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Writer's pictureKatie Berlin

Amiodarone-induced Interstitial Pneumonitis

Updated: Jul 11, 2019

Dr. Marong presented a fabulous case of a patient who presented in what seemed to be acutely decompensated heart failure. When she didn't improve with appropriate treatment, more workup was done revealing the true diagnosis of amiodarone-induced interstitial pneumonitis.


Amiodarone-induced interstitial pneumonitis fits into the broad category of diffuse parenchymal lung diseases.


From MKSAP 17. Pulmonary Medicine Chapter 03: Diffuse Parenchymal Lung Disease


The pathophysiology behind amiodarone-induced interstitial pneumonitis is unclear, but it is thought to either be direct injury to the lung parenchyma from the drug (where a metabolite disrupts cellular and metabolic pathways leading to tissue death) versus a hypersensitivity reaction.


Risk Factors

Several factors place patients at risk from lung disease secondary to amiodarone:

  • Age (most significant!)

  • Daily maintenance dose of > 400 mg (Up to 15% incidence of toxicity)

  • Greater than 6 months of therapy


It is important to note that existing lung disease, baseline DLCO, and loading dose were not found to be risk factors in a prior study.


Presentation

Symptoms will classically present within 6 to 12 months of starting amiodarone, although it has been reported as soon as 2 months and as late as years later.


Patients present with a slow progression of non-specific symptoms, such as cough, pleuritic chest pain, crackles , fatigue, and weight loss.


Diagnosis

This centers on the presence of clinical symptoms in addition to the following:

  • Current or recently (within 45 days) discontinued amiodarone therapy

  • Radiographic evidence

  • > 20 % reduction from baseline DLCO with restrictive pattern on PFT

  • Absence of eospinophilia (to rule out eosinophilic pneumonia)

  • Basic labs to rule out mimickers (including BNP, CBC, etc)

  • Foamy macrophages on BAL


There are multiple possible imaging findings consistent with the disease including:



  • ground-glass opacities

  • subpleural nodules

  • reticular abnormalities


Treatment

Remember: amiodarone has a VERY long half-life: this prevents clearance from the pulmonary parenchyma. Therefore, unlike other causes of drug-induced lung injury there is rarely improvement with discontinuation of the drug alone. You should still stop it.


If there is no severe respiratory distress, you can just monitor off amiodarone but if respiratory distress is present you should treat with steroids. Start Prednisone 40 mg po daily for at least 2 months.

  • Consider slow taper if clinically improving

  • Strongly consider PJP prophylaxis!

There is a high risk of recurrence with tapering of glucocorticoids so be cautious.


References

1. Adams PC, Holt DW, Storey GC, et al. Amiodarone and its desethyl metabolite: tissue distribution and morphologic changes during long-term therapy. Circulation 1985; 72: 1064–75

2. Seki S et al. Amiodarone increases the accumulation of DEA in a human alveolar epithelium-derived cell line. Biol Pharm Bull 2008; 31:1449

3. Lee KY et al. Activation of autophagy rescues amiodarone-induced apoptosis of lung epithelial cells and pulmonary toxicity in rats. Toxicol Sci 2013; 136:193

4. Akoun GM et al. Amiodarone-induced hypersensitivity pneumonitis. Evidence of an immunological cell-mediated mechanism. Chest 1984; 85:133.

5. Ernawati DK, Stafford L, Hughes JD. Amiodarone-induced pulmonary toxicity. Br J Clin Pharmacol 2008 July; 66(1): 82–7

6. Yamada Y et al. Incidence and predictors of pulmonary toxicity in Japanese patients receiving low dose amiodarone. Circ J 2007; 71:1610.

7. Chan et al. Amiodarone pulmonary toxicity. In: UptoDate., Post TW (Ed), UptoDate, Waltham, MA. (Accessed 6/30/2019.)






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