Abstract Introduction Hypersensitivity pneumonitis (HP) is exceptionally rare in children, with an estimated prevalence of 4 cases per 1,000,000. Its variable clinical presentation and often atypical, nonoccupational exposures pose a significant diagnostic challenge. We report a case of adolescent HP initially misattributed to an eating disorder and recurrent pneumonia, illustrating pitfalls in diagnosis and the importance of environmental history. Case A 17-year-old female with baseline sensory processing disorder and a recent diagnosis of eating disorder (20 lbs weight loss over 10 weeks) presented with progressive dyspnea and oxygen saturations in the 80s on room air. She had already been hospitalized twice at an outside facility for presumed pneumonia: the first admission treated with antibiotics, the second complicated by pneumomediastinum. Extensive workup (infectious, cystic fibrosis, immunology, rheumatology, echocardiography) was unrevealing. Chest CT demonstrated bilateral ground-glass opacities, interpreted as possible pneumonia or pulmonary edema. Her significant weight loss, attributed to psychosocial stressors (her father’s illness and death), led to their discharge diagnosis of “recurrent pneumonia in the setting of malnutrition,” and referral for behavioral and nutritional rehabilitation. On initial admission with us, CT findings persisted; she was weaned from supplemental oxygen over four days and discharged with plans for bronchoscopy the following week. She was readmitted four days later with further weight loss (6 lb), tachypnea, and SpO2 of 89%. Repeat rheumatologic and immunologic tests remained negative. A detailed review of her home environment revealed a history of mildew. This prompted sending an HP serologic panel and performing transbronchial lung biopsy, which showed lymphocytic infiltration with non-necrotizing granulomas, consistent with HP. The HP panel returned positive for Aspergillus fumigatus and aspergillus flavus precipitins. She was treated with prednisolone (1 mg/kg) for six weeks, with a taper planned over 2-4 months depending on response. She relocated to a new home environment, and over the subsequent four months experienced marked clinical improvement, weight gain, and no further hospitalizations. Conclusion HP in children can masquerade as other disorders—especially in the setting of weight loss or recurrent pneumonia. A high index of suspicion is critical. Meticulous environmental history to uncover antigen exposure should guide early testing (serologic precipitins, imaging, bronchoscopy). Delayed diagnosis risks progression to irreversible pulmonary fibrosis and poor long-term outcomes. Early removal of the offending antigen and initiation of anti-inflammatory therapy offer the best chance for recovery in pediatric HP. This abstract is funded by: None
Sahoo et al. (Fri,) studied this question.