Skip to main content

Table 2 Mechanism and incidence of hypertension associated with cancer drug class and proposed treatment recommendation

From: Etiology and management of hypertension in patients with cancer

Cancer Drug Class Mechanism of Hypertension Incidence of Hypertension Recommended Treatment
VEGF inhibitors endothelial dysfunction, decrease in nitric oxide and prostacyclin I, increase in endothelin, vascular remodeling, capillary rarefaction, decreased renal excretion of sodium All Grade: 17–80%
Grade 3–4: 6–9%
CCB (e.g., amlodipine)
ACEI (e.g., lisinopril)
TKI decrease in NOS activity, activation of RAAS All Grade: 17–47%
Grade 3–4: 4–6%
ACEI
CCB
Proteasome inhibitors angiotensin-induced hypertension, aortic vascular remodeling All Grade: 3–15% ACEI or ARB (e.g., losartan)
Alkylating agents oxidative damage to endothelial cells, increased intimal thickness, abnormal vascular remodeling, sodium retention All Grade: 36–50% ACEI or ARB
Steroids promoting sodium and water retention, intrinsic vasoconstricting properties, enhanced sensitivity to endogenous vasopressors All Grade: up to 13%a Diuretics (e.g., hydrochlorothiazide)
Mineralocorticoid antagonists (e.g., spironolactone)
Calcineurin inhibitors and other immunosuppressive agents sympathetic overactivity, increased renal sodium reabsorption (distal tubule ENaC activation), decrease in NO production, RAAS activation, altered renal PG synthesis All Grade: 30–80% CCB
Thiazide diuretics (especially for Tacrolimus)
Taxanes endothelial dysfunction, enhanced toxicity of bevacizumab and anthracyclines NA ACEI or ARB
CCB
Abiraterone increase in steroid precursors with mineralocorticoid properties (sodium and fluid retention) NA Mineralocorticoid antagonists
Diuretics
Recombinant human erythropoietin increased blood viscosity, direct vasoconstricting properties, increased sensitivity to endogenous vasopressors All Grade: 30–35% CCB
  1. aData on the incidence of steroid-induced hypertension comes mainly from pediatric population treated for acute lymphocytic leukemia (ALL)
  2. VEGF vascular endothelial growth factor, TKI tyrosine kinase inhibitor, NOS nitric oxide synthase, RAAS renin-angiotensin-aldosterone system, ENaC epithelial sodium channel, PG prostaglandin, CCB calcium channel blockers, ACEI angiotensin converting enzyme inhibitors, ARB angiotensin II receptor blocker, NA not available