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Kronik Myeloid Lösemi Tanılı Hastaların Klinik Özellikleri ve Tedaviye Yanıtlarının Değerlendirilmesi: Tek Merkez Deneyimi

Yıl 2021, , 35 - 39, 28.04.2021
https://doi.org/10.35440/hutfd.853074

Öz

Amaç: KML periferik kanda miyeloid hücreler, eritroid seri ve trombositlerin artmasına yol açan, kemik iliğinde de belirgin miyeloid hiperplazisine neden olan klonal hematopoetik bir kök hücre hastalığıdır. KML tanılı hastaların tedavi ve takip kriterleri son yıllarda önemli oranda değişmiştir. İmatinib öncesi dönemde KML hidroksiüre, interferon, kemoterapi ve en etkili şekilde de allojenik kök hücre nakli ile tedavi edilmiştir. Tirozin kinaz inhibitörü imatinib mesilatın tedaviye eklenmesi önceki standart tedavilere kıyasla daha üstün bir genel sağ kalım sağlamıştır. Bu çalışmadaki amacımız, kliniğimizde tedavi edilen KML hastalarının demografik özelliklerini, klinik özelliklerini, tedavi ve izleme stratejilerini, yanıt durumlarını ve genel sağ kalım oranlarını belirlemektir.
Materyal ve Metod: 2003 ve 2019 tarihleri arasında kronik faz KML tanısı koyulan ve dosya kayıtlarına ulaşılabilen 110 hasta çalışmaya dahil edildi. Hastaların demografik özellikleri, klinik bulguları, laboratuvar değerleri, ultrasonografi bulguları ve kemik iliği patoloji sonuçları değerlendirildi.
Bulgular: 110 tane hastanın 59 (%53.6) tanesi erkek, 51 (%46.4) tanesi kadındı. Tanı anındaki medyan yaş 49.5 (18-82) saptandı. Tanı anında sadece 32 (%29.0) hasta semptomatikti. Hastaların tanı anında 71 (%64.5) tanesinde splenomegali ve 51 (%46.4) tanesinde hepatomegali vardı. Tüm hastalara ilk basamakta imatinib 400 mg verilmişti. İmatinib tedavisi ile 12. ayda THY oranı %100, TSY oranı %72.5 ve MMR oranı ise %69.6 saptandı. Takiplerde 3 (%2.7) hastanın blastik faza progrese olduğu görüldü. Tüm hastaların OS oranı %86.4 saptandı.
Sonuç: KML hastalarının ilk basamak tedavisinde imatinib tolere edilebilir, etkili ve güvenli bir ajan olduğunu kanıtlamıştır. İmatinib sonrası tedavi değişikliği yapılırken hastaların komorbiditeleri göz önünde bulundurulmalıdır.

Destekleyen Kurum

yok

Proje Numarası

yok

Teşekkür

yok

Kaynakça

  • 1. Sawyers CL. Chronic myeloid leukemia. Vol. 340, New England Journal of Medicine. Massachusetts Medical Society ; 1999. p. 1330–40.
  • 2. Goldman JM, Melo J V. Mechanisms of disease: Chronic myeloid leukemia - Advances in biology and new approaches to treatment. Vol. 349, New England Journal of Medicine. Massachusetts Medical Society ; 2003. p. 1451–64.
  • 3. Corm S, Roche L, Micol JB, Coiteux V, Bossard N, Nicolini FE, et al. Changes in the dynamics of the excess mortality rate in chronic phase-chronic myeloid leukemia over 1990-2007: A population study. Blood. 2011;118(16):4331–7.
  • 4. Groffen J, Stephenson JR, Heisterkamp N, de Klein A, Bartram CR, Grosveld G. Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22. Cell. 1984;36(1):93–9.
  • 5. Davis RL, Konopka JB, Witte ON. Chromosomal Translocation Generates Altered c-abl Proteins with Similar In Vitro Kinase Properties. Vol. 5, MOLECULAR AND CELLULAR BIOLOGY. 1985.
  • 6. Ren R. Mechanisms of BCR-ABL in the pathogenesis of chronic myelogenous leukaemia. Vol. 5, Nature Reviews Cancer. Nature Publishing Group; 2005. p. 172–83.
  • 7. Vardiman JW. Chronic Myelogenous Leukemia, BCR-ABL1+. Am J Clin Pathol. 2009;132:250–60.
  • 8. Steinberg M. Dasatinib: A tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia and philadelphia chromosome-positive acute lymphoblastic leukemia. Clin Ther. 2007 Nov 1;29(11):2289–308.
  • 9. Sacchi S, Kantarjian HM, O’Brien S, Cortes J, Rios MB, Giles FJ, et al. Chronic myelogenous leukemia in nonlymphoid blastic phase: Analysis of the results of first salvage therapy with three different treatment approaches for 162 patients. Cancer. 1999;86(12):2632–41.
  • 10. Savage DG, Szydlo RM, Goldman JM. Clinical features at diagnosis in 430 patients with chronic myeloid leukaemia seen at a referral centre over a 16-year period. Br J Haematol. 1997 Jan 1;96(1):111–6.
  • 11. Tefferi A, Thiele J, Orazi A, Kvasnicka HM, Barbui T, Hanson CA, et al. Proposals and rationale for revision of the World Health Organization diagnostic criteria for polycythemia vera, essential thrombocythemia, and primary myelofibrosis: Recommendations from an ad hoc international expert panel. Blood. 2007;110(4):1092–7.
  • 12. Sokal JE, Cox EB, Baccarani M, Tura S, Gomez GA, Robertson JE, et al. Prognostic discrimination in "good-risk" chronic granulocytic leukemia. Blood. 1984 Apr;63(4):789-99.
  • 13. O’Brien SG, Guilhot F, Larson RA, Gathmann I, Baccarani M, Cervantes F, et al. Imatinib Compared with Interferon and Low-Dose Cytarabine for Newly Diagnosed Chronic-Phase Chronic Myeloid Leukemia. N Engl J Med. 2003 Mar 13;348(11):994–1004.
  • 14. Hughes TP, Saglio G, Kantarjian HM, Guilhot F, Niederwieser D, Rosti G, et al. Early molecular response predicts outcomes in patients with chronic myeloid leukemia in chronic phase treated with frontline nilotinib or imatinib. Blood. 2014;123(9):1353–60.
  • 15. Jabbour E, Kantarjian HM, Saglio G, Steegmann JL, Shah NP, Boqué C, et al. Early response with dasatinib or imatinib in chronic myeloid leukemia: 3-year follow-up from a randomized phase 3 trial (DASISION). Blood. 2014;123(4):494–500.
  • 16. Jabbour E, Kantarjian H. Chronic myeloid leukemia: 2018 update on diagnosis, therapy and monitoring. Am J Hematol. 2018 Mar 1;93(3):442–59.
  • 17. Saglio G, Kim D-W, Issaragrisil S, le Coutre P, Etienne G, Lobo C, et al. Nilotinib versus Imatinib for Newly Diagnosed Chronic Myeloid Leukemia. N Engl J Med. 2010 Jun 17;362(24):2251–9.
  • 18. Sahin F, Saydam G, Comert M, Uz B, Yavuz AS. Turkish Chronic Myeloid Leukemia Study: Retrospective Sectional Analysis of CML Patients. Turkish J Hematol. 2013;30(4):351–8.
  • 19. Smith A, Howell D, Patmore R, Jack A, Roman E. Incidence of haematological malignancy by sub-type: A report from the Haematological Malignancy Research Network. Br J Cancer. 2011;105(11):1684–92.
  • 20. Faderl S, Talpaz M, Estrov Z, O’Brien S, Kurzrock R, Kantarjian HM. The Biology of Chronic Myeloid Leukemia. N Engl J Med. 1999 Jul 15;341(3):164–72.
  • 21. Al-Amri AM. Outcome of Chronic Myeloid Leukemia-Chronic Phase Patients Treated With Imatinib: A Local Experience. Clin Lymphoma, Myeloma Leuk. 2018;18(3):199–203.
  • 22. Ben Lakhal R, Ghedira H, Bellaaj H, Ben Youssef Y, Menif S, Manai Z, et al. Chronic myeloid leukemia patients in Tunisia: epidemiology and outcome in the imatinib era (a multicentric experience). Ann Hematol. 2018;97(4):597–604.
  • 23. Hehlmann R. How I treat CML blast crisis. Vol. 120, Blood. American Society of Hematology; 2012. p. 737–47.

Evaluation of clinical features and treatment responses in patients with chronic myeloid leukemia: A single center experience

Yıl 2021, , 35 - 39, 28.04.2021
https://doi.org/10.35440/hutfd.853074

Öz

Background: Chronic myeloid leukemia is a clonal hematopoietic stem cell disorder that leads to an increase in myeloid cells, erythroid series, and platelets in peripheral blood and causes pronounced myeloid hyperplasia in the bone marrow. The treatment and follow-up criteria in patients with CML have changed significantly in the recent years. In the pre-imatinib period, CML has been treated with hydroxyurea, interferon therapy, chemotherapy, and most effectively, allogenic stem cell transplantation. The addition of imatinib mesylate, a tyrosine kinase inhibitor, to the treatment regime provided a superior overall survival rate compared to previous standard treatments. In this study, our aim is to demonstrate the demographic characteristics, clinical features, treatment and follow-up strategies, response status, and general survival rates of CML patients treated in our clinic.
Materials and Methods: 110 patients who were diagnosed with chronic phase CML during 2003–2019 were included in this study. The demographic characteristics and clinical findings including laboratory values, ultrasound findings, and bone marrow pathology results were evaluated retrospectively from their medical records
Results: Among the 110 patients included, 59 (53.6%) were male, and 51 (46.4%) were female, and the median age was 49.5 (18–82). At the time of diagnosis, only 32 (29.0%) patients were symptomatic, 71 (64.5%) had splenomegaly, and 51 (46.4%) had hepatomegaly. All patients were given 400 mg of imatinib as first-line therapy. With imatinib treatment, the rates of complete hematologic response (CHR), complete cytogenetic response (CyCR), and major molecular response (MMR) were 100.0%, 72.5% and 69.6%, respectively. In the follow-up, 3 (2.7%) patients were observed to progress to the blastic phase. The overall survival rate was 86.4%.
Conclusions: Imatinib has proven to be a tolerable, effective and safe agent in the first-line treatment of CML patients. Treatment choice after imatinib should take into consideration the patients' comorbidities.

Proje Numarası

yok

Kaynakça

  • 1. Sawyers CL. Chronic myeloid leukemia. Vol. 340, New England Journal of Medicine. Massachusetts Medical Society ; 1999. p. 1330–40.
  • 2. Goldman JM, Melo J V. Mechanisms of disease: Chronic myeloid leukemia - Advances in biology and new approaches to treatment. Vol. 349, New England Journal of Medicine. Massachusetts Medical Society ; 2003. p. 1451–64.
  • 3. Corm S, Roche L, Micol JB, Coiteux V, Bossard N, Nicolini FE, et al. Changes in the dynamics of the excess mortality rate in chronic phase-chronic myeloid leukemia over 1990-2007: A population study. Blood. 2011;118(16):4331–7.
  • 4. Groffen J, Stephenson JR, Heisterkamp N, de Klein A, Bartram CR, Grosveld G. Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22. Cell. 1984;36(1):93–9.
  • 5. Davis RL, Konopka JB, Witte ON. Chromosomal Translocation Generates Altered c-abl Proteins with Similar In Vitro Kinase Properties. Vol. 5, MOLECULAR AND CELLULAR BIOLOGY. 1985.
  • 6. Ren R. Mechanisms of BCR-ABL in the pathogenesis of chronic myelogenous leukaemia. Vol. 5, Nature Reviews Cancer. Nature Publishing Group; 2005. p. 172–83.
  • 7. Vardiman JW. Chronic Myelogenous Leukemia, BCR-ABL1+. Am J Clin Pathol. 2009;132:250–60.
  • 8. Steinberg M. Dasatinib: A tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia and philadelphia chromosome-positive acute lymphoblastic leukemia. Clin Ther. 2007 Nov 1;29(11):2289–308.
  • 9. Sacchi S, Kantarjian HM, O’Brien S, Cortes J, Rios MB, Giles FJ, et al. Chronic myelogenous leukemia in nonlymphoid blastic phase: Analysis of the results of first salvage therapy with three different treatment approaches for 162 patients. Cancer. 1999;86(12):2632–41.
  • 10. Savage DG, Szydlo RM, Goldman JM. Clinical features at diagnosis in 430 patients with chronic myeloid leukaemia seen at a referral centre over a 16-year period. Br J Haematol. 1997 Jan 1;96(1):111–6.
  • 11. Tefferi A, Thiele J, Orazi A, Kvasnicka HM, Barbui T, Hanson CA, et al. Proposals and rationale for revision of the World Health Organization diagnostic criteria for polycythemia vera, essential thrombocythemia, and primary myelofibrosis: Recommendations from an ad hoc international expert panel. Blood. 2007;110(4):1092–7.
  • 12. Sokal JE, Cox EB, Baccarani M, Tura S, Gomez GA, Robertson JE, et al. Prognostic discrimination in "good-risk" chronic granulocytic leukemia. Blood. 1984 Apr;63(4):789-99.
  • 13. O’Brien SG, Guilhot F, Larson RA, Gathmann I, Baccarani M, Cervantes F, et al. Imatinib Compared with Interferon and Low-Dose Cytarabine for Newly Diagnosed Chronic-Phase Chronic Myeloid Leukemia. N Engl J Med. 2003 Mar 13;348(11):994–1004.
  • 14. Hughes TP, Saglio G, Kantarjian HM, Guilhot F, Niederwieser D, Rosti G, et al. Early molecular response predicts outcomes in patients with chronic myeloid leukemia in chronic phase treated with frontline nilotinib or imatinib. Blood. 2014;123(9):1353–60.
  • 15. Jabbour E, Kantarjian HM, Saglio G, Steegmann JL, Shah NP, Boqué C, et al. Early response with dasatinib or imatinib in chronic myeloid leukemia: 3-year follow-up from a randomized phase 3 trial (DASISION). Blood. 2014;123(4):494–500.
  • 16. Jabbour E, Kantarjian H. Chronic myeloid leukemia: 2018 update on diagnosis, therapy and monitoring. Am J Hematol. 2018 Mar 1;93(3):442–59.
  • 17. Saglio G, Kim D-W, Issaragrisil S, le Coutre P, Etienne G, Lobo C, et al. Nilotinib versus Imatinib for Newly Diagnosed Chronic Myeloid Leukemia. N Engl J Med. 2010 Jun 17;362(24):2251–9.
  • 18. Sahin F, Saydam G, Comert M, Uz B, Yavuz AS. Turkish Chronic Myeloid Leukemia Study: Retrospective Sectional Analysis of CML Patients. Turkish J Hematol. 2013;30(4):351–8.
  • 19. Smith A, Howell D, Patmore R, Jack A, Roman E. Incidence of haematological malignancy by sub-type: A report from the Haematological Malignancy Research Network. Br J Cancer. 2011;105(11):1684–92.
  • 20. Faderl S, Talpaz M, Estrov Z, O’Brien S, Kurzrock R, Kantarjian HM. The Biology of Chronic Myeloid Leukemia. N Engl J Med. 1999 Jul 15;341(3):164–72.
  • 21. Al-Amri AM. Outcome of Chronic Myeloid Leukemia-Chronic Phase Patients Treated With Imatinib: A Local Experience. Clin Lymphoma, Myeloma Leuk. 2018;18(3):199–203.
  • 22. Ben Lakhal R, Ghedira H, Bellaaj H, Ben Youssef Y, Menif S, Manai Z, et al. Chronic myeloid leukemia patients in Tunisia: epidemiology and outcome in the imatinib era (a multicentric experience). Ann Hematol. 2018;97(4):597–604.
  • 23. Hehlmann R. How I treat CML blast crisis. Vol. 120, Blood. American Society of Hematology; 2012. p. 737–47.
Toplam 23 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular Klinik Tıp Bilimleri
Bölüm Araştırma Makalesi
Yazarlar

Mesut Göçer 0000-0002-0346-7154

Erdal Kurtoğlu 0000-0002-6867-6053

Proje Numarası yok
Yayımlanma Tarihi 28 Nisan 2021
Gönderilme Tarihi 4 Ocak 2021
Kabul Tarihi 9 Şubat 2021
Yayımlandığı Sayı Yıl 2021

Kaynak Göster

Vancouver Göçer M, Kurtoğlu E. Evaluation of clinical features and treatment responses in patients with chronic myeloid leukemia: A single center experience. Harran Üniversitesi Tıp Fakültesi Dergisi. 2021;18(1):35-9.

Harran Üniversitesi Tıp Fakültesi Dergisi  / Journal of Harran University Medical Faculty