AB0459 MORTALITY OF RHEUMATOID VASCULITIS AGGRAVATED BY CLINICALLY LATENT TUBERCULOSIS – A RETROSPECTIVE CLINICOPATHOLOGIC STUDY OF 161 AUTOPSY PATIENTS

Autor: Á. Apáthy, M. Bély
Rok vydání: 2020
Předmět:
Zdroj: Annals of the Rheumatic Diseases. 79:1528.2-1528
ISSN: 1468-2060
0003-4967
Popis: Background:Systemic vasculitis of autoimmune origin (e.g. rheumatoid vasculitis – RV) plays a pivotal role in the pathogenesis of rheumatoid arthritis (RA) [1]. RV may be characterized bynon-specific inflammation(nsRV) with or withoutfibrinoid necrosis(fnRV) or bygranulomatoustransformation of blood vessels (grRV) [1].The prevalence and mortality of tuberculosis (TB) is higher in rheumatoid arthritis (RA) than in the general population.Objectives:The aim of this study was to assess the influence of dormant (inactive), clinically latentTB (with or without subclinical atypical miliary exacerbation) on the mortality of rheumatoid vasculisit (RV).Methods:At the National Institute of Rheumatology9475patients died between 1969 and 1992; among them161withRAand all of them were autopsied [1].RAwas confirmed clinically according to the criteria of theARA.nsRValone or in combination withfnRVorgrRVwas diagnosed at autopsy, and confirmed by a detailed review of extensive histological material [1].The prevalence fibrous (fTB), fibrocaseous (fcTB) or miliaryTB(mTB) was diagnosed and characterized histologically, reviewing retrospectively the clinical and pathological reports [1].From each patient a total of 50-100 tissue blocks of 12 organs (heart, lung, liver, spleen, kidneys, pancreas, gastrointestinal tract, adrenal glands, skeletal muscle, peripheral nerve, skin and brain) were studied microscopically.The possible role offTB,fcTBor mTB on the mortality due tonsRV,fnRVorgrRVwas analyzed with Pearson’s chi-squared (χ2) test.Results:nsRVcomplicatedRAin33(20.49%) of 161 patients, in combination withfnRVin17(51.51%) or withgrRVin10(30.30%) of 33 cases.ThensRVled to death in19(57.57%) of 33 patients, in combination withfnRVin11(64.71% of 17) or withgrRVin7(70.0% of 10) cases; the mortality due tonsRV,fnRVorgrRVshowed an increasing tendency.Post-primaryTBwas associated withRAin21(13.04%) of 161 patients,12(57.14% of 21) werefTB, and9(42.86% of 21)fcTB.Oneof 12fTBand5of 9fcTBwere complicated with discrete miliary dissemination (mTB) in6(3.7% of 161; 28.57% of 21)RApatients.TB(n=21) was associated withfatal nsRVin5, withfnRVin3, withgrRVin3of 21 cases.ThefTB(n=12) was associated withfatal nsRVin1, withfnRVin1, withgrTBin1of 12 cases.ThefcTB(n=9) was associated withfatal nsRVin4, withfnRVin3, withgrTBin3of 9 cases.mTB(n=6) was associated withfatal nsRVin3, withfnRVin2, withgrTBin3of 6 cases.There was a significant and positive correlation betweenfcTBandmortalityofnsRV(c: 0.76,χ2=9.7593,p), betweenfcTBandmortalityoffnRV(c: 0.80,χ2=6.5701,p), betweenfcTBandmortalityofgrRV(c: 0.90,χ2=12.5835,p), The correlation was also positive and significant betweenmTBandmortalityofnsRV(c: 0.79,χ2=5.3406,p), betweenmTBandmortalityofgrRV(c: 0.95,χ2=20.8706,p),The relationships werenotsignificant betweenTBorfTBandmortalityofnsRV,fnRVorgrRV, nor betweenmTBandmortalityoffnRV.Conclusion:Recognition of indolentTBis a great challenge especially before starting immunosuppressive or biological therapy forRA.TBmay lead directly to death by arrosion of pulmonary arteries with massive pulmonary bleeding, by hematogenous miliary dissemination (Landouzy typhobacillos) or by canalicular spread as a cavernous chronic process (phthisis tuberculosa), etc. Discrete miliary dissemination may be also lethal caused by circulatory failure [1].The contribution ofTBto the mortality of complications ofRAor of allied disorders is plausible and can never be excluded.According to our data the risk of mortality due tonsRV,fnRVorgrRVshowed an increasing tendency, andfnRVorgrRVshould be regarded the most severe forms ofnsRVinRA.The positive and significant correlation betweenfcTBormTBandmortalityofnsRV,fnRVorgrRVrepresents a positive contribution to the fatal outcome due tonsRV,fnRVorgrRV.References:[1]Bély M, Apáthy Á: “Clinical pathology of rheumatoid arthritis.” Akadémiai Kiadó, Budapest (2012):1-144.http://www.akkrt.huISBN 978 963 05 93397Disclosure of Interests:None declared
Databáze: OpenAIRE
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