How are corticosteroids (steroids) prescribed for hypersensitivity pneumonitis?

Steroid Therapy for Hypersensitivity Pneumonitis

Corticosteroids should be prescribed for hypersensitivity pneumonitis (HP) at a dose of prednisone 0.5-1 mg/kg/day (maximum 60 mg/day) for non-fibrotic HP, with a gradual taper over 4-6 weeks, while fibrotic HP may require longer treatment courses with consideration of steroid-sparing agents. 1, 2, 3

Initial Treatment Approach Based on HP Classification

Non-Fibrotic HP

• Initial dosing: Prednisone 0.5-1 mg/kg/day (maximum 60 mg/day) 2, 3
• Duration: Typically 8 weeks of treatment 3
• Tapering: Gradual taper over 4-6 weeks to prevent recurrence 2
• Expected response: Significant improvement in lung function (FEV1, FVC), six-minute walk test, and oxygen saturation 3

Fibrotic HP

• Initial dosing: Same as non-fibrotic HP (prednisone 0.5-1 mg/kg/day)
• Duration: Longer courses may be necessary
• Response: Less dramatic improvement compared to non-fibrotic HP, but still beneficial 3
• Consider early addition: Steroid-sparing agents (mycophenolate mofetil or azathioprine) should be considered to reduce adverse events 4

Special Considerations

Severe Disease/Respiratory Failure

• For patients with severe disease or respiratory failure, consider higher doses:
  • Methylprednisolone 1-2 mg/kg/day IV 1
  • Consider hospitalization based on clinical status 2
  • Rule out infection through appropriate workup 2

Hot Tub Lung (Mycobacterial HP)

• Primary intervention: Complete avoidance of exposure to the antigen source is paramount 1
• Corticosteroid dosing: Prednisone 1-2 mg/kg/day tapered over 4-8 weeks 1
• Antimycobacterial therapy: Consider for immunocompromised patients or those with persistent disease despite antigen avoidance and steroids 1

Monitoring and Follow-up

• Before each treatment cycle:

  • Monitor for new or worsening cough (most important symptom) 1
  • Check renal function 1
  • Use a "toxicity checklist" to track symptoms 1

• Response assessment:

  • Improvement in pulmonary function tests (FVC and DLCO)
  • Resolution of radiologic abnormalities
  • Symptom improvement (especially cough and dyspnea)

Steroid-Sparing Strategies

• When to consider: For patients requiring prolonged therapy or experiencing significant steroid-related adverse events
• Options:
  • Mycophenolate mofetil: Associated with 66% fewer treatment-emergent adverse events compared to prednisone alone 4
  • Azathioprine: Associated with 54% fewer treatment-emergent adverse events compared to prednisone alone 4
  • Both agents may help stabilize lung function in fibrotic HP 1, 4

Pitfalls and Caveats

• Differential response: Non-fibrotic HP responds better to corticosteroids than fibrotic HP 1, 3
• Diagnostic confusion: Improvement with steroids supports but does not confirm HP diagnosis, as other interstitial lung diseases like NSIP may also improve with immunosuppressive treatment 1
• Antigen avoidance: Failure to identify and remove the causative antigen may lead to treatment failure despite appropriate steroid therapy 1
• Mortality risk: Fatal progression can occur despite appropriate treatment, particularly in fibrotic HP 5
• Steroid resistance: Approximately 10% of patients may develop steroid-resistant or refractory disease, which carries high mortality (67%) 6
• Alternative therapies: For progressive fibrotic HP despite immunosuppression, antifibrotic medications may be considered as second-line therapy 7

Administration Recommendations

• Timing: Administer prednisone in the morning before 9 am to minimize adrenal suppression 8
• GI protection: Take with food or milk to reduce gastric irritation; consider antacids between meals 8
• PCP prophylaxis: Consider for patients receiving ≥20 mg of methylprednisolone or equivalent for ≥4 weeks 2
• Calcium/Vitamin D: Supplement with prolonged corticosteroid use 2
• Gastric protection: Proton pump inhibitors for all patients with grade 2-4 pneumonitis receiving steroids 2

Remember that while corticosteroids are the mainstay of therapy for HP, the response varies significantly between non-fibrotic and fibrotic disease. Early identification and complete avoidance of the causative antigen remains the cornerstone of management.