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Heparin-induced hyperkalemia.

C M Thomas1, J Thomas, F Smeeton

  • 1Poole General Hospital, Poole, Dorset, UK; University of Liverpool, Liverpool, UK. drcecil@email.com

Diabetes Research and Clinical Practice
|March 18, 2008
PubMed
Summary
This summary is machine-generated.

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Heparin, a common anticoagulant, can cause dangerous hyperkalemia (high potassium) in patients with type 2 diabetes and peripheral neuropathy. This condition resolved upon heparin discontinuation, highlighting a critical drug-induced electrolyte imbalance.

Area of Science:

  • Endocrinology
  • Nephrology
  • Pharmacology

Background:

  • An 85-year-old female with a 32-year history of type 2 diabetes mellitus and peripheral neuropathy presented with lower limb gangrene.
  • Initial management included antibiotics and unfractionated heparin, revealing persistent hyperkalemia despite normal baseline electrolytes.

Observation:

  • Endocrine workup demonstrated normal adrenal response (short synacthen test), normal renin, and low aldosterone levels.
  • Hyperkalemia resolved upon heparin cessation and recurred with both unfractionated and low molecular weight heparin reintroduction.

Findings:

  • The patient developed significant hyperkalemia attributed to heparin administration.
  • Discontinuation of heparin led to normalization of serum potassium and aldosterone levels.

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Implications:

  • This case highlights a rare but serious adverse effect of heparin, inducing hyperkalemia potentially through aldosterone suppression.
  • Clinicians should consider heparin-induced hyperkalemia in diabetic patients with neuropathy presenting with electrolyte disturbances.
  • Careful monitoring of potassium levels is crucial in patients receiving heparin, particularly those with predisposing conditions.