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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