Antibiotic‐induced reduction of abnormal lung shadow in pulmonary nodular lymphoid hyperplasia

Pulmonary nodular lymphoid hyperplasia (PNLH) involves proliferative lymphatic tissues and is reportedly associated with inflammatory disease or autoimmune disorders. Herein, we describe a case of PNLH with difficult diagnosis because of antibiotics therapy‐induced reduction in the abnormal tumour s...

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Veröffentlicht in:Respirology case reports 2020-03, Vol.8 (2), p.e00522-n/a
Hauptverfasser: Tanino, Akari, Tsubata, Yukari, Hamaguchi, Shunichi, Sutani, Akihisa, Nagase, Mamiko, Isobe, Takeshi
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Sprache:eng
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Zusammenfassung:Pulmonary nodular lymphoid hyperplasia (PNLH) involves proliferative lymphatic tissues and is reportedly associated with inflammatory disease or autoimmune disorders. Herein, we describe a case of PNLH with difficult diagnosis because of antibiotics therapy‐induced reduction in the abnormal tumour shadow. An 86‐year‐old man was admitted for persistent cough and bloody sputum. Computed tomography (CT) revealed a mass in the right middle lobe, which got smaller on treatment with tosufloxacin for pneumonia. Unexpectedly, the tumour shadow remained one month later. Positron emission tomography depicted fluorodeoxyglucose uptake at the site. Although lung cancer was suspected, the mass was non‐diagnostic on transbronchial and CT‐guided biopsies. He was eventually diagnosed with PNLH on post‐surgical histological analysis of the lung mass. Neutrophil accumulation and bacterial lumps were present, indicating Actinomyces infection in the pulmonary alveolus, suggesting that PNLH was associated with pneumonia. Histopathological examination helped identify the aetiology of this rare case of PNLH. A case of pulmonary nodular lymphoid hyperplasia (PNLH) that was difficult to diagnosis because of an abnormal shadow that was reduced due to antibiotics use was described. Histopathological examination indicated a diagnosis of PNLH and the pathological evidence of bacteria suggested an infective aetiology for PNLH.
ISSN:2051-3380
2051-3380
DOI:10.1002/rcr2.522