Clinico Hematological Profile and Phase Distribution of Chronic Myeloid Leukemia
Authors/Creators
- 1. Junior Resident-3, Department of General Medicine, Government Medical College & Cancer Hospital, Aurangabad, Maharashtra, India
- 2. Associate Professor, Department of General Medicine, Government Medical College & Cancer Hospital, Aurangabad, Maharashtra, India
- 3. Professor & HOD, Department of General Medicine, Government Medical College & Cancer Hospital, Aurangabad, Maharashtra, India
Description
Chronic myeloid leukemia is a clonal hematopoietic stem cell disorder. CML is caused by the BCR-ABL1 chimeric gene product, which results from a reciprocal balanced translocation between the long arms of chromosomes 9 and 22, t (9; 22) (q34.1; q11.2), known as the Philadelphia chromosome (Ph) and its codes for a constitutively active tyrosine kinase. CML is a common hematological malignancy in adults and accounts for 15% of all hematological malignancies. Worldwide incidence of CML is 1-2 cases per 1 lakh population per year. Material and Methods: This was a cross sectional, observational and Descriptive study conducted in tertiary care centre & teaching institute during the period from November 2018 to December 2020. Total 100 patients of Chronic Myeloid Leukemia irrespective of etiology were included in this study. Results: In our study most of the patients were aged between 31-40 years. Majority of the patients were males (62%) and male to female ratio was1.6:1. Generalized weakness was the most common symptom (52%) followed by fatigue (35%), pain in abdomen (22%), Anemia (46%) and splenomegaly (58%) & 16% of the patients were Asymptomatic. Among 100 CML cases, Chronic phase (CP) cases were 95%, Accelerated phase (AP) cases were 3%, Blast crisis (BC) cases were 2%. But majority of patients were in chronic phase (95%) which is a good sign as the disease is completely treatable in the modern era. Conclusion: CML accounts for one of the most common leukemia which is treatable with oral medications when presented at an early stage. TKIs have revolutionized the treatment of CML.
Abstract (English)
Chronic myeloid leukemia is a clonal hematopoietic stem cell disorder. CML is caused by the BCR-ABL1 chimeric gene product, which results from a reciprocal balanced translocation between the long arms of chromosomes 9 and 22, t (9; 22) (q34.1; q11.2), known as the Philadelphia chromosome (Ph) and its codes for a constitutively active tyrosine kinase. CML is a common hematological malignancy in adults and accounts for 15% of all hematological malignancies. Worldwide incidence of CML is 1-2 cases per 1 lakh population per year. Material and Methods: This was a cross sectional, observational and Descriptive study conducted in tertiary care centre & teaching institute during the period from November 2018 to December 2020. Total 100 patients of Chronic Myeloid Leukemia irrespective of etiology were included in this study. Results: In our study most of the patients were aged between 31-40 years. Majority of the patients were males (62%) and male to female ratio was1.6:1. Generalized weakness was the most common symptom (52%) followed by fatigue (35%), pain in abdomen (22%), Anemia (46%) and splenomegaly (58%) & 16% of the patients were Asymptomatic. Among 100 CML cases, Chronic phase (CP) cases were 95%, Accelerated phase (AP) cases were 3%, Blast crisis (BC) cases were 2%. But majority of patients were in chronic phase (95%) which is a good sign as the disease is completely treatable in the modern era. Conclusion: CML accounts for one of the most common leukemia which is treatable with oral medications when presented at an early stage. TKIs have revolutionized the treatment of CML.
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IJPCR,Vol15,Issue3,Article185.pdf
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Additional details
Dates
- Accepted
-
2023-02-22
Software
- Repository URL
- https://impactfactor.org/PDF/IJPCR/15/IJPCR,Vol15,Issue3,Article185.pdf
- Development Status
- Active
References
- 1. Geary CG. The story of chronic myeloid leukaemia. Br J Haematol. 2000;10:2-11 2. Bhutani M, Kochupillai V. Hematological malignancies in India, in Kumar L (editor): Progress in Hematologic Oncology. Pub. TheAdvanced Research Foundation New York, New York 2003;10. 3. Ruchi Sinha, Iffat Jamal, Priyamvada, Punam Prasad Bhadani. Clinicohaematological Profile of Chronic Myeloid Leukaemia: An Institutional Based Study from Bihar. National Journal of Laboratory Medicine.2019, Jan, Vol-8(2):PO26-PO29 4. Baccarani M, Pileri S, Steegnmann JL, Muller M, Soverini S, Dreyling M. Chronic myeloid leukaemia: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow up. Ann Oncol.2012;23:72-75 5. Steven HS, Elias C, Nancy LH, Elaine SJ, Stefano AP, Herald S, et al. WHO Classification of Tumors of Haematopoietic and Lymphoid Tissues. Revised 4 th edition. 2017;32-35 6. Hagop K, Jorge C. Chronic Myeloid Leukemia. In: Jameson, Fauci, Kasoer, Hauser, Lango, Loscalzo, editors. Harrison's Principles of internal medicine. 20th ed. Newyork: McGraw Hill education; 2018, p748-757 7. Ahmed R, Naqi N, Hussain I, Khattak BK, Nadeem M, Iqbal J. Presenting phases of chronic myeloid leukaemia. J Coll Physicians Surg Pak. 2009;19 (8):469-72. 8. Malhotra H, Sharma R, Singh Y, Chaturvedi H. Report of chronic myeloid leukaemia SMS Medical College Hospital. Indian J Med Paediatr Oncol. 2013;34(3):177-79. 9. Bhatti F, Ahmed S, Ali N. Clinical and hematological features of 335patientss of chronic myelogenous leukaemia diagnosed at single centre in northern Pakistan. Clin Med Insights: Blood Disord.2014;5(5):15-24. 10. Prasad RR, Singh P. Report of chronic myeloid leukaemia from Indira Gandhi Institute of Medical Sciences, Regional Cancer Center, 2002-2009. Indian J Med Paediatr Oncol.2013;34 (3):172-74. 11. McClatchey, KD, MD, DDS. Clinical Laboratory Medicine, 2nd Edition. Philadelphia: Lippincott Williams & Wilkins, 2002. Copyright ©2002 Lippincott Williams & Wilkins. 12. Milojkovic D, Nicholson E, Apperley JF, et al. Early prediction of success or failure using second generation tyrosine kinase inhibitors for chronic myeloid le ukemia. Haematologica. 2010; 92:224– 231. 13. Soverini S, Hochhaus A, Nicolini FE, et al. BCR-ABL kinase domain mutation analysis in chronic myeloid leukemia patientss treated with tyrosine kinase inhibitors: recommendations from an expert panel on behalf of European Leukemia Net Blood. 2011;118(5):1208- 12 14. Beane Freeman LE, Blair A, Lubin JH, Stewart PA, HayesRB, Hoover RN, et al. Mortality from lymphohematopoietic malignancies among workers in formaldehyde industries: The National Cancer Institute Cohort. J Natl CancerInst. 2009;101(10):751-61. 15. Mishra P, Seth T, Mahapatra M, Saxena R. Report of chronic myeloid leukaemia in chronic phase from All India Institute of Medical Sciences,1990-2010.Indian J Med Paediatr Oncol. 2013; 34:159-63. 16. Chang F, Qazi RA, Khan M, Baloch S, Sahito MM, Mir A. Clinico hematological profile and phase distribution of chronic myeloid leukemia. Biology and Medicine. 2015;7(5):1. 17. Yagh maie M, Ghaffari SH, Ghavamzadeh A, Ali moghaddam K, Jahani M, Mousavi SA, et al. Frequency of BCR-ABL fusion transcripts in Iranian patientss with chronic myeloid leukaemia. Arch Iran Med. 2008; 11(3):247-51.