first indication ofdisease in 14(78%) of 18patients.The most common finding wasa solitary pulmonary nodule, seenin nine (50%) of 18patients. Other findings ...
Chest Radiography as a Predictor of Outcome in Posttransplantation Lymphoproliferative Disorder in Lung Allograft Recipients PerryJ. Pickhardt1
Marilyn J. Siegel1
@
0. Claire
RobertHayashi2 MichaelR.DeBaun2
OBJECTIVE. The radiologicfindingsof posttransplantation lymphoproliferativedisorder in lung transplant recipients have received little attention compared with the findings for re cipients of other solid organ transplants. We describe the intrathoracic findings and explore whether the radiographic presentation can predict outcome. MATERIALS AND METHODS. Twenty-sixpatients(mean age,32 years;range,2—63 years; 18 female, eight male) with histologically
proven lymphoproliferative
disorder were
identified from 5 18 lung transplantation patients, a 5.0% frequency. Chest radiographs, ob tamed within 1 week of diagnosis, were compared with baseline posttransplantation radio graphsfor all 26 patientsandwith chestCT scansfor 20 patients. RESULTS. The intervalbetweentransplantationanddiagnosisrangedfrom 6 weeksto 7 years (mean, 16 months; median, 6 months). The thorax was involved in 18 (69%) of 26 pa
tients. A new chest radiographic abnormality was present in all 18 patients and provided the first indication ofdisease in 14 (78%) of 18patients. The most common finding was a solitary pulmonary nodule, seen in nine (50%) of 18 patients. Other findings included multiple nod ules, multifocal alveolar infiltrates, and hilar and mediastinal adenopathy.CT scansdetected additional nodules and lymph nodesbut did not show occult diseasein any casethat appeared normal on radiography.
Eight (89%) of nine patients with solitary pulmonary
nodules at pre
sentation were alive 1 year after diagnosis, compared with six (35%) of 17 patients with other presentations(p < .01). CONCLUSION. Thoracicmanifestationsare presentin most lung transplantrecipients with lymphoproliferative disorder. Patients with solitary nodules have a better outcome in the first year after diagnosis than do patients with other presentations.
lymphoprolifer rience with lymphoproliferative disorder after ative disorder constitutes a spec lung transplantation to assess the imaging find trum of lymphoid hyperplasias and ings of this disease and the relationship be neoplasiasin solidorgantransplantrecipients tween the extent of intrathoracic diseaseand [1, 2]. The overall incidence of lymphoprolif the response to treatment. erative disorder among solid organ transplant patientsis approximately 2%, with thoracic in Materials and Methods volvement in less than 10% of cases [3, 4]. From July 1988 through July 1997, 518 lung P
ReceivedDecember2,1997;acceptedafterrevision February27,1998.
osttransplantation
Someserieshavesuggested thatboththemci
transplantationswere performed at our institution, in
cluding 144pediatriclung transplantations. During
UniversitySchoolof Medicine,5105. KingshighwayBlvd., St.Louis,MO63110.Addresscorrespondence to M.J.
denceof lymphoproliferative disorderandthe frequency of intrathoracicinvolvementare higher in lung transplant recipients than in other solid organ transplant recipients [5—7].
Siegel.
Imagingis importantin theevaluationof lym
2Divisionof HematologyOncology,Departmentof Pediatrics,WashingtonUniversitySchoolof Medicine, 1ChildrensPI.,St Louis,MO63110.
phoproliferativedisorderbecauseearly detec tion of this complication may result in an improved responseto therapy [3, 4, 8]. To date, the radiographic features of lymphoprolifera tive disorder in lung transplantrecipients have received little attention. We reviewed our expe
Presentedatthe annualmeetingofthe American RoentgenRaySociety,SanFrancisco,April—May 1998. 1Mallinckrodt
Institute of Radiology, Washington
AJR1998;171:375—382
0361—803X/98/1712-375 © American Roentgen RaySociety
AJR:171,August1998
this period. posuransplantation lymphoproliferative disorder developedin 26 lung transplantrecipients,a frequency of 5.0%. Patientswere 2—63 years old at
thetimeofdiagnosis(mean,32years).Twelve(46%) of26 patientswerelessthan18yearsold.Eightwere male, and 18 were female. Underlying lung diseases
leadingto transplantationincludedcystic fibrosis (n = 12),cz1-antitrypsin deficiency(n = 5), chronic obstructivepulmonarydisease(n = 3), pulmonary hypertension fromcongenitalheartdisease(n= 3),id iopathic pulmonary fibrosis (ii = 2), andsarcoidosis
375
Pickhardt et al. (n= I). Twentyof thetransplantations werebilateral, andsixwereunilateral. Posttransplantation lymphoproliferativedisorder wasdiagnosedthroughpercutaneous biopsyin 10 patients,open surgicalbiopsy in 14patients,and au topsy in two patients.Histopathologicdiagnoses werebasedon previouslyestablished criteria[3, 9]. The resultsof immunohistochemical testingof the specimens for Epstein-Barrviruswerepositivein 20 patients(77%) and negativein one patient(4%). Fivepatientswerenot tested.The intervalbetween radiologicdiagnosisand tissuediagnosiswasless than I week in all cases. Our standardprotocolin pediatriclung transplant recipients requireschestradiographsand 0' scansat
3, 6, and 12 monthsaftertransplantation andthen yearly. Imaging is performed at additional intervals if
infectionor rejectionis clinicallysuspected. In adult transplantrecipients.after the acuteperiod,radio graphsareobtainedatweeklyintervalsfor 3 months, thenmonthlyfor approximatelyI year,thenyearly unlesssymptomsarise.CT scansareobtainedonlyif radiographic findingsareabnormalor ifthe patientis symptomatic. Forthepurpose of ouranalysis, the baselineposttransplantation chestradiographswere comparedwith radiographs at thetimeof diagnosis of lymphoproliferative disorderto assess for interval change.Thebaselinestudywasdefinedasposttrans plantationradiographyfindingsthat were normal or near normal, showing minimal postoperative changes.Baselinechestradiographywasperformed 2 weeks to 6 years after transplantation (mean, 8
months)andapproximately8 monthsbeforediagno sis of lymphoproliferative disorder. CT scansat the time of diagnosis were available
for 20 patients.Chest CT scans were obtained with conventional or helicaltechniqueusing4-, 8-,or 10mm collimation with contiguousintervals.Addi tional 2-mm sections were obtained through most
lation (n = 518) was5.0%.The frequencyin the pediatricage group was 8.3% (12/144), versus3.7% (14/374) in adults(p < .05). The
Radiographic Findings
Findingsonchestradiographsversuspatient
of lymphoproliferativedisorderin the 26 pa tients in our series ranged from 6 weeks to 7
ageareshownin Table 1.In all 18patientswith thoracic involvement by lymphoproliferative disorder,chestradiographsshowedabnormali ties not seen on the baseline posttransplantation
years (mean, 16 months; median, 6 months).
radiographs.Seventeen patientshadparenchy
The diagnosisof lymphoproliferativedisorder was within 1 year of transplantation in 18 (69%) of 26 patients, including 10 (83%) of 12children. Eighteen(69%) of 26 patientshadintratho racic involvement by lymphoproliferative dis order; seven of these also had extrathoracic disease.Of these 18patients, 14 were asymp tomaticand the diseasewas detectedon sur
mal abnormalities,and one had only mediasti nal and hilar disease.Sevenpatientshad more than one abnormality. Nine (50%) of 18 pa tients had solitary pulmonary nodules,ranging in sizefrom 1.2to 4.0 cm (mean,2.5 cm) (Figs. I and 2). Two patients had multiple nodules (Fig. 3), four patientshadmultifocalair space
interval from lung transplantation to diagnosis
consolidation(Fig.4), andtwo hada combina tion of both findings (Fig. 5). When multiple
veillance chest radiographs.Four patients nodules were present, the mean number was presented with multiorgan failure from dis five andthe meandiameterwas2.6 cm. Two seminateddisease,which led to death within patientshad hilar and mediastinallymphade 2 weeks.
nopathy.One of thesepatientshad associated
Eightpatients(31%)hadonly extrathoracic lungdisease;in theotherpatient,theadenopa involvement.Four of the eight patientshad ab dominal symptoms,usually pain andfever.One patient eachpresentedwith seizuresfrom CNS involvement, sinusitis from sinonasal lympho
proliferativedisease,a paratesticular mass,and a cutaneouslymphoproliferativelesion. All patients except one received triple im munosuppressionwith corticosteroids,cy closporine, and azathioprine.Additional drugs included antithymocyte or antilymphocyte
thy was an isolatedfinding(Fig. 6). Four pa tients, all children, had pleural effusions occurring in association with parenchymal dis
ease (Fig. 3). Of the six patients with unilateral transplants, the native lung was involved in only onepatient with disseminatedlymphopro liferative disorder. ChestCT scanswere obtainedat the time of diagnosisof lymphoproliferative disorder in 20 patients, including 15 patients with thoracic in
globulinin nine,tacrolimusin four,andmarine volvement.No evidenceof lymphoproliferative monoclonal anti—humanCD3 antibody in two. disorderwasfoundon CT in patientswithout Antilymphocyte
globulin was used for induc
tion immunotherapybefore 1994 in our pro
radiographic findings of thoracic involvement.
However,of notewasthefactthatCT increased
gram, and antithymocyte globulin was used thereafter. Antithymocyte globulin and marine formedapproximatelyI monthafter institutionof therapy.includedchestradiographsfor 22 patients monoclonal anti—human CD3 antibody were
the sensitivity of nodule detection. In patients with abnormal radiographic findings, CT
used for steroid-refractory allograft rejection. Tacrolimus was used in place of cyclosporine ies, were obtained within I week of the diagnosis of in four patientswho receivedsecondsolidor lymphoproliferative disorder. gan engraftments. Chestradiographs andCF scanswerereviewedby Excluding the four patientswith a fulminant threeradiologists. Theradiologicstudieswereevalu coursewho died within 2 weeks,treatmentfor atedfor thepresence or absence of pulmonaryparen lymphoproliferativedisorderconsistedprima chymalnodulesandinfiltrates,pleuralandpericardial rily of reducing immunosuppression.Twelve disease,and mediastinaland hilar lymphadenopathy. Thedistribution andsizeof nodules, infiltrates, and patients(46%) died within 1 year of diagnosis lymphnodeswererecorded. Diagnosisofdiseasewas of lymphoproliferativedisorder. Of these, basedon consensus reading.Fisher'sexacttestwas death was attributed directly to lymphoprolif erativedisorderin sevenpatients(27%), bron usedfor statisticalanalysisof data.
0.2 to 1.5 cm, in 10 patients(sevenadults and
pulmonary nodules. Follow-up examinations, per
and chestCT scansfor 16patients.All imagingstud iesin thisseries,exceptbaselineandfollow-upstud
Medical records of the 26 patients were reviewed
showedadditionalnodules,rangingin sizefrom three children), including five patients with soli tat)' nodules on chest radiography. This addi
tional information did not alter clinical management in any patient. The nodules were typically of homogeneoussoft-tissue attenua
tion, althoughin threepatientsthenodulesex hibited centrallow attenuationsuggestiveof necrosis(Figs. 3B and 5C). In four patients,the
nodulesweresurrounded by a hazyrim or halo of infiltrate (Fig. 2B). All nodules were ran domly distributed throughout the lung al
chiolitis obliterans syndrome in three patients
lografts. Four patients had multifocal
infiltratesat CF scanning(Figs.4C and5C). Al
Results
(12%), and unrelated causes in two patients (8%). The remaining patientshavesurvived an average of 3 years to date, with a follow-up period ranging from 8 months to 5 years. In eight patients (3 1%) bronchiolitis obliterans
ClinicalFindings
developedafter reduction of immunosup
to determine clinical features and immunosuppres sive therapy at the time posttransplantationlympho proliferative diseasewas diagnosed. the subsequent
treatment, andtheresponse to therapy.
The frequency of lymphoproliferative dis
orderin our entirelung transplantationpopu 376
pression, and of these, three underwent a second transplantation.
alveolar
ternativeor concomitantcausesof infiltratesor nodules,suchasaspergillusor cytomegalovirus, were excluded by a combination of negative bi opsy findings for infection, clinical course,and responseof the lesionsto immunomodulation. Extrapulmonary intrathoracic involvement by lymphoproliferative disorderwaspresentin AJR:171,August1998
seven (27%) of 26 patients at CT and was al
ways associatedwith allograft involvement. Hilar and mediastinal lymph node enlargement was notedon CT scansfor five patients.In three patients. the adenopathy was not sus pected on radiographs. Pencarmnallymph nodes were most often involved. measuring
slightlylargerthan 1cm.Axillary lymphaden opathy was not present in any patient. Pleural
effusions were confirmed in four patients,and pericardial efflisions were observedin two pa tients by CT. The latter had not been suspected
on chestradiographs(Fig. SC). Intraabdominal involvement by lymphopro liferative disorder waspathologically provenin 11(42C/c)of26 patients.Specific sites included
liver (ii = 8), kidney (ii = 4). adrenal gland (n = 3), abdominal lymph nodes (ii = 3).
bowel (ti = 3), andspleen(,i = 2). Hepatic.re nal. and splenic involvement typically ap peared as focal parenchymal masses. Adrenal
involvement produced diffuse enlargementof the gland. whereas bowel involvement ap pearedaswall thickening or focal ulceration. Fourteenof 18 patientswith proven in trathoracic lymphoproliferative disorder un derwent follow-up chest radiography and CT scanningapproximately 1 month after diagno sis of lymphoproliferative
disorder and reduc
@Chest RadiographFindings .
Versus
Patient
Age
. .
FindingAdults
(n=12)Pulmonary
(n=14)Children
nodules Single
1 (7)
3(25)
Alveolar infiltratesa
1 (7)
5 (42)
Lymphadenopathyb
1 (7)
1 (8)
Pleural effusion6(43)
0 (0)3(25) 4 (33)
Multiple
Note—Numbers inparentheses arepercentages. aTWO patients had both multiple nodules and alveolar
tion of immunosuppression.Four patientsdied disease. before the I -month follow-up examination. bOne patient had associated lung disease. CAll four patients had concomitant lung disease. Regressionof diseasewas seenin I I patients
B
I
@
1!@.
,@
Fig. 1—38-year-oldman with solitary pulmonarynodule 4 months after left lung trans plantationfor idiopathic pulmonaryfibrosis.
A,Routine chestradiograph obtained 2 months aftertransplantation showsinterstitial diseaseconsistentwithfibrosisof nativerightlung.Leftlungallograftiswellexpanded and clear.
B,Radiograph obtained2monthsafterAshowsdevelopment ofsolitarypulmonary nod ule in lower lobe of allograft (arrow). This pattern of intrathoracic posttransplantation lymphoproliferativedisorder was seen in 50%of patients.
C,CTscanshowsfine-needlebiopsybywhichdiagnosisoflymphoproliferative disorder was confirmed.
AJR:171,August1998
377
Pickhardt et al.
@
-
—¿.@.,- .
--
Fig. 2—48-year-old woman inwhom solitary pulmonary nodule developed after bilateral lung
transplantation forcc1 -antitrypsin deficiency. A,Routine chestradiograph obtained 9 months aftertransplantation showsnewparenchymal
@ 4 .
@
@
nodule
. . . . . . .@‘.q-t@-@:;—
I
S
-a')t,
in right lower
lobe allograft
(arrow).
B,Corresponding CTscanshowssubtlehaloof infiltratearoundnodule(arrowheads). Diagno sis of posttransplantation lymphoproliferative disorderwas confirmedbyfluoroscopy-guided biopsy(notshown). C CT scan
after
immunomodulation
obtained
2 months
after
A and
B shows
cavitation
of nodule
(arrow).
@
.
(6 1C/@ ), with either obvious reduction or total resolutionol nodulesor infiltrates.Most nod ules became undetectable or left a residual
compared with only six (35%) of I 7 patients
pleural effusions. pericardial effusions. and
with all other presentations (p < .01).
central
scar: central cavitation ofa solitary nodule was
Lymphoproliferative disorder after lung
agnosis
of
lymphoproliferative
disorder.
seenin one patient after therapy(Fig. 2). Three
transplantation was twice as frequent in chil
patients had radiographic
dren as in adultsin our series,8.3% versus
progression
of al
thoracic imaging features in children included necrosis within
pulmonary
nodules.
Diseaseregression andsurvivalwerenotsignif icantly different between children and adults.
lograft lymphoproliferative disorder at 1
3.7% (p < .05). In general, children were less
month. Of the nine patients presenting with a
likelyto presentwith a solitarynoduleonchest radiographyand more likely to have alveolar
Discussion
solitary pulmonary nodule on chest radiogra phy. eight (89C/r) were alive I year after the di
lymphoproliferative
order is a seriouscomplication of organ trans
378
disease (Table I ). Unique
Posttransplantation lymphoproliferative
dis
AJR:171,August1998
Lymphoproliferative
Disorder After Lung Transplantation
Fig.3.—li-year-old girlpresenting withcoughandmultiple pulmonary nodules 4months afterbilateral lungtransplantation forcysticfibrosis. A,Chestradiograph showsmultiple, bilateral pulmonary nodules andleftpleuraleffusion (arrowhead), noneofwhichwereseenonbaseline posttransplantation study (not shown).
B,Corresponding unenhanced CTscanshowsleftpleuraleffusion (whitearrowhead) andenlarged lymph node(arrow)immediately posterior tocatheter withinsuperior vena cava. Faintcentral low attenuationin dominantright lung nodulesuggestsnecrosis(black arrowheads).Pleuralfluid obtainedfromthoracentesis and CT-guidedright upper lobe biopsywere diagnostic for lymphoproliferativedisorder.
cases.the disorderis believedto be the result of an atypical proliferation of Epstein-Barr vi
tral necrosisor a rim of hazy infiltrate, which equalrateof involvement[I 2]. The higherfre quencyof thoracicinvolvementby lyrnphopro can mimic fungal infection—in particular, in liferativedisorderin lungtransplantrecipients vasive aspergillosis 1131.In ourexperience. al
mis—induced lymphocytes
is due
plantation
and immunosuppression.
In most
[ 1—41.The
fre
to the
predilection
for
allograft
involve
quencyof lymphoproliferative disorder among our lung transplantpopulation was5.0%, corn pared with reported frequencies of 7% by
ment. becausernediastinal involvement does not appearto be significantly increased. Although our understanding of lympho
Armitage et al. 151and 20% by Montone et al.
proliferative disorder has steadily increased, this disease continues to cause significant mor bidity and mortality among solid organ trans
[61.both of whom describedsmaller seriesof patients. By comparison. the incidence of lyrn phoproliferative disorder after other solid or gan transplantations is approximately 2%. In
addition. our experience showed that the fre quency of diseasewas higher in children than
though
lymphoproliferative
disorder
is the
most frequent cause for single or multiple nodules in the lung transplant population.
bi
opsyremainstheonly reliablemethodof dis tinguishing lymphoproliferative disorder from opportunistic
infection.
An alveolar patternof allograft involvement was seenin six patientswith thoracic involve
plant recipients. Preliminary results have suggestedthateffortstowardearlierdetection ment by lymphoproliferative disorder, corre are paramountbecauseprompt reductionin sponding to 33% of cases. This appearance of immunosuppressionusually results in regres lung involvement in posttransplantationlym
in adults (8.3ck versus 37(/@) The increased
sion ofdisease [3. 4. 8]. In our series, we found
phoproliferative
frequencyof posttransplantation lymphopro liferativedisorderamongpediatriclungtrans plant recipients may be due to the higher incidenceof primary infection by the Epstein Barr virus after transplantationin children than
that chestradiography was a simple and accu rate surveillance method to detect lymphopro
othersolidorganrecipients.albeitinfrequently
liferative disorder in lung transplant recipients.
was bilateral in all instances and was accom panied by pulmonary nodules in only two pa tients at the time of diagnosis. Although focal air space consolidation may represent an in
CT of the chestis more sensitivethan chest radiography for evaluating the extent of intra
thoracic disease; however. this increased time oftransplantation 10. 11]. sensitivityfor detectingadditionallesionsdid Thoracic involvementwaspresentin 69Ckof not result in better prediction of survival. patientsin our serieswith lymphoproliferative We foundthat a new soft-tissuenodulein in adults, who are usually seropositive at the
disorder, a value that is slightly lower than the
100%frequencyamong lung transplantrecipi ents (nine of nine patients) reported by Mon tone et al. By comparison. in patients with
other solid organ transplants in whom lyrn phoproliferative disorder develops. the fre quency of thoracic involvement has been reportedto be only 7Ck[3. 4]. In this group of patients. the lung and rnediastinum have an
AJR:17l, August 1998
the allograft is the most common chest radio graph presentation of lymphoproliferative dis order after lung transplantation. Once a
nodule is detected,CT should be performed to determinethe full extentof disease.With CT scans. pulmonary
nodules tend to be ran
domly distributed throughout the allograft and are usually homogeneousand well defined. Occasionally, nodules seen on CT exhibit cen
disorder has been reported for
II2].The air spaceconsolidationin our series
fectious cause, lyrnphoproliferative disorder shouldalso be consideredin transplantpa tients. especially if the infiltrate persists de spiteantimicrobialtherapy[14). The mainstayof treatmentfor posttrans plantation lymphoproliferative disorder has consistedof reductionor cessation of immuno suppression 13.4, 8]. Regression rates of disease
after immunomodulation alone have ranged from 23% to 42% [3, 4, 15, 16). In the 18 pa tients with thoracic involvement by posttrans
plantation lymphoproliferative disorder in our
379
Pickhardt et al.
Fig.4—14-year-old girlwithworsening dyspnea andalveolar pulmonary infiltrates 2years afterbilaterallungtransplantation. A,Baseline radiograph obtained 6months aftertransplantation showsclearlungs. B,Chestradiograph obtained 2yearsaftertransplantation shows bilateral patchy, multifo cal alveolarinfiltrates.No discrete nodulesare present
C, Corresponding thin-sectionCTscanshowsareasof air spaceconsolidationand ground-glass opacity.Diagnosis ofalveolarlymphoproliferative disorderwasestablished byopenlungbiopsy.
C series,clinical and radiologic regressionof dis easewasnotedin 61%. Patientspresentingwith a dominant nodule on chest radiography showedimprovedsurvivalat I yearcompared with patientswith other presentations.A serious potentialcomplication of reducingimmunosup pressionis allograftrejectionwith bronchiolitis obliterans. Thisoccurredin 31% ofour patients. Severalexplanationsare possiblefor the im proved survival in patientspresentingwith soli tary noduleson chestradiography.Preliminary
representsthe monomorphic subtype,which is essentially indistinguishable from lymphoma. Alternatively. improved survival with solitary nodule diseasemay simply correspondto a de creasedtumor burden.
pathologic
patients with rejection. The intent of the protocol was not to identify posttransplan tation lymphoproliferative disorder. The ef fect that our standard imaging approach
data from our series suggest that
thesenodulesrepresentthe morebenignpoly morphic variant of lymphoproliferative disor der, whereas multifocal involvement more often
380
Our study hastwo limitations. First, the study was performed within a single insti tution, with the potential for bias related to the choice of immunosuppression and treatment protocols. Second, our routine imaging
protocol
was aimed at identifying
may have had on detecting
lymphoprolifer
ative diseaseis unknown. Our preliminary results strongly suggest that patients with solitary nodules due to posttransplantation lymphoproliferative dis order will more likely respond to a reduction in immunosuppression and have a better prognosis than patients with multifocal lung diseaseor other presentations. Future inves tigations are warranted to determine the po tential usefulnessof increasedsurveillance with chest radiography to identify patients with solitary lesions who may be earlier in the course of posttransplantation lympho proliferative
disorder.
AJR:171,August1998
Lymphoproliferative
Disorder After Lung Transplantation
B Fig.5—10-year-old girlwithpattern ofmixednodular andalveolar lymphoprolif erative disease2 monthsafter bilateral lung transplantation.
AandB,Frontal(A) andlateral(B)radiographs revealairspaceconsolidation in volving right middle lobe and nodulesin right upper and left lower lobes. C, Corresponding contrast-enhanced CT scan confirms right middle lobe air space disease (arrow) and left lower lobe noduleswith central necrosis (white arrowheads). Note pericardial effusion (black arrowheads). Posttransplantation lymphoproliferativedisorder was diagnosedby CT-guidedbiopsy.
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TE. Malignantlymphomasin transplantationpa tients. Transplant Proc 1969: 1:I06--112
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Fig.6—55-year-old womanwithmedi disorder.
3. Nalesnik MA. Jaffe R, Starzl TE, et al. The pathol ogy of posttransplant lymphoproliferative disorders
Routinechestradiograph obtained4
occurring in the setting of cyclosporine A-pred
astinal lymphoproliferative
monthsaftertransplantationshowshi lar and mediastinal enlargement (arrows) without parenchymalnod ules—findingthat was not seen on baselinestudy(notshown).Leftbasilar atelectasisresolvedon CTscan 1 day later (not shown).Posttransplantation lymphoproliferativedisorderwas con
firmedby mediastinoscopy withsub carinallymphnodebiopsy.
AJR:l71, August 1998
nisone immunosuppression. Am J Pathol 1988: 133: 173—192 4. Nalesnik MA, Makowka L, Staril TE. The diagnosis
and treatment of posttransplant lymphoproliferative disorders. Curr Probi Surg 1988:25: 367—472 5. Armitage JM, Kormos RL, Stuart RS. Posttrans plant lymphoproliferative disease in thoracic organ transplant patients: ten years of cyclosporine-based immunosuppression.
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