Valproic acid-induced eosinophilic pleural effusion: a case report and review of the literature

OBJECTIVE: To report a case of valproic acid-induced eosinophilic pleural effusion and to review the existing literature. CASE SUMMARY: A 25-year-old African-American man receiving valproic acid, 250 mg/d, had a moderate-sized right pleural effusion. Pleural fluid analysis revealed 75% eosinophils. The patient had no evidence of parasitic infection, hemothorax, or pneumothorax. One month after valproic acid was discontinued, there was no evidence of a pleural effusion by both chest radiography and thoracic ultrasonography. DISCUSSION: Valproic acid-induced pleural effusions have been reported in the medical literature in 5 case reports. Pleural fluid eosinophilia is almost always related to pneumothorax, hemothorax, parasitic infection, or drug toxicity; therefore, when the first 3 causes have been eliminated, a drug should be suspected. Only a few medications are known to cause pleural fluid eosinophilia, one being valproic acid. The Naranjo probability scale rated this adverse reaction as probably drug-related. CONCLUSIONS: In all 6 patients discussed in this review, the pleural effusions resolved after discontinuation of the valproic acid. None of these patients had associated pulmonary infiltrates. Valproic acid eosinophilia may be associated with peripheral blood eosinophilia. Valproic acid should be added to the list of medications that can cause an eosinophilic pleural effusion.     

Eosinophilic pleural effusion associated to Churg and Strauss syndrome

Eosinophilic pleural effusion (EPE) is defined as pleural eosinophilia greater than 10%. EPE can be seen in almost all conditions that can cause pleural effusion, but some aetiologies have to be investigated due to their frequency or potential severity. The most common aetiology of EPE is the presence of air or blood in the pleural cavity. Other frequent aetiologies include bacterial pneumonia, tuberculosis, parasitic disease and certain drugs. Although often considered to be a sign of a benign condition, pleural eosinophilia may be associated with malignancies. EPE may also indicate the presence of Churg and Strauss syndrome. We report the case of a 27-year-old man, in whom the exploration of EPE led to the diagnosis of Churg and Strauss syndrome with the association of asthma, blood and alveolar eosinophilia, myopericarditis and positive antineutrophil cytoplasmic antibodies (ANCA). This case report enables us to discuss the different causes of EPE and to illustrate how it may be a manifestation of Churg and Strauss syndrome.     

恶性胸膜间皮瘤致嗜酸细胞性胸腔积液1例报告并文献复习

目的提高对嗜酸细胞性胸腔积液的认识。方法对一例由恶性胸膜间皮瘤所致嗜酸细胞性胸腔积液的临床资料进行分析,并结合文献复习。结果嗜酸细胞性胸腔积液首次报道于1984年,其病因很复杂,由肿瘤引起的并不多见,机理也不十分清楚,大多预后良好。结论虽然嗜酸细胞性胸腔积液的病因大多数是良性的,但我们不能忽略恶性的情况,应尽可能查找原因,以免贻误病情。     

Hydatid cyst presenting as an eosinophilic pleural effusion

A 61-year-old woman presented with an eosinophilic pleural effusion, secondary to transdiaphragmatic intrapleural spread of an hepatic hydatid cyst. Right posterolateral thoracotomy and frenotomy revealed a loculated pleural effusion associated with a 10 x 8 cm hydatid cyst in the posterior segment of the liver. Hydatid disease should be included in the differential diagnosis of eosinophilic pleural effusions in endemic regions.     

A rare case of eosinophilic pleuritis due to sparganosis

A rare form of sparganosis with eosinophilic pleural effusion is reported. A 62-year-old man was admitted to our hospital with left pleural effusion, and diagnosed immunologically as having sparganosis. Eosinophilia was seen in both peripheral blood and pleural effusion. The level of interleukin (IL)-5 was elevated in the pleural effusion, but not in peripheral blood. The patient was treated successfully with three consecutive doses of praziquantel (75 mg/ kg/day). After the treatment, the antibody titer in serum decreased and the eosinophil number in the peripheral blood returned to the normal level. Thus, sparganosis should be included in the differential diagnosis for eosinophilic pleuritis. The immunoserological screening test using multiple-dot ELISA is helpful to identify the causative pathogen.     

Diagnostic utility of CYFRA 21-1 in malignant pleural effusion

OBJECTIVE: The diagnostic utility of the tumour marker CYFRA 21-1 in malignant pleural effusion is not yet clear. This study was designed to evaluate the diagnostic utility of serum and pleural fluid CYFRA 21-1 in malignant pleural effusion. METHODOLOGY: The validity of serum and pleural fluid CYFRA 21-1 was determined in 62 patients with exudative pleural effusion (27 malignant and 35 benign). The diagnosis of malignant pleural effusion was defined by cytological or histological results. RESULTS: A statistically significant difference between the geometric means of CYFRA 21-1 levels in pleural fluid of benign and malignant aetiologies was observed (11.2 vs 63.3 ng/mL, P < 0.0001). In addition, there was a significant difference in the serum levels (0.95 vs 5.55 ng/mL, P < 0.0001). The sensitivity and specificity of pleural fluid CYFRA 21-1 in malignant pleural effusion, at the cut-off value of 55 ng/mL, was 74.1% and 97.1%, respectively. The sensitivity and specificity of serum CYFRA 21-1, at the cut-off value of 2.5 ng/mL, was 81.5% and 97.1%, respectively. Using a combination of serum and pleural fluid CYFRA 21-1 level, the sensitivity increased to 88.9%. CONCLUSION: Serum and pleural fluid CYFRA 21-1 are useful as measures in differentiating malignant from benign pleural effusion.     

Pulmonary involvement, pleural effusion, and electrocardiographic abnormality in hypereosinophilic syndrome]

A 47-year-old man was admitted to our hospital with complaints of cough and shortness of breath. Chest radiography showed infiltration of the right lung and left pleural effusion, the eosinophil count increased notably in the peripheral blood, sputum, and pleural effusion. Transbronchial lung biopsy revealed the invasion of eosinophils like eosinophilic pneumonia. Heart failure easily developed in this patient after the intravenous infusion. Myocardial involvement was suspected, and hypereosinophilic syndrome was diagnosed. After prednisolone was administered, the peripheral blood eosinophil count normalized rapidly, and subsequently, the pleural effusion and infiltration shadows in the lung disappeared.     

Case of tuberculous pleurisy with eosinophilic pleural effusion and hematological eosinophilia

A 30-year-old man suffered from a chest-pain on his left side and was also having a low-grade fever though he actually neglected these symptoms for a while. Later, he was referred to our hospital due to the detection of chest abnormal shadows through the mass examination of chest X-ray taken on 18th October, 2005. His chest X-ray showed bilateral pleural effusion and it was confirmed that the right pleural effusion was encapsulated by his chest CT. The patient's hematological examination performed during his initial visit, showed an increased level of WBC with blood eosinophilia. He also had a puncture of pleural effusion at the time of admission to the center. Moreover, pleural effusion on both sides was exudative and elevations of ADA and eosinophil count as well were traced. In the patient's right pleural effusion, mycobacterium tuberculosis direct (MTD) test was positive. As there were no findings suggesting collagen disease, malignancy, parasite infection, and other complications, he was diagnosed as tuberculous pleurisy with eosinophilic pleural effusion and blood eosinophilia. He was treated with four antitubercular agents, namely, INH, RFP, EB and PZA. As the result, his pleural effusion and blood eosinophil counts were decreased along with an improvement in inflammatory reaction. The most common conditions associated with eosinophilic pleural effusion are described as malignancy, collagen disease, paragonimiasis, drug induced pleurisy, asbestosis, pneumothorax, and trauma, while there are only a few reports about such eosinophilic pleural effusion caused by tuberculous pleurisy. In this case, he also showed blood eosinophilia. Based on these findings, we finally came to the conclusion that the case is a very rare and significantly unique case of eosinophilic pleurisy with blood eosinophilia.     

Imidapril-induced eosinophilic pleurisy. Case report and review of the literature

We describe an unusual case of a patient with eosinophilic pleurisy associated with long-term administration of imidapril, an angiotensin-converting enzyme inhibitor (ACEI). An 81-year-old woman who had been given imidapril for the treatment of essential hypertension was admitted to our hospital for investigation of persistent low-grade fever, dry cough and difficulty in breathing. Left-sided eosinophilic pleurisy was diagnosed based on eosinophilic pleural effusion and peripheral eosinophilia. Soon after administration of imidapril was discontinued, her clinical symptoms subsided, and there was improvement in both diagnostic imaging and laboratory findings. So far, to our knowledge, this is the first reported case in which ACEI induced eosinophilic pleurisy.     

Rapidly recurring massive pleural effusion as the initial presentation of sarcoidosis: A case report

Rationale:Sarcoidosis is a multisystem granulomatous disease with unknown etiology. It affects mainly the lungs, but it can affect almost any other organ. Nevertheless, pleural involvement with the development of pleural effusion is relatively rare. It is usually mild and responsive to treatment with systemic steroids. Here we present a case of rapidly recurring massive unilateral pleural effusion caused by sarcoidosis that was resistant to systemic steroids.Patient concerns:A 55-year-old lady presented with shortness of breath of 2-months duration. No other respiratory symptoms were reported. On physical examination, there were signs of left-sided pleural effusion, splenomegaly, and inguinal lymph nodes. These findings were confirmed by chest x-ray showing massive pleural effusion. Work up of the effusion revealed an exudative effusion with lymphocyte predominance. Pan-computed tomography scan revealed multiple thoracic, abdominal and inguinal lymphadenopathy; additionally, a left-sided pleural effusion and an enlarged spleen; that contained variable hypodense nodular lesions. Positron emission tomography-computed tomography showed intense uptake in the spleen and the lymph nodes. Inguinal lymph node biopsy showed non-necrotizing granulomatous inflammation. Due to suspicion of malignancy, left medical thoracoscopy was done, and biopsy of the parietal pleura showed nonspecific inflammation without evidence of malignancy or tuberculosis.Diagnosis:Sarcoidosis was diagnosed based on the finding of the non-necrotizing granulomatous inflammation with no evidence of malignancy or infection on several microbiological and pathological samples.Interventions:The patient was treated with repeated pleural fluid drainage. Steroids failed to prevent pleural effusion recurrence. Surgical left side pleurodesis was eventually performed.Outcomes:At more than 1 year follow up, the patient showed no recurrence of pleural effusion or development of any other symptoms.Lessons:Sarcoidosis may rarely present with massive pleural effusion, as this presentation is rare; it is imperative to rule out other causes of massive pleural effusion. Massive pleural effusion in sarcoidosis may be steroid-resistant. Pleurodesis may have a role in such a scenario.     

Pleural fluid viscosity may help identifying malignant pleural effusions

Background and objective:   Cancer cells are larger in size and more rigid than blood cells. As the size and rigidity of cells contribute to blood viscosity, an association may exist between high pleural fluid viscosity and cancer cells in pleural effusions. The aim of this study was to determine the correlation between pleural fluid viscosity and cell constituents or laboratory data in pleural diseases with different aetiologies.
Methods:   Fluid viscosities were determined in pleural effusions obtained via thoracocentesis. Pleural fluid viscosities were correlated with the laboratory data and with the percentages of different cellular constituents as assessed by cytological examination.
Results:   Pleural fluid viscosity was highest in malignant pleural effusions with positive results on cytological examination, and was correlated with the percentages of tumour cells (Spearman's rho = 0.24, P  = 0.037) and mitotic figures (rho = 0.23, P  = 0.041) in the exudates. Multivariate logistic regression analysis showed that pleural fluid viscosity was a significant determinant of positive results on cytological examination (odds ratio (OR) 6.26, 95% confidence interval (CI) 1.32–29.8), as were the levels of protein (OR 1.48, 95% CI 1.01–2.16) and LDH (OR 1.001, 95% CI 1–1.002).
Conclusion:   High pleural fluid viscosity may suggest a potential diagnosis of malignant pleural effusion.     

Nodular lung disease with five year survival and unilateral pleural effusion in AL amyloidosis

A 67-year-old female patient with biopsy proven AL systemic amyloidosis developed rapidly progressive dyspnea. Chest roentgenogram and CT scan revealed a large right pleural effusion in addition to nodular lesions with bilateral hilar lymphadenopathy. The patient's serum showed IgG λ type monoclonal gammopathy and she also had Bence Jones proteinuria. The pleural effusion was an exudate that contained many mononuclear cells and a high concentration of protein. Cardiac function was not seriously disturbed Except for amyloidosis, no other causes for the severe pleural effusion were found. This patient was treated with chemical pleurodesis using Picibanil and a low dose of prednisolone. Eighteen months after this treatment, her right pleural effusion did not recur. Bronchopulrnonary tissues are known to be frequently involved by AL systemic amyloidosis, but a nodular pattern of pulmonary amyloid deposition and a unilateral large pleural effusion are rare clinical manifestations in this disease.     

肺癌患者胸水CA125、CEA测定及其临床意义

目的　探讨 CA1 2 5、CEA在良、恶性胸腔积液鉴别诊断中的价值。方法　对 36例恶性胸腔积液、34例良性胸腔积液于治疗前同时抽取血清及第一次胸腔积液标本进行 CA1 2 5、CEA测定。结果　恶性胸腔积液组血清和胸腔积液 CA1 2 5、CEA测定值高于良性胸腔积液组 (P<0 .0 1)。 CA1 2 5敏感度 5 8.3% (2 3/36 ) ,特异度 88.2 % (30 /34) ;CEA敏感度 6 8.3% (2 3/36 ) ,特异度 85 .3% (2 9/34)。CA1 2 5和 CEA联合检测敏感度 72 .2 % ,特异度 94 .1%。结论　胸腔积液 CA1 2 5和 CEA联合检测对恶性胸腔积液的诊断价值更大。     

胸膜活检对原因不明的渗出性胸腔积液的诊断价值

目的观察胸膜活检术在渗出性胸腔积液诊断中的价值。方法对146例渗出性胸腔积液患者行胸膜活检，同时取胸水及痰送检抗酸杆菌及癌细胞。结果146例胸膜活检第一次活检成功率71．9％，特异性病理诊断92例，病理诊断阳性率63％。恶性胸腔积液胸膜活检阳性率58％，胸水细胞学检查阳性率22％，痰找癌细胞阳性率16％。结核性胸腔积液胸膜活检阳性率66．6％，痰找抗酸杆菌阳性率5．2％。结论胸膜活检是一项安全、简单、有效的胸膜疾病的重要的内科确诊手段。     

尿激酶治疗结核性包裹性胸积液后外科手术治疗的疗效分析肖泽林 刘家杰 高健齐 连贵勇简

目的 探讨在结核性包裹性胸积液疾病治疗中如何选择胸腔内注入尿激酶与外科手术治疗.方法 分析我院651例诊断结核性包裹性胸积液病例,在入院后予常规抗痨治疗并予胸腔内注入尿激酶治疗,对有效组与效果不佳再转入外科行胸腔纤维板剥脱术治疗的手术组的疗效进行对比分析.结果 两组病例的发病病程、复发率比较无明显差异 （P〉0.05）,在体查及B超、CT检查、胸腔穿刺或置管后肺能否复张比较有明显差异（P＜0.05）.结论 在体查、B超和CT检查有阳性结果、胸腔穿刺或置管后肺不能复张的病例选择外科手术治疗效果较好,胸膜纤维板剥脱术仍是治疗胸膜增厚的结核性包裹性胸积液的有效方法.     

肺结节病合并胸腔积液14例诊治分析

目的对肺结节病合并胸腔积液的诊治进行分析。方法对我院1991~2009年间,肺结节病合并胸腔积液的14例患者进行分析。结果 8例为Ⅱ期,6例为Ⅰ期。13例口服醋酸泼尼松片（0.5 mg/kg）逐渐减量治疗。3例曾联合抗结核治疗。口服激素1个月后,4例胸腔积液消失,4例明显减少,3个月后14例患者胸腔积液均消失,1例留有胸膜肥厚。结论肺结节病出现胸腔积液的机制不明,激素治疗剂量与无胸腔积液患者用量相同,逐渐减量。     

流式细胞检测细胞胸腔积液中总数和白细胞介素-16的意义

目的 联合细胞技术检测恶性和结核性胸腔积液中的细胞总数和白细胞介素16(IL-16)的意义.方法 用流式细胞技术检测36例为结核性胸腔积液(PE)和32例为恶性积液患者的胸水中的细胞总数和IL16的水平.同时检测外周血的IL16水平.结果 恶性PE中细胞总数、淋巴细胞、中性粒细胞明显高于结核性PE(P<0.05),而结核性PE中巨噬细胞和间皮细胞明显高于恶性PE(P<0.05).胸腔积液中的IL-16在结核性PE中、高恶性PE(P=0.036),而外周血中的IL-16水平,结核性PE高于癌性PE(P=0.089).结论 恶性和结核性PE中细胞类型和IL-16表现出明显差别呈相关性,可作为鉴别诊断的参考.     

Derrame pleural e hipertensión pulmonar en un paciente con enfermedad de Parkinson en tratamiento con cabergolina

Cabergoline is a synthetic dopamine agonist used to treat Parkinson disease. The drug occasionally induces pleuropulmonary adverse effects, which manifest as pleural thickening or effusion, interstitial pneumonitis, pulmonary infiltrates, or fibrosis. We report a rare case of pleural effusion and severe pulmonary hypertension in a 79-year-old man with Parkinson disease who had been treated with cabergoline for 1 year. The symptoms disappeared 10 months after the drug was discontinued.     

Eosinophilic pleural effusion in adults at Srinagarind Hospital

The presence of pleural eosinophilia remains a controversy in etiology and prognosis. We conducted this study to evaluate the etiology of eosinophilic pleural effusion and to define the factors that determine malignancy in eosinophilic pleural effusion. Between 1 August 1994 and 1 July 2000, 50 patients were diagnosed with eosinophilic pleural effusion; 35 men and 15 women averaging 56.4 years of age. Most (96%) had exudative pleural effusion. Malignancy was the most common (46%) established cause followed by tuberculosis (10%), parapneumonic effusion (8%), and empyema thoracis (2%). We encountered only one case of pneumothorax and parasitic pleural effusion (from Strongyloides stercoralis). Unknown causes constituted 22% of cases. The etiology of those who had previously undergone thoracocentesis did not differ from those having their first thoracocentesis. Patients with malignant pleural effusion had significant longer duration of clinical symptoms (> or = 1 month) and weight loss than benign pleural effusion. The median duration of symptoms in benign pleural effusion was 14 days. Fever was more characteristic in patients with benign than in those with malignant pleural effusion. The percentage of eosinophils in pleural fluid and blood did not differ between the two groups. Pleural fluid eosinophils in malignant vs benign pleural effusion were 26.6% (range 10% to 63%), and 30.6% (range 10% to 93%), respectively. We concluded that, pleural eosinophilia did not indicate benign conditions which would spontaneously resolve. Malignant pleural effusion should be considered especially in areas malignancy is prevalent.     

Propylthiouracil-associated eosinophilic pleural effusion: a case report

We describe an unusual case of a patient with eosinophilic pleural effusion (EPE) associated with long-term propylthiouracil (PTU) administration. A 43-year-old woman was admitted to our hospital after complaining of chest pain. She had had Graves' disease, which had been treated with PTU for 11 years. Right-sided pleural effusion was detected and the result of thoracentesis confirmed an EPE. The patient's detailed medical evaluation failed to reveal any other cause of EPE. PTU was terminated since it was thought to be the cause. Despite withdrawal of the medication, however, the pleural effusion persisted for 6 weeks, and steroid therapy was planned for 15 days in decreasing dosages. During the control visit 10 days after the initiation of steroid therapy, no pleural effusion was observed, and the steroid was discontinued. Rechallenge with PTU produced recurrent pleural effusion. Therapy with PTU was again terminated, and treatment with methimazole and a brief course of low-dose corticosteroids were begun. Chest radiography revealed disappearance of the effusion within 10 days and it did not recur during a 1-year follow-up. To our knowledge, there is only 1 other case in the English-language literature describing EPE caused by PTU. Our report is of particular importance because it describes the development of that disorder in the 11th year of PTU treatment. It also shows that steroid therapy can be effective in treating drug-induced EPE.