Anaplastic large-cell lymphoma presenting as an endobronchial polypoid tumor.

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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
liverdisease(RILD;Fig1A,arrows).
RILD, previously termed radiation hepatitis, manifests 4 to 8
weeksafterradiationexposure.2-5SignificantRILDdevelopsin6%to
66% of patients exposed to an excess of 30 to 35 Gy of radiation,
depending on irradiated liver volume and hepatic functional re-
serve.3,5Patientsmaypresentwithatriadofascites,hepatomegaly,
andelevatedliverenzymes.2Themajorityofpatientsrecovercom-
pletely in 3 to 5 months, while a minority progress towards a
chronic stage, with worsening liver fibrosis and failure, only rarely
developingfulminanthepaticfailure.3,5Theterm“radiationhepatitis”
is a misnomer, since pathologic evaluation fails to reveal inflamma-
tion,instead showingnonspecific
Radiation-induced endothelial damage exposes the subendothelial
basement membrane, leading to platelet activation and aggregation,
and stimulation of dormant hepatic stellate cells. Fibrin thrombus
causesvenousocclusion,panlobularcongestion,diffusehemorrhagic
and necrotic foci, and distention of hepatic sinusoids.3-5Prolonged
obstructionandactivationofhepaticstellatecellsresultsinhepatocyte
loss and fibrosis mediated by transforming growth factor-?1
release.3-5Radiologically,RILDpresentswitha“straight-border”sign,
which is defined as any hepatic attenuation difference bordered by
straight lines.1Fatty infiltration, fibrosis, and vascular abnormalities
veno-occlusivedisease.3-5
canallpresentsimilarly.1RILDpresentsasdemarcatedareasofhypo-
or hyperattenuation in a nonanatomic distribution, contrasting with
vascularlesions.1OurpatientdevelopedRILDfollowinghepaticradi-
ation exposure during irradiation of right chest wall/axilla 6 weeks
earlier. Subsequent tests after 4 months and later imaging showed
completenormalizationofliverenzymesandhepaticappearance(Fig
1B).AsofMay2008,ourpatientwasfreeofrecurrentdisease.
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: Acti-
vation 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 radiation-
induced 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
leftmainbronchusandrightbronchialintermediates(Figs1A,1B,
2A,and2B;arrows).Endotrachealandendobronchialtuberculosis
wastheinitialimpression,sothepatientwasadmittedforisolation
and treated with isoniazid, rifampin, ethambutol, and pyrazin-
amide for high risk of transmission. However, serial sputum acid-
fast 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 malig-
nancy. 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
AB
Fig 1.
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exhibited tumor metastasis in both sides of the necks, left supra-
clavicular 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
showanymalignantcells.Thepatientthenreceivedchemotherapy
withcyclophosphamide,adrimycin,vincristine,andprednisolone,
and the lymphoma responded well. The collapsed lung and dys-
pneaalsoresolved.Hewassubsequentlydischargedandcontinued
receiving further chemotherapy.
Malignant lymphoma arising from endobronchial lesions is ex-
tremely rare and more often in Hodgkin’s disease than in non-
Hodgkin’slymphoma(NHL).1-3PrimarypulmonaryNHLcomprise
less than 1% of all NHL cases, 3.6% of extranodal lymphomas, and
only 0.5% to 1% of primary pulmonary malignancies.4Endobron-
chial lymphoma is classified into two types. Type I includes diffuse
submucosalinfiltratesspreadingfromthesystemiclymphomaviathe
hematogenousorlymphaticsystem.TypeIIincludesairwayinvolve-
mentbyalocalizedmassduetoadirectspreadofthelymphomafrom
adjacent lymph nodes or arising de novo from bronchus-associated
lymphoid tissue. Type II lesions are always associated with signs of
airwayobstruction,suchascoughingorwheezing,asinourpatient.4
ALCLcomprises2%to7%ofNHL,andthemostcommonmorphol-
ogy of endobronchial ALCL is polypoid lesion with airway obstruc-
tion.5As compared with endobronchial tuberculosis, the lesion can
AB
Fig 1.
AB
Fig 3.
AB
Fig 2.
Chen et al
4846
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JOURNAL OF CLINICAL ONCOLOGY

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be classified into four stages: exudative, ulcerative, cicatrative, and
broncho-glandular lesions.6Because of the extreme rarity of endo-
bronchial lymphoma and high incidence of pulmonary tuberculosis
in Taiwan, physicians may inadvertently delay diagnosis. Primary
lymphoma arising from the bronchus is usually a chemotherapy-
sensitive tumor, and it is necessary to add primary lymphoma to the
differentialdiagnosesofendobronchialpolypoidmasses.
Shuo-Chueh Chen
Division of Pulmonary and Critical Care Medicine, Department of Internal
Medicine, China Medical University Hospital; China Medical University,
Taichung, Taiwan
Chuen-Ming Shih
Division of Pulmonary and Critical Care Medicine, Department of Internal
Medicine, China Medical University Hospital, Taichung, Taiwan
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
AUTHORS’ DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST
The author(s) indicated no potential conflicts of interest.
REFERENCES
1. Kaira K, Ishizuka T, Tanaka H, et al: B-Cell Non-Hodgkin lymphoma present-
ing 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 chemother-
apy. Chest 103:673-677, 1993
DOI: 10.1200/JCO.2008.18.4325; published online ahead of print at
www.jco.org on September 8, 2008
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Fig 4.
Diagnosis in Oncology
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© 2008 by American Society of Clinical Oncology
4847
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Copyright © 2008 American Society of Clinical Oncology. All rights reserved.