oa Elevation of Alpha Acid Glycoprotein (AGP) does not Correlate with the Resistance of Chronic Myeloid Leukaemia (CML) to Imatinib Mesylate (IM)

Background: Despite the efficacy of IM in treating CML, high degree of resistance has already been noted.

AGP may reduce drug efficacy through its ability to interact with IM.

Objectives: Could the level of AGP be correlated with CML resistance/response to treatment and if it could be employed as a biological marker for CML resistance.

Methods: 25 CML patients were investigated for AGP level, serum samples were analysed to determine AGP level. Immunoturbidimetric assay is based on the formation of a precipitate of AGP with a specific antiserum. The mean, variance and significant difference between the means were determined using Student's t test and significance was determined when p value was ←0.05.

Results: Over 2 years a total of 89 serum samples were collected from 25 CML patients treated at Al Amal hospital in Qatar. Ten samples from 10 healthy volunteers were collected as a control group.

9 patients presented with CML at Chronic Phase (CP), 5 at Accelerated Phase (AP), 6 patients progressed while on treatment and five more patients were undergoing treatment and were at Complete Haematological Remission (CHR) at time of sample collection.

The mean AGP levels were 1.2 (±0.3), 1.61 (±0.4), 1.01 (±0.08), 1.07 (±0.09), and 0.72 (±0.04) for CP, AP, Poor Responders, CHR and controls respectively.

The mean AGP level for the control group was significantly lower when compared with any of the diseased group.

The significant differences amongst CP, AP, Poor Responders patients, CHR patients and control group were (p) 0.001, 0.03, 0.003, 0.005 respectively.

On the other hand, among these different CML groups there was no significant difference in AGP levels even when correlated with white blood cells, platelets and/or basophiles.

However, there was significant difference between CP and AP patients (P value 0.002) when AGP was correlated with WBC's.

Nonetheless AGP level could not be correlated with course of disease.

Conclusions: The noticed resistance in our CML patient population could not be correlated with AGP levels, as patients were responding or resisting treatment without any recognisable pattern of AGP; even when patients achieved CHR they might still had elevated AGP levels.