Salsalate (Disalcid, Salflex)
Indications
- 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
Contraindications
- 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]])
Pharmacology
Metabolism
Administration
Dose Adjustment
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]])
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
- Advanced Age
- Diabetes Mellitus (see Diabetes Mellitus, [[Diabetes Mellitus]])
- Volume Contraction
- 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
References