BCR-ABL Transcript Level as Compared to LDH and Uric Acid Among Chronic Myeloid Leukemic Patients.

BACKGROUND

Chronic myeloid leukemia is characterized by the presence of the Philadelphia chromosome, which is caused by the breakpoint cluster region-Abelson fusion or joined gene. A high concentration of BCR-ABL transcripts level can strongly forecast cytogenetic and hematologic reversion in CML patients. However, the molecular test for BCR-ABL is costly and hardly available in developing countries with low and middle-income. Owing to this, it is required to examine other cost-effective and best diagnostic (prognostic) biomarkers.

OBJECTIVE

The present study aimed to estimate the total LDH and uric acid level as compared to BCR-ABL transcript level among treated and treatment-naive Chronic Myeloid Leukemia (CML) patients.

METHODS

A comparative cross-sectional study design was used to include eighty-one (81) CML patients tested for BCR-ABL by GeneXpert RT-PCR transcript level at Tikur Anbessa Specialized Hospital. The current study correlates LDH with BCR-ABL and hematological parameters using the spearman correlation, Mann-Whitney U test, and roc curve data analysis tool.

RESULTS

A total of 81 CML patients were assayed; 46(56.8%) of them were in the medically treated group, and the remaining 35 (43.2%) were treatment-naive patients. Significant positive correlations were observed between LDH and BCR-ABL (r=0.79, P<0.001).The correlation coefficient value of uric acid (r=0.295, p<0.008) with BCR-ABL showed a weak correlation between the two test parameters. There was a statistically noteworthy (p<0.05) difference in the median level of BCR-ABL and LDH among patients in the treatment group (median=21%, 350 U/L) and the treatment- naive group (median=57%, 1246 U/L), respectively. For uric acid, there was no statistically significant (p<0.542) difference between the study group. The AUC for LDH, Basophil, and WBC was 0.881, 0.889, and 0.748, respectively, which showed better performance for the follow-up of patients with CML than uric acid (0.695) and platelets (0.70).

CONCLUSION

The CML LDH value strongly correlated with BCR-ABL transcript level, whereas uric acid was weakly correlated with BCR-ABL. Hence, in parallel with the BRC-ABL transcript level, these findings could be a patent for confirming the capability of LDH as an alternative cost-- effective diagnostic, prognostic biomarker, and a novel therapeutic target in CML disease.