Background Helicobacter Pylori (HP) has been studied in several autoimmune disorders but definite causality is perhaps restricted to MALT Lymphoma and some cases of ‘idiopathic’ immune thrombocytopenia (1,2). HP may suppress innate immune mechanisms yet promote antigen specific disease in autoimmune gastritis and increase IL 10 producing T- regs (3)
Objectives We postulate a possible link of HP infection to the pathogenesis of granulomatous diseases.
Methods We report a retrospective review of 7 cases of sarcoidosis / chronic undefined granulomatous disease.
Results Our index case is of multisystem Sarcoidosis in a 49-year-old Indian male who presented with ANA positive arthropathy, parotid swelling and sicca syndrome. Lip biopsy showed granulomatous inflammation. He was CLO positive on gastric biopsy at OGD and at the onset of HP eradication he deteriorated dramatically with orbital sarcoid myopathy, episcleritis and diplopia. His neurosarcoidosis, and restrictive inflammatory lung disease has responded to steroids. At 18 months systemic features of weight loss fevers and arthralgia/myalgia still require low dose Prednisolone and Mycophenolate. His immediate deterioration concurs with reports of transient arthralgias post HP eradication, possibly due to antigen load. A second case is of 40 year old Indian male, with limited but persistent granulomatous infiltration of a lachrymal gland and no further evidence of Sarcoidosis, had active HP which was eradicated successfully; but he still requires Prednisolone at 4 months. Review of one 41 year old Afro-Caribbean and 3 Asian females ages 51 -70 yrs and a 44 yr old Asian male confirmed active HP infection at the time of diagnosis or history of HP eradication prior to diagnosis of sarcoidosis. Further details of this incidental unique cohort of 3 males and 4 females with granulomatous disease will be presented.
Conclusions This incidental cohort suggests a role for H Pylori in granulomatous disorders. Reports in RA and Sjögren’s have not yet defined a specific mechanism or definite association. We propose H Pylori persistence may trigger or accelerate granulomatous disease by antigen specific or bystander cytokine milieu mechanisms.
Wotherspoon, A C ; Ortiz-hidalgo, C ; Falzon, M R ; Isaacson, P G.Helicobacter pylori-associated gastritis and primary B-cell gastric lymphoma. Lancet, 1991, Vol.338(8776), pp.1175-6
Pordeus V, Szyper-Kravitz M, Levy RA, Vaz NM, Shoenfeld Y (2008). Infections and autoimmunity: a panorama. Clin Rev Allergy Immunol 34: 283–299.
Mitchell, P J; Afzali, B; Fazekasova, H ; Chen, D ; Ali, N ; Powell, N ; Lord, G M ; Lechler, R I ; Lombardi, G Helicobacter pylori induces in-vivo expansion of human regulatory T cells through stimulating interleukin-1βproduction by dendritic cells Clinical and experimental immunology, 2012, Vol.170(3), pp.300-9
Disclosure of Interest None Declared