Systemic corticosteroid (glucocorticoid)
Dexamethasone is a potent corticosteroid used to reduce inflammation and modulate the immune system in many diseases (allergies, asthma, rheumatic diseases, tumours). Used in short or long courses; requires medical supervision, especially with prolonged use.
Also known as: Dexametasona, dexamethasone, Decadron
Corticosteroid + carbamazepine: CYP3A4 induction reduces corticosteroid effect.
Dexamethasone is metabolised by CYP3A4; carbamazepine, a potent inducer of this enzyme, can lower its concentrations and attenuate the anti-inflammatory/immunosuppressive effect. In patients on long-term corticosteroid therapy (e.g. autoimmune diseases, post-transplant) with epilepsy treated with carbamazepine, monitor the clinical response and consider increasing the dexamethasone dose or preferring a corticosteroid less dependent on CYP3A4.
Carbamazepine + dexamethasone: carbamazepine induces CYP3A4 and lowers dexamethasone levels, potentially reducing the corticosteroid effect. Consider dose adjustment.
Carbamazepine (CYP3A4 inducer) accelerates dexamethasone metabolism.
Clinical response to therapy.
Lack of control of inflammatory/allergic symptoms.
Watch clinical response; a higher corticosteroid dose may be needed.
DailyMed (FDA) — approved Dexamethasone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7cbd9005-7df2-47ee-adb3-7244c1c69bc3 ; approved Carbamazepine label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=97e6e175-75e8-437b-b457-ddb1ae4e857d — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Corticosteroid + ritonavir: CYP3A4 inhibition markedly increases corticosteroid exposure.
Dexamethasone is metabolised by CYP3A4, and ritonavir is a potent inhibitor of this enzyme: the combination raises corticosteroid exposure, with a risk of corticosteroid excess — Cushing syndrome, adrenal suppression, hyperglycaemia, sodium and fluid retention, potassium loss and immunosuppression (the dexamethasone label lists potassium loss, hypokalaemic alkalosis and adrenal axis suppression among the adverse reactions). The combination occurs mainly in HIV patients needing corticosteroids; use the lowest effective dose, watch for signs of corticosteroid excess and adrenal function, and consider reducing the dexamethasone dose. Note: dexamethasone also induces CYP3A4 — in ritonavir-boosted regimens, evaluate the impact on the protease inhibitors.
Dexamethasone + ritonavir: ritonavir inhibits CYP3A4 and raises dexamethasone levels. Watch for corticosteroid excess (Cushing, adrenal suppression).
Ritonavir (potent CYP3A4 inhibitor) reduces dexamethasone metabolism, risking Cushing syndrome.
Blood glucose, blood pressure, signs of corticosteroid excess.
Cushing syndrome, hyperglycaemia, oedema.
Avoid the combination; if unavoidable, reduce dexamethasone dose and monitor.
DailyMed (FDA) — approved Dexamethasone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7cbd9005-7df2-47ee-adb3-7244c1c69bc3 ; approved Ritonavir label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d2f8c6ba-5e06-4b03-8ca5-b4fd7e5a8925 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Corticosteroid + phenytoin: enzyme induction reduces the effect of both.
Phenytoin is a potent inducer of hepatic enzymes (the label states that "phenytoin is a potent inducer of hepatic drug-metabolising enzymes" and that it induces hepatic enzymes, increasing the metabolism of several drugs), and dexamethasone is metabolised by CYP3A4: the combination increases corticosteroid clearance and reduces its therapeutic effect — clinically relevant in epileptic patients treated with phenytoin who need corticosteroids (e.g. severe asthma, autoimmune disease, cerebral oedema). The phenytoin label also mentions interference with dexamethasone suppression tests. Monitor the clinical response to the corticosteroid and consider increasing the dexamethasone dose; if phenytoin is discontinued, reassess (the corticosteroid dose may need to be reduced to avoid excess).
Dexamethasone + phenytoin: phenytoin induces CYP3A4 and reduces dexamethasone efficacy. Monitor response and consider raising the corticosteroid dose.
Phenytoin induces CYP3A4 (dexamethasone metabolism) and dexamethasone alters phenytoin metabolism.
Clinical response and serum phenytoin levels.
Seizures, lack of allergic/inflammatory control.
Monitor response and, if feasible, phenytoin levels.
DailyMed (FDA) — approved Dexamethasone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7cbd9005-7df2-47ee-adb3-7244c1c69bc3 ; approved Phenytoin label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ef4e97a7-cd18-47a9-a016-2eca5481a87e — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Corticosteroid + thiazide: additive hypokalaemia and hyperglycaemia.
Both drugs cause renal potassium loss: hydrochlorothiazide (the exchange of sodium for potassium in the distal tubule can cause hypokalaemia and hypomagnesaemia, with a risk of ventricular arrhythmias and of potentiating digitalis toxicity) and dexamethasone (the label lists, among the fluid and electrolyte disturbances, sodium and fluid retention, potassium loss and hypokalaemic alkalosis). The hydrochlorothiazide label explicitly states that hypokalaemia may develop "during concomitant use of corticosteroid or ACTH" and that corticosteroids cause "intensified electrolyte depletion, particularly hypokalemia". The combination is common in practice (e.g. asthma/COPD with a corticosteroid + hypertension with a thiazide), but requires vigilance: monitor serum potassium (and magnesium), especially in the elderly, cirrhotics and digitalised patients, and replace potassium when indicated.
Dexamethasone + hydrochlorothiazide: additive potassium loss (hypokalaemia). Monitor potassium and replace if needed.
Both promote potassium loss and raised blood glucose.
Potassium, blood glucose and blood pressure.
Weakness, cramps, polyuria, glycaemic decompensation.
Monitor potassium and blood glucose; adjust therapy if needed.
DailyMed (FDA) — approved Dexamethasone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7cbd9005-7df2-47ee-adb3-7244c1c69bc3 ; approved Hydrochlorothiazide label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=0789baef-3424-43ab-a3fb-4908172da565 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Corticosteroid + loop diuretic: additive hypokalaemia risk.
Furosemide causes renal potassium loss (hypokalaemia, hypochloraemic alkalosis), and systemic corticosteroids such as dexamethasone increase potassium excretion and can cause hypokalaemic alkalosis, especially at high doses. Together, the risk of hypokalaemia is additive, with potential for arrhythmias, particularly in patients with cardiac disease, the elderly or those on other potassium-lowering drugs. The furosemide and corticosteroid labels recommend monitoring serum electrolytes and considering potassium supplementation during the combination.
Dexamethasone + furosemide: additive risk of hypokalaemia and hypokalaemic alkalosis. Monitor potassium and ECG.
Both increase renal potassium loss.
Serum potassium and hypokalaemia symptoms.
Weakness, cramps, arrhythmias.
Monitor serum potassium; consider supplementation if needed.
DailyMed (FDA) — approved Dexamethasone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7cbd9005-7df2-47ee-adb3-7244c1c69bc3 ; approved Furosemide label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=6d9caaab-d874-4cf1-b9fe-408452a18998 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Corticosteroid + aspirin: additive gastrointestinal risk (ulcer/bleeding).
Aspirin (especially at anti-inflammatory doses or with prolonged use) inhibits gastroprotective prostaglandins and can injure the mucosa; systemic corticosteroids such as dexamethasone inhibit mucosal repair and can mask signs of perforation. Together, the risk of ulcer, bleeding and digestive perforation increases, particularly in the elderly, at high doses and in prolonged treatment. Consider gastroprotection with a proton pump inhibitor in at-risk patients, use the lowest effective dose of each drug and monitor digestive symptoms.
Aspirin + dexamethasone: additive risk of peptic ulcer and gastrointestinal bleeding. Consider gastroprotection in at-risk patients.
Both weaken gastric mucosal protection.
GI symptoms and signs of bleeding.
Melena, haematemesis, abdominal pain.
Consider gastroprotection (PPI) in at-risk patients.
DailyMed (FDA) — approved Dexamethasone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7cbd9005-7df2-47ee-adb3-7244c1c69bc3 ; approved Aspirin label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=3ba0a9f2-062a-401e-82eb-54383a822366 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Corticosteroid + NSAID: additive gastrointestinal risk (ulcer/bleeding).
Both corticosteroids and NSAIDs can injure the gastrointestinal mucosa; the combination increases the risk of peptic ulcer, perforation and digestive bleeding, especially in the elderly, at high doses and in prolonged treatment. Dexamethasone can also mask signs of infection and alter metabolism, while ibuprofen adds platelet inhibition. Use the lowest corticosteroid dose for the shortest time, consider gastroprotection (proton pump inhibitor) in at-risk patients and monitor digestive symptoms.
Dexamethasone + ibuprofen: additive risk of peptic ulcer and gastrointestinal bleeding. Consider gastroprotection in at-risk patients.
Both weaken gastric mucosal protection.
GI symptoms and full blood count if bleeding.
Epigastric pain, melena, haematemesis.
Avoid the combination when possible; if needed, use gastroprotection.
DailyMed (FDA) — approved Dexamethasone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7cbd9005-7df2-47ee-adb3-7244c1c69bc3 ; approved Ibuprofen label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=291602fa-8ebe-4200-bba7-9798c90f8a50 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Corticosteroid + clarithromycin: CYP3A4 inhibition increases corticosteroid exposure.
Dexamethasone is metabolised by CYP3A4; clarithromycin inhibits this enzyme and can raise its concentrations, potentiating anti-inflammatory effects, hyperglycaemia and the risk of adrenal suppression in prolonged courses. In patients on corticosteroid therapy and a clarithromycin-treated infection, monitor blood glucose and corticosteroid excess signs and consider reducing the dexamethasone dose during the combination.
Dexamethasone + clarithromycin: clarithromycin raises dexamethasone levels (CYP3A4 inhibition), potentiating corticosteroid effects. Monitor corticosteroid effects.
Clarithromycin inhibits CYP3A4, reducing dexamethasone metabolism.
Blood glucose, blood pressure and signs of corticosteroid excess.
Weight gain, oedema, hyperglycaemia.
Watch for corticosteroid effects (hyperglycaemia, fluid retention, Cushing syndrome).
DailyMed (FDA) — approved Dexamethasone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7cbd9005-7df2-47ee-adb3-7244c1c69bc3 ; approved Clarithromycin label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d836ae7e-fdbf-4dcb-a90d-ede1dcbc3e67 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Corticosteroid + glucose: additive hyperglycaemia in patients on nutrition.
Systemic corticosteroids (dexamethasone) raise blood glucose by stimulating hepatic gluconeogenesis, reducing peripheral glucose uptake and increasing insulin resistance. In patients receiving glucose infusion (parenteral nutrition or hydration), the hyperglycaemic effect adds to the glucose load, potentially causing significant hyperglycaemia, especially in diabetics, but also in patients without known diabetes on high corticosteroid doses. Monitor capillary glucose (and diuresis), give insulin as needed and adjust the glucose load in nutrition when possible.
Corticosteroid + glucose: additive hyperglycaemia in patients on nutrition. Monitor blood glucose.
Corticosteroids raise glycaemia; glucose infusion adds a carbohydrate load.
Capillary/serum glucose.
Symptomatic hyperglycaemia, metabolic decompensation.
Monitor blood glucose and adjust insulin/antidiabetics during therapy.
DailyMed (FDA) — approved Dexamethasone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7cbd9005-7df2-47ee-adb3-7244c1c69bc3 ; approved Glucose (dextrose) label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=36e9478c-5df0-4b47-b97d-de3626d7cb29 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Corticosteroid + anticoagulant: altered INR and bleeding risk.
Corticosteroids, including dexamethasone, can modify the response to warfarin in both directions: most reports show an INR decrease (possibly through enzyme induction and fluid retention), but cases of increased effect exist, and the response is unpredictable between patients. The interaction is most relevant in prolonged courses or high doses. The INR should be monitored frequently when starting, adjusting and stopping dexamethasone and the warfarin dose adjusted accordingly; the INR must be re-evaluated after corticosteroid discontinuation.
Corticosteroids can alter the effect of warfarin (usually an INR decrease by induction, but variable). Monitor the INR when starting, adjusting and stopping dexamethasone.
Corticosteroids may potentiate or reduce warfarin effect (variable effect on haemostasis and GI mucosa).
Periodic INR and GI symptoms.
Melena, haematemesis, bleeding.
Monitor INR after starting/adjusting corticosteroids; consider gastroprotection.
DailyMed (FDA) — approved Dexamethasone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7cbd9005-7df2-47ee-adb3-7244c1c69bc3 ; approved Warfarin label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=541c9a70-adaf-4ef3-94ba-ad4e70dfa057 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Corticosteroid + digoxin: induced hypokalaemia increases digoxin toxicity.
Dexamethasone has mild mineralocorticoid activity that, at high doses or with prolonged use, can cause hypokalaemia and sodium/water retention. Hypokalaemia potentiates digitalis toxicity (ventricular arrhythmias, even at therapeutic digoxin levels), and fluid retention can decompensate the heart failure that prompted digoxin. Monitor serum potassium (keep ≥ 4.0 mEq/L) and weight, watch for decompensation and digitalis toxicity signs, and adjust accordingly.
Corticosteroids + digoxin: steroid-induced hypokalaemia increases digitalis toxicity; sodium/water retention may worsen heart failure. Monitor electrolytes.
Corticosteroid-associated potassium loss sensitises the myocardium to digoxin.
Serum potassium and ECG.
Nausea, arrhythmias, confusion, altered colour vision.
Monitor potassium and signs of digoxin toxicity.
DailyMed (FDA) — approved Dexamethasone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7cbd9005-7df2-47ee-adb3-7244c1c69bc3 ; approved Digoxin label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=e61d2108-d871-44c0-b12a-2e61fbb56967 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Alcohol may increase GI risk.
Limit alcohol during treatment.
EMC-UK (MHRA) — approved Dexamethasone SmPC: https://www.medicines.org.uk/emc/product/13196/smpc
Grapefruit (juice) inhibits CYP3A4 and increases dexamethasone exposure.
Avoid grapefruit juice during treatment.
EMC-UK (MHRA) — approved Dexamethasone SmPC: https://www.medicines.org.uk/emc/product/13196/smpc
Corticosteroids may worsen peptic ulcer and bleeding risk.
Use with caution; consider gastroprotection.
EMC-UK (MHRA) — approved Dexamethasone SmPC: https://www.medicines.org.uk/emc/product/13196/smpc
Corticosteroids may retain sodium and fluid and raise blood pressure.
Monitor blood pressure and adjust antihypertensives if needed.
EMC-UK (MHRA) — approved Dexamethasone SmPC: https://www.medicines.org.uk/emc/product/13196/smpc
Corticosteroids may raise intraocular pressure.
Monitor intraocular pressure on long-term therapy.
EMC-UK (MHRA) — approved Dexamethasone SmPC: https://www.medicines.org.uk/emc/product/13196/smpc
Long-term corticosteroids accelerate bone loss.
Use the lowest dose/duration; consider calcium + vitamin D.
EMC-UK (MHRA) — approved Dexamethasone SmPC: https://www.medicines.org.uk/emc/product/13196/smpc
Corticosteroids raise blood glucose.
Monitor blood glucose and adjust antidiabetics during therapy.
EMC-UK (MHRA) — approved Dexamethasone SmPC: https://www.medicines.org.uk/emc/product/13196/smpc
Corticosteroids may mask and worsen infections, including severe varicella.
Avoid in active systemic infections without antibiotic cover.
EMC-UK (MHRA) — approved Dexamethasone SmPC: https://www.medicines.org.uk/emc/product/13196/smpc
Corticosteroids cross the placenta; use in pregnancy only when clearly indicated (e.g. fetal lung maturation under guidance).
Use the lowest effective dose for the shortest duration.
Low doses are compatible with breastfeeding; high doses: wait 3-4 h after dosing.
No specific additional contraception.
EMC-UK (MHRA) — approved Dexamethasone SmPC: https://www.medicines.org.uk/emc/product/13196/smpc
Clinical and educational support tool. The information does not replace a medical prescription or the opinion of a qualified healthcare professional.
Synthetic glucocorticoid, readily absorbed from the gastrointestinal tract. At equipotent anti-inflammatory doses it almost completely lacks the sodium-retaining property of hydrocortisone. It causes varied metabolic effects and modifies the body immune responses to diverse stimuli; its main use is the anti-inflammatory effect in disorders of many organ systems.
It exerts anti-inflammatory and immunosuppressive effects by binding to the glucocorticoid receptor, with modulation of gene transcription (transactivation and transrepression), inhibiting the synthesis of inflammatory mediators and the immune response; it suppresses the hypothalamic-pituitary-adrenal axis, with potential adrenal insufficiency after withdrawal.
Well absorbed from the gastrointestinal tract after oral administration. Metabolic clearance is decreased in hypothyroidism and increased in hyperthyroidism; in cirrhosis the effect is enhanced due to decreased metabolism.
Metabolised in the liver, mainly by CYP3A4, and is also a moderate inducer of CYP3A4. CYP3A4 inducers (barbiturates, phenytoin, carbamazepine, rifampin) increase its metabolism and may require a dose increase; strong inhibitors (ketoconazole, itraconazole, clarithromycin, ritonavir) increase concentrations and the risk of systemic effects.
The biological half-life is prolonged (36 to 54 hours), allowing daily administration; relative adrenal insufficiency may persist for months after discontinuation, so withdrawal must be gradual.
Medicines from the same therapeutic group (ATC classification) or the same pharmacological class.
