Each week we will aim to bring out a concise email that provides 4-5 key pieces of information addressing a specific issue in clinical therapeutics. This week:
Many therapeutic agents cause a transient or persistent increase in BP. This secondary hypertension may present as new onset HT, worsening of existing HT, or as difficult to treat HT. A range of implicated agents are discussed here:
- Non-steroidal anti-inflammatory drugs (NSAIDs) including COX-2 inhibitors such as celecoxib can contribute to HT. A meta-analysis suggests that NSAIDs can produce an average increase in systolic blood pressure (SBP) of 5 mm Hg in patients without HT and up to 14 mm Hg in those with existing HT. Inhibited of prostaglandin synthesis by NSAIDs reduces vasodilatory & natriuretic effects. Increased sodium & water retention activates the renin-angiotensin-aldosterone system (RAAS), increasing BP, potentially reducing antihypertensive effects of ACE inhibitors, angiotensin receptor blockers (ARBs), beta-blockers and diuretics.
- Corticosteroids and hormone – mineralocorticoid receptor stimulation results in sodium and fluid retention. Cortisone and hydrocortisone, which have the highest activity, cause the greatest fluid retention. Combined oral contraceptives and hormone replacement therapy may increase BP through oestrogen activation of RAAS causing volume retention.
- Antidepressants – Venlafaxine, desvenlafaxine and reboxetine commonly contribute to HT through increased synaptic levels of serotonin and/or noradrenaline.
- Stimulants including caffeine, nicotine, alcohol, pseudoephedrine, phenylephrine (oral, nasal and ophthalmic instillations), modafanil, methylphenidate, and atomoxetine exert hypertensive effects through noradrenaline and or dopaminergic stimulation.
- Complementary medicines that have been reported to increase BP include coenzyme Q10, olive leaf, ginger, and Ma Huang. Ginseng has been reported to cause both increased and reduced blood pressure.
- Awareness of the potential for medication-induced HT is important to prevent the creation of prescribing cascades, where new medications are added to address the adverse effects of medications prescribed in an existing regimen.
Please consider these issues when preparing or interpreting RMMR reports or education sessions. Contributions of content or suggested topics are welcome and should be sent directly to email@example.com