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Global Translational Medicine AA amyloidosis in rheumatoid arthritis

organs (Figures 7 and 10), even in cases when some Ethics approval and consent to participate
structures are absent in a biopsy specimen. 41,43
This study was conducted in accordance with the local
A limitation of this study is that minimal amyloid legislation and institution requirements.
deposits may go undetected, and a small, randomly selected
tissue sample may provide misleading results, particularly Consent for publication
in early-stage amyloidosis. Not applicable.
It is essential to consider the following factors:
(i) The staining procedure should be appropriate 46,81 Availability of data
(ii) Illumination during histological examination is Data used in this work are available from the corresponding
crucial; a highly bright professional polarization author upon reasonable request.
microscope is required for reliable amyloid detection.
(iii) The staining intensity of Congo red may degrade over References
time; thus, freshly stained, high-quality tissue sections
are essential for accurate diagnosis. 1. Buxbaum JN, Eisenberg DS, Fändrich M, et al.
Amyloid nomenclature 2024: Update, novel proteins,
5. Conclusion and recommendations by the International Society of
Amyloidosis (ISA) Nomenclature Committee. Amyloid.
sAAa is one of the most significant and insidious 2024;31(4):249-256.
complications of RA, affecting multiple organs with doi: 10.1080/13506129.2024.2405948
varying prevalence and severity.
2. Sipe JD, Benson MD, Buxbaum JN, et al. Amyloid fibril
sAAa affects the cardiovascular system, and giAAa proteins and amyloidosis: Chemical identification and clinical
is closely associated with it. Compared to systemic AA classification international society of amyloidosis 2016
deposition, GI AA deposition occurs after a latent stage. Like nomenclature guidelines. Amyloid. 2016;23(4):209-213.
systemic amyloid deposition, GI amyloid deposition follows doi: 10.1080/13506129.2016.1257986
a progressive and cumulative trajectory, initially affecting
only a few structures in the GI tract before expanding to 3. Bély, M, Apáthy Á. Clinical Pathology of Rheumatoid
involve additional structures as the disease advances. AA Arthritis: Cause of Death, Lethal Complications and
deposition begins in the most frequently affected structures Associated Diseases in Rheumatoid Arthritis. Akadémiai
Kiadó, Budapest, Hungary; 2012. p. 1-440. Available from:
of the GI tract, where more extensive deposits are observed.
https://www.akkrt.hu [Last accessed on 2024 Oct 17].
In this study, giAAa did not play a direct role in the 4. Cohen AS. Amyloidosis associated with rheumatoid
mortality of 34 RA patients with sAAa. arthritis. Med Clin North Am. 1968;52:643-653.
Acknowledgment 5. Gillmore JD, Lovat LB, Persey MR, Pepys MB, Hawkins PN.
Amyloid load and clinical outcome in AA amyloidosis in
We wish to express our gratitude to Károly Balogh, MD, relation to circulating concentration of serum AA protein.
Associate Professor Emeritus of Pathology at Harvard Lancet. 2001;358(9275):24-29.
Medical School, for his invaluable contributions over the
years to our work with critical advice and professional 6. Lachmann HJ, Goodman HJ, Gilbertson JA, et al. Natural
history and outcome in systemic AA amyloidosis. New Engl
editing of the English text.
J Med. 2007;356(23):2361-2371.
Funding doi: 10.1056/NEJMoa070265

None. 7. Simons JP, Al-Shawi R, Ellmerich S, Speck I, Aslam S,
Hutchinson WL. Pathogenetic mechanisms of A amyloidosis.
Conflict of interest Proc Natl Acad Sci U S A. 2013;110(40):16115-16120.
The authors declare no conflicts of interest. doi: 10.1073/pnas.1306621110

Author contributions 8. Kennedy AC, Burton JA, Allison MEM. Tuberculosis as a
continuing cause of renal amyloidosis. Br Med J. 1974;3:395-397.
Conceptualization: Miklós Bély doi: 10.1136/bmj.3.5934.795
Investigation: Miklós Bély
Methodology: Miklós Bély, Ágnes Apáthy 9. Pasternack A. Fine-needle aspiration biopsy of spleen in
Writing – original draft: Miklós Bély diagnosis of generalized amyloidosis. Br Med J. 1974;3:30-33.
Writing – review & editing: Ágnes Apáthy doi: 10.1136/bmj.2.5909.20

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