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SAT0120 Multifocal recurrent pancreatitis caused by systemic secondary aa amyloidosis in rheumatoid arthritis - a postmortem clinicopathologic study of 161 patients
  1. î Apáthy1,
  2. M. Bély2
  1. 1Department of Rheumatology, St. Margaret Clinic
  2. 2Department of Pathology, Hospital of the Order of the Brothers of Saint John of God in Budapest, Budapest, Hungary

Abstract

Objectives The aim of this study was to describe the prevalence and formal pathogenesis of multi (micro) focal liponecrotic pancreatitis (LnP) caused by systemic secondary AA amyloidosis (AAa) in rheumatoid arthritis (RA).

Methods A randomized autopsy population of 161 in-patients with RA was studied. RA was confirmed clinically according to the criteria of the ACR. Tissue samples of pancreas were available for histologic evaluation in 111 of 161 patients. Pancreatitis and AAa were diagnosed histologically [1]. The possible role of AAa in the pathogenesis of LnP was analyzed by Pearson's chi-squared (χ2) test.

Results: AAa complicated RA in 29 (26.12%) of 111 patients. Amyloid A deposition on different tissue structures of pancreas was detected in 25 (86.2 %) of 29 cases. Marked amyloid A deposition was found in the walls of arterioles, small and medium size arteries, and on different tissue structures of the pancreas.

Acute or chronic LnP with or without AAa was present in different stages of the pathological process (necrotic foci with or without inflammatory reaction, and/or consecutive focal accentuated fibrosis) in 15 (13.51%) of 111 patients. Seven (46.66 %) of these 15 were associated with massive AAa. The correlation between LnP and prevalence of AAa was significant (c²=5.7939, p<0.016). Two (33.33%) of 15 LnP showed a special scattered multifocal appearance throughout the pancreas, characterized by necrotic foci of different size and stage of necrobiosis, without or with inflammation, and in association with severe AAa. The pancreatitis was basically not hemorrhagic, differing from hemorrhagic pancreatitis due to arterial erosions. Ductal changes were not present. The histological picture was dominated by more or less pronounced atrophy of pancreatic glands. The link between this special type of LnP and AAa very strong and significant (c²=16.2658, p<0.0005).

Conclusions The close relationship between AAa and LnP suggests a relationship between amyloidosis and the prevalence of pancreatitis, that even may lead to a special multi (mico) focal pancreatitis. Amyloid A deposition in the walls of the pancreatic arterioles, small and medium size arteries (branches of splenic artery, upper and lower gastroduodenal arteries) can lead to local ischemia and to regressive changes in the pancreatic gland. This process is more or less widespread and multifocal, depending on the number of involved vessels. The size of necrobiotic areas is determined by the size of involved bood vessels. Multi (micro) focal necrosis of the pancreas caused by diminished blood supply is followed by reactive inflammation, and later fibrosis, depending on the stages of the pathological process.

AAa is a progressive cumulative process involving more and more blood vessels of different sizes, thus the regressive changes accumulate in the pancreas with time, and exist in different stages at death. Different size and stage of focal necrosis, and the co-existent marked AAa may identify this type of pancreatitis. The progressive and cumulative process of AAa with multi (micro) focal necrosis in the pancreas may cause recurrent abdominal symptoms. This form of pancreatitis may be regarded a special manifestation of AAa or a new vasculogenic entity caused by AAa in RA. Plausible similar changes of pancreas may be expected in other autoimmune diseases complicated with AAa.

Reference: [1] Bély M. Apáthy Ágnes: Clinical pathology of rheumatoid arthritis. 1-440 pp. Akadémiai Kiadó, Budapest 2012 Budapest 2012. http://www.akkrt.hu

Disclosure of Interest: None declared

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