suggested a potential relationship to H. pylori infection
- 35. Endocrinal Insulin resistance DM type II Obesity Autoimmune thyroiditis
Editor's Notes
- In the world of medical research, it would be hard to find two individuals working together whose temperaments were more diametrically opposed than Robin Warren and Barry Marshall, the joint winners of this year's Nobel Prize in Physiology or Medicine. Warren a consultant pathologist now retired from Royal Perth Hospital in Australia, is a reserved man whose colleagues talk about his quiet persistence, thoughtfulness, and careful observation. Marshall, a gastroenterologist 14 years his junior from the University of Western Australia, has described himself as brash. Others list his creativity, determination, and entrepreneurial spirit. Warren's quiet persistence and Marshall's energetic enthusiasm complement one another. They make what both men describe as a “good team” and have together achieved, according to the Nobel Assembly at the Karolinska Institute, a remarkable and unexpected discovery that gastritis and peptic ulcers arise from an infection of the stomach caused by the bacterium Helicobacter pylori. In the process, the two researchers have overturned established medical dogma and revolutionised the treatment of peptic ulcers. The partnership began in 1981 when Marshall, a trainee doctor, asked Warren about the possibility of doing a research project with him. 2 years earlier, Warren had made a historic discovery—that gastric biopsy samples from patients with gastritis had an unexpected burden of curved bacteria. Since 1979, he had been gathering more and more samples. “As far as I was concerned the way they were arranged, they were associated with the gastritis”, Warren said. “But trying to convince other people of that was impossible.” Warren recalls: “Every time I spoke to a clinician they would say, ‘Robin, if these bacteria are causing it as you say, why hasn't it been described before?'.” Orthodox medical teaching at the time was that bacteria did not grow in a normal stomach. However, as Warren wrote in the 2002 book Helicobacter Pioneers, “I preferred to believe my eyes, not the medical textbooks or the medical fraternity.” Marshall also believed what he saw through Warren's microscope. “The first time I sat down with him he didn't really have any trouble convincing me there were these organisms in the stomach”, he told The Lancet. “As far as I was concerned he was right, and I thought this was a unique observation.” Soon the two became absorbed in a study of 100 patients, and Marshall had begun trying to culture the organism—a difficult task he finally achieved in early 1982. By the end of that year, armed with preliminary results, Marshall gave a presentation at a local meeting, where he earned a patronising and negative response. “I didn't have all my ammunition ready to go”, he says. “It allowed people to shoot holes in our hypothesis.” It was the kind of response he and Warren were to become familiar with. “I was out there fighting battles with the gastroenterologists”, he recalls. “But Robin's very persistent; I'm also a little the same. Neither of us would really care if there were 1000 people jeering on the sidelines; it would be like water off a duck's back.” Throughout this time, the two men took encouragement from talking to one another and valued the support of their wives—Win Warren and Adrienne Marshall. “In fact, there was only one doctor who did believe in what I was doing”, Warren wrote, “my wife Win, who was a psychiatrist and who encouraged me”. In 1983, the two published an unusual pair of correspondence letters in this journal, including photographs of the histology and electron microscope images of the organism (Lancet 1983; 1:1273–75). Later that year, at the recommendation of the campylobacter specialist Martin Skirrow from the UK's Public Health Laboratory Service, Marshall presented the findings to the 2nd International Workshop on Campylobacter Infections in Brussels, Belguim.“I think most microbiologists were convinced at the outset that this was linked to gastritis”, Skirrow recalls. “He's a good salesman is Barry. He carried most microbiologists with him in his work.” Whereas microbiologists had no dogma to overcome about the causes of gastritis and peptic ulcers, the wider medical community remained hard to convince. Even the first major publication of their results, in this journal in 1984, was a difficult hurdle (Lancet 1984; 1: 1311–15). The editors, Marshall recalls, found it difficult to find reviewers who could agree the paper was important, general, and interesting enough to be published. It was partly with the assistance of Skirrow that the article finally appeared. The same year, in an act born to some extent of frustration, Marshall deliberately infected himself by drinking a solution swimming with the bacterium, as part of a successful and widely reported experiment to prove Koch's postulates. But many clinicians still remained unmoved. It wasn't until the early 1990s that the evidence of Marshall and Warren became impossible to ignore, at which point pharmaceutical development and clinical practice underwent a shift towards eradication of H pylori to treat ulcers. The Nobel Prize came a decade later, and was richly deserved says Adrian Lee, a leading H pylori researcher who was among those microbiologists at the Brussels conference. Although other researchers had reported seeing spiral bacteria in the stomach before the west Australian duo, their achievement stands alone, he notes. “There was no accumulation of evidence”, he says. “What happened was that people had made observations, but had drawn no conclusions. This was a paradigm-shifting discovery.”
- ‘hygiene hypothesis’,
- Figure 5. Potential mechanisms by which FcγRIIB might contribute to the pathogenesis of systemic lupus erythematosus a | Fc receptor IIB for IgG (FcγRIIB) is important for the maintenance of B cell tolerance through inhibition of B cell activation, promotion of the exclusion of autoreactive cells from follicles and perhaps by mediating apoptosis of autoreactive B cells and plasma cells. In vitro, FcγRIIB cross-linking in pre-B cells can result in apoptosis. This has been proposed as a possible mechanism for the removal of autoreactive B cells that arise during development; however, studies in FcγRIIB-deficient mice do not confirm the importance of this mechanism in central tolerance in vivo. FcγRIIB operates at several stages during later peripheral B cell development, potentially inhibiting B cell receptor (BCR)-mediated activation of autoreactive B cells. In addition, it may be important for the follicular exclusion of low-affinity autoreactive B cells. Autoreactive B cells may arise during somatic hypermutation and affinity maturation. It has been proposed that FcγRIIB cross-linking in the absence of BCR ligation may mediate apoptosis of such autoreactive follicular B cells and may also be important for deleting autoreactive plasma cells. b | Breakdown of B cell tolerance and the emergence of autoantibodies does not necessarily result in autoimmune disease, as there are mechanisms that function to clear circulating immune complexes, Smith and Clatworthy Page 33 Nat Rev Immunol. Author manuscript; available in PMC 2014 August 29. Europe PMC Funders Author Manuscripts Europe PMC Funders Author Manuscripts preventing them from becoming deposited in tissues. Immune complex clearance is, in part, mediated by binding and internalization by activating FcγRs (particularly on macrophages of the reticuloendothelial system of the liver and spleen). FcγRIIB may enhance or inhibit FcγR-mediated immune complex internalization by phagocytes (depending on the isoform expressed) thus modulating the amount of circulating immune complex present. c | Tissue-deposited immune complexes may initiate inflammation owing to ligation of activating FcγRs on infiltrating macrophages and neutrophils. Pro-inflammatory cytokine release and neutrophil degranulation in response to immune complexes is negatively regulated by FcγRIIB. Thus, FcγRIIB dysfunction might contribute to the pathogenesis of systemic lupus erythematosus at several stages, including the breakdown of self-tolerance, decreased disposal of immune complexes and a failure to modulate the inflammatory response to deposited immune complexes. TCR, T cell receptor.
- *severity تتحسن مع eradication
- العد الوردي أو وردية الوجه أو حب الشباب الوردي Women, especially those who are menopausal, are more likely than men to develop rosacea.[33] Those of Caucasian descent, especially those of Northern or Eastern European descent appear more affected
- Rhinophyma Otophyma Gnathophyma Metophyma Blepharophyma otophyma
- H. pylori produces cytokines that contribute to inflammation in gastric mucosa and host response emerges which leads to infiltration of inflammatory cells[54] H. pylori is proposed to induce rosacea by cytotoxin mediated chronic inflammation and gastrin induced flushing[55] . Increased activity of reactive oxygen species have been reported in patients infected with H. pylori and rosacea is associated with genera-tion of reactive oxygen species that are released by inflammatory cells[56,57] . Since the first report of an association between rosacea and H. pylori by Rebora et al[58] in 1994, there have been numerous studies investigating the prevalence of H. pylori infection in
- H. pylori eradication can improve IR, although this resolution seems to be associated with a progressive increase in BMI and cholesterol levels, as H. pylori suppresses ghrelin, which is the hormone responsible for increased appetite, which may explain the weight gain associated with the eradication of Infection HBA1C-HOMAIR
- Blaser et al[173] showed the existence of an inverse relationship between H. pylori infection and the development of asthma or other allergic diseases, particularly in children and young people with an early onset of allergies. This relationship is controversial in adults
- To validate this hypothesis, Engler et al[179] demonstrated that the administration of VacA to mouse models was able to provide allergy protection that was comparable to that of active infection H. pylori influences the immune system by shifting the balance of cytokines to the Th1 type, which suppresses allergic diseases that are dependent on the Th2 cytotype