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Correspondence

Home Blood-Pressure Monitoring in Patients Receiving Sunitinib

N Engl J Med 2008; 358:95-97January 3, 2008

Article

To the Editor:

The use of sunitinib, an inhibitor of the split-kinase-domain family of receptor tyrosine kinases (including vascular endothelial growth factor receptor types 1 and 21), has been associated with a 15 to 25% incidence of hypertension in patients with advanced renal-cell carcinoma2,3; a similar incidence has been associated with other antiangiogenic drugs.3,4 We report on 14 consecutive patients with metastatic renal-cell carcinoma who were being treated with sunitinib and in whom home monitoring of blood pressure by teletransmission revealed a rapid, marked increase in blood pressure, an effect that was not detected by casual office measurement of blood pressure.

The 14 patients, all of whom had undergone unilateral nephrectomy, received two cycles of sunitinib at a dose of 50 mg daily for 4 weeks, followed by 2 weeks without treatment. The patients measured their blood pressure and heart rate at home with the use of a validated semiautomatic electronic device and teletransmitted the values weekly.

In seven patients who were initially normotensive, there was a substantial increase in both systolic and diastolic blood pressures by week 1 (mean [±SD] increase in systolic blood pressure, 13.6±8.4 mm Hg; mean increase in diastolic blood pressure, 10.9±4.7 mm Hg) (Figure 1AFigure 1Changes in Systolic and Diastolic Blood Pressure and Heart Rate.). Thereafter, the mean home blood-pressure values continued to rise, with increases of 22.2±6.4 mm Hg systolic and 17.2±6.0 mm Hg diastolic by week 4. All seven normotensive patients had become hypertensive by week 4. Home blood-pressure values decreased within 1 to 2 weeks after the withdrawal of sunitinib. The pattern in blood pressure that was observed during the second cycle was similar but even more marked than that during the first cycle. Office measurements of blood pressure during scheduled visits at weeks 4, 6, 10, and 12 revealed a pattern similar to that at home, but the changes in blood pressure were much smaller and more variable than those measured by home monitoring (data not shown).

In the seven patients who were initially hypertensive, the mean home blood pressure increased from 146±11.9 mm Hg systolic and 80.9±6.9 mm Hg diastolic at baseline to 162±14.2 mm Hg systolic and 92.1±11.5 mm Hg diastolic by week 1 (Figure 1B). Thereafter, from week 2 to week 12, blood pressure tended to plateau at values that were not substantially different from baseline values, probably because additional antihypertensive drugs were prescribed to control hypertension in these patients. Office measurements of blood pressure did not show substantial changes (data not shown).

The pattern of changes in the heart rate was the opposite of the pattern of changes in home blood pressure: when the blood pressure increased, the heart rate decreased in both initially normotensive and initially hypertensive patients (Figure 1A and 1B). The changes in blood pressure and heart rate were significantly and negatively correlated in both groups (r=0.47, P=0.003) (data not shown).

Our study suggests that rapid and large increases in blood pressure should be anticipated in patients who are treated with sunitinib; consequently, close monitoring of blood pressure through home measurement is indicated. The routine use of home blood-pressure monitoring may be valuable in standard care for early detection and accurate assessment of blood-pressure changes in patients treated with antiangiogenic drugs.

Michel Azizi, M.D., Ph.D.
Antoine Chedid, M.D.
Stéphane Oudard, M.D., Ph.D.
Hôpital Européen Georges Pompidou, 75015 Paris, France

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