Triple therapy term is used in management of pulmonary artery hypertension, COPD and cystic fibrosis. Let us now read in next 2 minutes a quick recap of this must asked topic for your forthcoming competitive examinations.

Triple Therapy for Pulmonary Arterial Hypertension (PAH)

1. Endothelin Receptor Antagonists (ERAs)
   • Example: Bosentan, Ambrisentan, Macitentan
   • Action: Blocks endothelin, a vasoconstrictor, to reduce pulmonary vascular resistance.
2. Phosphodiesterase-5 (PDE-5) Inhibitors or Soluble Guanylate Cyclase (sGC) Stimulators
   • Example (PDE-5): Sildenafil, Tadalafil
   • Example (sGC stimulator): Riociguat
   • Action: Increases nitric oxide (NO) signaling to promote vasodilation.
3. Prostacyclin Analogues or Prostacyclin Receptor Agonists
   • Example: Epoprostenol, Treprostinil, Selexipag
   • Action: Mimics prostacyclin to dilate blood vessels and inhibit platelet aggregation.

This combination targets multiple pathways involved in PAH pathophysiology, offering better control of the disease.

Triple Therapy for COPD

Triple therapy for Chronic Obstructive Pulmonary Disease (COPD) involves a combination of inhaled medications to manage symptoms and reduce exacerbations.

1. Long-Acting Beta-2 Agonists (LABA)
   • Example: Salmeterol, Formoterol, Indacaterol
   • Action: Broncho dilates airways for symptom relief and improved airflow.
2. Long-Acting Muscarinic Antagonists (LAMA)
   • Example: Tiotropium, Glycopyrrolate, Umeclidinium
   • Action: Reduces bronchoconstriction by blocking muscarinic receptors in the airways.
3. Inhaled Corticosteroids (ICS)
   • Example: Budesonide, Fluticasone, Beclomethasone
   • Action: Reduces airway inflammation and frequency of exacerbations.

Triple therapy (LABA + LAMA + ICS) is recommended for patients with moderate to severe COPD who have frequent exacerbations despite dual therapy.

Triple Therapy for Cystic Fibrosis (CF)

For patients with Cystic Fibrosis, triple therapy specifically refers to the combination of CFTR modulators targeting different aspects of the CFTR protein defect (commonly associated with the F508del mutation).

1. Elexacaftor
   • Action: Facilitates the movement of defective CFTR protein to the cell surface.
2. Tezacaftor
   • Action: Improves CFTR protein processing and stability.
3. Ivacaftor
   • Action: Potentiates the function of the CFTR protein at the cell surface, enhancing chloride ion transport.

This combination therapy significantly improves lung function and quality of life in CF patients with the F508del mutation.

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