A 56-year-old caucasian male patient, with history of active cigarette smoking (35 pack/years), hypertension and coronary heart disease (for which he underwent a double coronary artery stenting), presented with recurrent hemoptysis of mild abundance which first occurred no less than 4 months before. He also reported fatigue and weight loss amounting to 6 kg in 4 months. There was no associated history of fever, night sweats or extra-thoracic symptoms and no household contact of tuberculosis.
Upon admission, the physical examination showed a patient in a good condition (performance status 1) with no fever and no chest abnormalities except for few rhonchi on lung auscultation and a slightly enlarged supraclavicular lymph node. There was no clubbing, no extra-thoracic signs and no other superficial lymph nodes meeting size criteria for lymphadenopathy.
Frontal chest x-ray revealed a mediastinal widening probably due to grossly enlarged right paratracheal and left paratracheal nodes as well as a mild left parahilar infiltrate with irregular borders (Fig. 1). 
Electrocardiogram was in sinus rhythm, with a heart rate at 90 bpm. PR and QT intervals were normal, axis at 90 , without ST segment abnormalities or other waves and intervals. Blood tests showed an elevated white cell count exceeding 21,000 cells/mm3 with a lymphocyte count amounting to 13,750 and mild thrombocytosis. An elevated C reactive protein level (41 mg/l) was also noted, hinting to a biological inflammatory syndrome. Tests for hemostasis and blood biochemistry yielded a normal result. Lipid tests revealed hypertriglyceridemia (2.48 g/l). Urinalysis showed proteinuria (400 mg per day) with albumin presence, as well as hematuria. Serum protein electrophoresis was normal though.
Chest x-ray findings urged us on performing a chest computed tomography (CT) scan. On the mediastinal window, it showed bilateral mediastinal and axillary lymphadenopathies, as well as enlarged supraclavicular lymph nodes on the left side. On the parenchymal window, CT revealed an ill-defined heterogeneous attenuation in the left upper lobe with blurred margins, as well as a solitary contralateral pulmonary nodule (Fig. 2). Abdominal and pelvic CT showed an adenoma of the left adrenal gland, bilateral simple kidney cysts and a subrenal aortic aneurysm. Brain CT scan showed no anomalies. Bone scintigraphy showed no evidence of osseous metastatic disease. 
Hepatitis B and C serologic tests were negative. Immunological blood tests (antinuclear antibodies, extractable nuclear antigen antibodies, anti-dsDNA, anti-neutrophil cytoplasmic antibodies, cryoglobulin) were negative. Total immunoglobulins E level was normal.
Looking for histological evidence of a potential tumoral process, fibrobronchoscopy was performed, showing a mild bronchial stenosis of the upper lobe branch and thickening of the bifurcation between culmen and lingula branches with no evidence of endoluminal tumor. Aspiration cytology was benign. Bronchial biopsy examination could not prove malignancy, showing an inflammatory mucosa.
We eventually came to terms with performing a surgical biopsy of Virchow's node. Pathology slides showed a B cell lymphomatous process that might tally with lymphocytic lymphoma of CLL type (tumoral subtype of old Kiel classification). Immunohistochemistry confirmed the B phenotype with CD5, CD20 and CD23 expression and a Ki-67 index exceeding 50% which heralds a transformation into diffuse large B cell lymphoma (DLBCL), also known as Richter syndrome (RS) or transformation. Additionally, one of the nodes was infiltrated by a malignant epithelial process with poorly differentiated large tumoral cells, hinting to a non-small cell carcinoma (NSSC). The latter were cytokeratin, TTF1, Napsin A positive and p40 negative in immunohistochemistry, which corroborated nodal metastatic disease of an adenocarcinoma. Taking into consideration that no clinical or radiological signs apart from the left upper lobe pulmonary lesion were found, we concluded to a pulmonary origin of the carcinomatous process thus making the diagnosis of primary adenocarcinoma of the lung.
Flow cytometry immunophenotyping was carried out showing normal proportions of B cell lymphocytes (CD19+ CD5- CD20+ CD22+) and T cell lymphocytes (CD3+ CD5+), amounting to 6% and 80% respectively, which are normal proportions for B and T populations.
Bone marrow aspiration and biopsy were then performed. Pathology examination showed massive infiltration of medullary spaces by small-sized lymphocytes with a few large atypical prolymphocytic cells, highly suggestive of CLL, which corroborates the lymph node biopsy examination findings. Besides, BCR-ABL transcript molecular testing was negative.
The diagnosis of metastatic adenocarcinoma of the lung associated with RS was made. Treatment consisted in chemotherapy, associating carboplatin, docetaxel and cyclophosphamide in the scope of a multidisciplinary approach.
The course was unfavorable since the first days of therapy. In fact, the patient's condition worsened swiftly after the first course of chemotherapy as he presented with severe dyspnea in relation to a superior vena cava (SVC) syndrome. CT showed an obstruction of the SVC, a major increase in the mediastinal lymph nodes enlargement, an extension of the left upper lobe mass as well as a left adrenal gland metastasis (Figs. 3 and 4). Echocardiography revealed a small pericardial effusion.  
These findings urged us on prescribing corticosteroids and palliative radiation therapy. Within a fortnight, the patient showed further signs of deterioration with the onset of atrial fibrillation and a severe fatal infectious process.