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SAT0281 Prevalence of Amyloidosis in Polymyalgia Rheumatica and in Temporal Arteritis
  1. M. Bély1,
  2. Ά. Apáthy2
  1. 1Department of Pathology, Hospital of the Order of the Brothers of Saint John of God
  2. 2Department of Rheumatology, St. Margaret Clinic, Budapest, Hungary

Abstract

Background Polymyalgia rheumatica (PMR) or temporal arteritis (TA) may be complicated by systemic secondary AA amyloidosis (AAa). Legault and coworkers (2012) confirm this statement in a comprehensive review, although they did not found amyloid A deposition in temporal artery of their own patient and do not mention amyloid deposition in this localization in the cited papers [1].

Objectives The aim of this study was to determine the prevalence of amyloidosis in the temporal artery of PMR patients with or without TA.

Methods Surgical biopsy specimens of the temporal artery of 299 patients with clinically diagnosed PMR were studied. PMR was clinically diagnosed at the National Institute of Rheumatology between 1991 and 2005 according to the criteria of Bird et al. [2].

TA and amyloid deposits were histologically diagnosed.

The types of amyloid deposits were analysed by the histochemical method according to Bély and Apáthy [3] and confirmed by immunohistochemical techniques. The link between prevalence of amyloidosis and PMR with or TA was determined by c2-test.

Results Segmental or sectoral TA was present in 71 (23.8%) of 299 patients, and was accompanied with amyloid deposits in 18 (25.35%) of 71 patients. PMR existed without TA in 228 (76.3%) of 299 patients, and was accompanied with amyloid deposits in 37 (16.23) of 228 patients.

Amyloid deposits were localized – as small globular or linear deposits – along the partially damaged internal elastic lamina. Amyloid deposits were negative for anti-human amyloid A, b2 microglobulin (Ab2M), and AL l- or κ-light chain. The origin of amyloid deposits – based on the histochemical analysis – proved to be dystrophic. There was no significant correlation between dystrophic amyloid deposition and PMR with TA (c2=3.0025; NS), or without TA (c2=0.9349; NS).

Conclusions Systemic secondary AAa – like any type of systemic amyloidosis – involves the blood vessels at an early stage of the disease (3) and spreeding via bloodstream – sooner or later – may be present in the wall of the temporal artery as well.

The temporal artery was not involved by systemic AAa in any of 299 PMR patients with or without TA. AAa seems to be – based on our biopsy material – a rare complication of PMR with or without TA.

Dystrophic amyloidosis is basically an ageing phenomenon. The low value of correlations coefficients support the assumption, that dystrophic amyloid deposits in the wall of the temporal artery are independent of the inflammation of PMR patients. The higher, but not significant, value of correlations coefficient between dystrophic amyloidosis and TA shows that the inflammation of the temporal artery contributes to the development of this type of amyloidosis by causing structural damage of the temporal artery. The localization of amyloid deposits along the fragmented elastic lamina and the close connection between them indicates that the dystrophic amyloid deposits derive from the damaged elastic lamina.

References

  1. Legault K, Shroff A, Crowther M, Khalidi N: Amyloidosis and Giant Cell Arteritis/Polymyalgia Rheumatica. J Rheumatol 2012; 39:878-880 PMID: 22467956.

  2. Bird HA, Esselinckx W, Dixon AS, Mowat AG: An evaluation of criteria for polymyalgia rheumatica. Ann Rheum Dis 1979; 38:434-439.

  3. Bély M, Apáthy Άgnes: Clinical Pathology of rheumatoid arthritis: Cause of death, lethal complications and associated diseases in rheumatoid arthritis. Academiai Kiadό, Budapest 2012 http://www.akkrt.hu.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.2322

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