Salsalate (Disalcid, Salflex)


  • Arthritis
    • Acute Gout (see Gout, [[Gout]])
    • Osteoarthritis (see Osteoarthritis, [[Osteoarthritis]])
    • Rheumatoid Arthritis
  • Dysmenorrhea (see Dysmenorrhea, [[Dysmenorrhea]])
  • Fever (see Fever, [[Fever]])
  • Pain
    • Post-Operative Pain
    • Soft Tissue/Musculoskeletal Injury
  • To Decrease the Risk of Malignancy


  • Chronic Kidney Disease (CKD) (see Chronic Kidney Disease, [[Chronic Kidney Disease]])
    • Due to Risk of Worsening Chronic Kidney Disease
  • Chronic Liver Disease (see End-Stage Liver Disease, [[End-Stage Liver Disease]])
    • Due to Frequent Co-Existing Chronic Kidney Disease (and Risk of Hepatorenal Syndrome) (see Hepatorenal Syndrome, [[Hepatorenal Syndrome]])
    • Due to Risk of Gastrointestinal Hemorrhage (see Gastrointestinal Hemorrhage, [[Gastrointestinal Hemorrhage]])



  • Hepatic: predominantly


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Dose Adjustment

  • Hepatic:
  • Renal:

Adverse Effects

Endocrinologic Adverse Effects

Drug-Induced Hyporeninemic Hypoaldosteronism (see Hypoaldosteronism, [[Hypoaldosteronism]])

  • Physiology
    • Class effect, common to all NSAID’s
    • Dose-dependent COX-inhibition -> decreased renal prostaglandin synthesis -> results in drug-induced hyporeninemic hypoaldosteronism
  • Clinical

Gastrointestinal Adverse Effects

Peptic Ulcer Disease (PUD) (see Peptic Ulcer Disease, [[Peptic Ulcer Disease]])

  • Physiology: class effect, common to all NSAID’s

Pulmonary Adverse Effects

Aspirin-Intolerant Asthma (see Asthma, [[Asthma]])

  • Physiology: class effect, common to multiple NSAID’s

Renal Adverse Effects

Acute Kidney Injury (see Acute Kidney Injury, [[Acute Kidney Injury]])

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Acute Interstitial Nephritis (see Acute Interstitial Nephritis, [[Acute Interstitial Nephritis]])

  • Physiology: class effect, common to all NSAID’s

Hyperkalemia (see Hyperkalemia, [[Hyperkalemia]])

  • Mechanism: due to drug-induced hyporeninemic hypoaldosteronism

Increased Renal Sodium Reabsorption with Peripheral Edema

  • Risk Factors
  • Physiology: decreased PGE2 -> increased renal sodium reabsorption
    • Class Effect: common to all NSAID’s
    • Dose-Dependent Effect
  • Clinical: typically occurs during the first week of therapy

Type 4 Renal Tubular Acidosis (RTA) (see Type 4 Renal Tubular Acidosis, [[Type 4 Renal Tubular Acidosis]])

  • Physiology: due to NSAID-induced hyporeninemic hypoaldosteronism
  • Clinical

Other Adverse Effects

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