The analysis of secondary AA-amyloidosis current etiology and its influence on the approaches for diagnosis and treatment

Aim. To investigate an influence of the currently changed etiologic structure of AA-amyloidosis on the diagnosis and treatment tactics. Materials and methods. In 110 patients with АА-amyloidosis followed during full disease duration (1 month 29 years) etiology, clinical manyfestations and approaches...

Full description

Saved in:
Bibliographic Details
Published inTerapevtic̆eskii arhiv Vol. 93; no. 6; pp. 672 - 678
Main Authors Rameev, Vilen V., Kozlovskaya, Lidiia V., Rameeva, Anna S., Novikov, Aleksandr V., Barsuk, Mariia V.
Format Journal Article
LanguageEnglish
Russian
Published "Consilium Medicum" Publishing house 15.06.2021
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Aim. To investigate an influence of the currently changed etiologic structure of AA-amyloidosis on the diagnosis and treatment tactics. Materials and methods. In 110 patients with АА-amyloidosis followed during full disease duration (1 month 29 years) etiology, clinical manyfestations and approaches to diagnose and treatment of AA-amyloidosis were evaluated. With ELISA levels of amyloid precursor acute phase inflammation reactant SAA and neutrophil activity marker S100A12 were measured. Results. Among the most common causes of AA-amyloidosis at the present stage, in addition to RA (40.3%), a significant place is occupied by a group of diseases with a predominantly autoinflammatory mechanism (53.73%). To confirm the autoinflammatory mechanism of the predisposing disease it is recommended to study a highly sensitive parameter serum protein S100A12. An effective marker of the risk of AA-amyloidosis progression, especially in patients with subclinical activity of inflammatory disease, is a high level of production of amyloidogenic protein-a precursor of SAA.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0040-3660
2309-5342
DOI:10.26442/00403660.2021.06.200851