(Radiographics. 1999;19:601-614.)
© RSNA, 1999
Parathyroid Imaging with Tc-99m Sestamibi Planar and SPECT Scintigraphy1
Ba D. Nguyen, MD
1 From the Department of Radiology, Mayo Clinic Scottsdale, 13400 E Shea Blvd, Scottsdale, AZ 85259. Presented as a scientific exhibit at the 1997 RSNA scientific assembly. Received June 17, 1998; revision requested July 13 and received September 11; accepted September 14. Address reprint requests to the author.
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Abstract
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Technetium-99m sestamibi planar and single-photon-emission computed tomographic scintigraphy is useful in the diagnosis of parathyroid gland disease. To understand the various patterns of parathyroid disease, it is important to understand parathyroid embryology and anatomy. The spectrum of parathyroid disease demonstrated with Tc-99m sestamibi scintigraphy includes eutopic disease, ectopic disease, solitary adenoma, double or multiple adenomas, cystic adenoma, lipoadenoma, multiple endocrine neoplasia, hyperfunctioning parathyroid transplant, entities with atypical washout, and nonparathyroid entities that take up Tc-99m sestamibi. The diagnosis of parathyroid tumors with Tc-99m sestamibi scintigraphy is based on the difference in clearance rates between the thyroid and diseased parathyroid glands, and any condition that interferes with radiotracer clearance will limit the effectiveness of the study. The technique is most clearly indicated for the preoperative evaluation of recurrent or persistent hyperparathyroidism, but it is increasingly being used before the initial surgical exploration as well. Subtraction Tc-99m sestamibi and iodine-123 scintigraphy may be helpful in difficult cases. Parathyroid hyperplasia, multisite parathyroid disease, and concomitant thyroid and parathyroid disease remain potential hurdles for this scintigraphic technique, and optimal handling of these problems still relies heavily on the skill and experience of the endocrine surgeon.
Index Terms: Parathyroid, hyperparathyroidism, 274.531 • Parathyroid, neoplasms, 274.363 • Parathyroid, radionuclide studies, 274.12175
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INTRODUCTION
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Sestamibi is a cationic, lipophilic isonitrile derivative that was first used for myocardial scintigraphy. The usefulness of sestamibi in imaging the parathyroid gland and the time-related differential clearance of the thyroid-parathyroid tumor complex make dual-phase technetium-99m sestamibi scintigraphy an effective noninvasive modality for imaging hyperparathyroidism.
In this article, different facets of parathyroid disease are reviewed, including parathyroid embryology and anatomy, clinical features of hyperparathyroidism, and surgical treatment of hyperparathyroidism. Imaging of parathyroid disease is also discussed along with the most recent trends and the effect on treatment. Finally, the spectrum of parathyroid disease demonstrated with Tc-99m sestamibi scintigraphy is presented.
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PARATHYROID EMBRYOLOGY AND ANATOMY
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The organogenesis of the parathyroids determines the definitive location in adulthood. Familiarity with the formation and migration of these glands is necessary if one is to understand the different patterns of parathyroid disease. Parathyroid IV, or the superior parathyroid, derives from the dorsal portions of the fourth pharyngeal pouch. Parathyroid III, or the inferior parathyroid, and the thymus arise from the third pharyngeal pouch complex. Parathyroid III and the thymus migrate caudally with parathyroid III located inferior to the less mobile parathyroid IV. The thymus reaches the normal mediastinal location behind the manubrium of the sternum (1–3).
The normal position of the superior parathyroids is at the cricothyroid junction, above the anatomic demarcation of the inferior thyroid artery and the recurrent laryngeal nerve (1–3). The inferior parathyroids are more widely distributed with most of them anterolateral or posterolateral to the lower thyroid gland (2). Aberrant migration of parathyroid III may expand the potential site from the upper neck to the mediastinum. A normal parathyroid has average dimensions of 5 x 3 x 1 mm and an average weight of 30–40 mg (1,2). The color is reddish brown in young adults and yellowish tan in older patients. Among healthy adults, 80%–97% have four parathyroids (2), approximately 5% have fewer than four glands, and 3%–13% have supernumerary glands (2).
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CLINICAL FEATURES OF HYPERPARATHYROIDISM
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Hyperparathyroidism can be primary, secondary, or tertiary. Primary hyperparathyroidism is of unknown origin and has a sporadic prevalence of 0.2% among women over the age of 40 years and 0.05% among men (4). Approximately 100,000 new cases of primary hyperparathyroidism are detected annually in the United States (5). Eighty percent of patients with primary hyperparathyroidism have a solitary adenoma. Multiple adenomas occur in 3%–5% of cases, and parathyroid hyperplasia occurs in 15%. In addition, a hyperfunctioning parathyroid may have a familial origin, as in multiple endocrine neoplasia (MEN), or be secondary to metabolic disorders such as chronic renal insufficiency. Only about 1% of cases of hyperparathyroidism are related to parathyroid carcinoma (4).
Clinical symptoms include fatigue, weakness, depression, polydipsia, and polyuria (4). Common associated skeletal, renal, or abdominal manifestations are osteoporosis, osteitis fibrosa cystica, renal lithiasis, nephrocalcinosis, peptic ulcer disease, and pancreatitis (5). Elevated serum ionized calcium and parathyroid hormone levels are key laboratory findings in the diagnosis of hyperparathyroidism (4,6).
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SURGICAL TREATMENT OF HYPERPARATHYROIDISM
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Surgery is the most effective treatment for symptomatic hyperparathyroidism. The success rates of experienced endocrine surgeons exceed 95% (3–5,7,8). The recommended approach is bilateral neck exploration with identification of all of the parathyroids (4,6,9). Removal of the tumor is indicated in cases of a solitary parathyroid neoplasm. Subtotal parathyroidectomy is recommended in cases of primary hyperplasia. Bilateral neck exploration is performed in cases of parathyroid disease at multiple sites with excision of the thymus or thyroid to exclude ectopic, supernumerary, and intrathymic or intrathyroid hyperfunctioning parathyroid tissue (4). Total parathyroidectomy and autotransplantation are useful for familial, secondary, recurrent, and persistent hyperparathyroidism. In selected high-risk patients, surgery may be replaced by ablation of the parathyroid tumor with angiographic contrast material or alcohol (4).
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IMAGING OF PARATHYROID DISEASE
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Multiple imaging modalities are available for the detection of parathyroid disease. Selective angiography and venous parathyroid hormone sampling have sensitivities of 60%–85% (5,7). However, these techniques are somewhat too aggressive to be used as the initial imaging approach. Computed tomography (CT) performed with intravenously administered contrast material has a disappointing overall sensitivity of 45%–55% with a slightly better detection rate for mediastinal parathyroid tumors (5,7). Cost-effective ultrasonography (US) demonstrates a wide sensitivity range (36%–76%), which is related to the skill of the sonographer (5,7). In experienced hands, US performed with high-frequency probes and Doppler assessment is an excellent technique for imaging upper cervical parathyroid disease. US is of limited value in detection of mediastinal and tracheoesophageal lesions. Magnetic resonance (MR) imaging with three-dimensional evaluation of the neck and upper chest has an excellent overall sensitivity of 78% (5,7). The sensitivity is higher in the mediastinum (almost 88%), a rate equivalent to that of dual-phase Tc-99m sestamibi scintigraphy (5,10).
An isonitrile derivative first used in myocardial imaging, sestamibi is now used in parathyroid imaging. Tc-99m sestamibi scintigraphy has the following advantages over thallium-technetium subtraction scintigraphy: simplified handling of a single radiotracer, dual-phase acquisition capability, and the capability for three-dimensional assessment with single photon emission computed tomography (SPECT) (8,10,11). Planar and SPECT parathyroid scintigraphy is performed 15–30 minutes and 2–4 hours after intravenous administration of 20–25 mCi (740–925 MBq) of Tc-99m sestamibi (Fig 1) (10). The field of view encompasses the neck and thorax. For planar imaging, anterior, lateral, and oblique views are obtained with a low-energy, high-resolution collimator. Additional pinhole images may be helpful. Dual-phase SPECT acquisition in a 128 x 128 matrix with cine display of the reprojection images appears to be the optimal way to evaluate parathyroid disease (8). Dual-phase Tc-99m sestamibi scintigraphy is based on the time-related differential washout of radioactivity between the thyroid gland and a parathyroid tumor (Fig 2) (10). The characteristic retention of Tc-99m sestamibi within the diseased parathyroid has been attributed to the high metabolic activity and mitochondria-rich oxyphil cell content of the tumor (11,12).
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Figure 1. Healthy subject. Top: Ten-minute scintigrams show normal uptake of Tc-99m sestamibi in the thyroid, submandibular glands, heart, and liver. Bottom: Two-hour scintigrams show normal clearance of sestamibi from the thyroid. There is no focus of radiotracer retention to suggest parathyroid disease. p.i. = post injection.
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Figure 2a. Differential washout between thyroid gland and parathyroid adenoma. (a) Early-phase scintigram shows a focus of increased activity in the middle of the left thyroid lobe (arrow). (b) Two-hour scintigram shows persistence of the focus (arrow), a finding consistent with parathyroid adenoma.
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Figure 2b. Differential washout between thyroid gland and parathyroid adenoma. (a) Early-phase scintigram shows a focus of increased activity in the middle of the left thyroid lobe (arrow). (b) Two-hour scintigram shows persistence of the focus (arrow), a finding consistent with parathyroid adenoma.
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The use of preoperative imaging for first-time parathyroid exploration remains controversial. Because of the high success rate of exploration performed by expert endocrine surgeons, imaging has been considered unnecessary, especially in the context of cost-conscious health care management (7). Improved imaging with dual-phase Tc-99m sestamibi SPECT may change the diagnostic approach to hyperparathyroidism with a potential reduction in surgical time and morbidity (8,13,14). Subtraction Tc-99m sestamibi and iodine-123 scintigraphy may be helpful in difficult cases (15). Preliminary results of positron emission tomography with 2-[fluorine-18]fluoro-2-deoxy-D-glucose appear promising, even though the cost and availability of this technique limit use (16). Consensus has already been achieved on the use of preoperative imaging in the planning of repeat surgery for hyperparathyroidism or in high-risk patients (7,8).
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SPECTRUM OF PARATHYROID DISEASE DEMONSTRATED WITH TC-99M SESTAMIBI SCINTIGRAPHY
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Eutopic Disease
Eutopic parathyroid disease represents 80%–90% of all cases (9). As described in the section on anatomy, there is a relatively fixed location for the superior parathyroids. They are found close to the dorsal aspect of the upper thyroid (1,2). The inferior parathyroids have a more widespread distribution, which is closely related to the migration of the thymus. Most inferior parathyroids are located inferior, posterior, or lateral to the lower thyroid (1,2). They are sometimes adjacent to or surrounded by remnant thymic tissue. The parathyroids may be very close to the thyroid and may be covered by or attached to the thyroid capsule (2). The parathyroids demonstrate a remarkably constant symmetry, which is helpful in the surgical exploration of eutopic disease (2).
Ectopic Disease
There are two types of ectopic parathyroid disease. The first type is due to mechanical factors and is seen with large adenomas of the superior parathyroids (3,9,17). The second type is due to abnormal organogenesis and mainly involves the inferior parathyroids.
The larger a superior parathyroid adenoma is, the more likely it is that it will have an abnormal superoposterior mediastinal position, such as a retropharyngeal, retroesophageal, or paraesophageal site or the tracheoesophageal groove (Fig 3). The right and left superior parathyroids have a similar frequency of ectopia (up to 36%–39%) (9). Intrathyroid superior parathyroid adenomas are rare. Truly ectopic superior parathyroid tumors from undescended parathyroids are exceptional.
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Figure 3a. Parathyroid adenoma in the tracheoesophageal groove. Twenty-minute (a) and 2-hour (b) scintigrams show a focus of activity in the middle of the mediastinum (arrow). The focus appeared to be posterior on the SPECT reprojection image.
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Figure 3b. Parathyroid adenoma in the tracheoesophageal groove. Twenty-minute (a) and 2-hour (b) scintigrams show a focus of activity in the middle of the mediastinum (arrow). The focus appeared to be posterior on the SPECT reprojection image.
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Ectopic inferior parathyroid tissue is a well-established entity responsible for 10%–13% of all cases of hyperparathyroidism (2,9). Such tissue can occur from the angle of the mandible to the mediastinum according to the developmental and migratory aberrations. Rare sites include the carotid sheath (Fig 4), vagus nerve, thyroid (Fig 5), retroesophageal region (Fig 6), thymus (Fig 7), thyrothymic ligament (Fig 8), mediastinum, aortopulmonary window, and pericardium (Fig 9) (3,5,9,18). When routine exploration for parathyroid disease yields inconclusive results, a thorough search must be conducted along the line of descent of the inferior parathyroids with possible excision of the thymus and thyroid.
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Figure 6a. Retroesophageal parathyroid adenoma. (a) Delayed scintigram shows a focus of uptake just superior and to the left of the suprasternal notch (arrow). (b) Left lateral SPECT image shows that the focus has a middle to posterior location (arrow).
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Figure 6b. Retroesophageal parathyroid adenoma. (a) Delayed scintigram shows a focus of uptake just superior and to the left of the suprasternal notch (arrow). (b) Left lateral SPECT image shows that the focus has a middle to posterior location (arrow).
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Figure 7a. Intrathymic parathyroid adenoma. (a) Delayed-phase scintigram shows an elongated focus of uptake in the left substernal region (arrow). (b) Left lateral SPECT image of another patient shows an abnormal focus of activity in the right mediastinum (arrow).
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Figure 7b. Intrathymic parathyroid adenoma. (a) Delayed-phase scintigram shows an elongated focus of uptake in the left substernal region (arrow). (b) Left lateral SPECT image of another patient shows an abnormal focus of activity in the right mediastinum (arrow).
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Figure 8a. Parathyroid adenoma within the thyrothymic ligament. (a) Delayed scintigram shows a questionable focus of activity inferior to the inferior pole of the left thyroid lobe (arrow). (b) Left lateral SPECT image shows the lesion (arrow).
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Figure 8b. Parathyroid adenoma within the thyrothymic ligament. (a) Delayed scintigram shows a questionable focus of activity inferior to the inferior pole of the left thyroid lobe (arrow). (b) Left lateral SPECT image shows the lesion (arrow).
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Figure 9. Mediastinal parathyroid adenoma attached to the upper aspect of the pericardium. Early-phase scintigram shows a left mediastinal lesion (arrow), which was nearly overlooked due to the restricted field of view.
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Solitary Adenoma
A solitary adenoma is found in 80%–85% of patients with hyperparathyroidism (2). There is no significant predominance in location among the four parathyroids with each responsible for approximately 25% of all adenomas (9). Small adenomas weighing less than 100 mg are less likely than larger ones to be demonstrated with Tc-99m sestamibi scintigraphy (16).
Double or Multiple Adenomas
Double adenomas occur in up to 11.8% of cases of primary hyperparathyroidism (Fig 10) (19,20). Double adenomas are bilateral in 55%–88% of cases and are seen mainly in patients beyond the 6th decade of life. These patients present with more prominent symptoms than those with a solitary parathyroid adenoma or hyperplasia and usually have higher parathyroid hormone and alkaline phosphatase levels than patients with single-site parathyroid disease. However, clinical symptoms and laboratory values do not enable the diagnosis of double adenoma. Preoperative detection of double or multiple adenomas with any imaging modality is not reliable (4). Tc-99m sestamibi scintigraphy has a sensitivity of up to 37% for detection of multisite disease (Fig 11) (15,21).
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Figure 11. Multisite parathyroid disease. Delayed-phase scintigram shows mediastinal parathyroid hyperplasia (arrow). In addition to this lesion, four eutopic sites of parathyroid hyperplasia not seen with Tc-99m sestamibi scintigraphy were found at surgery.
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Cystic Adenoma
Parathyroid cysts may be of two types. The first type, termed a true cyst, is due to embryologic vestiges of the third and fourth pharyngeal pouches or enlargement of microcysts within the parathyroid as a manifestation of colloid retention (22,23). Most true cysts are asymptomatic and may simulate "cold" thyroid nodules at scintigraphy. The second type of parathyroid cyst is frequently associated with hyperparathyroidism. These lesions are thought to represent central necrosis or cystic degeneration of adenomas (Fig 12) and account for less than 9% of all parathyroid adenomas (23).
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Figure 12. Cystic parathyroid adenoma in a patient with multinodular goiter. Delayed-phase scintigram shows a focal defect (arrow) in the inferior aspect of an enlarged right thyroid lobe. The focal defect represented cystic degeneration of a right inferior parathyroid adenoma.
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Lipoadenoma
Parathyroid lipoadenoma is a rare entity that occurs in patients beyond the 4th decade of life (24). It is composed of hyperfunctioning parathyroid tissue and fatty stroma (24,25). There is no gender predilection and no difference in terms of symptoms between this condition and typical parathyroid adenoma. Parathyroid lipoadenoma is sometimes demonstrated on the basis of the space-occupying appearance at scintigraphy (Fig 10). The target-to-background signal ratio may be low due to the high adipose content of the tumor (24).
Multiple Endocrine Neoplasia
MEN is a hereditary syndrome that involves hyperfunctioning of two or more endocrine organs. Primary hyperparathyroidism, pancreatic endocrine tumors, and anterior pituitary gland neoplasms characterize type 1 MEN, an autosomal dominant disorder with a prevalence of 0.02–0.2 cases per 1,000 persons (26–28). The causative genes, yet to be identified, are located on chromosome 11q13 (27,28). Primary hyperparathyroidism is the most common manifestation with onset in the 2nd decade of life followed by pancreatic islet cell tumors (Fig 13) and involvement of the pituitary gland (26–29). The hyperparathyroidism is multiglandular with an asynchronous and steadily progressive course (28,29). There is a high frequency of carcinoid tumors of foregut origin with male predominance for thymic involvement and female predominance for bronchial lesions (27,30). Type 1 MEN has a potentially lethal outcome with hemorrhagic peptic ulcer disease and metastatic pancreatic neoplasms (27). Treatment of hyperparathyroidism due to type 1 MEN is surgical with an exhaustive search for all possible diseased glands, including supernumerary and ectopic parathyroids (4,26,28,29). Subtotal parathyroidectomy or total parathyroidectomy with autotransplantation are indicated (28,29). Combined Tc-99m sestamibi and indium-111 pentetreotide scintigraphy is helpful in assessment of type 1 MEN (Fig 14).
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Figure 13a. Type 1 MEN. (a) Delayed-phase scintigram shows a right inferior parathyroid adenoma (arrow). (b) Fast spin-echo T2-weighted MR image (4,000/117) shows an islet cell tumor of the pancreas (arrow).
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Figure 13b. Type 1 MEN. (a) Delayed-phase scintigram shows a right inferior parathyroid adenoma (arrow). (b) Fast spin-echo T2-weighted MR image (4,000/117) shows an islet cell tumor of the pancreas (arrow).
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Figure 14a. Type 1 MEN. (a) Delayed-phase scintigram shows multiple sites of parathyroid disease with mediastinal involvement (arrow). (b) In-111 pentetreotide anterior reprojection SPECT image shows an islet cell tumor of the pancreas (open arrow) and a carcinoid tumor of the duodenum (solid arrow).
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Figure 14b. Type 1 MEN. (a) Delayed-phase scintigram shows multiple sites of parathyroid disease with mediastinal involvement (arrow). (b) In-111 pentetreotide anterior reprojection SPECT image shows an islet cell tumor of the pancreas (open arrow) and a carcinoid tumor of the duodenum (solid arrow).
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Type 2A MEN is also an autosomal dominant disorder and is characterized by pheochromocytoma, medullary thyroid carcinoma, and hyperparathyroidism (26). The parathyroid disease in type 2A MEN is also multiglandular but has a later onset, less severe effects at clinical evaluation and surgery, and a lower morbidity (26,28,29).
Hyperfunctioning Parathyroid Transplant
Autotransplantation of parathyroid tissue into the sternocleidomastoid muscle or into the brachioradial muscle or flexor muscle group of the forearm is performed in association with total parathyroidectomy in cases of recurrent, persistent type 1 MEN and symptomatic secondary hyperparathyroidism (29). After total parathyroidectomy, the most normal glands, usually one or two, are chosen for the graft. They are diced into small pieces approximately 1–2 x 1 x 1 mm with each fragment placed in an individual bed beneath the muscle sheath and between muscle fibers (29,31). The graft consists of a cluster of 10–25 parathyroid fragments. The remainder of the healthy gland (or glands) is cryopreserved for potential retransplantation (4,29,31). A graft site in the forearm is preferred for accessibility for laboratory work-up of parathyroid hormone levels and surgical reexploration in cases of recurrent hyperparathyroidism (29). The graft may be functional 8–9 days after surgery.
Recurrent hyperparathyroidism after autografting of parathyroid tissue occurs in approximately 14% of cases (32). A hyperfunctioning transplant is a possible cause as is residual or ectopic diseased parathyroid tissue. A hyperfunctioning autograft in the forearm is easily demonstrated with Doppler US or Tc-99m sestamibi scintigraphy (Fig 15) (17,29).
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Figure 15. Hyperfunctioning parathyroid autograft in a patient with recurrent hyperparathyroidism. Scintigram of the right forearm shows hypervascularity as activity within the vessels of the extremity (arrow). The radiotracer was injected into the opposite upper extremity.
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Entities with Atypical Washout
The diagnosis of parathyroid tumor with Tc-99m sestamibi scintigraphy is based on the differential washout rate between the thyroid and diseased parathyroids. Any interference with radiotracer clearance will limit the efficacy of detection of parathyroid disease with dual-phase Tc-99m sestamibi scintigraphy.
Early washout is frequently seen in parathyroid hyperplasia; the detection rate for this entity is approximately half of that for parathyroid adenoma (17). Scintigraphy performs worse in cases of multisite hyperplasia, in which only the most prominent radiotracer-avid gland is visualized. In addition, rapid washout from a parathyroid adenoma has been attributed, without unanimous confirmation, to the histologic composition of the adenoma (Fig 16) (21,33). A delay in radiotracer clearance from the thyroid parenchyma makes dual-phase scintigraphic assessment difficult. Tc-99m sestamibi could be retained in thyroid diseases such as multinodular goiter (Fig 17), Hashimoto thyroiditis (Fig 18), thyroid adenoma, and thyroid carcinoma owing to the hypermetabolic characteristics of these diseases (10,15,17,34). Changes in the imaging protocol with additional interval scanning between the standard 15-minute and 2–4-hour acquisitions may be helpful in demonstrating rapid washout. Extended delayed-phase imaging in combination with in-depth clinical examination may be useful in diagnosis of concomitant thyroid and parathyroid disease (Fig 19) (34).
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Figure 16a. Parathyroid adenoma with rapid clearance of Tc-99m sestamibi. (a) Early-phase scintigram shows a possible lesion within the inferior region of the left thyroid lobe (arrow). (b) Delayed-phase scintigram shows no focus of persistent activity.
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Figure 16b. Parathyroid adenoma with rapid clearance of Tc-99m sestamibi. (a) Early-phase scintigram shows a possible lesion within the inferior region of the left thyroid lobe (arrow). (b) Delayed-phase scintigram shows no focus of persistent activity.
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Figure 18. Hashimoto thyroiditis. Delayed-phase scintigram shows diffuse retention of the radiotracer. The focus of increased activity in the medial aspect of the right thyroid lobe is a parathyroid adenoma (solid arrow). The focal defect in the lateral aspect of the left thyroid lobe is a papillary thyroid carcinoma (open arrow).
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Figure 19a. Parathyroid adenoma in a patient with multinodular goiter. (a) Early-phase scintigram shows a probable lesion of the right superior parathyroid (arrow). (b) Extended delayed-phase scintigram shows clearance of Tc-99m sestamibi from the thyroid and persistent activity in the right superior parathyroid (arrow).
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Figure 19b. Parathyroid adenoma in a patient with multinodular goiter. (a) Early-phase scintigram shows a probable lesion of the right superior parathyroid (arrow). (b) Extended delayed-phase scintigram shows clearance of Tc-99m sestamibi from the thyroid and persistent activity in the right superior parathyroid (arrow).
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Nonparathyroid Entities That Take up Tc-99m Sestamibi
Any focus of incidental Tc-99m sestamibi uptake may be mistaken for parathyroid disease, especially when the site of such uptake is within the pathway of descent of the parathyroid in patients with recurrent or persistent hyperparathyroidism. Tc-99m sestamibi can become indiscriminately fixed in normal and pathologic cervical, supraclavicular, and axillary lymph nodes (15). A hyperplastic thymus may be confused with an intrathymic or mediastinal parathyroid adenoma (Fig 20) (35). Diffuse or focal soft-tissue uptake in the thorax from a sarcoid or carcinoid tumor may complicate the evaluation of parathyroid disease (17,36).
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Figure 20. Hyperplastic thymus. Delayed-phase scintigram shows a left inferior parathyroid adenoma (solid arrow) and a mediastinal focus of increased activity (open arrow), which was shown to represent thymic hyperplasia at surgery.
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CONCLUSIONS
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Dual-phase Tc-99m sestamibi SPECT scintigraphy is an excellent modality for imaging parathyroid adenoma. This technique may be supplemented with subtraction Tc-99m sestamibi and I-123 scintigraphy or positron emission tomography in difficult cases. The role of Tc-99m sestamibi scintigraphy in preoperative evaluation of recurrent or persistent hyperparathyroidism is unanimously established. There is increasing acceptance among endocrine surgeons of the use of Tc-99m sestamibi scintigraphy in the planning of first-time parathyroid exploration. Parathyroid hyperplasia, multisite parathyroid disease, and concomitant thyroid and parathyroid disease remain potential hurdles for this scintigraphic technique, and optimal handling of these problems still relies heavily on the skill and experience of the endocrine surgeon.
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Footnotes
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See the commentary by Kotlyarov
following this article.
Abbreviations: MEN = multiple endocrine neoplasia
SPECT = single photon emission computed tomography
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References
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-
Wang CA. The anatomic basis of parathyroid surgery. Ann Surg 1976; 183:271-275.[Medline]
-
Akerstrom G, Malmaeus J, Bergstrom R. Surgical anatomy of human parathyroid glands. Surgery 1984; 95:15-21.
-
Simeone DM, Sandelin K, Thompson NW. Undescended superior parathyroid gland: a potential cause of failed cervical exploration for hyperparathyroidism. Surgery 1995; 118:949-956.[Medline]
-
Clark OH, Duh QY. Primary hyperparathyroidism: a surgical perspective. Endocrinol Metab Clin North Am 1989; 18:701-714.[Medline]
-
Shen W, Duren M, Morita E, et al. Reoperation for persistent or recurrent primary hyperparathyroidism. Arch Surg 1996; 131:861-869.[Abstract]
-
Summers GW. Parathyroid exploration: review of 125 cases. Arch Otolaryngol Head Neck Surg 1991; 117:1237-1241.
-
Mitchell BK, Merrell RC, Kinder BK. Localization studies in patients with hyperparathyroidism. Surg Clin North Am 1995; 75:483-498.[Medline]
-
Udelsman R. Parathyroid imaging: the myth and the reality (editorial). Radiology 1996; 201:317-318.[Free Full Text]
-
Thompson NW, Eckhauser FE, Harness JK. The anatomy of primary hyperparathyroidism. Surgery 1982; 92:814-821.[Medline]
-
Taillefer R, Boucher Y, Potvin C, Lambert R. Detection and localization of parathyroid adenomas in patients with hyperparathyroidism using a single radionuclide imaging procedure with technetium-99m-sestamibi (double-phase study). J Nucl Med 1992; 33:1801-1807.[Abstract/Free Full Text]
-
Coakley AJ, Kettle AG, Wells CP, et al. 99m Tc-sestamibi: a new agent for parathyroid imaging. Nucl Med Commun 1989; 10:791-794.[Medline]
-
Moinuddin M, Whynott C. Ectopic parathyroid adenomas: multi-imaging modalities and its management. Clin Nucl Med 1996; 21:27-32.[Medline]
-
Perez-Monte JE, Brown ML, Shah AN, et al. Parathyroid adenomas: accurate detection and localization with Tc-99m sestamibi SPECT. Radiology 1996; 201:85-91.[Abstract/Free Full Text]
-
Casas AT, Burke GJ, Mansberger AR, Wei JP. Impact of technetium-99m-sestamibi localization on operative time and success of operations for primary hyperparathyroidism. Am Surg 1994; 60:12-17.[Medline]
-
McHenry CR, Lee K, Saadey J, et al. Parathyroid localization with technetium-99m-sestamibi: a prospective evaluation. J Am Coll Surg 1996; 183:25-30.[Medline]
-
Neumann DR, Esselstyn CB, MacIntyre WJ, et al. Comparison of FDG-PET and sestamibi-SPECT in primary hyperparathyroidism. J Nucl Med 1996; 37:1809-1815.[Abstract/Free Full Text]
-
Lee VS, Wilkinson RH, Leight GS, et al. Hyperparathyroidism in high-risk surgical patients: evaluation with double-phase technetium-99m sestamibi imaging. Radiology 1995; 197:627-633.[Abstract/Free Full Text]
-
Doppman JL, Skarulis MC, Chen CC, et al. Parathyroid adenomas in the aortopulmonary window. Radiology 1996; 201:456-462.[Abstract/Free Full Text]
-
Tezelman S, Shen W, Shaver JK, et al. Double parathyroid adenomas: clinical and biochemical characteristics before and after parathyroidectomy. Ann Surg 1993; 218:300-309.[Medline]
-
Bartsch D, Nies C, Hasse C, et al. Clinical and surgical aspects of double adenoma in patients with primary hyperparathyroidism. Br J Surg 1995; 82:926-929.[Medline]
-
Bergenfelz A, Tennvall J, Valdermarsson S, et al. Sestamibi versus thallium subtraction scintigraphy in parathyroid localization: a prospective comparative study in patients with predominantly mild primary hyperparathyroidism. Surgery 1997; 121:601-605.[Medline]
-
Fallon MD, Haines JW, Teitelbaum SL. Cystic parathyroid gland hyperplasia-hyperparathyroidism presenting as a neck mass. Am J Clin Pathol 1982; 77:104-107.[Medline]
-
Rogers LA, Fetter BF, Peete WPJ. Parathyroid cyst and cystic degeneration of parathyroid adenoma. Arch Pathol 1969; 88:476-479.[Medline]
-
Turner WJD, Baergen RN, Pellitteri PK, Orloff LA. Parathyroid lipoadenoma: case report and review of the literature. Otolaryngol Head Neck Surg 1996; 114:313-316.[Medline]
-
van Hoeven KH, Brennan MF. Lipothymoadenoma of the parathyroid. Arch Pathol Lab Med 1993; 117:312-314.[Medline]
-
Fitzpatrick LA. Hypercalcemia in the multiple endocrine neoplasia syndromes. Endocrinol Metab Clin North Am 1989; 18:741-752.[Medline]
-
Skogseid B, Rastad J, Oberg K. Multiple endocrine neoplasia type 1. Endocrinol Metab Clin North Am 1994; 23:1-17.[Medline]
-
Herfarth KK, Wells SA. Parathyroid glands and the multiple endocrine neoplasia syndromes and familial hypocalciuric hypercalcemia. Semin Surg Oncol 1997; 13:114-124.[Medline]
-
Mallette LE. Management of hyperparathyroidism in multiple endocrine neoplasia syndromes and other familial endocrinopathies. Endocrinol Metab Clin North Am 1994; 23:19-36.[Medline]
-
Duh QY, Hybarger CP, Geist R, et al. Carcinoids associated with multiple endocrine neoplasia syndromes. Am J Surg 1987; 154:142-148.[Medline]
-
Kilgore EJ, Teigen EL, Cowan RJ. Imaging of transplanted parathyroid tissue in a patient with recurrent hyperparathyroidism. Clin Nucl Med 1996; 21:383-386.[Medline]
-
Chen CC, Premkumar A, Hill SC, et al. Tc-99m sestamibi imaging of a hyperfunctioning parathyroid autograft with Doppler ultrasound and MRI correlation. Clin Nucl Med 1995; 20:222-225.[Medline]
-
Benard F, Lefebvre B, Beuvon F, et al. Rapid washout of technetium-99m-sestamibi from a large parathyroid adenoma. J Nucl Med 1995; 36:241-243.[Abstract/Free Full Text]
-
Caixas A, Berna LB, Hernandez A, et al. Efficacy of preoperative diagnostic imaging localization of technetium 99m-sestamibi scintigraphy in hyperparathyroidism. Surgery 1997; 121:535-541.[Medline]
-
Mudun A, Kocak M, Unal S, Cantez S. Tc-99m MIBI accumulation in remnant thymus: a cause of false-positive interpretation in parathyroid imaging. Clin Nucl Med 1995; 20:379-380.[Medline]
-
Desai S, Yuille DL. Visualization of a recurrent carcinoid tumor and an occult distant metastasis by technetium-99m-sestamibi. J Nucl Med 1993; 34:1748-1750.[Abstract/Free Full Text]
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Abstract
INTRODUCTION
