Journals / İstanbul Kanuni Sultan Süleyman Tıp Dergisi / 2018 / Cilt: 10 - Sayı: 3

Retrospective Evaluation of the Etiologies of the Patients Diagnosed as AA Amyloidosis

AA Amiloidoz Tanısı Alan Hastaların Etiyolojisinin Retrospektif Olarak Değerlendirilmesi

Pages
113–116
Publication Date
2022-10-18
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: Further studies with large sample size are needed to confirm the results of our study and determine etiology of AA amyloidosis.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Amyloidosis is a systemic disease that occurs when abnormally folded fibrils of amyloid protein, accumulate in the extracellular area in various organs and tissues of the body.
📊
Key Findings & Data:Material and Method: In this study, we retrospectively evaluated the data of 63 patients with AA amyloidosis and tried to determine the primary underlying etiologic factors.
💡
Conclusion & Impact:Conclusion: Further studies with large sample size are needed to confirm the results of our study and determine etiology of AA amyloidosis.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: Amyloidosis is a systemic disease that occurs when abnormally folded fibrils of amyloid protein, accumulate in the extracellular area in various organs and tissues of the body. Amyloidosis is definitively diagnosed by demonstration of abnormal amyloid deposition in the tissues. Biopsies are taken from various tissues when clinically amyloidosis is conceived. In this study, we wanted to investigate the distribution of underlying diseases in AA amyloidosis in our country. Material and Method: In this study, we retrospectively evaluated the data of 63 patients with AA amyloidosis and tried to determine the primary underlying etiologic factors. Results: The most common primary etiologic factor was Familial Mediterranean Fever (FMF) (57%). In addition, rheumatoid arthritis, chronic bronchitis, tuberculosis, Crohn’s disease, sarcoidosis, ankylosing spondylitis and bronchiectasis were other etiologic causes. The most commonly used biopsy for diagnosis in this study was renal biopsy (63%). Conclusion: Further studies with large sample size are needed to confirm the results of our study and determine etiology of AA amyloidosis.

Özet

Amaç: Amiloidozis, anormal şekilde katlanmış amiloidproteininin vücudun çeşitli organ ve dokularında ekstraselüler alanda, fibriler şekilde birikmesiyle oluşan sistemikbir hastalıktır. Dokularda amiloid birikiminin gösterilmesiile amiloidozis kesin tanısı konur. Klinik olarak amiloidozisdüşünüldüğünde çeşitli dokulardan biyopsi alınır. Bu çalış-mada, AA amiloidozisin altında yatan diğer hastalıklarınülkemizdeki dağılımını araştırmak istedik.Gereç ve Yöntem: Bu çalışmada, AA amiloidoz tanılı 63hastanın verilerini resrospektif olarak değerlendirilerek,altta yatan primer etiyolojik nedenleri belirlemeye çalış-tık.Bulgular: En sık primer etyolojik neden, Ailevi AkdenizAteşi (AAA) (%57) olarak belirlendi. Bunun dışında romatoid artrit, kronik bronşit, tüberküloz, Crohn hastalığı,sarkoidoz, ankilozan spondilit ve bronşektazi diğer primeretiyojik nedenlerdi. Bu çalışmada, tanı için en sık böbrekbiyopsisi (%63) yapıldı.Sonuç: AA amiloidozis etiyolojisiyle ilgili yapmış olduğumuz bu çalışmanın daha büyük örneklemli çalışmalarladesteklenmesi gerekmektedir

🔖

Cite This Article

ELÇİOĞLU, Ö. C., ORAL, A., BAKAN, A., ECDER, S. A., ÖZKÖK, A., KUZGUN, G. Ş., BAHAT, K. A., ODABAŞ, A. R. (2022). Retrospective Evaluation of the Etiologies of the Patients Diagnosed as AA Amyloidosis. İstanbul Kanuni Sultan Süleyman Tıp Dergisi, Cilt: 10 - Sayı: 3, 113–116. https://ajindex.com/articles/551070

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Simms RW, Prout MN, Cohen AS. The epidemiology of AL and AA amyloidosis. Bailliere’s Clinical Rheumatology. 1994;8(3):627-34.
  2. Merlini G, Bellotti V. Molecular mechanisms of amy- loidosis. New England Journal of Medicine. 2003;349(6):583-96.
  3. Sait Ş, Alkanat MB, Akalın T, Özsan N. Amiloidozis tanısında zorluklar: Böbrek iğne biyopsisinden kaçını- labilir mi? Ege Tıp Derg. 2002;41(4)
  4. Pettersson T, Konttinen YT, editors. Amyloidosisrecent developments. Seminars in arthritis and rheumatism; 2010: Elsevier
  5. Röcken C, Shakespeare A. Pathology, diagnosis and pathogenesis of AA amyloidosis. Virchows Archiv. 2002;440(2):111-22.
  6. Büyükberber S, Dumlu Ş, Örmeci N. Amiloidozis ve gastrointestinal sistem tutulumu. Turkiye Klinikleri Journal of Medical Sciences. 1992;12(5):346-54
  7. Kyle R, Greipp P, editors. Amyloidosis (AL). Clinical and laboratory features in 229 cases. Mayo Clinic Proceedings; 1983
  8. Lachmann HJ, Goodman HJ, Gilbertson JA, Gallimore JR, Sabin CA, Gillmore JD, et al. Natural historyandoutcome in systemic AA amyloidosis. New England Journal of Medicine. 2007;356(23):2361-71.
  9. De Asúa DR, Costa R, Galván JM, Filigheddu MT, Trujillo D, Cadi-anos J. Systemic AA amyloidosis: epidemiology, diagnosis, and management. Clinical Epidemiology. 2014;6:369.
  10. Yıldız A, Tekinalp A, Hoyrazlı A, Bülent G, Aktaş N, Ayşegül O, et al. Böbrek biyopsisi ile reaktif amiloidoz tanısı alan hastaların retrospektif analizi. Uludağ Üniversitesi Tıp Fakültesi Dergisi. 38(2):63-5
  11. Yıldız A, Tekinalp A, Hoyrazlı A, Gül B, Aktaş N, Oruç A, et al. Böbrek biyopsisi ile reaktif amiloidoz tanısı alan hastaların retrospektif analizi
  12. Ensari C, Ensari A, Tümer N, Ertug E. Clinicopathological and epidemiological analysis of amyloidosis in Turkish patients. Nephrology Dialysis Transplantation. 2005;20(8):1721-5.
  13. Kocyigit I, Yilmaz MI, Şimşek Y, Unal A, Sipahioglu MH, Eroglu E, et al. The role of platelet activation in determining responseto therapy in patients with primary nephrotic syndrome. Platelets. 2013;24(6):474-9.
  14. Tuglular S, Yalcinkaya F, Paydas S, Oner A, Utas C, Bozfakioglu S, et al. A retrospective analysis for aetiology and clinical findings of 287 secondary amyloi