Dexamethasone as an antiemetic
Dexamethasone is a corticosteroid (a steroid drug related to cortisol) that is also a powerful antiemetic (a drug that prevents nausea and vomiting) in chemotherapy and after surgery.
Remember
In chemotherapy and after surgery, dexamethasone probably works by reducing inflammation near the chemoreceptor trigger zone (a small area in the lower brainstem that senses drugs and toxins in the blood) and by inhibiting prostaglandin synthesis. It is kept to a short course to avoid the chronic side effects of steroids.
Memory aid
calming the inflamed neighbourhood around the trigger zone
Picture dexamethasone as calming the inflamed area near the trigger zone, rather than as blocking one named receptor.
Dexamethasone is a corticosteroid, a drug related to cortisol (the steroid hormone the body makes itself) and used mainly to dampen inflammation and allergy. It is also a powerful antiemetic (a drug that prevents nausea and vomiting) in chemotherapy and after surgery.
Its exact mechanism is not fully understood. It probably reduces inflammation around the chemoreceptor trigger zone, or CTZ, a small area in the lower brainstem called the area postrema. The CTZ sits outside the blood-brain barrier (the tightly sealed lining of the brain's blood vessels), so it can sense drugs and toxins in the blood, including chemotherapy, and pass the signal on to the vomiting centre in the medulla (the part of the brainstem that coordinates vomiting). Dexamethasone is also thought to inhibit prostaglandin synthesis, and prostaglandins are inflammatory chemical messengers made by the body.
Many antiemetic drug classes are named for the receptor they block: ondansetron blocks serotonin 5-HT3 receptors and metoclopramide blocks dopamine D2 receptors. Dexamethasone stands apart from them, so it is combined with them in chemotherapy regimens rather than being a substitute.
The course is kept short because prolonged steroid exposure is linked with infection, osteoporosis (thinning of the bones), raised blood glucose and suppression of the adrenal glands (the glands that make the body's own cortisol). A short course gives the antiemetic benefit while keeping the risk of these chronic complications low, although even short courses can cause high blood glucose.
Key facts
- Class and use
- a corticosteroid given short term to prevent nausea and vomiting after chemotherapy and surgery.
- Proposed mechanism
- probably less inflammation around the chemoreceptor trigger zone and inhibition of prostaglandin synthesis, although the exact action is not fully understood.
- Not a receptor blocker
- unlike ondansetron (which blocks serotonin 5-HT3 receptors) or metoclopramide (which blocks dopamine D2 receptors), its antiemetic action is not simply the block of one named receptor.
- Why the course is short
- prolonged steroid exposure is linked with infection, osteoporosis, raised blood glucose and suppression of the adrenal glands.
- Usual partner
- it is usually combined with a 5-HT3 receptor antagonist (a drug that blocks serotonin receptors) such as ondansetron.
Exam traps
- Blocking dopamine D2 receptors at the chemoreceptor trigger zone, with movement side effects such as acute dystonia (sudden involuntary muscle spasm) limiting use, is the profile of metoclopramide and prochlorperazine, not of dexamethasone, which is not a dopamine blocker.
- Speeding the emptying of the stomach is the job of a prokinetic drug (one that speeds up gut movement) such as metoclopramide, not dexamethasone. A falling response to repeated doses (tachyphylaxis) is also not why steroid antiemetics are kept to short courses.
- Blocking serotonin 5-HT3 receptors is the mechanism of ondansetron, one of the drugs most often given together with dexamethasone, so it is easily mistaken for the mechanism of dexamethasone, which is not a 5-HT3 antagonist.
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