Response of Elevated Serum Soluble Interleukin-2 Receptor (sIL-2R) and Overexpression of Glucose-6-Phosphate Dehydrogenase (G6PD) in Patients with Chronic Myelogenous Leukemia Treated with Imatinib Mesylate.

Regulation of intracellular redox potential is important for regulation of cell growth. G6PD functions to catalyze the first step in the pentose phosphate pathway physiologically providing the NADPH required for reductive biosynthesis and detoxification of free-radicals and peroxides in mature red blood cells. We present two cases of patients (pts) with Chronic Myelogenous Leukemia-chronic phase (CML-cp) with significant overexpression of sIL-2R and G6PD. Serum elevated levels of sIL-2R and G6PD correlated to CML stage and response to therapy with imatinib; one male pt and one female pt with white blood cell counts of 80 and 21,000 X 10⁹ per liter and a mean sIL-2R and G6PD levels of 26.975 X 10³ pg/ml and 14.10 units/gHb respectively. Both pts had BCR/abl-RT-PCR positive gene rearrangements with b2a2 in peripheral blood and bone marrow. Chromosomal abnormalities of female pt was consistent with CML-cp (t 9; 22) ( q34;q11.2) philadelphia chromosome. Treatment of both pts with imatinib 400 mg orally daily resulted in reduction toward normal levels of sIL-2R and G6PD. Our female pt had to have therapy interrupted due to severe gastrointestinal and myelosuppression with cardiac irritation, edema, headaches and arthralgia. She was changed to 300 mg of imatinib with a proton-pump inhibitor, growth factor G-CSF, and a cox-2 inhibitor with excellent tolerance and response to therapy ( see table I).

Response of sIL-2R and G6PD To Treatment With Imatinib Mesylate

CONCLUSIONS: Overexpression of sIL-2R and G6PD in CML-cp pts treated with tyrosine kinase inhibitor imatinib mesylate were significantly reduced to levels within normal limits after twelve months of therapy. Peripheral blood sera sIL-2R and erythrocyte G6PD levels in CML-cp pts may be useful clinical and prognostic indicators of leukemic cell burden.