Abstract
Background As2O3, on the one hand is successful in the treatment of acute promyelocytic leukemia (APL), on the other hand many side effects may occur during the early arsenic treatment. We assessed the effectiveness and security of two As2O3 administration methods in acute promyelocytic leukaemia treatment.
Methods seventy-four cases of APL treated using As2O3 in two administration methods have been studied randomly. Thirty-two cases were administrated As2O3 with routine method as control, the other 42 cases were given As2O3 with a ‘continuous and slowing intravenous infusion’ method. Firstly, we calculated the total quantity of As2O3 needed every day of every patient according to the criteria of 0.16mg/kg, then gave half of the total amount of As2O3 in the morning and the other half in the afternoon, diluted each half of total amount of As2O3 with 5% glucose 250ml and infused at the speed of 8 drops/min, collected the blood serums of the patients treated with the two methods respectively at different time points, and finally we assayed arsenic concentration in blood serums.
Results Most of the APL treated by As2O3 gained complete remission at the time of 4th week with the two administrated methods. The total effective rate in ‘continuous and slowing intravenous infusion ‘ group was 93.75%, while that in control group was 83.3%. The effective arsenic level in blood circulation in ‘continuous and slowing intravenous infusion’ group was lasted at least 18.38±3.27 hours, while in control group was lasted 9.38 ±1.58 hours, the average hospitalization duration in ‘continuous and slowing intravenous infusion ‘ group was26.4±2.04 days, while that in control group was 35.7±4.78 days.
Conclusions The ‘continuous and slowing intravenous infusion’ method can relieve leukocytosis, increase complete remission (CR) rate of APL, and accelerate to CR.
Table1 arsenic concentration, its lasting time and the average time reaching CR (mean± SD)
| Group . | (n) . | The peakconcentration in 24h μmol/L) ( . | The lasting time above μmol/L(h / 24h) 1 . | The average time reaching CR(d) . |
|---|---|---|---|---|
| Experiment | 42 | 3.32±0.55 | 18.38±3.27 | 26.4±2.04 |
| control | 32 | 5.84±1.05 | 9.38 ±1.58 | 35.7±4.78 |
| t-value | 6.08 | 3.64 | 4.78 | |
| P -value | < 0.01 | < 0.01 | < 0.01 |
| Group . | (n) . | The peakconcentration in 24h μmol/L) ( . | The lasting time above μmol/L(h / 24h) 1 . | The average time reaching CR(d) . |
|---|---|---|---|---|
| Experiment | 42 | 3.32±0.55 | 18.38±3.27 | 26.4±2.04 |
| control | 32 | 5.84±1.05 | 9.38 ±1.58 | 35.7±4.78 |
| t-value | 6.08 | 3.64 | 4.78 | |
| P -value | < 0.01 | < 0.01 | < 0.01 |
Table2 The incidence of side effects in As2O3 therapy ( %)
| peripheral WBC↑ | DIC | QTc prolongation | nerve conductspeed ↓ | cerebral vasospasm | liver disfunction | |
| experiment (n=42) | 31.3(15) | 16.7(8) | 8.1(4) | 8.1(4) | 14.6(7) | 14.6(7) |
| control (n=32) | 71.2(34) | 35.4(17) | 25.0(12) | 6.3(3) | 33.3(16) | 22.9(11) |
| X2 - value | 17.64 | 4.38 | 4.80 | 0.14 | 4.62 | 1.08 |
| P - value | <0.001 | < 0.05 | < 0.05 | > 0.1 | < 0.05 | > 0.05 |
| peripheral WBC↑ | DIC | QTc prolongation | nerve conductspeed ↓ | cerebral vasospasm | liver disfunction | |
| experiment (n=42) | 31.3(15) | 16.7(8) | 8.1(4) | 8.1(4) | 14.6(7) | 14.6(7) |
| control (n=32) | 71.2(34) | 35.4(17) | 25.0(12) | 6.3(3) | 33.3(16) | 22.9(11) |
| X2 - value | 17.64 | 4.38 | 4.80 | 0.14 | 4.62 | 1.08 |
| P - value | <0.001 | < 0.05 | < 0.05 | > 0.1 | < 0.05 | > 0.05 |
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