Joint bone spine · 2026
AA amyloidosis in inflammatory joint diseases in the era of biological therapies: Prevalence, manifestations, management and evolution.
СтатьяМногоцентровое исследованиеНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
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Raymond Anna, Savadogo Binta, Bourguiba Rim, Dellal Azeddine, Buob David, Savey Léa, Grateau Gilles, Assaraf Morgane, Boffa Jean-Jacques, Cez Alexandre, Michel Pierre-Antoine, Sellam Jérémie, Georgin-Lavialle Sophie, Fautrel Bruno, Mitrovic Stéphane
Аннотация
OBJECTIVES: AA amyloidosis (AAA) is a complication of chronic inflammation whose burden is expected to decrease in the era of biological therapies. We assessed the prevalence, clinical and laboratory manifestations, management and evolution of AAA in patients with inflammatory joint diseases (IJDs).
METHODS: We retrospectively assessed adults followed from 2008 to 2025 in 2 French tertiary university hospitals. AAA had to be histologically confirmed and related to one of the following IJDs: rheumatoid arthritis, spondylarthritis, juvenile idiopathic arthritis, undifferentiated arthritis or gout.
RESULTS: The prevalence of rheumatoid arthritis- and spondylarthritis-related AAA was low, estimated at 0.6‰ and 0.5‰, respectively. We identified 15 patients with IJD-related AAA: 5 rheumatoid arthritis, 4 spondylarthritis, 2 juvenile idiopathic arthritis, 3 undifferentiated arthritis and 1 gout. Ten (66.7%) patients were from developing countries. All patients experienced delays in diagnosis and treatment. At AAA diagnosis, most patients (80%) were not receiving any treatment for IJD. AAA clinical manifestations were mainly renal and digestive; the median (interquartile range) C-reactive protein level was 41.5 (16.8-59.5) mg/L, serum amyloid A level 31 (13-44) mg/L and proteinuria/creatinuria ratio 3.5 (1.3-5.2) g/mmol. Biological disease-modifying anti-rheumatic drugs were started in 14 patients (1 patient lost to follow-up) and resulted in clinically inactive disease in 57.2%; normal C-reactive protein and serum amyloid A and proteinuria negativity in 71.4%.
CONCLUSION: In the last 2 decades, AAA occurred in only patients with IJDs who experienced long diagnostic and therapeutic delays, mainly related to country of origin and difficulties in access to care.
METHODS: We retrospectively assessed adults followed from 2008 to 2025 in 2 French tertiary university hospitals. AAA had to be histologically confirmed and related to one of the following IJDs: rheumatoid arthritis, spondylarthritis, juvenile idiopathic arthritis, undifferentiated arthritis or gout.
RESULTS: The prevalence of rheumatoid arthritis- and spondylarthritis-related AAA was low, estimated at 0.6‰ and 0.5‰, respectively. We identified 15 patients with IJD-related AAA: 5 rheumatoid arthritis, 4 spondylarthritis, 2 juvenile idiopathic arthritis, 3 undifferentiated arthritis and 1 gout. Ten (66.7%) patients were from developing countries. All patients experienced delays in diagnosis and treatment. At AAA diagnosis, most patients (80%) were not receiving any treatment for IJD. AAA clinical manifestations were mainly renal and digestive; the median (interquartile range) C-reactive protein level was 41.5 (16.8-59.5) mg/L, serum amyloid A level 31 (13-44) mg/L and proteinuria/creatinuria ratio 3.5 (1.3-5.2) g/mmol. Biological disease-modifying anti-rheumatic drugs were started in 14 patients (1 patient lost to follow-up) and resulted in clinically inactive disease in 57.2%; normal C-reactive protein and serum amyloid A and proteinuria negativity in 71.4%.
CONCLUSION: In the last 2 decades, AAA occurred in only patients with IJDs who experienced long diagnostic and therapeutic delays, mainly related to country of origin and difficulties in access to care.