Background <p>Interferon (IFN)-induced interstitial lung disease (ILD) is a rare but potentially fatal complication. While predominantly reported in patients with chronic hepatitis C, its occurrence during therapy for chronic hepatitis B is exceedingly rare. Although steroids are widely used empirically, the optimal therapeutic regimen remains to be elucidated.</p> Case presentation <p>We reported a case of a middle-aged, non-smoking Asian female patient with chronic hepatitis B who received weekly subcutaneous injection of pegylated interferon-alpha (Peg-IFNα) (alternating 135&#xa0;μg or 180&#xa0;μg). One month after treatment initiation (following the fifth dose), she developed exertional dyspnea, dry cough, and a low-grade fever. High-resolution computed tomography revealed bilateral interlobular septal thickening with subpleural ground-glass opacities. Pulmonary function tests demonstrated a reduced diffusion capacity, however, uncommon in ILD, the patient also exhibited pulmonary hyperinflation. Serological tests did not reveal any abnormalities in white blood cell count, C-reactive protein, procalcitonin, autoantibodies, or anti-respiratory virus antibodies. Echocardiography confirmed structurally normal cardiac chambers and preserved left ventricular systolic function (ejection fraction of 71%). After excluding infectious, autoimmune, and cardiogenic causes, the IFN-induced ILD was diagnosed. After discontinuation of Peg-IFNα and initiation of methylprednisolone therapy, the patient’s respiratory symptoms improved markedly within 24&#xa0;h and resolved completely within a week. During follow ups, no respiratory symptom reoccurred, and chest imaging and the pulmonary function resolved gradually.</p> Conclusion <p>In this study, we reported a female case who developed an IFN-induced ILD while monotherapy with IFN for chronic hepatitis B, and who experienced rapid clinical improvement after initiation of steroid therapy. To our knowledge, IFN-induced ILD is exceedingly rare in the context of PEG-IFNα monotherapy for chronic hepatitis B, particularly in female patients. Clinicians should maintain a high index of suspicion for IFN-induced ILD when unexplained pulmonary symptoms arise during therapy. Early recognition and appropriate steroid administration appear to be effective strategies for managing disease progression.</p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Interferon-induced interstitial lung disease: a rare adverse effect induced by pegylated interferon-alpha in a patient with chronic hepatitis B-case report

  • Haoyue Yu,
  • Shuangshuang Zhang,
  • Yu Zhou,
  • Qingqing Wen,
  • Yan Wang,
  • Xuemei Yang

摘要

Background

Interferon (IFN)-induced interstitial lung disease (ILD) is a rare but potentially fatal complication. While predominantly reported in patients with chronic hepatitis C, its occurrence during therapy for chronic hepatitis B is exceedingly rare. Although steroids are widely used empirically, the optimal therapeutic regimen remains to be elucidated.

Case presentation

We reported a case of a middle-aged, non-smoking Asian female patient with chronic hepatitis B who received weekly subcutaneous injection of pegylated interferon-alpha (Peg-IFNα) (alternating 135 μg or 180 μg). One month after treatment initiation (following the fifth dose), she developed exertional dyspnea, dry cough, and a low-grade fever. High-resolution computed tomography revealed bilateral interlobular septal thickening with subpleural ground-glass opacities. Pulmonary function tests demonstrated a reduced diffusion capacity, however, uncommon in ILD, the patient also exhibited pulmonary hyperinflation. Serological tests did not reveal any abnormalities in white blood cell count, C-reactive protein, procalcitonin, autoantibodies, or anti-respiratory virus antibodies. Echocardiography confirmed structurally normal cardiac chambers and preserved left ventricular systolic function (ejection fraction of 71%). After excluding infectious, autoimmune, and cardiogenic causes, the IFN-induced ILD was diagnosed. After discontinuation of Peg-IFNα and initiation of methylprednisolone therapy, the patient’s respiratory symptoms improved markedly within 24 h and resolved completely within a week. During follow ups, no respiratory symptom reoccurred, and chest imaging and the pulmonary function resolved gradually.

Conclusion

In this study, we reported a female case who developed an IFN-induced ILD while monotherapy with IFN for chronic hepatitis B, and who experienced rapid clinical improvement after initiation of steroid therapy. To our knowledge, IFN-induced ILD is exceedingly rare in the context of PEG-IFNα monotherapy for chronic hepatitis B, particularly in female patients. Clinicians should maintain a high index of suspicion for IFN-induced ILD when unexplained pulmonary symptoms arise during therapy. Early recognition and appropriate steroid administration appear to be effective strategies for managing disease progression.