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THU0130 Systemic aa amyloidosis in rheumatoid arthritis – the influence of septic infection, tuberculosis or associated malignant tumours. a retrospective study
  1. AJ Apathy1,
  2. M Bely2
  1. 1Department of Rheumatology, National Institute of Rheumatology, Budapest, Hungary
  2. 2Department of Pathology, Policlinic of the Hospitaller Brothers of St. Johns of God in Budapest, Budapest, Hungary

Abstract

Background Systemic secondary (reactive) AA amyloidosis (AAa) is one of the most important complications of rheumatoid arthritis (RA). The AA amyloid precursors are produced by the liver, basically determined by the chronic relapsing inflammation of RA. The disease may be complicated by other inflammatory phenomena, such as generalised septic infection, chronic active tuberculosis, or may be accompanied by malignant tumours and consequent inflammation.

Objectives The aim of this study was to determine the role of lethal, generalised septic infection, or associated diseases like tuberculosis, and malignant tumours on the development and course of amyloidosis.

Methods A randomised autopsy population of 161 in-patients (female 116, average age of 64.9 years; male 45, average age of 66.2 years at death) with rheumatoid arthritis (RA) was studied.1

AA amyloidosis (AAa), lethal septic infection (SI), inactive post-primary tuberculosis (Tb), or active miliary tuberculosis (mTb), and malignant tumours (mTu) was post mortem diagnosed histologically.

The links between AAa and coexisting complications (SI, Tb, mT, and mTu) were analysed by chi2-test.

Results AAa was observed in 34 (21.1%), SI in 22 (13.7%), Tb in 13 (8.1%), mTb in 6 (3.7%) and mTu in 13 (8.1%) of 161 RA patients.

AAa was associated with SI in 1, with Tb in 2, with mTb in 2, with mTu in 3 of 34 cases.

There was a negative association between AAa and SI (value of association coefficient was negative: -0.7346).

There was no significant correlation between AAa and SI (chi² = 3.1279, p < 0.07), Tb (chi² = 0.0302, p < 0.86), mTb (chi² = 0.05638, p < 0.81), or mTu (chi² = 0.0302, p < 0.86).

Conclusion AAa may be considered a direct consequence of RA.

Coexistent inflammatory complications (SI, Tb, or mTb, mTu) did not influence statistically the frequency of AAa in our autopsied RA patients. Post-primary tuberculotic scars did not represent an active inflammation, and did not have a statistically significant influence on amyloidosis. Miliary dissemination of tuberculosis (endogenous reactivation of post-primary tuberculosis) must be considered a terminal pre-mortem phenomenon, which ? because of its terminal onset – did not have a statistically significant effect on prevalence of AAa.

Based on the negative value of association coefficient between AAa an SI may guess a diminished reactivity of the vessels and tissues infiltrated by amyloid. This effect is nearly significant (chi² = 3.1279, p < 0.07).

Reference

  1. Bély M. Krankheitsmodifizierende Faktoren bei chronischer Polyarthritis. D. Sc. Acad. Sci. Hung. Thesis. Budapest, 1993

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