High blood pressure. A side effect of drugs, poisons, and food

Grossman, Ehud; Messerli, Franz H.

doi:10.1001/archinte.155.5.450

Cited by 35 publications

(46 citation statements)

References 86 publications

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“…In the past, treatment-related hypertension was seldom a concern in anticancer therapeutics (38). During the development of the VSP inhibitors, hypertension surveillance, rating, and structured adverse event reporting to the NCI were through the standardized Common Terminology Criteria for Adverse Events (CTCAE) (39).…”

Section: Principles For Bp Management In Patients Receiving Vsp Inhibmentioning

confidence: 99%

Initial Assessment, Surveillance, and Management of Blood Pressure in Patients Receiving Vascular Endothelial Growth Factor Signaling Pathway Inhibitors

Maitland¹,

Bakris²,

Black³

et al. 2010

JNCI: Journal of the National Cancer Institute

385

248

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Hypertension is a mechanism-based toxic effect of drugs that inhibit the vascular endothelial growth factor signaling pathway (VSP). Substantial evidence exists for managing hypertension as a chronic condition, but there are few prospectively collected data on managing acute hypertension caused by VSP inhibitors. The Investigational Drug Steering Committee of the National Cancer Institute convened an interdisciplinary cardiovascular toxicities expert panel to evaluate this problem, to make recommendations to the Cancer Therapy Evaluation Program on further study, and to structure an approach for safe management by treating physicians. The panel reviewed: the published literature on blood pressure (BP), hypertension, and specific VSP inhibitors; abstracts from major meetings; shared experience with the development of VSP inhibitors; and established principles of hypertension care. The panel generated a consensus report including the recommendations on clinical concerns summarized here. To support the greatest possible number of patients to receive VSP inhibitors safely and effectively, the panel had four recommendations: 1) conduct and document a formal risk assessment for potential cardiovascular complications, 2) recognize that preexisting hypertension will be common in cancer patients and should be identified and addressed before initiation of VSP inhibitor therapy, 3) actively monitor BP throughout treatment with more frequent assessments during the first cycle of treatment, and 4) manage BP with a goal of less than 140/90 mmHg for most patients (and to lower, prespecified goals in patients with specific preexisting cardiovascular risk factors). Proper agent selection, dosing, and scheduling of follow-up should enable maintaining VSP inhibition while avoiding the complications associated with excessive or prolonged elevation in BP.

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Section: Principles For Bp Management In Patients Receiving Vsp Inhibmentioning

confidence: 99%

Initial Assessment, Surveillance, and Management of Blood Pressure in Patients Receiving Vascular Endothelial Growth Factor Signaling Pathway Inhibitors

Maitland¹,

Bakris²,

Black³

et al. 2010

JNCI: Journal of the National Cancer Institute

385

248

View full text Add to dashboard Cite

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“…A detailed medical history should include inquiries concerning foods, poisons, and medications that patients do not consider to be drugs and therefore frequently omit from their history. Identification of the intake of these substances is important; their elimination might obviate the need for unnecessary evaluations or treatments 1,2 …”

Section: List Of Mmedications That May Increase Bpmentioning

confidence: 99%

Secondary Hypertension: Interfering Substances

Grossman

Messerli

2008

J of Clinical Hypertension

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A variety of therapeutic agents or chemical substances can induce either a transient or persistent increase in blood pressure or interfere with the blood pressure‐lowering effects of antihypertensive drugs. Some agents either cause sodium retention and extracellular volume expansion or directly or indirectly activate the sympathetic nervous system. Other substances act directly on arteriolar smooth muscle or do not have a defined mechanism of action. Some medications that usually lower blood pressure may paradoxically increase blood pressure, and an increase in pressure may be encountered after their discontinuation. In general, these pressure increases are small and transient; however, severe hypertension involving encephalopathy, stroke, and irreversible renal failure have been reported. Careful evaluation of a patient's drug regimen may identify chemically induced hypertension and obviate unnecessary evaluation and direct to the optimal antihypertensive therapy. The present review summarizes the therapeutic agents or chemical substances that elevate blood pressure and their mechanisms of action.

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“…1 The list of compounds capable of increasing blood pressure (BP) is quite extensive and continues to grow. Drugs that cause hypertension do so by either stimulating pressor responses, increasing extracellular volume, and/or by decreasing vascular compliance.…”

mentioning

confidence: 99%