eMedicine Specialties > Radiology > Musculoskeletal
Hyperparathyroidism, Primary: Imaging
Updated: Jan 24, 2008
Radiography
Findings
Hyperparathyroidism is a disease of increased bone resorption and bone formation. Subsequently, plain radiographic findings may include resorption and sclerosis of numerous sites in the skeletal system.
Historically, osteitis fibrosa cystica was used to describe the advanced skeletal disease in primary hyperparathyroidism. Bone findings were characterized by the osteoclastic resorption of bone, osteoblastic bone formation, and fibrous replacement of marrow, with radiographic findings of subperiosteal resorption, brown tumors, bone cysts, and sclerosis.
These days, the most common radiologic finding in primary hyperparathyroidism is osteopenia, which may be generalized or asymmetric (see Image 1). Fine trabeculations are initially lost, with resultant coarse and thickened trabeculae. The disease may progress with further destruction that results in a ground-glass appearance in the trabeculae. About 30-50% of the bone density must be lost to show changes on radiographs. Other methods for the quantification of bone density, such as QCT scanning and DXA, are more sensitive in the evaluation of osteopenia.
Additional findings include bone resorption, which may occur at many different anatomic sites. Bone resorption may be classified as subperiosteal, intracortical, trabecular, endosteal, subchondral, subligamentous, or subtendinous. Subperiosteal bone resorption is an early and virtually pathognomonic sign of hyperparathyroidism, and this finding is marked by marginal erosions with adjacent resorption of bone and sclerosis. An unusual lacelike appearance may be seen beneath the periosteum with an occasional spiculated external cortex. The underlying resorptive process may progress to complete cortical disappearance. Although subperiosteal bone resorption can affect many sites, the most common site in hyperparathyroidism is the middle phalanges of the index and middle fingers, primarily on the radial aspect (see Images 2-3).
Other sites of subperiosteal resorption include the phalangeal tufts (acro-osteolysis) (see Images 4 and 23), the lamina dura around the teeth, the medial aspect of the tibia, the humerus (see Images 5-6), the femur (see Images 10-11), and the distal clavicle (see Images 7-8). When the resorption extends to the margins of joints, particularly in the hands, wrists, and feet, findings may appear articular.
Other areas of resorption, such as cortical or endosteal regions, are usually accompanied by subperiosteal findings. Intracortical bone resorption is an indicator of rapid bone turnover and is described as linearly oriented striations in the cortex. The linear lucencies are produced by resorption of bone in the haversian canals and are best seen on the cortical surface of the second metacarpal.
Trabecular bone resorption may occur throughout the skeleton and usually accompanies advanced disease. In the skull, areas of decreased radiopacity are intermingled with sclerotic radiopaque areas, resulting in a classic appearance called the salt-and-pepper skull (see Image 9).
In endosteal resorption, the medullary cavity widens, with thinning of the inner cortex (see Images 10-11). Changes are usually best seen in the hands and appear as scalloped lucencies on the inner aspect of the bony cortex. Endosteal changes are usually accompanied by subperiosteal or cortical resorption.
Subchondral bone resorption is most common in the joints of the axial skeleton, such as the sacroiliac, acromioclavicular (see Image 12), discovertebral, sternoclavicular, and symphysis pubis, but it may also occur in the joints of the appendicular skeleton. Subchondral bone is resorbed; collapse with subsequent new bone formation and fibrous replacement may result. On radiographs, areas of subchondral lucency are noted with surrounding sclerosis. In the sacroiliac joint, bilateral findings affect the ilium more than the sacrum and may produce an irregular articular margin with the appearance of a widened joint. At the acromioclavicular joint, bilateral erosions affect the clavicle side more than the acromion, whereas the sternum and clavicle are equally affected at the sternoclavicular joint.
Subligamentous and subtendinous resorption occurs at insertion sites on bones. Common sites are the plantar aspect of the calcaneus, dorsal aspect of the patella, inferior margin of the distal clavicle, trochanters, and ischial and humeral tuberosities.
Brown tumors are well-circumscribed lytic lesions of bone that represent the osteoclastic resorption of a confluent area of bone with subsequent fibrous replacement (see Images 13-16). The lesions may be single or multiple, with expansion of overlying bone, and they may be present in any site, although the lesions usually occur in cortical bone. Common sites include the mandible, clavicle, ribs, pelvis, and femur. After resection of an adenoma, lesions may become sclerotic on radiographs. Once considered a finding that was characteristic of primary hyperparathyroidism, brown tumors are more common in secondary hyperparathyroidism because of the increasing population and life expectancy of patients undergoing dialysis.
Calcium pyrophosphate dihydrate crystal deposition disease (CPPD) is more common in association with primary hyperparathyroidism than with secondary hyperparathyroidism. Chondrocalcinosis may affect the menisci of the knee, the triangular cartilage of the wrist, and the symphysis pubis. CPPD arthropathy is less common in these patients than in patients with idiopathic disease.
Other radiographic findings in primary hyperparathyroidism include varying degrees of sclerosis, although generalized sclerosis is more common in secondary hyperparathyroidism. Soft-tissue and vascular calcification is more common in secondary disease, as is superior and inferior band sclerosis of the spine, which is called rugger-jersey spine. The laxity of ligaments and tendons primarily affects the sacroiliac and acromioclavicular joints, whereas rupture may be seen at several sites, including the quadriceps, triceps, and patellar tendons.
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Degree of Confidence
In the setting of elevated serum calcium levels and elevated PTH levels, the diagnosis of primary hyperparathyroidism is certain. However, radiographic findings of subperiosteal resorption are most specific for the disease and should prompt consideration of the primary hyperparathyroidism.
Computed Tomography
Findings
With parathyroid imaging, ectopic adenomas can be assessed by using contrast-enhanced CT scan studies. However, sestamibi and MRI are more sensitive, and these are the imaging studies of choice in most patients.
In musculoskeletal imaging, QCT scanning is another method of bone densitometry. This modality offers the advantage of selective evaluation of the mineral content in trabecular bone, which makes QCT scanning more sensitive in detecting small changes in bone density.
Magnetic Resonance Imaging
Findings
MRI is one diagnostic modality that can be used to evaluate ectopic parathyroid adenomas. On T1-weighted images, adenomas appear as low-signal-intensity masses, whereas intermediate or high signal intensity is seen on T2-weighted images. Gadolinium enhancement with fat suppression results in diffuse enhancement of the adenoma.
Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans.
As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.
MRI findings of brown tumors are nonspecific. Bony expansion can be visualized, and the extent of the lesion can be determined. The imaging characteristics depend on the amount of fibrous tissue, hemorrhage, and cystic changes that are present in the lesion. Lack of an associated soft-tissue mass is a pertinent negative finding that can be demonstrated on MRIs.
Ultrasonography
Findings
Ultrasonography is one of the primary modalities used to localize parathyroid tumors. The size of the adenoma is usually correlated with the degree of parathyroid elevation. Adenomas appear as well-defined hypoechoic lesions with potential cystic or necrotic areas. Ultrasonography offers the advantage of depicting potential concomitant thyroid disease, which is present in approximately 40% of patients with parathyroid disease.
In renal imaging, ultrasonography can demonstrate bilateral hyperechoic medullary pyramids that are consistent with medullary nephrocalcinosis; this is a nonspecific finding (see Image 17).
Degree of Confidence
Ultrasonography is approximately 75% sensitive in identifying adenomas, but this technique has low sensitivity in identifying ectopic lesions.
Nuclear Imaging
Findings
In parathyroid imaging, localization of the parathyroid glands may be accomplished with 99m Tc MIBI scanning (see Image 18). Both thyroid and parathyroid tissues demonstrate radionuclide uptake, but sestamibi washes out of thyroid tissue early after its injection, leaving only parathyroid tissue that demonstrates activity at 2-4 hours.
In musculoskeletal imaging, bone densitometry is extremely valuable in assessing primary hyperparathyroidism because it can be used to quantify bone loss, and it may help making predictions regarding the fracture risk. DXA helps in evaluating the mineral content of all bone in the path of the beam. Bone mineral density is expressed as either a T score, which is based on the standard deviations from a young-adult mean, or as a Z score, which is compared with an age-matched mean. The T score is used to clinically diagnose osteopenia or osteoporosis and to predict the fracture risk. DXA may also be used after an intervention to document improvements in bone density.
The diagnosis of primary hyperparathyroidism is based on biochemical determinations, and bone scanning has a limited role in making the diagnosis. In addition, a few patients with hyperparathyroidism have insufficient disease for its demonstration on bone scans. However, bone scanning may assist in differentiating hyperparathyroidism from metastatic disease in the setting of elevated calcium levels. Because bone turns over significantly in hyperparathyroidism, findings on bone scans include generalized increased radionuclide uptake throughout the skeleton in contrast to soft tissues; this observation is called a superscan. Because the contrast of the skeletal system is increased, renal activity may not be apparent.
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References
Albright F, Aub JC, Bauer W. Hyperparathyroidism, a common and polymorphic condition as illustrated by seventeen proved cases from one clinic. JAMA. 1934;102:1276-87.
Albright F, Reifenstein EC Jr. Clinical hyperparathyroidism. In: Albright F, Reifenstein EC Jr, eds. The Parathyroid Glands and Metabolic Bone Disease: Selected Studies. Baltimore, Md: Williams & Wilkins; 1948:46-134.
Mihai R, Wass JA, Sadler GP. Asymptomatic hyperparathyroidism--need for multicentre studies. Clin Endocrinol (Oxf). Feb 2008;68(2):155-64. [Medline].
Silverberg SJ. Natural history of primary hyperparathyroidism. Endocrinol Metab Clin North Am. Sep 2000;29(3):451-64. [Medline].
Marx SJ. Hyperparathyroid and hypoparathyroid disorders. N Engl J Med. Dec 21 2000;343(25):1863-75. [Medline].
Bringhurst FR, Demay MB, Kronenberg HM. Hormones and disorders of mineral metabolism. In: Williams RH, Foster DW, Kronenberg HM, Larsen PR, eds. Williams Textbook of Endocrinology. 9th ed. Orlando, Fla: Harcourt Brace & Co; 1998:1172-80.
Lenchik L, Sartoris DJ. Orthopedic aspects of metabolic bone disease. Orthop Clin North Am. Jan 1998;29(1):103-34. [Medline].
Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, Pa: WB Saunders Co; 1994:1144-6.
Mankin HJ. Metabolic bone disease. J Bone Joint Surg. 1994;76-A:760-88. [Full Text].
Hayes CW, Conway WF. Hyperparathyroidism. Radiol Clin North Am. Jan 1991;29(1):85-96. [Medline].
Resnick D, Niwayama G. Parathyroid disorders and renal osteodystrophy. In: Resnick D, Niwayama G, eds. Diagnosis of Bone and Joint Disorders. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1988:2219-49.
Genant HK. Quantitative bone mineral analysis. In: Resnick D, Niwayama G, eds. Diagnosis of Bone and Joint Disorders. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1988:2006-17.
Gleason DC, Potchen EJ. The diagnosis of hyperparathyroidism. Radiol Clin North Am. Aug 1967;5(2):277-87. [Medline].
Inoue Y, Kaji H, Hisa I, et al. Vitamin D status affects osteopenia in postmenopausal patients with primary hyperparathyroidism. Endocr J. Jan 10 2008;epub ahead of print. [Medline]. [Full Text].
Moosgaard B, Christensen SE, Vestergaard P, et al. Vitamin D metabolites and skeletal consequences in primary hyperparathyroidism. Clin Endocrinol (Oxf). Jan 8 2008;epub ahead of print. [Medline].
Fogelman I, Cook GJ. Scintigraphy in metabolic bone disease. In: Favus MJ, Goldring SR, Christakos S, eds. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 4th ed. Hagerstown, Md: Lippincott Williams & Wilkins; 1999:150-2.
Jergas MD, Genant HK. Radiology of osteoporosis. In: Favus MJ, Goldring SR, Christakos S, eds. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 4th ed. Hagerstown, Md: Lippincott Williams & Wilkins; 1999:160-5.
Mayo-Smith W, Rosenthal DI. Radiographic appearance of osteopenia. Radiol Clin North Am. Jan 1991;29(1):37-47. [Medline].
Reynolds WA, Karo JJ. Radiologic diagnosis of metabolic bone disease. Orthop Clin North Am. Nov 1972;3(3):521-43. [Medline].
Pugh DG. Subperiosteal resorption of bone; a roentgenologic manifestation of primary hyperparathyroidism and renal osteodystrophy. Am J Roentgenol Radium Ther Nucl Med. Oct 1951;66(4):577-86. [Medline].
Rodgers SE, Lew JI, Solórzano CC. Primary hyperparathyroidism. Curr Opin Oncol. Jan 2008;20(1):52-8. [Medline].
Erbil Y, Kapran Y, Issever H, et al. The positive effect of adenoma weight and oxyphil cell content on preoperative localization with 99mTc-sestamibi scanning for primary hyperparathyroidism. Am J Surg. Jan 2008;195(1):34-9. [Medline].
Gupta Y, Ahmed R, Happerfield L, et al. P-glycoprotein expression is associated with sestamibi washout in primary hyperparathyroidism. Br J Surg. Dec 2007;94(12):1491-5. [Medline].
Carlier T, Oudoux A, Mirallié E, et al. (99m)Tc-MIBI pinhole SPECT in primary hyperparathyroidism: comparison with conventional SPECT, planar scintigraphy and ultrasonography. Eur J Nucl Med Mol Imaging. Oct 25 2007;epub ahead of print. [Medline].
Siegel A, Mancuso M, Seltzer M. The spectrum of positive scan patterns in parathyroid scintigraphy. Clin Nucl Med. Oct 2007;32(10):770-4. [Medline].
Prasannan S, Davies G, Bochner M, Kollias J, Malycha P. Minimally invasive parathyroidectomy using surgeon-performed ultrasound and sestamibi. ANZ J Surg. Sep 2007;77(9):774-7. [Medline].
Gotway MB, Reddy GP, Webb WR, et al. Comparison between MR imaging and 99mTc MIBI scintigraphy in the evaluation of recurrent of persistent hyperparathyroidism. Radiology. Mar 2001;218(3):783-90. [Medline]. [Full Text].
Gritzmann N, Koischwitz D, Rettenbacher T. Sonography of the thyroid and parathyroid glands. Radiol Clin North Am. Sep 2000;38(5):1131-45, xii. [Medline].
Weber AL, Randolph G, Aksoy FG. The thyroid and parathyroid glands. CT and MR imaging and correlation with pathology and clinical findings. Radiol Clin North Am. Sep 2000;38(5):1105-29. [Medline].
Gabbe SG, Neibyl JR, Simpson JL, eds. Obstetrics: Normal and Problem Pregnancies. 3rd ed. London, England: Churchill Livingstone; 1996:1065-8.
Eigelberger MS, Clark OH. Surgical approaches to primary hyperparathyroidism. Endocrinol Metab Clin North Am. Sep 2000;29(3):479-502. [Medline].
Townsend CM Jr, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery: The Biological Basis of Modern Surgical Practice. 16th ed. Philadelphia, Pa: WB Saunders Co; 2001:632-7.
Further Reading
Keywords
von Recklinghausen's disease of bone, von Recklinghausen disease of bone, generalized osteitis fibrosa cystica, PTH, parathyroid glands, multiple endocrine neoplasia syndrome type 1, MEN 1 / MEN-1, brown tumor
