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Eosinophilic pneumonia: case report A 57-year-old woman developed eosinophilic pneumonia (EP) during treatment with valproate semisodium for bipolar disorder. The woman was hospitalised in February 2017 for exploration of dyspnoea on exertion. Her medical history was significant for atopic asthma, which was diagnosed in childhood and not very symptomatic, and bipolar disorder with autolytic attempt in 2014. Cannabis use and alcohol were weaned off in 2014. She had stopped smoking (an estimated at 40 packs-year) 2 months previously. Her usual treatment included valproate semisodium [sodium divalproate] [dosage and route not stated], zopiclone, hydroxyzine, budesonide in combination with formoterol and salbutamol. Five months previously, non-febrile dyspnoea on exertion emerged. It was gradually worsening and was associated with 10kg weight-loss and wet cough. The lack of improvement following two successive courses of antibiotic therapy with pristinamycin and levofloxacin then led to her hospitalisation. Upon admission, she had a grade 3 dyspnoea with no evidence of acute respiratory distress. Her body temperature was 36.2°C. Lung auscultation revealed signs of squeaking sound wheeze and bilateral sibilant. No associated extra-respiratory sign was observed. Her SpO2 was 96% under 3 L/min oxygen and the blood gases sampling confirmed the severity of hypoxaemia in room air. Her chest x-ray did not find any obvious pleuroparenchymal abnormality. The spirometry found severe airway obstruction (AO). The blood count found hyperleukocytosis with polymorphonuclear neutrophils and hypereosinophilia, with no other abnormal blood cell lines. Her Creactive protein was 27 mg/L. A suspicion of an acute exacerbation of an unrecognised chronic obstructive pulmonary disease was made. Aerosol treatment with unspecified β-2-mimetic and anticholinergic agents, combined with systemic corticosteroid therapy at 0.5 mg/kg/day of prednisone equivalent for 5 days, was proposed. As no clinical improvement was noted, she underwent a chest CT scan, which showed diffuse bilateral ground glass opacities with peripheral and central location, affecting the 5 lobes, associated with interlobular septa thickening, with crazy paving appearance. An increase in the blood eosinophil count was also observed under the systemic corticosteroid therapy. The bronchoalveolar lavage fluid (BAL) fluid collected from the middle lobe found mixed alveolitis with 420000 cells/mL, predominantly polymorphonuclear eosinophils (PNE). In this context, after excluding other drugs, a diagnosis of EP secondary to valproate semisodium was considered, since this was the only drug retained as potentially able to induce such disorder. Retrospectively, it was specified that valproate semisodium was introduced in June 2014 when the blood count of PNE was 0.134 g/L. Secondly, a gradual increase in blood eosinophil count was noted, respectively at 0.717 g/L and 1536 g/L in April 2015 and January 2017. Therapy with valproate semisodium was withdrawn and changed to lamotrigine. No