The efficacy of interleukin-1 antagonist drugs in combination with colchicine in patients with FMF-AA with colchicine resistance after kidney transplantation: A study with histopathologic evidence
Clinical Transplantation, cilt.35, sa.6, 2021 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 35 Sayı: 6
- Basım Tarihi: 2021
- Doi Numarası: 10.1111/ctr.14309
- Dergi Adı: Clinical Transplantation
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, CAB Abstracts, EMBASE, MEDLINE
- Anahtar Kelimeler: colchicine, FMF‐, amyloidosis, IL‐, 1 antagonist, kidney transplantation
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Background: The efficacy of anti-interleukin-1 (IL-1) drugs in kidney transplant patients with FMF-AA who developed colchicine resistance has not been clearly demonstrated. Method: Thirty nine kidney transplant recipients with FMF-AA were evaluated. Group 1 consisted of patients who were in remission after transplantation with colchine and Group 2 included those who developed colchicine resistance. Results: The mean follow-up of the patients was 88.5 ± 61.9 months. Following the treatment with IL-1 antagonists; serum Amyloid A (SAA) averages (79.4 ± 35.3 mg/L) as well as the average number of hospitalizations per month due to FMF episodes (1.4 ± 0.5 times/month) decreased significantly (26.6 ± 25.9 mg/L and 0.1 ± 0.3 times/month) (p <.001). Rates of death with a functional graft were 30% and 0% in group 1 and 2 (p =.086). Biopsy-proven AA amyloidosis recurrence in the allograft was observed in 11 of 19 (58%) and seven of nine (78%) patients in group 1 and 2, respectively. Interestingly, glomerular amyloid deposition was not present in the vast majority of biopsies. De novo vasculer amyloid deposition was observed during treatment. Conclusion: IL-1 antagonist drug and colchicine combination almost completely prevented acute FMF attacks in kidney transplant patients with colchicine resistance. However, amyloid accumulation did not cease during IL-1 antagonist drug treatment.