Unilateral hilar sarcoidosis with anemia and low T3 syndrome: a case report.

BACKGROUND

Sarcoidosis is a systemic granulomatous disease that typically presents with bilateral hilar or mediastinal lymphadenopathy. Unilateral hilar involvement is uncommon and may closely mimic lung cancer, lymphoma, or tuberculosis. Inflammatory activation in sarcoidosis may also disrupt iron metabolism and thyroid hormone homeostasis, but these extra-radiological clues are often overlooked in routine practice.

CASE PRESENTATION: A 53-year-old woman was admitted with fever, chest tightness, and a left hilar mass with mediastinal lymphadenopathy. Laboratory tests showed pancytopenia and markedly elevated inflammatory markers, including interleukin-6 at 60.7 pg/mL and C-reactive protein at 98.7 mg/L. Iron studies showed a discordant profile: low serum iron of 6.3 μmol/L, reduced transferrin, and markedly elevated ferritin of 955.2 μg/L. Total T3 was also low at 0.57 nmol/L. She had a 2-year history of anemia with poor response to oral iron therapy. Initial endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) of station seven lymph nodes was non-diagnostic. Because malignancy and infection remained possible, repeat EBUS-TBNA targeting stations 4L and 11L was performed and showed non-caseating granulomatous inflammation. Microbiological tests for tuberculosis and fungal infection were negative, and tumor markers did not support malignancy. Intrathoracic sarcoidosis with atypical unilateral hilar and mediastinal lymphadenopathy was diagnosed. The anemia was interpreted as mixed absolute iron deficiency and inflammation-related iron restriction, accompanied by low T3 syndrome in the setting of systemic inflammation. Treatment with intravenous iron sucrose and inhaled budesonide-formoterol was followed by regression of the hilar and mediastinal lesions, normalization of hemoglobin, and recovery of T3 levels.

CONCLUSION

The case highlights the diagnostic challenge of unilateral hilar sarcoidosis, which may mimic malignancy or infection. When initial EBUS-TBNA is non-diagnostic but clinical suspicion persists, repeat multi-station sampling should be considered in selected cases to reduce false-negative interpretation. The accompanying anemia and low T3 syndrome may provide supportive evidence of systemic inflammation, but they should not be regarded as central diagnostic features. Continued follow-up is warranted to monitor the clinical course.