|Year : 2015 | Volume
| Issue : 2 | Page : 66-68
Massive pleural effusion and associated pulmonary embolism in a case of Gefitinib responsive lung cancer
Rajiv Garg1, Ashwini Kumar Mishra1, Ankit Bhatia1, Laxmi Devi2, Rahul Kumar1, Jyoti Bajpai1
1 Department of Pulmonary Medicine, King George Medical University, Lucknow, Uttar Pradesh, India
2 Department of Radiodiagnosis, King George Medical University, Lucknow, Uttar Pradesh, India
|Date of Web Publication||16-Jun-2015|
Department of Pulmonary Medicine, King George Medical University, Lucknow, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Pulmonary embolism (PE) and venous thrombosis is a common complication in lung cancer patients with a high misdiagnosis rate and high mortality. However, when an undiagnosed lung cancer patient presents as PE, cancer as a cause may not always be explored. We present a case of a young male patient presenting with venous thromboembolism causing massive pleural effusion, leading to the diagnosis of epidermal growth factor receptor mutation positive adenocarcinoma, showing good response to gefitinib therapy.
Keywords: Gefitinib, lung cancer, pleural effusuion, pulmonary embolism
|How to cite this article:|
Garg R, Mishra AK, Bhatia A, Devi L, Kumar R, Bajpai J. Massive pleural effusion and associated pulmonary embolism in a case of Gefitinib responsive lung cancer. J Assoc Chest Physicians 2015;3:66-8
|How to cite this URL:|
Garg R, Mishra AK, Bhatia A, Devi L, Kumar R, Bajpai J. Massive pleural effusion and associated pulmonary embolism in a case of Gefitinib responsive lung cancer. J Assoc Chest Physicians [serial online] 2015 [cited 2021 Jul 30];3:66-8. Available from: https://www.jacpjournal.org/text.asp?2015/3/2/66/158866
| Introduction|| |
Venous thromboembolism (VTE) and lung cancer are associated by a two-way clinical association: VTE may be the presenting feature of an occult cancer and patients with clinically visible cancer may develop a venous thromboembolic complication at any stage of their disease. Apparently, idiopathic pulmonary embolism (PE) may be a presenting complication of underlying undiagnosed lung cancer. Additionally, the occurrence of a VTE with cancer has been associated with a worse prognosis and a poor quality of life.
| Case Report|| |
A 34-year-old smoker male with no significant medical history presented with insidious onset breathlessness associated with a sharp, retrosternal left-sided chest pain. The patient was noted to be in respiratory distress and shock with markedly decreased breath sounds on the left. Chest X-ray [Figure 1] revealed massive left-sided pleural effusion, which on pleurocentesis revealed hemorrhagic exudative effusion (TLC-700, DLC-L70 N21 Meso7, protein 5.2 g/dL, albumin 3.2 g/dL, sugar 67 mg/dL, ADA 24 IU/L, hematocrit 18%). On routine clinical examination, the patient was found to have dilated thrombosed veins over both lower limbs. D-dimer (82 mg/dL) was found to be elevated. Venous Doppler of the lower limbs confirmed the presence of a complete thrombus of the bilateral posterior tibial vein and popliteal vein. Computed tomography (CT) thorax and pulmonary angiogram [Figure 2]a and b confirmed the presence of a pulmonary embolus in the left main pulmonary artery. Pulmonary embolus was confirmed as the cause of pleural effusion. The patient was started on therapeutic anticoagulation. Initially, the patient was started on low molecular weight heparin (Enoxaparin) in a dose of 1 mg/kg for 5 days then patient was shifted to warfarin 5 mg daily. After the patient got relieved and was stable and effusion also decreased, to assess the cause of embolism pleural biopsy was performed which confirmed the diagnosis of adenocarcinoma of lung origin [Figure 3]. The epidermal growth factor receptor (EGFR) mutation investigation of the histopathological specimen revealed an EGFR point mutation at exon 21 (L858R). Gefitinib treatment was started, and his levels of plasma D-dimer immediately decreased. Follow-up chest X-ray [Figure 4] showed nearly complete resolution of pleural effusion. The patient got relief from his complaints and showed an excellent clinicoradiological response to the treatment and is now free from any symptoms and is in our regular follow-up and treatment.
|Figure 4: Follow-up chest X-ray showing nearly complete resolution of pleural effusion|
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| Discussion|| |
Pleural effusions secondary to PE are usually small, manifest only as blunting of costophrenic angle, rarely do the effusions occupy more than one-third of the hemithorax.  Pulmonary infarctions are associated with large effusions, clear more slowly and appear hemorrhagic in appearance.
Venous thromboembolism and lung cancer are associated by a two-way clinical association: VTE may be the presenting feature of an occult cancer and patients with clinically visible cancer may develop a venous thromboembolic complication at any stage of their disease. Apparently, idiopathic PE may be a presenting complication of underlying undiagnosed lung cancer.  Additionally, the occurrence of a VTE with cancer has been associated with a worse prognosis and a poor quality of life.
It is generally thought that malignancy is the most common cause of a pleural effusion occupying the entire hemithorax especially in older patients.
The mechanism of lung cancer and PE risk factors not yet fully understood. Most of the events associated with PE occur in patients at the same time of cancer diagnosis or during early phases of first-line chemotherapy, most cases being of adenocarcinoma type, in advanced stages and poor performance status.  Cancer can lead to a prothrombotic or hypercoagulable state by an altered balance between the coagulation and fibrinolytic systems.  The hypercoagulable state is the result of the complex interaction of various mechanisms. There is activation of coagulation and fibrinolytic pathways by either vascular endothelium, monocytes, platelets or by their complex interaction.  Tumor cells interact with all parts of the hemostatic system. Tumor cells have the potential to create a hypercoagulable state either by directly activating the coagulation cascade by producing their own procoagulant factors or by stimulating the prothrombotic properties of other blood cell components.  Additional mechanisms of clotting activation are initiated by cytotoxic chemotherapy or other cancer therapies. Underlying cancer biological features such as tumor mutations may contribute to VTE risk and cancer prognosis. EGFR activating mutations are more frequently found in this histological subtype than in other lung cancers.  Gefitinib is observed to be a very effective treatment in PE due to lung cancer with reports of complete tumor regression and no recurrence after treatment. ,
Computed tomography-pulmonary angiography as used in our case is a highly specific and sensitive for diagnosis of PE, it provides important ancillary additional information and helps in making an alternative clinical diagnosis. The diagnosis of PE is based on the presence of partial or complete filling defects in the pulmonary artery on the contrast enhanced CT.
| Conclusion|| |
Investigating for underlying malignant disease in patients with idiopathic venous thrombosis presenting with PE is beneficial. The potential use of tyrosine kinase inhibitors in adenocarcinoma with PE needs to be studied further and promoted. Anticoagulant therapy should be initiated in patients of lung Adenocarcinoma with PE as soon as possible as it creates a difference in the outcome.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]