Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1382_Библиотеки_им_академика_М_И_Перельмана.pdf
ENDOCRINE SURGERY
60
focus of increased uptake is seen on thyroid
scanning. Solitary toxic thyroid nodules are
rarely malignant and generally standard I-123
thyroid scanning is not used in patients with
solid nodules unless the serum TSH is suppressed. In those patients with TSH suppression, when a ‘‘hot’’ solitary functioning nodule
is seen with suppression of extranodular uptake
in thyroid tissue, the ‘‘hot’’ nodule is rarely
malignant. There can be exceptions to the rule
andbothendocrinologistandsurgeons
may still wish to further work up ‘‘hot’’ nodules
on occasion, since there is a small chance
(<1–2% at most) of malignancy in this type
of nodule [15].
Thyroid Scanning in Patients with a Substernal
Goiter
I-123 scintigraphy can be helpful in identifying
large intrathoracic/mediastinal masses as functioning thyroid [80] thus differentiating these
from other lesions such as lymphoma [67].
Whole-Body Scintigraphy in Patients
with Thyroid Cancer
Diagnostic Whole-Body Scanning and Thyrogen
Scanning
The application of most important nuclear
medicine techniques in the follow-up and for
delineation of treatment in patients withthyroid
cancer is mainly represented by thyroid scintigraphy and whole-body iodine scintigraphy.
The ATA guidelines allow clinicians to decide
whether whole-body scanning is necessary prior
to a therapeutic dose of I-131[27]. Some nuclear
medicine departments use diagnostic scanning
routinely and others almost never use it. I-123 is
considered an optimal agent for diagnostic purposes before therapy with I-131; it may be a
better initial diagnostic agent to be used or
I-131 can be used for whole-body scanning
prior to radioablation therapy [81]. I-123 is
used for diagnostic whole-body scanning
(acquiring images at 6, 24, 48 h after injection)
in patients with DTC reducing the risk for
‘‘stunning’’ (a controversial phenomenon
whereby a diagnostic dose of radioiodine, possibly I-131, may decrease uptake of a subsequent therapeutic dose by remnant thyroid
tissue or by functioning metastases), and
improving improves image quality because of
its shorter half-life more favorable gamma
energy [82]. In fact, for postablation follow-up,
the use of I-131 doses of several mCi for scans
can stun the thyrocytes and thyroid cancer cells
[83, 84].
Low-iodine diet and a high-serum TSH (gen-
erally >25–30 mU/ml) are required for effective
use of this technique [67]. Achieving high TSH
serum levels slowly using thyroid hormone
withdrawal can affect the patient’s quality of
life and at least theoretically may result in
increased growth of metastatic thyroid tissue
[85]. Recently, several clinical trials have proven
that intramuscular injection of rhTSH (Thyrogen) is effective in achieving radioiodine uptake
during nuclear scan imaging of thyroid cancer
similar to a T4 withdrawal strategy thus allowing the patient to remain euthyroid during testing [85]. Most clinicians will have the patient
stop T4 for a few days prior to scanning given
the nonnegligible amount of iodine present in
T4 preparations. One common standard protocol for using rhTSH in patients with thyroid
cancer is the following: a single 0.9 mg (intramuscular injection) of rhTSH daily for two consecutive days (Monday and Tuesday); a dose of
I-131 or I-123 is administered on the day after
the second injection of rhTSH (Wednesday); a
total body scan is performed 24–48h after
radioiodine administration (Thursday or Friday); serum Tg detection is quantified 3–4 days
after the second injection of rhTSH (Thursday
and/or Friday) [85]; serum TSH may be
assayed in order to verify that rhTSH has
been injected. During this protocol a
patient can continue to use thyroid hormone
except for the few days prior to scanning. AntiTg antibodies must be assayed along with Tg to
avoid false negatives due to antibody interference withthe Tg measurement assay [51]. AntiTg antibodies will generally decrease and
disappear in patients in complete remission
[51]. rhTSH represents an important clinical
tool to identify residual or metastatic thyroid
tissue [85]. WBS findings (after rhTSH injection) must be correlated with serum Tg
levels because different physiological and
pathological conditions can result in misinterpreted WBS imaging results producing false
positives that can be mistaken as metastases
(Table 4.5) [67].
61
THYROID IMAGING
Table 4.5. Causes of false positives on whole-body scan
radioiodide imaging misdiagnosed as metastasis from thyroid cancer
Physiological causes Pathological causes
Salivary Glands
Nasopharynx Meningioma
Esophagus Artificial eye
Thymus Dacrocystitis
Breast Parotid tumor
Stomach Sinusitis
Liver Dental caries
Gall Bladder Tracheostomy
Intestine Inflammatory lung
disease
Urinary tract Lung carcinoma
Contamination with saliva, stool
or urine
Pleuropericardial cyst
Struma cordis
Hiatal hernia
Zenker’s diverticulum
Barrett’s esophagus
Gastric
adenocarcinoma
Renal cyst
Meckel’s diverticulum
Ovarian
cystoadenoma
ATA management guidelines for patients
with DTC propose that Tg unstimulated or stimulated levels greater than 2 ng/ml that increase
over time may represent recurrent disease [27].
The presence of detectable Tg levels after total
thyroidectomy and remnant ablation can be
used to identify patients with persistent and
recurrent disease (Fig. 4.6) [86]. I-131-WBS is
also more sensitive after I-131 ablation of normal thyroid remnants because identification of
neoplastic foci (which often have low radioiodine uptake) may be masked in the presence of
thyroid remnants with a high uptake [86]. However, it is possible to obtain accurate Tg measurements for the follow-up of patients with
DTC (after thyroidectomy) even without I-131
ablation treatment [86]. Serum Tg and diagnostic WBS have been considered complementary
in identifying residual tumor for patients with a
serum Tg below 1 ng/mL during thyroid hormone suppression [87, 88]. Undetectable levels
of Tg with TSH stimulated (whether by thyroid
hormone withdrawal or rhTSH) by itself may be
all that is necessary in follow-up of patients at
low risk for recurrence [87]. Diagnostic wholebody scanning (demonstrating functioning tissue, remnant, and/or metastasis, following thyroidectomy for DTC) can be performed by the
absorbed radiation from 3 to 10 mCi (dose of I-
131), causing suppression of iodine uptake
function [81].
a
Fig. 4.6. Whole-body scanning with I-131 showing multiple foci of metastatic thyroid cancer throughout the body (A) and with
detailed images of the patient’s lungs (B).
b
ENDOCRINE SURGERY
62
PostTreatment Whole-Body Scans
Posttreatment whole-body scans are more sensitive than diagnostic whole-body scans; this
phenomenon is related to much higher doses
of I-131 used for treatment than for the diagnostic scans and helps detect additional metastatic foci in the bone, mediastinum, and lungs
in approximately 10% of patients [89, 90]. Posttreatment WBS can show the lesions that produce Tg in patients with a negative diagnostic
WBS for iodine uptake and detectable serum Tg
levels [90, 91]. Posttreatment WBS generally is
performed 5–7 days after treatment [67]. Posttreatment whole-body scanning allows the clinicians to tell whether any I-131 localizes into the
malignant thyroid tissue and whether this agent
will be helpful in future intervention (Fig. 4.6).
Use of Thyroid Scintigraphy in Congenital Thyroid
Disorders
Congenital hypothyroidism (CH) (the overall
incidence is 1 of 3,000–4,000 newborns) is
related to developmental defects of the thyroid
gland including agenesis, hypoplasia, and
arrested migration of the embryonic thyroid
cells. Other less-frequent causes of CH are functional thyroid cell defects, such as TSH resistance or dyshormonogenesis, alterations of
secretion and action of thyrotropin-releasing
hormone (TRH), and the action of T3 [92].
Work up of CH is based on clinicalexamination,
biochemical tests, thyroid USS [93], and also on
thyroid scintigraphy, using Tc-99m-pertechnetate or I-123 [94]. Imaging is centered on distinguishing between transient and permanent
hypothyroidism [92]. Tc-99m pertechnetate is
trapped, not organified, so thyroid uptake is
similar to salivary uptake. Therefore, I-123 scintigraphy is preferable in the case of ectopic
thyroid (usually a small sublingual gland) [94]
Recently, it has been reported that rhTSH
stimulation followed by I-123 thyroid scintigraphy can be used for diagnosis of CH during
infancy [93].
Positron Emission Tomography
Patients with DTC that have a negative diagnostic WBS (by I-131 or I-123) and a negative head
and neck ultrasound yet have detectable serum
Tg need other diagnostic methods, such as positron emission tomography utilizing
fluoro-2-deoxyuse of
18
D-glucose (
FDG-PET as the positron-emitting
18
FDG-PET). The
18
F-2-
radiopharmaceutical has become increasingly
common in the management of various malignancies of the head and neck [95]. This imaging
technique is based on the principle that many
malignancies metabolize glucose at a much
higher rate than normal tissues. The images
are made 1 h after injection of 10–20 mCi
(370–740 MBq)
the cell to
to glucose. However, unlike glucose, which continues along the glycolytic pathway,
cannot be metabolized any further, and
PO
4
18
18
FDG.18FDG is converted in
FDG-6-PO4by hexokinase, similar
18
FDG-6-
thus accumulates in the cell. Tumor cells will
accumulate more of this radioisotope, which
can then be visualized during PET scanning.
One limitation of PET scanning was the lack of
anatomic information. More recently, imaging
18
with
FDG-PET has been refined further with
the introduction of a combined PET scan and
computed tomography scans (PET/CT), where
the PET images are fused with CT images. This
is extremely important because PET/CT provides a detailed anatomic context for areas of
increased uptake seen on PET scanning, allowing spatial localization of worrisome areas of
increased metabolic activity [96] (Fig. 4.7). In
order to supplement visual interpretation in
PET exam, some investigators calculate a standardized uptake value (SUV) [also defined as
the dose uptake ratio (DUR)] from the equation
SUV [T
act/Vmax
ity (in mCi or MBq), corrected for decay; V
the volume of tumor (in grams); D
]/[D
inj
/B]; T
is the tumor activ-
act
inj
max
is the
injected dose (in mCi or MBq), and B is the
body weight (in grams). If there is no excretion
of activity and if the activity is uniformly distributed over the whole body, then the SUV is 1.
In some cases an empirical value for SUV is
selected, typically 2.0 – 2.5, and lesions with
values greater than that are considered to be
malignant, but this has not yet been adapted to
DTC. Currently both benign (chronic thyroiditis or benign nodules) and malignant thyroid
lesions can have SUVs which are indistinguishable or at least overlapping.
More recently with the recognition of many
‘‘incidentally’’ detected thyroid nodules
(Fig. 4.7) on PET imaging done for work up of
other malignancies (such as lymphoma or lung
is
63
THYROID IMAGING
Fig. 4.7. PET/CT imaging of thyroid cancer. A small 7-mm
incidentally detected papillary carcinoma in the thyroid marked
by black arrow.
cancer) there has been some interest in whether
18
FDG-PET can be used to differentiate between
benign and malignant thyroid lesions preoperatively, and consequently be used as a tool to
select those who should undergo thyroidectomy. The results from these studies have
shown that this imaging modality has the potential to be useful in differentiating benign from
malignant lesions preoperatively showing a
high negative predictive value for thyroid
malignancy, especially in those patients with
an indeterminate/microfollicular cytologic pattern on FNAB of the thyroid nodule [97–102]. In
contrast, other findings were inconsistent with
those of studies that have considered the usefulness of preoperative FDG-PET in the evaluation
of cytologically indeterminate thyroid nodules
for selecting patients for surgery because the
glucose metabolic activities of benign thyroid
follicular nodules were as high as those of malignant nodules [103]. Studies examining the usefulness of FDG-PET in differentiating malignant
from benign nodules have reported conflicting
results; most found considerable overlap in glucose metabolic activities between malignant and
benign nodules [97, 99, 100, 102, 104]. Careful
selection of patients who could most benefit
from the additional information this test provides will be crucial and additional studies with
larger sample sizes need to be performed to
clearly establish the true efficacy and utility of
this test in the preoperative management of
thyroid nodules.
PET/CT has mainly been used for postoperative surveillance of patients with known thyroid
cancer, especially those with poor differentiation
or negative WBS despite Tg positivity
[95, 105–107]. Poorly differentiated or dedifferentiated thyroid carcinomas have more limited
abilities to concentrate radioiodine, leading to
negative I-131 scans despite significant increases
in thyroglobulin. However, these poorly differentiated lesions tend to be more metabolically
active, and therefore take up
18
FDG which can
be visualized during PET scanning [95, 105, 108]
(Fig. 4.8). If the extent of disease recurrence can
be identified in these patients with PET/CT then
surgical excision or other therapeutic interventions may become possible.
Computed Tomography Scan
and Thyroid Imaging
CT is occasionally used for the diagnosis of thyroid disorders [24], though it is not able to distinguish benign nodules from carcinoma [24]. CT is
better than USS for evaluating the mediastinal
extension of thyroid masses [24], and is also very
accurate to evaluate the spread of thyroid carcinoma, especially into certain lymph node basins
or in patients with local invasion of adjacent
structures. CT has some limitations such as
cost, artifacts caused by swallowing or breathing,
difficulty with foreign objects such as metal scatter from surgical clips and exposure to ionizing
irradiation [24, 109, 110]. Density value is quantified in CT numbers and the Hounsfield scale
(HU) is a quantitative scale for describing radiodensity. Sometimes contrast materials such as
ENDOCRINE SURGERY
64
Fig. 4.8. Utility of PET/CT scanning in patients with non-I-131 avid disease. (A) I-123 diagnostic scan in patient with a fractured
right humerus suspicious for metastatic Hurthle cell thyroid cancer shows no uptake in thyroid bed or humerus. (B) Posttherapy scan
after administration of I-131 shows some uptake in thyroid only. (C) PET/CT images with detail shows intense uptake in left thyroid
bed (arrow), right humerus (arrowhead), and left ribs.
intravenous iodinated contrast are used. This is
useful to highlight structures such as blood vessels that otherwise would be difficult to delineate
from their surroundings. CT with contrast
should not be used in patients who may need
treatment with radioiodine within a few months
since the iodine load reduces the iodine uptake of
any thyroid tissues for 8 weeks or longer. Moreover, it has been reported that in normal thyroid
tissues without calcifications CT density values
correlate linearly withiodine concentration [111]
and based on this demonstration, the decrease in
CT values not only could reveal a reduction of
iodine concentration in the thyroid follicles but
also represent a decrease in follicular content and
subsequently an increase of follicular cells [112].
Seventy-five to eighty percent of retrosternal
goiters have an extension in the anterior
mediastinum and 20–25% in the posterior mediastinum [24]. In addition, CT can provide
anatomical informations such as compression
of the trachea, esophagus, and great vessels
[113]. Features of substernal thyroid gland
include anatomic continuity with the cervical
thyroid, focal calcifications, relatively high CT
number, rise in CT number after administration
of iodinated contrast material, and prolonged
enhancement after contrast material administration. However, these features are not always
observed in patients with intrathoracic goiter
but a combination of these should be accurate
to have an appropriate diagnosis [114].
CT can be used in the follow-up of patients
with thyroid carcinoma as useful adjuvant imaging method to detect loco-regional recurrence
of thyroid carcinoma in the neck and/or metastases [115]. Pathognomonic signs of metastatic
lymph nodes can be recognized by size, shape,
and/or presence of nonenhancing areas after
contrast medium injection. This latter
65
THYROID IMAGING
phenomenon may be due to tumour necrosis,
tumour keratinization, or cystic areas inside the
tumor [116]. In patients with thyroid cancer,
mediastinal lymph-node metastases are often
associated with lung metastases and the preoperative localization with CT with injection of
contrast medium is an important diagnostic
phase and should be realized six weeks before
any administration of I-131 [115]. CT is elective
in the diagnosis of the aero-digestive tract invasion from thyroid carcinoma [115]. Finally, it is
also helpful in the identification of hepatic
metastases from medullary thyroid carcinoma
[24].
CT shows a hypodensity in nonautoimmune
nontoxic diffuse goiters with a homogeneous
enlargement of thyroid gland. In Graves’ disease
and autoimmune thyroiditis is reported a hypodensity of thyroid gland on CT [117]. On CT
scan, primary thyroid lymphoma should be
included in the differential diagnosis when a
homogeneous thyroidal mass is seen isoattenuating to muscles, with a strong tendency to
compress normal remnant thyroid and the surrounding structures without invasion [118].
References
1. Crocker E, Jellins, J. Grey scale ultrasonic examination
of the thyroid gland. Med J Aust. 1978;2(6):244–8.
2. Scheible W, Leopold GR, Woo VL, Gosink BB. Highresolution real-time ultrasonography of thyroid
nodules. Radiology. 1979;133(2):413–7.
3. Blum M, Weiss, B, Hernberg, J. Evaluation of thyroid
nodules by A-mode echography. Radiology. 1971;101(3):
651–6.
4. Solbiati L, Osti V, Cova L, Tonolini M. Ultrasound of
thyroid, parathyroid glands and neck lymph nodes. Eur
Radiol. 2001;11(12):2411–24.
5. Jarlov AE, NygardB, HegedusL, Karstrup S, Hansen JM.
Observer variationin ultrasoundassessment of thethyroid gland. Br J Radiol. 1993;66(787):625–7.
6. Yousem D, Scheff AM. Thyroid and parathyroid. In:
Som PM, Curtin HD, editors, Head and Neck Imaging.
St Louis: Mosby; 1996. 953–75.
7. Yousem DM, ScheffAM. Thyroid and parathyroid gland
pathology. Role of imaging. Otolaryngol ClinNorth Am.
1995;28(3):621–49.
8. Ying M, Brook F, Ahuja A, Metreweli C. The value of
thyroid parenchymal echogenicity as an indicator of
pathology using the sternomastoid muscle for comparison. Ultrasound Med Biol. 1998;24(8):1097–105.
9. Frates MC, Benson CB, Charboneau JW, et al. Management of thyroid nodules detected at US: Society of Radiologists in Ultrasound consensus conference statement.
Radiology. 2005;237(3):794–800.
10. Papini E, Guglielmi R, Bianchini A, et al. Risk of malignancy in nonpalpable thyroid nodules: predictive value
of ultrasound and color-Doppler features. J Clin Endocrinol Metab. 2002;87(5):1941–6.
11. Radecki PD, Arger PH, Arenson RL, et al. Thyroid imaging: comparison of high-resolution real-time ultrasound and computed tomography. Radiology. 1984;
153(1):145–7.
12. Tan GH, Gharib H. Thyroid incidentalomas: management approaches to nonpalpable nodules discovered
incidentally on thyroid imaging. Ann Intern Med.
1997;126(3):226–31.
13. Knudsen N, Bulow I, Jorgensen T, Laurberg P, OvesenL,
Perrild H. Goitre prevalence and thyroid abnormalities
at ultrasonography: a comparative epidemiological
study in two regions with slightlydifferent iodine status.
Clin Endocrinol (Oxf) 2000;53(4):479–85.
14. Gharib H, Papini E. Thyroid nodules: clinical importance, assessment, and treatment. Endocrinol Metab
Clin North Am. 2007;36(3):707–35, vi.
15. Hegedus L. Clinicalpractice. The thyroid nodule. N Engl
J Med. 2004;351(17):1764–71.
16. Takashima S, Fukuda H, Nomura N, Kishimoto H, Kim
T, Kobayashi T. Thyroid nodules: re-evaluation with
ultrasound. J Clin Ultrasound. 1995;23(3):179–84.
17. Solbiati L, Volterrani L, Rizzatto G, et al. The thyroid
gland with low uptake lesions: evaluation by ultrasound.
Radiology. 1985;155(1):187–91.
18. Gharib H. Fine-needle aspiration biopsy of thyroid
nodules: advantages, limitations, and effect. Mayo Clin
Proc. 1994;69(1):44–9.
19. Danese D, Sciacchitano S, Farsetti A, Andreoli M, Pontecorvi A. Diagnostic accuracy of conventional versus
sonography-guided fine-needle aspiration biopsy of
thyroid nodules. Thyroid. 1998;8(1):15–21.
20. Carmeci C, Jeffrey RB, McDougall IR, Nowels KW, Weigel RJ. Ultrasound-guided fine-needle aspiration biopsy
of thyroid masses. Thyroid. 1998;8(4):283–9.
21. Hegedus L, Bonnema SJ, Bennedbaek FN. Management
of simple nodular goiter: current status and future perspectives. Endocr Rev. 2003;24(1):102–32.
22. Jarlov AE, Nygaard B, Hegedus L, Hartling SG, Hansen
JM. Observer variation in the clinical and laboratory
evaluation of patients with thyroid dysfunction and
goiter. Thyroid. 1998;8(5):393–8.
23. Hegedus L. Thyroid size determined by ultrasound.
Influence of physiological factors and non-thyroidal
disease. Dan Med Bull. 1990;37(3):249–63.
24. Naik KS, Bury RF. Imaging the thyroid. Clin Radiol.
1998;53(9):630–9.
25. Gotway MB, Higgins CB. MR imaging of the thyroid and
parathyroid glands. Magn Reson Imaging Clin N Am.
2000;8(1):163–82, ix.
26. American Association of Clinical Endocrinologists and
Associazione Medici Endocrinologi medical guidelines
for clinical practice for the diagnosis and management
of thyroid nodules. Endocr Pract. 2006;12(1):63–102.
27. Cooper DS, DohertyGM, Haugen BR, et al. Management
guidelines for patients with thyroid nodules and differentiated thyroid cancer. Thyroid. 2006;16(2):109–42.
28. Pedersen OM, AardalNP, Larssen TB, Varhaug JE,Myking O, Vik-Mo H. The value of ultrasonography in predicting autoimmune thyroid disease. Thyroid. 2000;
10(3):251–9.
ENDOCRINE SURGERY
66
29. Raber W, Gessl A, Nowotny P, Vierhapper H. Thyroid
ultrasound versus antithyroid peroxidase antibody
determination: a cohort study of four hundred fiftyone subjects. Thyroid. 2002;12(8):725–31.
30. Matsuzuka F, Miyauchi A, Katayama S, et al. Clinical
aspects of primary thyroid lymphoma: diagnosis and
treatment based on our experience of 119 cases. Thyroid. 1993;3(2):93–9.
31. Hiromatsu Y, Ishibashi M, Miyake I, et al. Color Doppler
ultrasonography in patients with subacute thyroiditis.
Thyroid. 1999;9(12):1189–93.
32. Bennedbaek FN, Hegedus L. The value of ultrasonography in the diagnosis and follow-up of subacute thyroiditis. Thyroid. 1997;7(1):45–50.
33. Vitti P, RagoT, MancusiF, et al. Thyroid hypoechogenic
pattern at ultrasonography as a tool for predicting
recurrence of hyperthyroidism after medical treatment
in patients with Graves’ disease. Acta Endocrinol
(Copenh) 1992;126(2):128–31.
34. Zingrillo M, D’Aloiso L, Ghiggi MR, et al. Thyroid
hypoechogenicity after methimazole withdrawal in
Graves’ disease: a useful index for predicting recurrence? Clin Endocrinol (Oxf) 1996;45(2):201–6.
35. Boi F, Loy M, Piga M, Serra A, Atzeni F, Mariotti S.
The usefulness of conventional and echo colour Doppler sonography in the differential diagnosis of toxic
multinodular goitres. Eur J Endocrinol. 2000;143(3):
339–46.
36. Bogazzi F, Bartalena L, Vitti P, Rago T, Brogioni S,
Martino E. Color flow Doppler sonography in thyrotoxicosis factitia. J Endocrinol Invest. 1996;19(9):603–6.
37. Bogazzi F, Bartalena L, Brogioni S, et al. Color flow
Doppler sonography rapidly differentiates type I and
type II amiodarone-induced thyrotoxicosis. Thyroid.
1997;7(4):541–5.
38. Gharib H, Goellner JR. Fine-needle aspiration biopsy of
the thyroid: an appraisal. Ann Intern Med. 1993;118(4):
282–9.
39. Hall TL, Layfield LJ, Philippe A, Rosenthal DL. Sources
of diagnostic error in fine needle aspiration of the thyroid. Cancer. 1989;63(4):718–25.
40. Akerman M, Tennvall J, Biorklund A, Martensson H,
Moller T. Sensitivity and specificity of fine needle
aspiration cytology in the diagnosis of tumors of the
thyroid gland. Acta Cytol. 1985;29(5):850–5.
41. Cochand-Priollet B, Guillausseau PJ, Chagnon S, et al.
The diagnostic value of fine-needle aspiration biopsy
under ultrasonography in nonfunctional thyroid
nodules: a prospective study comparing cytologic and
histologic findings. Am J Med. 1994;97(2):152–7.
42. Mittendorf EA, Tamarkin SW, McHenry CR. The results
of ultrasound-guided fine-needle aspiration biopsy for
evaluation of nodular thyroid disease. Surgery.
2002;132(4):648–53; discussion 53–4.
43. Sutton RT, Reading CC, Charboneau JW, James EM,
Grant CS, Hay ID. US-guided biopsy of neck masses in
postoperative management of patients withthyroid cancer. Radiology. 1988;168(3):769–72.
44. Baskin H. Ultrasound of thyroid nodules. In: Baskin H,
Thyroid ultrasound and ultrasound-guidedFNA biopsy.
Boston: Kluwer Academic; 2000:71–86.
45. Cappelli C, Castellano M, Pirola I, et al. Thyroid nodule
shape suggests malignancy. Eur J Endocrinol. 2006;
155(1):27–31.
46. Mandel SJ. Diagnostic use of ultrasonography in
patients with nodular thyroid disease. Endocr Pract.
2004;10(3):246–52.
47. Kim EK, Park CS, Chung WY, et al. New sonographic
criteria for recommending fine-needleaspiration biopsy
of nonpalpable solid nodules of the thyroid. AJR Am J
Roentgenol. 2002;178(3):687–91.
48. Papini E. Thedilemma of non-palpable thyroid nodules.
J Endocrinol Invest. 2003;26(1):3–4.
49. Frasoldati A, Valcavi R. Challenges in neck ultrasonography: lymphadenopathy and parathyroid glands.
Endocr Pract. 2004;10(3):261–8.
50. Baskin HJ. New applications of thyroid and parathyroid
ultrasound. Minerva Endocrinol. 2004;29(4):195–206.
51. Pacini F, Schlumberger M, Dralle H, Elisei R, Smit JW,
Wiersinga W. European consensus for the management
of patients with differentiated thyroid carcinoma of the
follicular epithelium. Eur J Endocrinol. 2006;154(6):
787–803.
52. Frasoldati A, Pesenti M, Gallo M, Caroggio A, Salvo D,
Valcavi R. Diagnosis of neck recurrences in patients
with differentiated thyroid carcinoma. Cancer. 2003;
97(1):90–6.
53. Pacini F, Molinaro E, Castagna MG, et al. Recombinant
human thyrotropin-stimulated serum thyroglobulin
combined with neck ultrasonography has the highest
sensitivity in monitoring differentiated thyroid carcinoma. J Clin Endocrinol Metab. 2003;88(8):3668–73.
54. Torlontano M, Attard M, Crocetti U, et al. Follow-up of
low risk patients with papillary thyroid cancer: role of
neck ultrasonography in detecting lymph node metastases. J Clin Endocrinol Metab. 2004;89(7):3402–7.
55. Tohnosu N, Onoda S, Isono K. Ultrasonographic evaluation of cervical lymph node metastases in esophageal
cancer with special referenceto therelationship between
the short to long axis ratio (S/L) and the cancer content.
J Clin Ultrasound. 1989;17(2):101–6.
56. Steinkamp HJ, Cornehl M, Hosten N, Pegios W, Vogl T,
Felix R. Cervical lymphadenopathy: ratio of long- to
short-axis diameter as a predictor of malignancy. Br J
Radiol. 1995;68(807):266–70.
57. van den Brekel MW, Castelijns JA, Snow GB. The size of
lymph nodes in the neck on sonograms as a radiologic
criterion for metastasis: how reliable is it? AJNR Am J
Neuroradiol. 1998;19(4):695–700.
58. Kessler A, Rappaport Y, Blank A, Marmor S, Weiss J,
Graif M. Cystic appearance of cervical lymph nodes is
characteristic of metastatic papillary thyroid carcinoma.
J Clin Ultrasound. 2003;31(1):21–5.
59. Ahuja AT, Chow L, Chick W, King W, Metreweli C.
Metastatic cervical nodes in papillary carcinoma of the
thyroid: ultrasound and histological correlation. Clin
Radiol. 1995;50(4):229–31.
60. Kuna SK, Bracic I, Tesic V, Kuna K, Herceg GH, Dodig
D. Ultrasonographic differentiation of benign from
malignant neck lymphadenopathy in thyroid cancer. J
Ultrasound Med. 2006;25(12):1531–7; quiz 8–40.
61. Pacini F, Fugazzola L, Lippi F, et al. Detection of thyroglobulin in fine needle aspirates of nonthyroidal neck
masses: a clue to the diagnosis of metastatic differentiated thyroid cancer. J Clin Endocrinol Metab. 1992;
74(6):1401–4.
62. Leboulleux S,Girard E,Rose M,et al. Ultrasoundcriteria
of malignancy for cervical lymph nodes in patients
67
THYROID IMAGING
followed up for differentiated thyroid cancer. J Clin
Endocrinol Metab. 2007;92(9):3590–4.
63. Carrasco N. Thyroid Iodine Transport. In: Braverman
LE, Utiger RD, eds. Werner & Ingbar’s the Thyroid: a
fundamental and clinical text, 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2005:37–52.
64. Dai G, LevyO, CarrascoN. Cloning and characterization
of the thyroid iodide transporter. Nature. 1996;
379(6564):458–60.
65. De La Vieja A, Dohan O, Levy O, Carrasco N. Molecular
analysis of the sodium/iodide symporter: impact on
thyroid and extrathyroid pathophysiology. Physiol
Rev. 2000;80(3):1083–105.
66. Meller J, Becker W. The continuing importance of thyroid scintigraphy in the era of high-resolution ultrasound. Eur J Nucl Med Mol Imaging. 2002;29 Suppl
2:S425–38.
67. McDougall IR. In vivo Radionuclide Tests and Imaging.
In: Braverman LE, Utiger RD, eds. Werner & Ingbar’s
the Thyroid: a fundamental and clinical text, 9th ed.
Philadelphia: Lippincott Williams & Wilkins; 2005:
37–52.
68. Atkins HL. Technetium-99m pertechnetate uptake and
scanning in the evaluation of thyroid function. Semin
Nucl Med. 1971;1(3):345–55.
69. Iida Y, Hidaka A, HatabuH, KasagiK, KonishiJ. Followup study of postoperative patients with thyroid cancer
by thallium-201 scintigraphy and serum thyroglobulin
measurement. J Nucl Med. 1991;32(11):2098–100.
70. Almeida-Filho P, Ravizzini GC, Almeida C, Borges-Neto
S. Whole-body Tc-99m sestamibi scintigraphy in the
follow-up of differentiated thyroid carcinoma. Clin
Nucl Med. 2000;25(6):443–6.
71. Tenenbaum F, Lumbroso J, Schlumberger M, Caillou B,
Fragu P, Parmentier C. Radiolabeled somatostatin analog scintigraphy in differentiated thyroid carcinoma. J
Nucl Med. 1995;36(5):807–10.
72. Morris LF, Waxman AD, Braunstein GD. Accuracy considerations when using early (four- or six-hour) radioactive iodine uptake to predict twenty-four-hour values
for radioactive iodine dosage in thetreatment of Graves’
disease. Thyroid. 2000;10(9):779–87.
73. Abdel-Razzak M, Christie JH. Thyroid carcinoma in an
autonomously functioning nodule. J Nucl Med. 1979;
20(9):1001–2.
74. Bitterman A, Uri O, Levanon A, Baron E, Lefel O, Cohen
O. Thyroid carcinoma presenting as a hot nodule. Otolaryngol Head Neck Surg. 2006;134(5):888–9.
75. De Rosa G, Testa A, Maurizi M, et al. Thyroid carcinoma
mimicking a toxic adenoma. Eur J Nucl Med. 1990;
17(3–4):179–84.
76. Majima T, Doi K, Komatsu Y, et al. Papillary thyroid
carcinoma without metastases manifesting as an autonomously functioning thyroid nodule. Endocr J. 2005;
52(3):309–16.
77. Iwata M, Kasagi K, Misaki T, Iida Y, Konishi J. A patient
with two thyroid papillary carcinomas demonstrating
hot and cold lesions on 113I thyroid scintigraphy. Ann
Nucl Med. 2002;16(5):355–8.
78. Rubenfeld S, Wheeler TM. Thyroid cancer presenting as
a hot thyroid nodule: report of a case and review of the
literature. Thyroidology. 1988(1):63–8.
79. Sarkar SD. Benign thyroid disease: what is the role of
nuclear medicine? Semin Nucl Med. 2006;36(3):185–93.
80. Sandler MP, Patton JA, Sacks GA, Shaff MI, Kulkarni
MV, Partain CL. Evaluation of intrathoracic goiter with
I-123 scintigraphy and nuclear magnetic resonanceimaging. J Nucl Med. 1984;25(8):874–6.
81. Park HM, Perkins OW, Edmondson JW, Schnute RB,
Manatunga A. Influence of diagnostic radioiodines on
the uptake of ablative dose of iodine-131. Thyroid.
1994;4(1):49–54.
82. Gerard SK, Cavalieri RR. I-123 diagnosticthyroid tumor
whole-body scanning with imaging at 6, 24, and 48
hours. Clin Nucl Med. 2002;27(1):1–8.
83. Park HM, Park YH, Zhou XH. Detection of thyroid
remnant/metastasis without stunning: an ongoing
dilemma. Thyroid. 1997;7(2):277–80.
84. Park H, Gerard SK. Stunning: untoward effect of 131I
thyroid imaging prior to radioablation therapy.In: Wartofsky L, Van Nostrand D, editors. Thyroid Cancer: a
Comprehensive Guide to Clinical Management. Totowa,
NJ: Humana Press; 2006:337–45.
85. Schlumberger M, Pacini F. Epidemiology. In: Thyroid
Tumors, 2nd ed. Paris: Nucleon; 2003. 165–80.
86. Schlumberger M, Pacini F, editors., Epidemiology. In:
Thyroid Tumors. Paris: Nucleon; 2003. 128–46.
87. Mazzaferri EL, Robbins RJ, Spencer CA, etal.A consensus
report of the role of serum thyroglobulin as a monitoring
method for low-risk patients with papillary thyroid carcinoma. J Clin Endocrinol Metab. 2003;88(4):1433–41.
88. Torrens JI, Burch HB. Serum thyroglobulin measurement. Utility in clinical practice. Endocrinol Metab
Clin North Am. 2001;30(2):429–67.
89. Sherman SI, Tielens ET, Sostre S, Wharam MD, Jr.,
Ladenson PW. Clinical utility of posttreatment radioiodine scans in the management ofpatients with thyroid
carcinoma. J Clin Endocrinol Metab. 1994;78(3):629–34.
90. Pacini F, Lippi F, Formica N, et al. Therapeutic doses of
iodine-131 reveal undiagnosed metastases in thyroid
cancer patients with detectable serum thyroglobulin
levels. J Nucl Med. 1987;28(12):1888–91.
91. Pineda JD, Lee T, Ain K, ReynoldsJC, Robbins J. Iodine131 therapy for thyroid cancer patients with elevated
thyroglobulin and negative diagnosticscan. JClin Endocrinol Metab. 1995;80(5):1488–92.
92. Vulsma T, DeVijlder JM. Genetic defects causing
hypothyroidism. In: Braverman LE, Utiger RD, editors.
Werner & Ingbar’s the Thyroid: a fundamental and
clinical text, 9th ed. Philadelphia: Lippincott Williams
& Wilkins; 2005. 35–72.
93. Fugazzola L, Persani L, Vannucchi G, et al. Thyroid
scintigraphy and perchlorate test after recombinant
human TSH: a new tool for the differential diagnosis of
congenital hypothyroidism during infancy. Eur J Nucl
Med Mol Imaging. 2007;34(9):1498–503.
94. Schoen EJ, ClappW, ToTT, FiremanBH. The key role of
newborn thyroid scintigraphy with isotopic iodide
(123I) in defining and managing congenital hypothyroidism. Pediatrics. 2004;114(6):e683–8.
95. Chisin R, Macapinlac HA. The indications of FDG-PET
in neck oncology. Radiol Clin North Am. 2000;38(5):
999–1012.
96. Bockisch A, Brandt-Mainz K, Gorges R, Muller S,
Stattaus J, Antoch G. Diagnosis in medullary thyroid
cancer with [18F]FDG-PET and improvement using a
combined PET/CT scanner. Acta Med Austriaca. 2003;
30(1):22–5.
ENDOCRINE SURGERY
68
97. Kresnik E, Gallowitsch HJ, Mikosch P, et al. Fluorine18-fluorodeoxyglucose positron emission tomography
in the preoperative assessmentof thyroidnodules inan
endemic goiter area. Surgery. 2003;133(3):294–9.
98. BloomAD, AdlerLP, ShuckJM.Determination of malignancy of thyroid nodules with positron emission tomography. Surgery. 1993;114(4):728–34; discussion 34–5.
99. Uematsu H, SadatoN, OhtsuboT,et al.Fluorine-18-fluorodeoxyglucose PET versusthallium-201 scintigraphyevaluation of thyroid tumors. J Nucl Med. 1998;39(3):453–9.
100. Mitchell JC, Grant F, Evenson AR, Parker JA, Hasselgren PO, Parangi S. Preoperative evaluation of
thyroid nodules with 18FDG-PET/CT. Surgery. 2005;
138(6):1166–74; discussion 74–5.
101. Sebastianes F, Cerci, JJ, Zanoni, PH, Soares, J Jr, Chibana, LK, Tomimori, EK, de Camargo, RY, Izaki, M,
Giorgi, MC, Eluf-Neto, J, Meneghetti, JC, Pereira, MA.
Role of 18F-fluorodeoxyglucose positron emission
tomography in preoperative assessment of cytologically indeterminate thyroid nodules. J Clin Endocrinol
Metab. 2007;92(11):4485–8.
102. de Geus-Oei L, Pieters, GF, Bonenkamp, JJ, Mudde,
AH, Bleeker-Rovers, CP, Corstens, FH, Oyen, WJ 18FFDG PET reduces unnecessary hemithyroidectomies
for thyroid nodules withinconclusive cytologic results.
J Nucl Med. 2006;47(5):770–5.
103. Kim J, Ryu, JS, Kim, TY, Kim, WB, Kwon, GY, Gong, G,
Moon, DH, Kim, SC, Hong, SJ, Shong, YK. 18F-fluorodeoxyglucose positron emission tomography does
not predict malignancy in thyroid nodules cytologically diagnosed as follicular neoplasm. J Clin Endocrinol Metab. 2007;92(5):1630–4.
104. Sasaki M, Ichiya, Y, Kuwabara, Y, Akashi, Y, Yoshida,
T, Fukumura, T, Masuda,K. Anevaluation of FDG-PET
in the detection and differentiation of thyroid tumours.
Nucl Med Commun. 1997;18(10):957–63.
105. Larson SM, Robbins R. Positron emission tomography
in thyroid cancer management. Semin Roentgenol.
2002;37(2):169–74.
106. Shammas A, Degirmenci, B, Mountz, JM, McCook,BM,
Branstetter, B, Bencherif, B, Joyce, JM, Carty, SE, Kuffner, HA, Avril, N. 18F-FDG PET/CT in patients with
suspected recurrent or metastatic well-differentiated
thyroid cancer. J Nucl Med. 2007;48(2):221–6.
107. Iagaru A, Kalinyak, JE, McDougall, IR. F-18 FDG PET/
CT in the management of thyroid cancer. Clin Nucl
Med. 2007;32(9):690–5.
108. Lind P, Kumnig G, Matschnig S, et al. The role of F18FDG PET in thyroid cancer. Acta Med Austriaca.
2000;27(2):38–41.
109. Loevner LA. Imaging of the thyroid gland. Semin
Ultrasound CT MR. 1996;17(6):539–62.
110. Bashist B, Ellis K, Gold RP. Computed tomography of
intrathoracic goiters. AJR Am J Roentgenol. 1983;
140(3):455–60.
111. Imanishi Y, Ehara N, Mori J, et al. Measurement of
thyroid iodine by CT. J Comput Assist Tomogr. 1991;
15(2):287–90.
112. Imanishi Y,Ehara N, Shinagawa T, etal.Correlation of CT
values, iodine concentration, and histological changes
in the thyroid. J Comput Assist Tomogr.
2000;24(2):322–6.
113. Jennings A. Evaluation of substernal goiters using
computed tomography and MR imaging. Endocrinol
Metab Clin North Am. 2001;30(2):401–14, ix.
114. Glazer GM, Axel L, Moss AA. CT diagnosis of mediastinal thyroid. AJR Am J Roentgenol. 1982;138(3):495–8.
115. Schlumberger M, Pacini F, editors. Epidemiology. In:
Thyroid Tumors. Paris: Nucleon; 2003. 181–92.
116. van den Brekel MW. Lymph node metastases: CT and
MRI. Eur J Radiol. 2000;33(3):230–8.
117. Hegedus L., Bennedbaek FN. Nonisotopic techniques
of thyroid imaging. In: Werner & Ingbar’s the Thyroid:
a fundamental and clinical text, 9th ed. Philadelphia:
Lippincott Williams & Wilkins; 2005:373–83.
118. Kim HC, Han MH, Kim KH, et al. Primary thyroid
lymphoma: CT findings. Eur J Radiol. 2003;46(3):
233–9.
5
Multinodular Goiter
Abdullah N. Hisham
Introduction
Goiter is a general definition of any enlargement
of the thyroid gland; multinodular goiter is the
name given where multiple nodular enlargements have developed within the thyroid
gland. David Marine was the first to postulate
the formation of multinodular goiter, which is
caused by inadequate production of thyroid
hormones coupled with the increase in thyroid-stimulating hormone (TSH) response. This
led to the initial phase of hyperplastic changes
in the thyroid gland. Subsequently, when there
is iodide repletion or decreased requirement of
thyroid hormone, the thyroid gland responded
into a resting phase of colloid storage. It is the
repetition of these two phases of the cycle that
would eventually lead to formation of multinodular goiter [1]. Selwyn Taylor supported this
concept and believed that the initial formation
is diffuse thyroid hyperplasia, but with time
discrete nodules develop [2].
Multinodular goiter is the most common
thyroid disorder worldwide. The prevalence of
multinodular goiter varies according to geographical regions; it is estimated that 4–5% of the
normal female population over the age of 50 has
a palpable multinodular goiter [3]. The prevalence is much higher when ultrasonography is
used to detect multinodular goiter [4]. Multinodular goiter may be endemic or sporadic in
origin. Endemic goiters are mainly attributed to
iodine deficiency in the dietary intake and lack
of exogenous iodine supplementation. By and
large, in iodine-sufficient countries the prevalence of goiter is not higher than 4% [5]. On the
other hand, the prevalence of endemic goiter is
much higher in iodine-deficient countries, estimated to be 15% in mild and 22.6% in moderate
iodine-deficient regions. The increase in the size
of goiter is in parallel with the severity of iodine
deficiency [6]. Overall it has been estimated that
over 12% of the world’s population live in
iodine-deficient regions. In Malaysia at least
7% of the population is at risk of developing
endemic goiter, particularly aborigines and
Malays in remote inland areas and natives living
in Borneo (in Sabah and Sarawak) away from
the seacoast [7].
On the other hand, sporadic goiters may be
attributed to the endogenous factors and defect
in thyroid hormone synthesis. Goitrogenic
substances in the diet and certain medications
such as lithium, sulfonamides, and aminoglutethimide have been implicated to cause a prolonged fall in serum T4 levels, which led to the
feedback response of high TSH levels to the
thyroid glands [8]. Both endemic and sporadic
goiters are caused by increased TSH response
due to low thyroid hormone production.
Sporadic goiter, which is also known as nonendemic goiter or colloid goiter, occurs in about
5% of population for which there is no apparent cause found. It was earlier hypothesized
that sporadic goiter was due to prolonged
J.G.H. Hubbard et al. (eds.), Endocrine Surgery, Springer Specialist Surgery Series,
DOI 10.1007/978-1-84628-881-4_5, Springer-Verlag London Limited 2009
69