BACKGROUND: Q fever is a zoonosis caused by Coxiella burnetii. Acute infection is mainly asymptomatic. In other cases it mainly causes a flu-like illness, a pneumonia, or an hepatitis. We present an atypical case of an acute Q fever revealed by a massive pleural effusion.
METHODS: We report the case of a 43-year-old man referred to our hospital for an acute respiratory distress. Further analyses showed an exudative eosinophilic pleural effusion, associated with a pulmonary embolism and a deep femoral vein thrombosis. Aetiologic explorations revealed an acute Q fever (IgM and IgG against C. burnetii phase II antigens) associated with anti-phospholipids. The outcome was favorable with vitamin K antagonists, doxycycline, and hydroxychloroquine, till the negativation of the anti-phospholipid antibodies.
CONCLUSIONS: During acute C. burnetii infections, anti-phospholipid antibodies are highly prevalent but thrombotic complications are rare. The 2023 ACR/EULAR APS criteria restricts the diagnosis of APS, as in our case of acute severe infection. In front of an atypical pneumonia and/or thrombotic events, screening of C. burnetii and anti-phospholipid antibodies could be useful. Given its low level of evidence, prolongated treatment by doxycycline, hydroxychloroquine ± anticoagulant for C. burnetii\'s associated anti-phospholipid syndrome is discussed, but succeeded in our case.

We present a rare case of a 45-year-old woman with pseudo-Meigs\' syndrome and eosinophilic pleural effusion (EPE). She experienced cough, sputum, and dyspnea with a large right pleural effusion. Laboratory tests showed eosinophilia in the blood and pleural fluid. An ovarian tumor and ascites were also detected. After left salpingo-oophorectomy, the tumor was diagnosed as a mature cystic teratoma of the left ovary. The right-sided pleural effusion gradually resolved. Pseudo-Meigs\' syndrome is characterized by benign ovarian tumor, ascites, and pleural effusion. Typically, it is associated with exudate pleural effusion characterized by a predominance of mononuclear cells. The occurrence of eosinophilic pleural effusion in our patient may be exceptionally rare.

The diagnosis of unilateral eosinophilic pleural effusion (EPE) is difficult, especially for the elderly. IgG4-related disease (IgG4-RD) is a rare cause of EPE.
An 81-year-old man was admitted to the hospital for dyspnea due to right pleural effusion. Laboratory examination shows elevated IgG4 and eosinophils in both serum and pleural fluid. The patient was diagnosed with IgG4-RD by video-assisted thoracoscopy and pleural biopsy. We found no evidence of other organ involvement except for the EPE and history of prurigo. He was treated with prednisolone 40 mg daily orally and pleural effusion decreased significantly.
IgG4-RD should be considered in the differential diagnosis of EPE in the elderly. High effusion IgG4 concentration may be an indication of IgG4-related pleural lesions.

Eosinophilic pleural effusions are defined by an eosinophil count ≥ 10% in pleural fluid and represent approximately 10% of exudative pleural effusions. They are associated with a large spectrum of etiologies, both benign and malignant. Drug-induced eosinophilic pleural effusions remain rarely described.
After ruling out other causes with a careful diagnostic assessment, we retain paliperidone as the etiology, given the disappearance of the pleural effusion after drug discontinuation.
We report the first case of eosinophilic pleural effusion induced by paliperidone palmitate treatment.
After considering other etiologies, drug-induced eosinophilic pleural effusion should be sought.

BACKGROUND: Pleural fluid effusion is a possible harmful effect of sodium valproate. It most often consists in polynuclear eosinophilic pleurisy and occurs within months of treatment initiation.
METHODS: We report on a case of sodium valproate-induced pleural effusion occurring more than 12years after initiation of treatment. The original formula was variegated and not eosinophilic. The patient exhibited contralateral recurrence with continued treatment. Once treatment was discontinued, there was no recurrence during three-year follow-up.
CONCLUSIONS: Sodium valproate-induced pleural effusion can present an atypical polymorphous picture leading to erroneous diagnoses.

BACKGROUND: Eosinophilic pleural effusion (EPE) is a distinct entity among pleural effusions, but its diagnostic and prognostic significance is still controversial. This study aimed to evaluate the incidence and aetiological distribution of EPE in our institution and to assess the relationship between EPE and malignancy and other underlying diseases and the relevance of the percentage of eosinophils and other laboratory parameters.
METHODS: A retrospective study was conducted by reviewing the medical records of 252 patients with PE from September 2017 to January 2021.
RESULTS: EPE was found in 34 (13.49%) out of 252 patients. There were 20 (58.82%) males and 14 (41.18%) females in the EPE group. The mean percentage of eosinophils in EPE (21.7%, range (10.0-67.5%)) was significantly higher than the percentage of eosinophils in peripheral blood (5.65%, range (0-34.60%); p < 0.05). The most common cause of EPE was malignant disease (52.94%), followed by idiopathy (14.71%), parasites (8.82%), pneumonia (8.82%) and others (14.71%). Comparative analysis of patients with malignant versus nonmalignant EPE showed that patients with malignant EPE were significantly older, and had a lower white blood cell (WBC) count in the pleural fluid (1.8 vs 4.7 cells × 109/L, p < 0.05). However, the percentage of eosinophils in PE was not significantly different between malignant EPE and nonmalignant EPE (p = 0.66). There was no correlation between the percentage of eosinophils in PE and peripheral blood (r = 0.29; p = 0.09).
CONCLUSIONS: Malignant disease ranks as the leading cause of EPE. The presence of EPE should not be considered as a predictive factor of benign conditions. Pleural parasitic infestation (PPI) should be emphasized in areas with a high incidence of parasitic disease.

Eosinophilic pleural effusion can be the first presenting feature of a wide range of diseases, with malignancy being the commonest cause. Elevated levels of eosinophils could be an indicator of a favourable prognosis. In clinical practice, malignant lymphomas have been rarely associated with eosinophilic pleural effusions. In this report, we present the case of a 37-year-old otherwise healthy woman, who initially presented with a cough of five months\' duration. Diagnostic workups including pleural and lymph node biopsies confirmed the diagnosis of nodular lymphocyte-predominant Hodgkin\'s lymphoma.

Coronavirus disease 2019 (COVID-19) has become a global pandemic since its discovery in December 2019, and as the disease continues to evolve, varying complications associated with it continue to arise. In this regard, computed tomography has played an extremely important role in the diagnosis and evaluation of COVID-19 pneumonia and its complications. We encountered a case of a male patient with neurofibromatosis (type I) who developed concurrent pneumothorax and pleural effusion during his recovery period from severe COVID-19 pneumonia. Pulmonary fibrosis and emphysema were also confirmed. Furthermore, an eosinophil pleural effusion appeared and was prolonged during the healing process of COVID-19. This clinical presentation suggests that fibrosis and emphysema formation due to neurofibromatosis may have caused pneumothorax and pleural effusion.

A 37-year-old man with fever, cough, and dyspnea with no medical history developed an eosinophilic pleural effusion and blood eosinophilia. No evidence of malignancy or pathogens was detected in the pleural effusion, and the pleural specimen obtained by thoracoscopy showed eosinophilic infiltration with inflammatory granulation tissue without fibrinoid necrosis or malignant cells. Since a myeloproliferative disorder was also excluded, the diagnosis was idiopathic eosinophilic pleurisy. Corticosteroid treatment was started and then slowly tapered, and the eosinophilic pleural effusion resolved. Considering the various etiologies of eosinophilic pleurisy, a practical clinical approach to the investigation and diagnosis of eosinophilic pleurisy is presented.

UNASSIGNED: Prolonged air leakage after pulmonary resection is a common complication, and fibrin glue is used as a sealant to reduce this. Fibrin glue-induced adverse events are generally rare. Herein, we describe a rare case of fibrin glue-induced eosinophilic pleural effusion (EPE).
METHODS: A 77-year-old man underwent partial pulmonary resection for right lower lobe lung cancer, and the pulmonary staple stump was subsequently covered with fibrin glue. Antibacterial drugs were administered for the treatment of postoperative pneumonia. However, re-elevation of the inflammatory cell number was observed, and computed tomography revealed an increase in right pleural effusion. Although thoracoscopy was performed based on a possibility of empyema, no empyema was observed. The eosinophil count in the pleural effusion was 11%; thus, the patient was diagnosed with EPE, which was resolved after thoracic drainage, without corticosteroid administration. Fibrin glue was identified as the causative agent, using a drug-induced lymphocyte stimulation test.
UNASSIGNED: EPE is defined as an eosinophil count of ≥10% in the pleural effusion. If pleural effusion on the surgical side, with fever or an elevated inflammatory cell number, is observed in the early postoperative period after pulmonary resection, empyema should be considered foremost. In this case, the administration of antibacterial drugs was ineffective, and the patient was eventually diagnosed with EPE.
CONCLUSIONS: EPE should be considered as a rare fibrin glue-induced adverse event after pulmonary resection. It is recommended that the leukocyte fraction be examined, if pleural effusion is collected for postoperative pleural effusion.