Fludrocortisone

Fludrocortisone

Generic Name

Fludrocortisone

Mechanism

Fludrocortisone acts as a high‑affinity agonist of the mineralocorticoid receptor (MR) in renal cortical cells, vascular smooth muscle, and intestinal epithelium.
• ↑ Na⁺/Cl⁻ absorption in the distal nephron → ↑ plasma volume, ↑ systolic BP
• ↑ K⁺ and H⁺ excretion → ↓ serum potassium, ↓ acidemia
• Relatively weak glucocorticoid activity (≈ 5‑10 % of cortisol potency) – the drug’s therapeutic effects rely mainly on its mineralocorticoid properties.

In contrast to aldosterone, fludrocortisone has a longer duration of action (~30 h) and oral bioavailability of ~90 %.

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Pharmacokinetics

ParameterTypical ValueNotes
AbsorptionOral bioavailability ~90 %Rapid absorption; peak plasma 1–2 h
DistributionVolume of distribution ≈ 12 LProtein‑binding ~80 % (α‑1‑acid glycoprotein)
MetabolismHepatic CYP3A4 mainly → 4‑hydroxy metaboliteMinimal renal excretion; metabolite inactive
Elimination half‑life11–18 h (clinical)Clinical effect may last 20–30 h
Excretion70–80 % biliary, 10–20 % renalNo dose adjustment for mild‑moderate renal disease

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Indications

  • Addison’s disease (primary adrenal insufficiency) – maintenance and adrenal crisis rescue.
  • Secondary adrenal insufficiency when mineralocorticoid replacement is needed (e.g., post‑adrenalectomy).
  • Orthostatic hypotension secondary to low plasma volume (post‑tropic).
  • Hypovolemia and sodium‑loss disorders (e.g., Bartter syndrome, loop‑diuretic side effects).
  • Low‑dose “Addisonian challenge” in endocrinology work‑ups to evaluate endogenous cortisol production.

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Contraindications

  • Absolute Contraindications
  • Known hypersensitivity to fludrocortisone or excipients.
  • Untreated or severe hypertension—risk of exacerbation.
  • Cushing syndrome or any condition of hypercortisolism.
  • SIADH (syndrome of inappropriate ADH secretion).
  • Fluid‑overload states (CHF, cirrhosis); risk of edema, pulmonary congestion.
  • Warnings
  • Hypernatremia and hyponatremia – monitor sodium; adjust dose.
  • Hypokalemia – risk of arrhythmia, especially with concomitant diuretics.
  • Glucose intolerance/diabetes mellitus – may worsen glycemic control.
  • Osteoporosis & bone fractures with prolonged use.
  • Pregnancy – category C; use only if benefits outweigh risks.
  • Concomitant CYP3A4 inhibitors (ketoconazole, clarithromycin) ↑ exposure → monitor signs of hypertension, electrolyte imbalance.

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Dosing

  • Addison’s disease
  • Oral tablets (0.1 mg) once daily (preferably in the evening).
  • Rescue (adrenal crisis): 0.2 mg IV or IM, repeat every 6 h until stabilization, then bridge to oral.
  • Orthostatic hypotension / other indications
  • 0.05 – 0.1 mg daily; titrate to BP/weight changes.
  • Administration tips
  • Swallow whole; do not chew or crush to avoid dose variability.
  • Consistently take at the same time of day to reduce circadian fluctuations.

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Adverse Effects

Adverse EffectFrequencyNotes
Hypertension↑ 7–12 %Dose‑dependent; monitor BP.
Hypokalemia↑ 5–10 %Can precipitate arrhythmias; monitor K⁺.
Edema / weight gain≤ 5 %Fluid retention, especially in elderly.
Mood changes, insomnia, anxiety≤ 3 %Corticosteroid spectrum.
Hyperglycemia≤ 3 %Worsens pre‑existing diabetes.
Mastitis / milk engorgementRareIn lactating patients.
Serious: Severe electrolyte disturbances, congestive heart failure exacerbation, adrenal crisis if discontinued acutely.

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Monitoring

ParameterFrequencyRationale
Serum sodium & potassiumBaseline, then 1–2 wk after dose change, then monthlyDetect hypo/hypernatremia, hypokalemia.
Serum creatinine & eGFRBaseline, then every 3 moRenal function influences clearance.
Blood pressureEach clinic visit; home BP as neededHypertension risk.
WeightEach visitFluid retention.
Morning serum cortisol levelsBefore titration; every 6–8 wk if clinical suspicionVerify adequate adrenal replacement.
Bone density (DEXA)After ≥ 1 yr of therapy, especially > 50 yEvaluate osteoporosis risk.
Pregnancy screeningFor women of childbearing ageAvoid teratogenic exposure if possible.

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Clinical Pearls

  • Low‑dose Challenge Test – A single 15 mg dose of hydrocortisone or 0.1 mg fludrocortisone can unmask adrenal insufficiency; useful when ACTH is unreliable.
  • Fluid‑balanced Regimen – Combine fludrocortisone with a low‑dosage β‑blocker if hypertension is problematic; this preserves electrolyte balance while controlling BP.
  • Avoid Abrupt Discontinuation – Sudden withdrawal may precipitate adrenal crisis; consider tapering over 3–5 days if dose reduction is needed.
  • Kidney Function Doesn’t Necessarily Require Dose Adjustment – Most patients with mild–moderate CKD tolerate same dosing; however, monitor electrolytes closely.
  • CYP3A4 Inhibitors – Double‑check drug interactions; when co‑administered with potent inhibitors, reduce dose and monitor serum electrolytes/ BP.
  • High‑altitude Use – In climbers with impaired adrenal function, fludrocortisone at 0.05–0.1 mg/day can prevent orthostatic hypotension and maintain plasma volume.
  • Pregnancy – If pregnancy is confirmed, switch to hydrocortisone 15 mg/day + chlorothiazide 12.5 mg (to mimic mineralocorticoid effect safely) until delivery.

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Key Takeaway:

Fludrocortisone is a reliable mineralocorticoid replacement for adrenal insufficiency and fluid‑balance disorders. Careful dose titration, vigilant monitoring of electrolytes & BP, and attention to drug interactions are essential for safe, effective therapy.

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Medical Disclaimer: Medical definitions are provided for educational purposes and should not replace professional medical advice, diagnosis, or treatment.

AI Content Disclaimer: Some definitions may be AI-generated and may contain inaccuracies. Always verify with authoritative medical references.

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