Fosinopril (Monopril)
Indications
Pharmacology
Metabolism
Administration
Dose Adjustment
Adverse Effects
Allergic/Immunologic Adverse Effects
Anaphylaxis (see Anaphylaxis, [[Anaphylaxis]])
- Epidemiology: xxx
- Treatment: see Anaphylaxis, [[Anaphylaxis]]
Angioedema (see Urticaria-Angioedema, [[Urticaria-Angioedema]])
- Epidemiology: occurs in 0.1-0.2% of ACE-Inhibitor treated patients
- Physiology: class effect (common to all ACE inhibitors)
- Mediated by bradykinins (and possibly by autoantibodies and complement activation)
- Clinical
- Time of Onset: onset can occur from hours-months after starting ACE-Inhibitor
- However, most cases within hrs-1 week after starting ACE-Inhibitor
- Lingual Edema (see Lingual Edema, [[Lingual Edema]])
- Facial Edema (see Facial Edema, [[Facial Edema]])
- Treatment
- Airway Protection: as required
- Antihistamines (see H1-Histamine Receptor Antagonists, [[H1-Histamine Receptor Antagonists]])
- Diphenhydramine (Benadryl) (see Diphenhydramine, [[Diphenhydramine]]): 25-50 mg IV PRN
- Epinephrine (see Epinephrine, [[Epinephrine]])
- Corticosteroids (see Corticosteroids, [[Corticosteroids]])
- Icatibant (Firazyr) (see Icatibant, [[Icatibant]])
- Withdrawal of ACE-Inhibitor: rechallenge is contraindicated
Cardiovascular Adverse Effects
Hypotension (see Hypotension, [[Hypotension]])
- Physiology: class effect (common to all ACE inhibitors)
Endocrinologic Manifestations
Hypoaldosteronism (see Hypoaldosteronism, [[Hypoaldosteronism]])
- Physiology: class effect (common to all ACE inhibitors)
Gastrointestinal Adverse Effects
Elevation of Hepatic Transaminases with Hepatocellular Injury (see Drug-Induced Hepatotoxicity, [[Drug-Induced Hepatotoxicity]])
Pulmonary Adverse Effects
Cough (see Cough, [[Cough]])
- Epidemiology: occurs in 5-20% of treated patients
- Physiology: class effect (common to all ACE inhibitors)
- Likely related to accumulation of kinins and substance P (which are usually degraded by ACE and other endopeptidases)
- Clinical: dry cough with onset typically wihtin the first few weeks of therapy (although some cases do not present with cough until months later)
- Treatment: 50% of cases with cough ultimately need to have ACE-I discontinued -> cough usually stops within 4 days of discontinuation of ACE-I
- Rechallenge with ACE-I is not recommended, as cough will usually recur
- However, since ARB’s have much lower incidence of cough, one of these may be substituted
Drug-Induced Pulmonary Eosinophilia (see Drug-Induced Pulmonary Eosinophilia, [[Drug-Induced Pulmonary Eosinophilia]])
- Physiology: class effect
- Associated Agents
- Captopril (see Captopril, [[Captopril]])
- Fosinopril (see Fosinopril, [[Fosinopril]])
- Perindopril (Coversyl, Coversum, Preterax, Aceon) (see Perindopril, [[Perindopril]])
Exacerbation of Bronchospasm (see Obstructive Lung Disease, [[Obstructive Lung Disease]])
- Epidemiology: very rare
- Physiology: class effect (common to all ACE inhibitors)
Renal Adverse Effects
Acute Kidney Injury (AKI) (see Acute Kidney Injury, [[Acute Kidney Injury]])
Hyperkalemia (see Hyperkalemia, [[Hyperkalemia]])
- Physiology: class effect (common to all ACE inhibitors)
- Due to drug-induced hypoaldosteronism (see above)
Rheumatologic Adverse Effects
Drug-Induced Systemic Lupus Erythematosus (SLE) (see Systemic Lupus Erythematosus, [[Systemic Lupus Erythematosus]])
- Epidemiology: low-moderate risk of developing drug-induced SLE
- Physiology: class effect (common to all ACE inhibitors)
References