Anaplastic Large-Cell Lymphoma Presenting As an Endobronchial Polypoid Tumor

Diagnosis in Oncology

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AST and ALT of 72 U/L and 92 U/L, respectively (normal, 3 to 48 U/L and 30 to 65 U/L). These were normal 4 months earlier. Abdominal computed tomography scan revealed an abnormal “straight-border”1—attenuation of the liver along the trajectory of radiation beam used previously—representing radiation-induced liver disease (RILD; Fig 1A, arrows). RILD, previously termed radiation hepatitis, manifests 4 to 8 weeks after radiation exposure.2-5 Significant RILD develops in 6% to 66% of patients exposed to an excess of 30 to 35 Gy of radiation, depending on irradiated liver volume and hepatic functional reserve.3,5 Patients may present with a triad of ascites, hepatomegaly, and elevated liver enzymes.2 The majority of patients recover completely in 3 to 5 months, while a minority progress towards a chronic stage, with worsening liver fibrosis and failure, only rarely developing fulminant hepatic failure.3,5 The term “radiation hepatitis” is a misnomer, since pathologic evaluation fails to reveal inflammation, instead showing nonspecific veno-occlusive disease.3-5 Radiation-induced endothelial damage exposes the subendothelial basement membrane, leading to platelet activation and aggregation, and stimulation of dormant hepatic stellate cells. Fibrin thrombus causes venous occlusion, panlobular congestion, diffuse hemorrhagic and necrotic foci, and distention of hepatic sinusoids.3-5 Prolonged obstruction and activation of hepatic stellate cells results in hepatocyte loss and fibrosis mediated by transforming growth factor-␤1 release.3-5 Radiologically, RILD presents with a “straight-border” sign, which is defined as any hepatic attenuation difference bordered by straight lines.1 Fatty infiltration, fibrosis, and vascular abnormalities

can all present similarly.1 RILD presents as demarcated areas of hypoor hyperattenuation in a nonanatomic distribution, contrasting with vascular lesions.1 Our patient developed RILD following hepatic radiation exposure during irradiation of right chest wall/axilla 6 weeks earlier. Subsequent tests after 4 months and later imaging showed complete normalization of liver enzymes and hepatic appearance (Fig 1B). As of May 2008, our patient was free of recurrent disease.

Radwan F. Khozouz, Syed Z. Huq, and Michael C. Perry University of Missouri, Columbia, Columbia, MO

AUTHORS’ DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST

The author(s) indicated no potential conflicts of interest. REFERENCES 1. Itai Y, Murata S, Kurosaki Y: Straight border sign of the liver: Spectrum of CT appearances and causes. Radiographics 15:1089-1102, 1995 2. Yamasaki SA, Marn CS, Francis IR, et al: High-dose localized radiation therapy for treatment of hepatic malignant tumors: CT findings and their relation to radiation hepatitis. A J Roentgenol 165:79-84, 1995 3. Sempoux C, Horsmans Y, Geubel A, et al: Severe radiation-induced liver disease following localized radiation therapy for biliopancreatic carcinoma: Activation of hepatic stellate cells as an early event. Hepatology 26:128-134, 1997 4. Jeffrey RB Jr, Moss AA, Quivey JM, et al: CT of radiation-induced hepatic injury. Am J Roentgenol 135:445-448, 1980 5. da Silveira EB, Jeffers L, Schiff ER: Diagnostic laparoscopy in radiationinduced liver disease. Gastrointest Endosc 55:432-434, 2002

DOI: 10.1200/JCO.2008.18.2931; published online ahead of print at www.jco.org on September 8, 2008

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Anaplastic Large-Cell Lymphoma Presenting As an Endobronchial Polypoid Tumor A 17-year-old previously healthy male student had chronic dry cough and low-grade fever for 6 weeks. Body weight loss of about 10 kg was also noted in the last 4 months. There were multiple palpable lymph nodes with tenderness over the bilateral sides of the neck and supraclavicular areas noted when the patient consulted at our pediatric clinic. He was then referred to the chest medicine clinic for his refractory cough and progressive dyspnea on exertion. Right middle lobe and left lower lobe atelectasis was seen on chest x-ray. Chest computed tomography revealed a polypoid lesion in the trachea and soft tissue lesions occluding the www.jco.org

left main bronchus and right bronchial intermediates (Figs 1A, 1B, 2A, and 2B; arrows). Endotracheal and endobronchial tuberculosis was the initial impression, so the patient was admitted for isolation and treated with isoniazid, rifampin, ethambutol, and pyrazinamide for high risk of transmission. However, serial sputum acidfast stain showed negative findings. Flexible bronchoscopy demonstrated polypoid lesions in the distal trachea, left main bronchus, and right bronchus intermedius (Figs 3A and 3B). Broncho-alveolar lavage fluid acid–fast stain also showed no pathogens, but cytology examination revealed suspicious malignancy. Bronchoscopic electrocautery tumor dissection was then performed to resolve his dyspnea. Biopsy confirmed a CD30⫹ anaplastic large-cell lymphoma (ALCL; Fig 4). Positron emission tomography and whole body computed tomography for staging © 2008 by American Society of Clinical Oncology

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Chen et al

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less than 1% of all NHL cases, 3.6% of extranodal lymphomas, and only 0.5% to 1% of primary pulmonary malignancies.4 Endobronchial lymphoma is classified into two types. Type I includes diffuse submucosal infiltrates spreading from the systemic lymphoma via the hematogenous or lymphatic system. Type II includes airway involvement by a localized mass due to a direct spread of the lymphoma from adjacent lymph nodes or arising de novo from bronchus-associated lymphoid tissue. Type II lesions are always associated with signs of airway obstruction, such as coughing or wheezing, as in our patient.4 ALCL comprises 2% to 7% of NHL, and the most common morphology of endobronchial ALCL is polypoid lesion with airway obstruction.5 As compared with endobronchial tuberculosis, the lesion can

exhibited tumor metastasis in both sides of the necks, left supraclavicular regions, sternum, mediastinum, left lower lung, spine, celiac region, para-aortic region, pelvis, iliac bones with bony destruction, and right buttock region. Bone marrow study did not show any malignant cells. The patient then received chemotherapy with cyclophosphamide, adrimycin, vincristine, and prednisolone, and the lymphoma responded well. The collapsed lung and dyspnea also resolved. He was subsequently discharged and continued receiving further chemotherapy. Malignant lymphoma arising from endobronchial lesions is extremely rare and more often in Hodgkin’s disease than in nonHodgkin’s lymphoma (NHL).1-3 Primary pulmonary NHL comprise

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© 2008 by American Society of Clinical Oncology

JOURNAL OF CLINICAL ONCOLOGY

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Diagnosis in Oncology

Jen-Liang Su China Medical University, Taichung, Taiwan

Su-Peng Yeh Division of Hematology and Oncology, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan

Chia-Hung Chen Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan

Guan-Chin Tseng Department of Pathology, China Medical University Hospital, Taichung, Taiwan

Wu-Huei Hsu, Wei-Erh Cheng, and Yu-Sheng Lin Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan

Yu-Lin Tsai Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Tungs’ Taichung MetroHarbor Hospital, Taichung, Taiwan Fig 4.

AUTHORS’ DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST

The author(s) indicated no potential conflicts of interest.

be classified into four stages: exudative, ulcerative, cicatrative, and broncho-glandular lesions.6 Because of the extreme rarity of endobronchial lymphoma and high incidence of pulmonary tuberculosis in Taiwan, physicians may inadvertently delay diagnosis. Primary lymphoma arising from the bronchus is usually a chemotherapysensitive tumor, and it is necessary to add primary lymphoma to the differential diagnoses of endobronchial polypoid masses.

Shuo-Chueh Chen Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, China Medical University Hospital; China Medical University, Taichung, Taiwan

REFERENCES 1. Kaira K, Ishizuka T, Tanaka H, et al: B-Cell Non-Hodgkin lymphoma presenting as an endobronchial polypoid mass. J Thorac Oncol 3:530-531, 2008 2. Berkman N, Breuer R, Kramer MR, et al: Pulmonary involvement in lymphoma. Leuk Lymphoma 20:229-237, 1996 3. Ferraro P, Trastek VF, Adlakha H, et al: Primary non-Hodgkin’s lymphoma of the lung. Ann Thorac Surg 69:993-997, 2000 4. Solomonov A, Zuckerman T, Goralnik L, et al: Non-Hodgkin’s lymphoma presenting as an endobronchial tumor: Report of eight cases and literature review. Am Journal of Hematol 83:416-419, 2008 5. Kim DH, Ko YH, Lee MH: Anaplastic large cell lymphoma presenting as an endobronchial polypoid mass. Respiration 65:156-158, 1998 6. Kim YH, Kim HT, Lee KS, et al: Serial fiberoptic bronchoscopic observations of endobronchial tuberculosis before and early after antituberculosis chemotherapy. Chest 103:673-677, 1993

Chuen-Ming Shih Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan

DOI: 10.1200/JCO.2008.18.4325; published online ahead of print at www.jco.org on September 8, 2008 ■ ■ ■

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© 2008 by American Society of Clinical Oncology

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