Case

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Multiple

Brown

ma

Tumors

and THOMAS

Brown

tumor

thyroidism. tumor roidism

W.

for

or

HARRY

until

1963,

During

patients

with

with

secondary

the

past end-stage

secondary a

demonstrable

with brown

chronic

brown

least

has

the

tests

and

azotemia.

the

third

Failure

been

We

cadaver

was

than

the

measured

#zl eq/mI).

then,

Case first

seen

and

in November

dehydration.

1972

Serum

be-

labona-

magnification)

[5]

was

obtained

during

1975) right

1. -

the

5, 1976;

I

Department

of

2

Department

of Pediatrics.

accepted

Radiology.

128:131-134.

after

University University

January

revision of California. of California,

1977

August San San

27,

Magnification

showing ischium,

Francisco.

California California

131

94143. 94143.

Address

reprint

requests

hips

brown left

1976.

Francisco.

rejection

(A) and left (B)

left supraacetabular

J Roentgenol

greater

Since

Subpeniosteal resorption of bone in the phalanges was first demonstrated in November 1973 on conventional nadiognaphs of the hands and then 1 year later on fine-detail films (type M film). A roentgenognaphic bone survey (with selective

Fig.

Am

100-200

continued.

night

May

=

tumors.

A 17-year-old girl was cause of vomiting, malaise,

Received

Alkaline

(normal

hormone

65

=

vigorous

rejection.

lU/liter

pade-

a kidney from a One month later,

acute

to 228

(normal has

and

chronic

Report

rejection

to

despite

1974, patient.

panathyroid

eq/mI

urognam

failure,

December underwent

rose

serum

intravenous

renal In

levels p1

An

cystic disease. onset of symptoms, the times because of vomiting,

five

kidney

and 600

age.

medullary after the

transplanted

transplanted

lU/liter),

re-

delayed

progressive

management.

phosphatase

radiographically

for

hospitalized and

hyponatremia, hyperkalemia, and growth was below

was

revealed the 2 years

medical the

acidosis,

percentile

was

HATTNER,’

Puberty

hydration,

frewith

S.

POTTER2

revealed

biopsy

During

tumors

unusual.

E.

tory

tient

presence

brown

eight

Renal

ROBERT

DONALD

renal

hemodial-

been observed more tumors in a patient remain

at

a

disease and with

has brown

been

hyperparathy-

renal

hyperparathyroidism patient

was

frequency

hypenparathyroidism

long

GENANT,’

AND

hyperpana-

secondary decade,

increasing

and renal osteodystrophy quently [2-4]. Multiple port

primary

however,

with

K.

ORLOFF,2

has

of

Chronic

Hyperparathyroidism

BROWN,1

osteoclastoma,

complication

in association

[11.

employed of

bone, a

Not noted

ysis

of as

Patientwith

Secondary

SHELDON

recognized

Reports

to H. K. Genant.

femoral

region.

episode

views (February

tumors neck,

of

in and

CASE

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132

Fig.

2.-Pelvicfilm

left supraacetabular

in May

1975.

region show varying

Browntumorin

degrees

rightiliacwing

REPORTS

hasdisappeared;

brown

tumors

of

right

schium,

left

femoral

head.

and

of sclerosis.

r.

Fig.

gressive

3.

-

Radiographs showing prohealing over 3 month

A, Expansile brown tumor in fibula (magnification view) in February 1975. 8, Increased scleperiod.

proximal

rosis by May 1975. Subperiosteal resorption is seen at proximal medial border of tibial metaphysis.

CASE

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. .-. .

133

Dihydnotachystenol therapy was instituted, and by August 1975, the alkaline phosphatase measured 73 lU/liter. Bone surveys and nadiographs with magnification, repeated in May and August 1975, showed disappearance of the lesion in the right iliac wing. A sclerotic change appeared in several of the other lesions (figs. 2 and 3). In May 1975, skeletal scintigraphy using ‘9Tc-pyrophosphate [6] was performed. Anterior and posterior whole-body scans (fig. 4) showed abundant generalized bony perfusion with focally increased activity that corresponded to the nadiognaphically defined brown tumors. A single ectopic

#{149}ir*t.,

“.1

REPORTS

kidney

(renal

allograft)

was

Radiographically, sharply

sis,

brown

demarcated

part of the or expanded.

and

skeleton. Healing

[9]

defect and

of

[7,

8].

[10]

in

Brown

tumors

rarely

[11].

the

frequent

manifestation

12-14].

and ..,

JB

A

4.-Anterior

and

in areas

posterior

whole

of brown

tumors.

bone

scans

showing

Gniffiths

et

as

1.5%

lesions

were

demonstrated

patients

with

brown

the

multiplicity

Although

the

patients

with

common, a patient The

lucent

lesions

in

the

left

survey femoral

showed neck,

well left

circumscribed, supnaacetabular

region, right ischium, night iliac wing, right proximal fibula, right distal femur, left acromion, left distal ulna, and a questionable small lesion in the left distal clavicle (figs. 1-3). Those lesions in the night fibula, right ischium, and left ulna were mildly expansile. A mild “ruggen jersey” appeanance of the spine, subpeniosteal resorption of the proximal medial humeri and tibia, and resorption of the distal clavicles were also noted.

well 20]

demonstrated.

Our

of et

advanced

with

tumors

Other

possible

(in

plasia,

and

histiocytosis

X),

healing

in

3 months

with

cludes

these

other

processes.

specific

tumors [18].

in

osteoof

bone,

in

resorption

for

polyostotic but

un-

presence of

After of

causes

particular,

in

not

renal the

parathyroid

levels [21]. evidence

be-

patient.

such

lesions

serum

those

unusual

is

subpeniosteal

elevated

single

a single

on

destructive

brown

in

brown

based

aswith since

patients al. [16] of

is

in

to

held

Only

case

tumor

first

only has

incidence

multiple

was

a

secondary

series Katz

lesions

brown

defined

considered

large

one report of hyperparathynoidism

patient

and

the

previously

the

of

and alkaline phosphatase therapy [22], radiographic were

with

hyperparathyroidism

of

with

fibrosa

nadiographically

occurrence

in our

[19,

were

patient

respectively.

of

only

hyperparathyreported as

been

the

cited

of skull.

osteitis of

were associated A single case

1.7%

primary

the

described

in 1963 a

tumors.

diagnosis

conjunction bone

[17] and

we found only with secondary

multiple This

al.

shown

uptake

hyperpanathyroidism

[1 5], and in two hypenparathyroidism,

tumors

of

been

a

primary

and

that

dispelling

reported secondary

dystrophy 1975.

in

that brown tumors hyperparathyroidism.

cause

body

[1]

tumor

of

with have

primary

any

persistence

regions have

et aI.

brown

in

be thinned sciero-

prominent

proof

of

hyperpanathyroidism,

been with

or

with

scans

appear

appear

in patients

a manifestation tumors have

Fordham a

sumption primary

lesion, scans

experimental

of bone was [1 2], brown

may

cortex may in calcification,

metaphyseal

cystica roidism

describe

February

pelvis.

usually

and

activity

in bone

Following

in

the

hyperparathyroidism

increased

radionuclide

[1,

the

Bone

secondary

generalized

activity

in

tumors

lytic,

The overlying may result

disappearance

cystic

increased

visible

Discussion .

Fig.

faintly

the therapy

of

hormone appropriate healing was these fibrous

lesions dys-

appearance

of

virtually

cx-

CASE

134

REFERENCES

Downloaded from www.ajronline.org by 50.126.135.151 on 11/11/15 from IP address 50.126.135.151. Copyright ARRS. For personal use only; all rights reserved

1.

Fordham CC, Williams TF: Brown tumor and secondary hyperparathyroidism. N EngI J Med 269:129-131, 1963 2. Johnson C, Graham CB, Kings F, Curtis FK: Roentgenographic manifestations of chronic renal disease treated by periodic hemodialysis. Am J Roentgenol 101:915926, 1967 3. Meema HE, Rabinovich 5, Meema S. Lloyd GJ, Oreopoulos DG: Improved radiological diagnosis of azotemic osteodystrophy. Radiology 1 02: 1-1 0, 1972 4. Potter DE, Wilson CJ, Ozonoff MB: Hyperparathynoid bone disease in children undergoing long-term hemadialysis: treatment with vitamin 0. J Pediatr 85:60-66, 1974. 5. Genant HK, Doi K, Mall JC: Optical versus radiographic magnification for fine-detail skeletal radiography. Invest Radio!

6.

10:160-172,

REPORTS

12. 13.

14. 1 5.

16.

17.

1975

Huberty JP, Hattnen RS, Powell MR: A 9911Tcpyrophos phate kit: a convenient, economical, and high-quality skeletal-imaging agent. J NucI Med 15:124-126, 1974 7. Robbins SL: Pathology, 3rd ed. Philadelphia, Saunders, 1967 8. Steinbach HL, Gondan GS, Eisenberg E, Crane JT, Silverman 5, Goldman L: Primary hypenparathyroidism: a correlation of roentgen, clinical, and pathologic featunes. Am J Roentgenol 86:329-343, 1961 9. Sy WM: Bone scan in primary hyperpanathyroidism. J NucI Med 15:1089-1091, 1974 1 0. Rosenthall L, Kaye M : Technetium-99m-pyrophosphate kinetics and imaging in metabolic bone disease. J Nucl Med 16:33-39, 1975 11. Evens RG, Ashburn W, Bantter FC: Strontium 85 scanning of a “brown tumour’S in a patient with panathynoid carcinoma. Br J Radiol 42:224-225, 1969

18.

Jaffe HL: Hyperparathynoidism (Aecklinghausen’s disease of bone). Arch Pathol 16:63-1 12, 236-258, 1933 Bartlett NL, Cochran D: Reparative processes in primary hypenpanathyroidism. Radiol Clin North Am 12:261-279, 1974 Teng CT, Nathan MH: Primary hyperpanathyroidism: Am J Roentgenol 83:716-731, 1960 Friedman

WH,

Gniffiths

20.

N,

Schwartz

HJ,

Ennis

JT,

Bailey

G:

Brown

tumor

of

Skeletal

changes

fol-

1974

Genant HK, Heck LL, Lanzl LH, Rossmann K, Vanden Horst J, Paloyan E: Primary hypenpanathynoidism; a cornprehensive study of clinical, biochemical and radiographic manifestations. Radiology 1 09 :51 3-524, 1973 Doyle

FH:

Radiological

patterns

sociated with renal glomenulan Bull 28:220-224, 1972 21 . Shapiro

A:

The

biochemical

of

bone

failure basis

of

disease

in adults. the

skeletal

as-

Br Med changes

uremia. Am J Roentgenol 111:750-761, 1971 Kaye M, Chattenjee G, Cohen GF, Sagan 5: Arrest of hypenparathynoid bone disease with dihydrotachysterol in patients undergoing chronic hemodialysis. Ann Intern Med 73:225-233, 1970 in

22.

AE:

lowing renal transplantation. Radiology 113:621-626, 1974 Idelson BA, Audikoff J, Smith GW: Renal osteodystrophy: unusual roentgenologic manifestation. JAMA 230: 870-872,

19.

Pervez

the maxilla in secondary hyperparathynoidism. Arch Otolaryngol 100:1 5-1 59, 1974 Katz Al, Hampers CL, Merrill JP: Secondary hyperparathynoidism and renal osteodystrophy in chronic renal failure. Analysis of 195 patients, with obsenations on the effects of chro&c dialysis, kidney transplantation and subtotal parathynoidectomy. Medicine 48:333-374, 1969

chronic