Dexamethasone

Mechanism

Additive ulcerogenic effect. Dexamethasone suppresses GI mucosal repair; aspirin blocks protective prostaglandins.

Symptoms

Epigastric pain, nausea, heartburn. With prolonged therapy: peptic ulcer and GI bleeding risk (black stools, vomiting blood or coffee-ground material). Older patients and prior peptic ulcer disease: higher risk.

Management

For short dexamethasone courses, cardioprotective aspirin is acceptable with pantoprazole cover. For prolonged systemic glucocorticoid therapy, watch dyspepsia symptoms; consider stool occult blood testing as needed.

Mechanism

Dexamethasone is a weak CYP3A4 inducer and may slightly reduce amiodarone levels in long-term therapy. The additive QT effect is minimal but persists in predisposed patients.

Symptoms

Short dexamethasone pulses usually cause no symptoms. QT prolongation on ECG. Dizziness, syncope, palpitations. Rarely: polymorphic ventricular tachycardia (torsades de pointes). Risk is higher with hypokalaemia, hypomagnesaemia, bradycardia, and ischaemic heart disease.

Management

For short dexamethasone courses (3–7 days), no specific adjustment needed. For long-term therapy, check ECG every 3 months. In atrial fibrillation with uncontrolled rate, consider raising amiodarone by 50–100 mg/day.

Mechanism

Dexamethasone is a weak CYP3A4 inducer. With prolonged therapy, amlodipine plasma levels may modestly fall and the antihypertensive effect weaken.

Symptoms

Gradual blood pressure rise 2–4 weeks after starting the glucocorticoid. In heart failure: oedema, weight gain.

Management

For short dexamethasone courses (up to 7 days), no adjustment. For prolonged systemic therapy, monitor blood pressure every 2 weeks; increase amlodipine if needed.

Mechanism

Dexamethasone induces CYP3A4. With prolonged therapy, atorvastatin plasma levels may fall modestly and lipid-lowering effect weakens.

Symptoms

The patient feels nothing. Laboratory: LDL cholesterol and total cholesterol rise during prolonged systemic glucocorticoid therapy.

Management

For short dexamethasone courses, no adjustment. For prolonged systemic therapy, monitor lipid profile every 2–3 months; increase atorvastatin by 25–50% if needed.

Mechanism

Dexamethasone causes sodium and water retention via mineralocorticoid effect, reducing the antihypertensive effect of the beta-blocker.

Symptoms

Gradual blood pressure rise 2–4 weeks after starting the glucocorticoid. In heart failure: oedema, weight gain.

Management

For short dexamethasone courses (up to 7 days), no adjustment. For prolonged systemic therapy, increase bisoprolol or add a diuretic (hydrochlorothiazide, indapamide) with blood pressure monitoring.

Mechanism

Dexamethasone has minimal mineralocorticoid activity but, at high doses and prolonged use, blunts the ACE inhibitor's antihypertensive effect. The effect is weaker than with prednisolone.

Symptoms

Possible rise in blood pressure with long-term therapy. Weakness, fatigue, paraesthesias, arrhythmia. Symptoms develop at potassium above 5.5 mmol/L; life-threatening above 6.5 mmol/L.

Management

For short dexamethasone courses, no specific adjustment needed. For long-term therapy, check BP every 1–2 weeks. If BP rises, intensify antihypertensive therapy (increase enalapril or add a thiazide). Potassium and creatinine monthly.

Mechanism

Dexamethasone stimulates gluconeogenesis and reduces tissue insulin sensitivity. The glycaemic effect is stronger than with prednisolone due to long half-life and high potency.

Symptoms

Return of thirst and polyuria, rising fasting glucose, fatigue. In type 2 diabetes, possible decompensation with HbA1c rise of 0.5–1.5%.

Management

For short dexamethasone pulses (1–3 days, e.g. cerebral oedema or post-chemotherapy), no metformin adjustment needed — transient hyperglycaemia is tolerated. For long-term therapy, increase metformin or add long-acting insulin. Check glucose twice daily in the first week.

Mechanism

Dexamethasone is a weak CYP3A4 inducer and a potential weak CYP2C9 inhibitor. Effect on INR is unpredictable and usually mild: INR may fall in some patients and rise in others.

Symptoms

Gum bleeding, epistaxis, bruising without trauma, black or tarry stools, haematuria. Higher risk in older patients, prior peptic ulcer disease, and chronic kidney disease.

Management

For short dexamethasone courses (3–5 days), no special monitoring needed. For longer therapy, check INR at one week, then every 2 weeks. Beyond the INR effect, glucocorticoids add gastrointestinal bleeding risk via mucosal ulcerogenic action.