A 64-year-old patient, chronic smoker for 40 years, had a dry cough since 6 months along with mMRC stage 2 dyspnea which became complicated 1 month ago by the worsening of dyspnea resulting in mMRC stage 3, all evolving in a context of preservation of general condition. On clinical examination, his desaturation level was at 78% in ambient air with polypnea at 25 cycles per minute, cyanosis of the extremities and signs of respiratory struggle. The pleuropulmonary examination revealed crackles on the left.
The chest X-ray showed bilateral alveolar opacities.
At the biological level: hypereosinophilia was noted on several occasions (going up to 1170), a hemoglobin level at 15.9g/l, white blood cells at 13,700/mm3 and platelets at 320,000/mm3, a correct renal function, a negative covid 19 PCR test, a negative genexpert for tuberculosis in the sputum and a negative cytobacteriological examination of the sputum. The total IgE level was not done.
Faced with hypereosinophilia, a stool parasitology was requested which returned negative.
The thoracic CT scan (Fig. 1) showed diffuse foci of pulmonary parenchymal condensation, involving the various pulmonary lobes with areas of ground glass.
A bronchial fibroscopy was performed showing a normal endoscopic appearance. Staged bronchial biopsies returned to normal, fibroaspiration in search of neoplastic cells was done but did not detect tumor cells and the patient did not tolerate BAL.
A spirometry objectified a ventilatory disorder of restrictive pace with a forced vital capacity at 3.02l or 43% and an arterial blood gas: hypoxia at 40 mmHg.
The diagnosis of the eosinophilic lung was retained on the radiological aspect and hypereosinophilia and the patient was put on a bolus of corticosteroids followed by an oral corticosteroid therapy at a dose of 1mg/kg/day. The initial evolution after 15 days was marked by an improvement in the patient's dyspnea with an increase in saturation to 83% in ambient air, a slight decrease in the eosiniphil level to 1000/mm3 and radiological stability. The patient was discharged on oral corticosteroid therapy and oxygen therapy 3l per minute.
The follow-up at 2 months showed reaggravation of symptoms with stage 3 dyspnea, 78% desaturation on AA and the appearance of recurrent episodes of low abundance hemoptysis. Eosinophil count increased to 3630/mm3. A thoraco-abdomino-pelvic CT scan was redone showing the same radiological appearance with no lesions outside the lung. The diagnosis of eosinophilic lung was questioned, therefore a CT-guided biopsy was performed, and the result showed tumoral proliferation consisting of atypical cells cohesively colonizing the alveolar structures without signs of stromal invasion which is histological appearance of a non mucinous lepidic adenocarcinoma (Fig. 2).
The case of our patient was presented in a multidisciplinary consultation meeting (RCP) and the diagnosis of invasive lepidic adenocarcinoma was retained because of the radiological presentation. It was decided to put the patient on chemotherapy and to search for the EGFR mutation.
The patient received his first course of carboplatin - pemetrexed.