without thyroid hormone replacement results in subsequent remnant growth, normal hormone secretion andradioiodine accumulation (4—6).Unfortunately, the adrenal cortex by virtue of its location deep within the retroperitoneum is accessible only through invasive or highresolution imaging with computed tomography (CT) orangiography. However, even with finely detailed anatomicimaging, only changes in glandular contour and anatomy,such as the presence ofadrenal masses or gross hyperplasia,can be appreciated with these modalities (7—10).Theaccumulation ofthe cholesterol analog ‘311-6$-iodomethyl19-norcholesterol (NP-59) has been shown to depict adrenocortical function (1 1). Both the pattern and level of NP59 uptake can serve as a functional map of adrenocorticaltissues, and were used in the present study to documentalterations in adrenal cortical function in the remainingadrenal after unilateral adrenalectomy and in the unaffected, normal adrenal gland in patients in whom thecontralateral gland had been replaced by a nonfunctioning(in terms of adrenal cortical function), mass lesion.

PATIENTS AND METHODS

Seventeen patients were referred for study based upon anabnormal CT scan done for reasons other than suspected adrenaldisease (10 patients), as follow-up for previously resected adrenalneoplasms (2 patients) or for the evaluation of abnormal plasmaand/or urinary catecholamines (5 patients). CT was performedusing both oral and intravenous contrast. Contiguous slices of 1cm or less taken through the region ofthe adrenals were obtainedon each patient and the scans were interpreted by experiencedradiologists. In each patient, a combination of blood and urinebiochemical measurements of adrenal function were performed.These included basal determination of plasma catecholamines,plasma and urinary cortisol, 17-hydroxycorticosteroids, 17-ketosteroids, and catecholamines; and plasma cortisol responses todexamethasone and adrenocorticotrophic hormone administration. Plasma and urinary free cortisol levels were measured byradioimmunoassay (12) Plasma epinephrine and norepinephrinewere determined by radioenzymatic methods (13) and 24-hrurine 17-hydroxycorticosteroids, 17-ketosteroids, catecholaminesand metabolites were determined fluorometrically (14—16).Allmedications that might interfere with the scintigraphic or biochemical evaluations were omitted prior to study. Three of the

To assess the compensatory functional and anatomicchangesin the remainingadrenalcortex after unilateraladrenalectomyor in the unaffected adrenal in patients withunilateral adrenal destruction by neoplasm, i 7 patients witha single,functioningadrenalglandand normalindicesofadrenocortical function, nine after adrenalectomy and eightwitha unilateral,destructiveadrenallesionwere studiedwith131I-6@3-iodomethyI-i9-norcholesterol(NP-59)scintigraphyandcomputed tomography. Adrenal masses with a mean (±s.d.)diameterof 2.8 ±1.0 cm; (range 1—4cm; 95% confidenceinterval(CI),2.5—3.1cm)wereidentifiedbycomputedtomographyinsevenof ninepatientsinthe remainingadrenalcortexat variabletimes(6.1 ±5.9 y; range0.5—i9 y) after unilateraladrenalectomy.Mean (±s.e.m.)NP-59 uptake was elevated(p < 0.01) in both adrenalectomyand adrenal destructiongroups,mean uptake (±s.e.m.)was 0.32% ±0.04% administered dose (95% Cl, 0.24%—0.4%administereddose) ascomparedto normal (0.16% ±0.05% administereddose,95% CI, 0.06%—0.26%administereddose). The remainingadrenal cortex may be anatomically abnormal after unilateraladrenalectomy and demonstrate compensatory, increasedNP-59 uptake in the presenceof overall,normaladrenocortical function.

J NucIMed 1991;32:1882—1887

he compensatory changes seen in endocrine organsafter subtotal resection are well recognized and in theabsence of exogenous hormone replacement, the remaining functioning tissues may increase their capacity toproduce sufficient hormone(s) for endocrine homeostasis(1). Substrate accumulation by the remaining tissues increases to support a greater biosynthetic effort necessaryto meet demand and glandular hormone reserve; suchresponses have been demonstrated for many endocrinetissues (1-3). These compensatory changes have beendocumented in the thyroid, where subtotal thyroidectomy

Received Dec. 17, 1990; revision accepted Apr. 2, 1991.For reprints contact: Milton D. Gross, MD, Nuclear Medicine Service (115),

Dept. of Veterans Affairs Medical Center, 2215 Fuller Rd., Ann Arbor, MI48105.

1882 The Journalof NuclearMedicine•Vol. 32 •No. 10 •October1991

Clinical Significance of the Solitary FunctioningAdrenal GlandMilton D. Gross, Brahm Shapiro, John E. Freitas, Laura Meyers, Isaac Francis, Norman W. Thompson, andJacobo Wortsman

Division ofNuclear Medicine, Department oflnternal Medicine, Departments ofSurgery and Radiology, University ofMichigan and the VA Medical Centers, Ann Arbor, Michigan; and Division ofEndocrinology and Metabolism, Departmentoflniernal Medicine, Southern Illinois University, Springfield, Illinois

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Age Sex Dx (cm)Adrenal

massinterval

(side)(y)Urine(,@mol/d)PlasmaNP-59UPTAKE

(%admin.dose)l7OHtCORTISOLt17KS UFC (,anol/liter)E(pmol/liter)NE(pmol/Iiter)

HN= hypemephroma;AD= adrenaladenoma;P = pheochromocytoma;andACA= adrenocorticalcarcinoma.e No mass lesions detected in remaining gland.

t After 1 mg p.o. dexamethasone at 2,000 hr and cortisol at 800 hr, normal greater than 138 ,@mol/Iiter.

* 17 hydroxycorticosteroids(14—29@moI/d);17KS= 17 ketosteroids(25—28zmol/d);UFC= urinaryfreecortisol(55—276nmol/d).E =epinephrine(0—545pmol/liter); NE = norepinephnne(0—2955pmou/Iiter).

seventeen patients described in this study have been included inprevious reports dealing with the correlation of CT and ‘@‘I-6$-iodomethyl-l9-norcholesterol imaging in oncologic patients, andthe efficacy of 13I-6f3-iodomethyl-l9-norcholesterolscintigraphyin the evaluation of the incidentally discovered, euadrenal mass(17,18).

Scintigraphic studies were performed after institutional approval and with the informed consent of the patients. One millicurie of NP-59 was injected intravenously 48 hr after the administration of Lugols' or saturated potassium iodide solution tosuppress the thyroidal accumulation of free ‘@‘I(19). Adrenalscintigraphy was performed 5—7days after NP-59 injection usingmethods previouslydescribed(19). Posteriorand lateralabdominal images (50,000 counts/image) were obtained from eachprojection. A mild laxative (bisacodyl) was also given (10 mgdaily) beginning 2 days before and on the day ofimaging in mostofthe patients(20).AdrenalglandNP-59uptake(%administereddose/gland) was measured using a semi-operator-independentcomputer algorithm designed specifically for this purpose (21).Adrenal gland uptakes were compared to normal single andcombined, bilateral gland values reported previously (22). Statistical analyses were performed using Student's t-test and theconfidenceintervalestimationfor the binomial parameter(23).

RESULTS

Computed tomography was performed in nine patientsafter unilateral adrenalectomy as follow-up for previouslytreated malignancies (hypernephroma in five), previousadrenocortical disease (non-functioning cortical adenomain 2, a nonfunctioning adrenocortical carcinoma and apheochromocytoma (Table 1). Preoperative studies thatinclude nephrotomography and angiography in the earlierand CT in the latter cases did not demonstrate anatomicabnormalities in the contralateral adrenal cortex (the adrenal cortex that was not removed and is the subject ofthis report). The mean (±s.d.)interval from adrenalectomy

A.@

FIGURE 1. (A)PosteriorNP-59scintiscandepictstheremaining left adrenal cortex as a focal collection of@ il radioactivity(arrow) in a patient nineteen years after right radical nephrectomyand adrenalectomyfor hypernephroma(B) AbdominalCT identifles the left adrenalmass(arrow).

to the present study was 6. 1 ±5.9 yr (range 0.5—19yr). Inseven of these nine patients an incidental adrenal masswas discovered by CT in the remaining adrenal gland (Fig.1). Adrenal mass diameter (mean ±s.d.) in these patientswas 2.8 ±1.0 cm (range 1—4cm; 95% CI, 2.5—3.1cm).An additional eight patients were studied while harboringa nonadrenocortical mass of sufficient size to cause ipsilateral adrenocortical destruction and non-visualization onan NP-59 scan (Fig. 2). The contralateral unaffected glandwas considered anatomically normal by CT. This groupwas comprised of five patients with sporadic, unilateralpheochromocytoma, two with metastatic lung cancer andone with an adrenal cyst (Table 2). Mean (±s.d.)lesiondiameter in this group was 4.7 ±1.2 cm (range 3—7cm;95% CI, 4.4—5.0cm). In the five patients with pheochromocytoma, adrenal cortical function was normal whileplasma and/or urinary catecholamines were elevated(Table 2). The serum cortisol response to cortrosyn (250@Lgi.v.) was also normal in the remaining three patientswith unilateral, destructive adrenal lesions (Table 2). Inthe five patients with pheochromocytoma a thin band of

TABLE IEffect of UnilateralAdrenalectomy Upon Adrenal Function and NP-59 Uptake

54FHN3L1919.110.6145.841.7119.92807.30.5846FHN2R1216.935.866.70.2266MAD@‘A41

7.240.0239.341.7245.3862.90.2638FP3.5L4116.930.6457.8969.20.2343FHN4L5151.347.20.3467MHN3L620.836.416.70.2865FAD3L0.5137.527.80.3669FACA—L321

.37.00.3056MHN1A121.729.41 25.00.27

1883The Solitary Adrenal Gland •Gross et al

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FIGURE 2. (A)CT-guidedneedle(smallarrows)biopsyof a 5cmleft adrenalmass(largearrow)from metastaticlungcarcinoma(B)PosteriorNP-59scintiscanidentifiestherightadrenal(arrow),noleftadrenalcorticalactivityisseen.

cortical tissue was recognized in the excised adrenal whileno gross anatomic abnormalities were noted in the contralateral gland at abdominal exploration. The diagnoses ofthe remaining two cases of metastatic lung cancer and anadrenal cyst were made by CT-guided adrenal biopsy.

Adrenal gland iodocholesterol uptake (mean ±s.e.m.)in the unilateral adrenalectomy and adrenal destructiongroups was 0.32% ±.04% administered dose (95% CI,0.24%—0.4% administered dose) (Fig. 3). There was nodifference in NP-59 uptake between these groups (p = ns).Adrenal ‘31I-6f@-iodomethyl-l9-norcholesteroluptake ofboth groups was elevated (p < 0.01) as compared to theunilateral uptake of normal subjects (0. 16% ±0.05%administered dose; 95% CI, 0.06%—0.26% administereddose), and similar (p = ns) to the total (bilateral) uptakeof normal controls (Fig. 3) (22).

DISCUSSION

Post-adrenalectomy compensatory changes are well recognized in the adrenal. In both acute (hours) and subacute(days) intervals after unilateral adrenalectomy, a combination ofadrenocortical hypertrophy and hyperplasia havebeen noted (24—26).Early studies had suggested that adrenocorticotrophin or other pituitary/hypothalamic-derived trophic substances may be responsible for theseanatomic and histologic changes, but more recent investigations with concomitant dexamethasone suppression ofACTH, in a variety of animal models did not inhibit thecompensatory response after unilateral adrenalectomy (25,27-29). In hypophysectomized rats compensatory adrenalchanges can be blocked by the administration of aldosterone, even in the presence ofadrenocorticotrophin (25,30).This effect ofaldosterone may be related to suppression ofangiotensin II and its recently described participation inthe stimulation of platelet-derived (31) and other growthfactors in the adrenal zona glomerulosa and elsewhere (32,33). Others have suggestedthat a major stimulus foradrenal growth after unilateral adrenalectomy is neural(34,35). Interruption of the neural circuit by hemisectionofthe spinal cord has been shown to inhibit compensatoryadrenal changes in animals when performed on the con

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adrenal destruction consistently exhibited normal anatomy of the unaffected gland by CT. It is not surprisingthat in the unaffected gland, small hypertrophic and/orhyperplastic changes might not be appreciated by multi,thin slice, high resolution CT at an early time wherefunctional changes in that gland manifested as increased‘31I-6@-iodomethyl-l9-norcholesterol (substrate) uptakewould be detected by scintigraphy.

We used adrenal non-visualization on the ‘31I-NP-59scintiscan as a means to identify the absence of unilateraladrenocortical function. The rationale for this approach isdrawn from our previous studies which have demonstratedthe efficacy of scintigraphy in identifying the sources ofabnormal adrenal function (37—40).Although we cannotbe assured of complete functional obliteration of the affected adrenal in the group with destructive lesions, giventhe absence ofdiscernible NP-59 uptake, the contributionto circulating hormones from this gland must be verysmall. The uptake of ‘31I-NP-59has been used to characterize physiological changes of adrenal cortical function inboth man and animals (41,42). Furthermore, the patternsof iodocholesterol accumulation can be used to discerndifferential adrenal function in the context of overall normal hormone secretion in patients harboring incidentallydiscovered, adrenal masses (43—45).That a second pheochromocytoma occurring in the remaining adrenal at aremote time after the removal of a primary lesion wouldbe an alternative explanation for an intraadrenal masslesion and must be a diagnostic consideration in the evaluation of these particular patients. However, in our seriesthe presence of normal biochemistry and increased adrenocortical iodocholesterol accumulation makes this a mostunlikely possibility, as a pheochromocytoma would bedepicted as a cortical defect or space occupying adrenallesion on iodocholesterol scintigraphy (46).

In the present study we believe that the increased uptakeof iodocholesterol in these remaining, intact adrenals reflects the integrated effect of compensatory process(es)triggered by contralateral adrenalectomy or unilateral adrenal destruction. Mean adrenocortical NP-59 uptake issignificantly elevated over that of the normal single glandand in some instances exceeds normal total (right + left)adrenocortical NP-59 uptake (22). Thus, not only cananatomic changes after unilateral adrenalectomy be appreciated, but chronic functional changes can also be documented in the remaining adrenocortical tissues after adrenalectomy or unilateral adrenal destruction by neoplasmin man.

The consequences of prolonged replacement therapywith gluco- and/or mineralocorticoids are well defined.These may include symptoms and signs of glucocorticoidexcess or deficiency following abrupt cessation of therapy.Most important is the suppression of the hypothalamicpituitary-adrenal axis with its attendant risks during medical or surgical emergencies. Viewed in this context, thecurrent work suggests that after adrenalectomy the de

FIGURE 3. AdrenocorticalNP-59uptakeinadrenalectomy(S)andadrenaldestruction(0) groupscomparedto normal,singleadrenalglanduptake(p< 0.01 comparedto normal)(ref.22).

tralateral side of the remaining adrenal (24). Unilateral,hypothalamic lesions have been shown to abolish ipsilateral, but not contralateral adrenal growth in adrenalectomized rats (36).

There are no morphologic or biochemical studies ofadrenal activity and growth and/or anterior pituitary orhypothalamic function in intact animals maintained eitheron or off chronic adrenocortical suppression after unilateral adrenalectomy. The present investigation examined amore chronic, post adrenalectomy condition, where theshortest interval of study after operation was six months,and where replacement adrenal steroids were not given(Table 1). In all but two of the post-adrenalectomy groupadrenal masses were noted. Whether the formation ofadrenal masses represents a chronic tissue response toadrenalectomy mediated by angiotensin II and/or othergrowth factors cannot be established in the present study,but the high proportion, seven of nine patients with discrete adrenal masses, is suggestive of such an effect. Theparticipation of the renin-angiotensin system cannot unfortunately be assessed in these cases as an evaluation ofaldosterone and its secretogogues was not performed. Thelevel of NP-59 uptake in the remaining adrenal in theadrenalectomy group was related to neither the size of theadrenal mass nor the interval after operation, albeit thesample size is small.

The normal remaining adrenal of the adrenal destruction group represents the result ofprogressive, and in somecases, rapid loss of functioning contralateral cortex in oneadrenal gland. Like adrenalectomy, this situation shouldalso result in a compensatory response(s) of ihe contralateral gland with increased size, function and substrate (NP59) accumulation. That stress due to the primary nonadenocortical lesion (for example, a pheochromocytomaor other neoplastic process) was not a factor in the compensatory response of these patients is suggested by thelack of a difference in NP-59 uptake between the adrenalectomy versus the adrenal destruction groups. Furthermore, the non-adrenalectomized patients with unilateral

1885The SolitaryAdrenalGland•Grosset al

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creased“adrenalreserve―of the solitaryfunctioningadrenal gland has no effect upon either basal adrenal functionor the response to stress (ACTH challenge). Therapy withgluco-or mineralocorticoids would not therefore be mdicated in these patients. The anatomic distortion (adrenalmasses) developing in the remaining adrenal cortex afterunilateral adrenalectomy, poses interesting mechanisticand etiologic questions that remain unanswered at thispoint, but based upon the present study appear to be ofliule pathologic significance.

CONCLUSIONCompensatory anatomic and functional changes can be

depicted in the remaining adrenal cortex after adrenalectomy. These changes appear to have little effect uponadrenocortical function, but when accompanied by significant alterations of adrenal contour or the development ofan adrenal mass then it may require further diagnosticevaluation.

ACKNOWLEDGMENTSThe authors thank Thomas Mangner, PhD for the synthesis

ofNP-59, the Phoenix Memorial Laboratories for the use of theirradiochemistry facilities, and Leann C. Beird and Christine Mancik for manuscript preparation.

Supported in part by grants ROl-CA-43300-Ol, NC! CA90915, NIAMDD ROl-AM-2147702 RAD, and GCRC-HEW 2MOl RR-0042-2lSI CLR fromthe National Institutesof Health;and the Department of Veterans Affairs Research Service andthe Nuclear Medicine Research Fund ofThe Division of NuclearMedicine, The University of Michigan.

REFERENCESI . LogothetopoulosJH, Doniach I. Compensatoryhypertrophyof the rat

thyroid after partial thyroidectomy. Br J Exp Pathol 1955;36:617—627.2. Mackay EM, Mackay LL. Compensatory hypertrophy of the adrenal

cortex. J Exp Med l924;43:395-402.3. ClarkOH, LambertWR,CavalieriRR,RapoportB,HammondME,

Ingbar SH. Compensatory thyroid hypertrophy after hemithyroidectomyin rats. Endocrinology 1976:99:988—995.

4. Matte R, Ste-Mane LG, ComtoisR, et al. The pituitary-thyroidaxisafterhemithyroidectomyin man.J C/in Endocrino/Metab198l;53:277—380.

5. Wollman SH, HerveyJP, ZeligsJD, EricsonCE. Bloodcapillaryenlargement duringthe developmentof thyroid hyperplasiain the rats.Endocrinologv1978;103:2306—2314.

6. MichalkiewiczM, ConnorsJM, Huffman U, HedgeGA. Increasesinthyroidglandbloodflowafterhemithyroidectomyin therat.Endocrinology1989:124:1118—I123.

7. El-Sherief MA, Hemmingsson A. Computed tomography of the normaladrenal gland. Ada Radiol 1982:23:433—442.

8. Goldman SM, Badghdassanan-GatewoodM, Walsh PC, Dornhorst A,SiegelmanSS.CT configuration of the enlargedadrenal gland. J CompulAssistTomogr 1982:6:276—280.

9. MontagneJ-P, KresselHY, Korobkin M, MossAA. Computedtomographyofthe normaladrenalglands.AmJ Roenigeno/1978;30:963—966.

10.SchultzA, HaagaJR. FletcherBO, Alfide Ri, SchultzM. Magneticresonanceimaging of the adrenal glands: A comparison with computedtomography. Am J Roenzgeno/1984;143:1235—1240.

I 1. GrossMD, Valk TW, SwansonDP, Thrall JH, Grekin Ri, BeierwaltesWH. Pharmacologicmanipulation in the contralateraladrenal gland.SeminNuc/Med 1981:11:128—148.

12. DashAJ, EnglandBH, Midgley AR Jr. et al. A specificnon-chromatographic radioimmunoassay for human plasma cortisol. Steroids1975:26:647—661.

13. PeulerJD, JohnsonGA. Simultaneoussingleradioenzymaticassayofplasmanorepinephrine,epinephrineanddopamine.LjfeSci 197l;2l:625—636.

14. SilberBH, PorterCC. The determinationof I7,21-dihydroxy-20-ketosteroids in urine and plasma.J Biol Chem 1954;210:923—928.

IS. Von Euler OS, LishajkoF. The estimationof catecholaminesin urine.Ada PhysiolScand1959:45:122—132.

16. TaniguchiK, Kakimoto Y, ArmstrongM. Quantitativedeterminationofmetenephnne and normetanephrine in urine. J Lab C/in Med1964;64:469—484.

17. FrancislR, Smid A, Gross MD, et al. Adrenal massesin oncologic patientsfunctional and morphological evaluation. Radiology l988;l66:353—356.

18. GrossMD, Shapiro B, BouffardJA, et al. Distinguishingbenignfrommalignanteuadrenalmasses.Ann Intern Med l988;109:613—661.

19. Thrall JH, FreitasJE, BeierwaltesWH. AdrenalScinitgraphy.SeminNuclMed 1978;8:23—4l.

20. ShapiroB, NakajoM, GrossMD, FreitasJE,CoppJ, BejerWaItesWFI.Value of bowelpreparationin adrenocorticalscintigraphywith NP-59. JNuc/Med 1983;24:732—734.

21. Koral KF, Sarkar SD. An operator-independent method for backgroundsubtractionin adrenaluptakemeasurements:concisecommunication.INuc/Med 1977;18:925—928.

22. Freitas JE, Thrall JH, Swanson DP, Rifai A, Beierwaltes WH. Normaladrenal asymmetry. Explanation and interpretation. I NucI Med1978;I9:149—l54.

23. Remmington RD. Schork MA. Statistics with applications to biologicalandhealthsciences.EngelwoodCliffs,NJ.PrenticeHall; 1970:183-185.

24. Holzwarth MA, Wilkinson CW, Dallman MF. Compensatory adrenalgrowth in immature and mature male rats. Neuroendocrinologyl980;31:34—38.

25. Dunlap NE, Grizzle WE. Golden syrian hamsters: a new experimentalmodel for adrenal compensatory hypertrophy. Endocrinology1984;l14:1490—1495.

26. Reiter Ri, Pizzarello DJ. Radioautographic study of cellular replacementin the adrenal cortex of male rats. Tex Exp Rep Biol Med l966;24:189—194.

27. Mc Nicol AM, Duffy AE, Penmran ID. Compensatory adrenal growth indexamethasonetreated rats. VirchowsArchiv B Cell Patho/ l989;56:3l7—320.

28. Vaughan MK, Vaughan GM, Reiter Ri, Benson B. Effect of melatomnand other pineal indoleson adrenalenlargementproducedin male andfemale mice by pinealectomy,unilateraladrenalectomy,castrationandcold stress. Neuroendocrino/ogy 1972:10:139—154.

29. England WC, Shinsako J, Dallman MF. Corticosteroids and ACTH arenot required for compensatory adrenal growth. Am I Phsyio/1975;229:1461—1464.

30. Grizzle WE, Dunlop NE. Aldosteroneblocksadrenalcompensatoryhypertrophyin therat.AmI Physioll984;246:E306—E3010.

31. GeisterferA, PeachMi, OwensGK. AngiotensinII induceshypertrophy,not hyperplasiaof cultured rat aortic smooth muscle cells. Circ Res1988;62:749—756.

32. Simonian MH, Gill GN. Regulation ofdeoxyribonucleic acid synthesisinbovineadrenocorticalcellsinculture.Endocrinology1979;l04:588—595.

33. Horiba N, Nomura K. Effectofexogenousand locallysynthesizedanglotensin II on adrenalglomerulosacell growth and aldosteronesecretion[Abstract]. Proceedings 70th annual meeting of the Endocrine Society,1988:102.

34. Dallman MF, Engeland WC, Shinsako J. Compensatory adrenal growth: aneurally mediated reflex. Am I Physiol 1976;23l:408—414.

35. HolzworthMA, DallmanMF.Theeffectofhypothalamichemi-islandsoncompensatoryadrenal growth. Brain Res l979;162:33—43.

36. Dallman MF, EngelandWC, HotzworthMA, ScholzPM. Adrenocorticotrophin inhibitscompensatoryadrenalgrowthafter unilateraladrenalectomy.Endocrinology1980;107:1397—1405.

37. Gross MD, Shapiro B, Grekin Ri, Meyers L Swanson DP, BelerwaltesWH. The relationshipof adrenalglandiodomethylnorcholesteroluptaketo zonaglomerulosafunctionin primaryaldosteronism.I C/in EndocrinolMetab1983;57:477—481.

38. Gross MD, Shapiro B. Scintigraphic studiesin adrenalhypertension. SeminNuc/Med 1989;19:122—143.

39. GrossMD, Valk TW, FreitasiE, SwansonDP, SchteingartDE, BeierwaltesWH. Therelationshipof adrenaliodomethylnorcholesteroluptaketo indicesofadrenal cortical function in Cushing'ssyndrome.IClin EndocrinolMetab 198l;52:1069—1072.

40. GrossMD, ShapiroB, FreitasSE,et al. The relationshipof “I-6fl

1886 The Journal of Nuclear Medicine •Vol. 32 •No. 10 •October1991

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iodomethyl-l9-norcholesterol (NP-59) adrenal cortical uptake to indices ofandrogen secretion in women with hyperandrogenism. C/in Nuc/ Med1984:9:264—270.

41. Gross MD, Shapiro B, Thrall JH, Freitas iE, Beierwaltes WH. The scintigraphic imaging ofendocrine organs. Endo Rev 1984;5:22l—28l.

42. Gross MD, Grekin Ri, Brown LE, Marsh DD, Beierwaltes WH. Therelationship ofadrenal iodocholesterol uptake to adrenal zona glomerulosafunction. J C/in Endocrino/Metab l981;52:612—6l5.

43. Beierwaltes WH, Sturman MF, Ryo U, Ice RD. Imaging functional nodulesofthe adrenal glandswith ‘311-l9-iodocholesterol.JNuc/Med 1974:15:246—

257.44. RizzaRA, WahnerWH, SpelsbergTC, Northcutt RC, MosesHL. Visual

ization of nonfunctioning adrenal adenomas with iodocholesterol: possiblerelationship to subcellular distribution oftracer. J Nuc/Med 1978:19:458—463.

45. Gross MD, Wilton GP, Shapiro B, et al. Functional and scintigraphicevaluation ofthe silent adrenal mass. J NucI Med l987;28:l401—l407.

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(continuedfrom page 5A)

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FIGURE1. Galliumscan48 hr postinjectionshowsintenselung activityandabsent liveractivity.

FIGURE2. Normalliver-spleenscanwith‘@mTcsulfurcolloid.

FIGURE3.Galliumscan7wkaftertheinitial scan shows normal liver uptakeand absentlung activity.

exposure and chemotherapeutic agents (6-8) and, recently,gandolinum contrast for MRI (9).

In this patient, no significant liver pathology or hematologic abnormalities were demonstrated throughout thehospital course nor did he receive any chemotherapeuticor contrast agents. Consequently, the poor liver uptake wasascribed to a “steal―phenomenon by the acutely inflamedlungs.

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In: Hoffer HB, Bekerman C, Henkin RE, eds. Gal1iu@n-67imaging.New York:JohnWileyandSons;1979:23-38.

2. Hayes.RL, Byrd, BL, RafterJJ, et al. The effectofscandiumon the tissuedistribution ofGa-67 in normal and tumor-bearing rodents.J Ni,clMed 1980:21:361-365.

3. Hayes RL, Edwards CL. The effect of stable scandium on red blood cells andon the retentionand excretionof'7Ga in humans.SouthMedJ l973;66:1339-l340.

4. Ford-Hutchinson AW,Perkins Di. The binding of scandium ions to transferrinin vivo and in vitro. Ear J Biochem 1971:21:55-59.

5. Lentle BC, Castor WR, Khalig A, et al. The effectofcontrast lymphangiographyon localization of “Ga-citrate.J Nuc! Med 1975:16:374-376.

6. BekermanC,HofferPB.Salivaryglanduptakeof‘1Ga-citratefollowingradiation therapy. J Nucl Med l976;l7:685-687.

7. Bradley WP, Alderson P0. Eckelman WC. et al. Decreased tumor uptake ofgallium-67 in animals after whole-body irradiation. JNuclMed 1978:19:204-209.

8. BekermanC, PavelD,BitranJ,etal. Effectsofinadvertentadministrationofantineoplastic agents prior to Ga-67 injection. J Nuci Med 1984:25:430-435.

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1887The SolitaryAdrenalGland•Grosset al

FIRST IMPRESSIONS

Case Report: Hepatopulmonary Steal In PCPJoseph Charalel and Zev W. ChayesNuclear Medicine/Ultrasound, Veterans AffairsMedical Center, Bronx, New York

A gallium scan was performed on a 49-yr-old male HIVpositive patient admitted with fever, weight loss and respiratory distress that required intubation. The chest x-rayshowed diffuse interstitial infiltration and his sputum waspositive for PCP. The gallium scan (48 hr postinjection)showed massive uniform lung uptake bilaterally and nonvisualization ofthe liver (Fig. 1). All standard lab test resultswere unremarkable except for mild elevation of liver function values. A liver-spleen scan with 99mTc@sulfurcolloid(Fig. 2) and a hepatobiliary scan with 99mTc@Mebrofenin®were found to be normal. The patient was treated with Pentamidine and Septra, which induced a dramatic clinical improvement. A follow-upgallium scan performed after 6 wkshowed no lung uptake and normal liver activity (Fig. 3).

DISCUSSIONAbsent or faint liver activity on gallium scans has beenascribed to hemochromatosis and other causes of serum ironelevation that block the binding sites. Other reduction ingallium uptake includes competitive uptake by tumor orinflammatory sites (1), prior administration of scandium(2—4),lymphangiographic contrast agents (5), radiation

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1991;32:1882-1887.J Nucl Med.   WortsmanMilton D. Gross, Brahm Shapiro, John E. Freitas, Laura Meyers, Isaac Francis, Norman W. Thompson and Jacobo  Clinical Significance of the Solitary Functioning Adrenal Gland

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