Although the natural history of autonomous hyperfunc tioning thyroid nodules is a variable one, they usually main tam their size and autonomous hyperactive ...
Disappearance
of a Hyperfunctioning Following
TSH
Thyroid
Nodule
Stimulation
Huldrick Kammer and Mark 0. Loveless
Providence Medical Center and the University of Oregon Health Sciences Center, Portland, Oregon Following functioning
stimulation autonomous
roidism
decreased
and
with exogenous TSH, a patient with a large hyper thyroid nodule developed transient hyperthy radioiodine
uptake,
and
subsequently
the
nodule
disappeared.
J NuciMed19: 1149—1150, 1978 Although the natural history of autonomous hyperfunc tioning thyroid nodules is a variable one, they usually main tam their size and autonomous hyperactive function if left untreated (1,2). The response of such nodules to thyro tropin (TSH) stimulation is also variable, for both a decrease in sensitivity (3) and hyperresponsiveness (4) have been demonstrated. We have observed a patient whose
11.8), T3-RIA 2 10 ngm% (N 80—220). The patient was thought to be mildly toxic and was placed on antithyroid
drugs in preparation for surgery. He improved rapidly, and at the end of 3 wk was considered euthyroid. The previous 2½- x 3-cm nodule was no longer palpable. Examination by several physicians confirmed this new finding. The anti thyroid
medication
was
discontinued
and
the
previously
autonomous hyperfunctioning thyroid nodule responded in a most unusual manner. It not only showed a marked de
planned surgery was cancelled. The patient was seen 2 mo
crease in radioiodine uptake, but disappeared following administration of TSH.
evidence of nodularity. He remained euthyroid clinically. A serum T4 was 10.7 @ig%(N 4.5—11.8), and T3-RIA was
completely
later.
His thyroid
was normal
in size and shape,
with no
113 ngm% (N 80—220).Thyroidal radioiodine uptake was CASEREPORT
In June, 1976 a 44-year-old white man sought medical attention because of a mass on the right side of his neck.
repeated and showed 18% of the dose in 24 hr, with the tracer distributed uniformly (Fig. 3 ) . The patient has been seen at regular
intervals
over
the past
1½ yr. His thyroid
On physicalexaminationhis physicianfound a 2½-x 3-cm continues to function normally and no nodules can be pal solitary, nontender, movable nodule located in the right lower pole of the thyroid. There were no palpable regional lymph nodes, and the patient was euthyroid clinically. Laboratory data revealed a T3 resin uptake of 48.4% (N 37—65%), T4 9.2 @g% (N 3.8—12). An uptake test
pated. Thyroid image remains normal (Fig. 4).
revealed
the histologic pattern showed the majority to be true ade
25%
at 24 hr (N
8—30%). The
thyroid
image
, showed essentially all theradioactivity to belocatedin the nodule (Fig. 1). The patient was given 10 units of thyrotropin
intramuscu
larly on each of three consecutive days. Following this, a 24-hr uptake of radioiodine was 17.5%. The nuclide was distributed throughout both lobes, with a decreased con centration in the nodule (Fig. 2). Although a T3 suppression test was not performed, the diagnosis of a hyperfunctioning thyroid nodule was considered established. An ultrasound tracing was not obtained. One week following the injections of TSH, the patient complained
of heat
intolerance,
anorexia,
diarrhea,
weak
DISCUSSION
The solitary thyroid nodule is a clinically important le sion. In a comprehensive
study by Ferriman
et al. (5),
noma, while most of the rest showed nodular hyperplasia, autoimmune thyroiditis, cystic degeneration, or carcinoma. These lesions possess varying degrees of physiologic ac tivity, and when they function independently of endogenous
TSH, they are referred to as autonomously functioning nodules. Should a nodule produce sufficient hormone to suppress endogenous TSH secretion, the surrounding thy roid tissue is rendered functionless. When this occurs the patient need not be hyperthyroid clinically, for hormone secretion may be only sufficient to suppress pituitary func tion but inadequate to promote clinical hyperthyroidism (Fig. 1). It has been shown that extranodular thyroid tis sue will respond to TSH stimulation only if the patient is
ness, sleeplessness, nervousness, palpitations, and weight euthyroid, while there is little or no response if hyper loss. Physical examination revealed blood pressure to be thyroidism is present (6). Following TSH stimulation, our 108/68, pulse 96 per minute, and regular cardiac rhythm. The skin was warm and moist, and there was a fine tremor of the extended fingers. Deep reflexes were brisk. No lid lag was noted. The nodule showed no change from the Received Jan. 25, 1978; revision accepted May 3, 1978. initial examination. The remainder of the gland felt nor For reprints contact : Huldrick Kammer, Providence mal. Laboratory data revealed a T4 of 11.9 @g%(N 4.5— Medical Ctr., 700 NE 47th Ave., Portland, OR 97213.
Volume 19, Number 10
1149
KAMMER AND LOVELESS
@.--
FIG. 1. Initialthyroidimageshowingsolitaryhyperfunction ing thyroid
nodule
at right
FIG. 3. Twomonths following TSHstimulation.
lower pale.
I
F1G.4. Fourteen-month followup scan.
FIG. 2. Following 10 unitsTSHi.m.dailyfor3 days.
patient's thyroid image demonstrated preferential uptake in the paranodular tissue with less concentration of the radio nuclide in the nodule (Fig. 2) . We have been able to find only one case showing a similar response (3). One week following TSH injections, our patient appeared mildly toxic. His serum T4 was minimally elevated. Plasma levels of free T4 and T3 were not determined. Hyperthy roidism
could
have
resulted
from
synthesis
and
release
of
hormone by stimulated normal tissue or possibly by release of preformed hormone from the nodule. Thyroid imaging at intervals more frequent than 24 hr might have demon strated a difference in the rate of hormone turnover in various portions of the gland. It is also conceivable that TSH
could
have
induced
tissue
changes
within
the nodule
like those of subacute thyroiditis; in such an event increased release of hormone along with decreased radionuclide up take would be expected.
At the time of his initial examination our patient had a thyroid nodule of substantial size. Although a cystic corn ponent was not definitely excluded by ultrasound, the scan was compatible with a solid lesion. It was a surprise to find the nodule
had disappeared
completely
in the short
interval
of 3 wk between examinations. Long-term studies of a large number of patients indicate that it is most unusual for untreated thyroid nodules to ever decrease in size, even if they undergo partial cystic degeneration (2,9,10). The part played by TSH, if any, in causing regression of the nodule is purely speculative. Could such stimulation have compromised the nodule's blood supply, thereby in viting infarction or hemorrhage? Since the patient never experienced pain, tenderness, or acute swelling of his gland, it is unlikely that any of these phenomena occurred. If infarction of the nodule following TSH stimulation was responsible for its resolution, it would represent a rare occurrence indeed, for it has not been reported in over 200 patients submitted to TSH testing (1—3,9). Moreover, in a few instances where it has been known to occur, the
1150
nodule
has
regressed
in size
only
over
a long
period
of
time (8,10) . It would seem a short period of treatment with methirnazole and iodide would not account for dis appearance
of this nodule.
Followup examination at 1½ yr reveals the thyroid gland to be normal to palpation, and the scan shows no focal or irregular areas of uptake (Fig. 4). The thyroid function tests are normal at this time, indicating re-estab lishment of the pituitary-thyroid axis. REFERENCES
1. SILVERSTEIN GE, BURKE G, COGAN R: The natural history of the autonomous hyperfunctioning thyroid nod ule. Ann Inter,; Med 67: 539—548,1967 2. MCCORMACKKR, SHELINEGE: Long-term studies of solitary autonomous thyroid nodules. I NucI Med 8 : 701— 708, 1967 3. S0IN JS, BEAL W, BURDINE JA: Disappearance of autonomous thyroid nodule under TSH stimulation. I NucI Med 15:1209—1211, 1974 4. BURKE G, SZABO M : Dissociation of in vivo and in vitro “autonomy―in hyperfunctioning thyroid nodules. I Cliii Endocrinol Metab 35: 199—202,1972 5. FERRIMAN D, HENNEBRY TM, TASSOPOULOSCN: True thyroidadenoma.QuartI Med 41: 127—139, 1972
6. HORNET, REICHE, EHRENFELD EN, et al: The thy rotropin-stimulation ules of the thyroid
test in patients with solitary hot nod gland.
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