Hyperpara

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Hyperparathyroidism, Primary
Bonnie Freitas, MD, Assistant Professor, Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland
Alex Freitas, MD, Assistant Professor, UCLA Department of Radiology, Assistant Chief of Musculoskeletal Radiology, Renaissance Imaging Medical Associates
Updated: Jan 24, 2008
Introduction
Background
In 1891, von Recklinghausen described the classic bone disease termed osteitis fibrosa cystica. In 1925, the Viennese surgeon Mandl performed the first parathyroid exploration and adenoma resection. Mandl noted improvement
of the patient's severe skeletal abnormalities postoperatively, thereby linking hyperparathyroidism with bone disease. Albright later described the clinical entity of classic primary hyperparathyroidism in the 1930s on the basis of 17
[1 ] [2 ]
cases from his clinical practice. Historically, the disorder was marked by characteristic skeletal changes, nephrolithiasis, and neuromuscular dysfunction.
[3,4,5,6,7,8,9,10,11,12,13 ]
Primary hyperparathyroidism is now a different entity. Since the advent of chemical screening with an autoanalyzer in the 1960s, most cases are discovered in asymptomatic patients with hypercalcemia. Patients
[14,15,16,17,18,19,20 ]
may also present with nonspecific complaints of back pain, or they may have osteopenia, as depicted on radiographic studies. Primary hyperparathyroidism is the most common cause of hypercalcemia in the
[21 ]
outpatient population, and it is second only to malignancy as an etiology of hypercalcemia in the inpatient population. The natural progression of disease in asymptomatic patients is unclear.
For excellent patient education resources, visit eMedicine's Bone, Joint, and Muscle Center, Osteoporosis and Bone Health Center, and Endocrine System Center. Also, see eMedicine's patient education articles Bone Mineral
Density Tests and Vitamin D: Vital Role in Your Health.
Related eMedicine topics:

Hyperparathyroidism, Secondary
Osteoporosis
Related Medscape topics:

Resource Center Chronic Kidney Disease: Mineral and Bone Disorders
Resource Center Osteoporosis
Resource Center Thyroid Disease
CME ASN 2007: Emerging Therapies for Management of Mineral Bone Disorders in Chronic Kidney Disease
CME Expert Interview - The Role of Hyperphosphatemia and Phosphate Binders in Vascular Calcification: An Expert Interview With Keith A. Hruska, MD
Pathophysiology
Normal parathyroid glands function to maintain appropriate serum calcium concentrations and to regulate bone metabolism by means of the production of parathyroid hormone (PTH). In the nonpathologic state, PTH secretion
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Hyperparathyroidism, Primary: [Print] - eMedicine Radiology http://emedicine.medscape.com/article/390728-print
increases in response to low serum calcium concentrations and enhances the synthesis of 1,25-dihydroxyvitamin D. PTH and 1,25-dihydroxyvitamin D act together to increase calcium reabsorption in the gut and kidney and to
promote osteoclastic resorption and the demineralization of bone.
Primary hyperparathyroidism is caused by an overproduction of PTH, in excess of the amount required by the body. In contrast, secondary hyperparathyroidism involves an increase in PTH levels to meet some bodily requirement.
In 75-80% of cases of primary hyperparathyroidism, one or more adenomas account for the overproduction, whereas approximately 20% of cases are secondary to diffuse hyperplasia of all glands. Carcinoma accounts for less
than 2% of all cases.
The effects of hyperparathyroidism on bone are numerous. Excess PTH results in an increase in bone breakdown by means of osteoclastic resorption with subsequent fibrous replacement and reactive osteoblastic activity. The
bone may have microfractures, with subsequent hemorrhage and growth of fibrous tissue and an influx of macrophages. The resulting mass is called a brown tumor because of the brown color of the vascular elements and blood in
the mass. The process of bone resorption and fibrous replacement results in the characteristic radiologic features of generalized bone demineralization, resorption, cysts, brown tumors, erosion of the dental lamina dura, and
pathologic fractures (see Images 13-16).
Other effects of hypercalcemia include nephrolithiasis or nephrocalcinosis, neurologic changes, peptic ulcer disease, and pancreatitis.

Disorders of Bone Mineralization
Hypocalcemia
Pancreatitis, Chronic
Parathyroid Adenoma

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Resource Center Peptic Ulcer Disease
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Frequency
United States
The incidence of primary hyperparathyroidism is approximately 25-30 cases per 100,000 people. In individuals aged 15-65 years, the incidence increases to 70-150 cases per 100,000 people. The disease is rare in children.
International
In Europe, the overall incidence of primary hyperparathyroidism is similar to the incidence in the United States.
Mortality/Morbidity
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There is supportive evidence of an increase in the morbidity and mortality rates in patients with hyperparathyroidism that is primarily related to cardiac disease. This topic is controversial, with the results of some studies refuting the
increased risk. Differences in mortality data may reflect the different clinical profiles of classic primary hyperparathyroidism and the modern asymptomatic cohort of patients. (See also Special Concerns.)
Sex
The incidence of primary hyperparathyroidism in women is 2-3 times the incidence in men.
Age
The average patient age at diagnosis is 55 years.
The incidence peaks in those aged 40-70 years.
The disease is rare in children.
Anatomy
Usually, 4 parathyroid glands develop, although approximately 10% of people may have 2, 3, or 5 parathyroid glands. The superior glands are typically located on the posterior aspect of the upper thyroid, whereas the location of
the inferior glands is more variable. The inferior glands may be posterior to the inferior aspect of the thyroid or ectopically located in the thyroid gland, along the carotid sheath, or attached to the thymus. The superior glands may
also be ectopic and in a retroesophageal, retrotracheal, or retropharyngeal location. Typical parathyroid glands are approximately 5 X 3 X 1 mm.
Related eMedicine topic:

Thyroid Anatomy
Presentation
Historically, in classic primary hyperparathyroidism, nephrolithiasis was noted in 50% of patients, and this condition was the most common clinical presentation of the disease. Currently, stone disease is present in 10-20% of
patients and continues to be the most common complication that is clearly attributable to primary hyperparathyroidism. However, patients typically present without symptoms after routine laboratory testing reveals hypercalcemia.
Patients may also report nonspecific back pain.
Additional manifestations of primary hyperparathyroidism include a wide range of neuromuscular and neuropsychiatric symptoms, pancreatitis, peptic ulcer disease, and cardiovascular abnormalities. Symptomatic bone disease
may be present in 10-25% of patients. The diagnosis is based on an elevated PTH level in the setting of elevated calcium levels. Other chemical alterations that support the diagnosis include hypophosphatemia,
hyperphosphaturia, elevated uric acid levels resulting from tissue destruction, and increased alkaline phosphatase levels resulting from bone formation.
Hereditary hyperparathyroidism is seen in multiple endocrine neoplasia type 1 syndrome (MEN 1) in association with tumors of the anterior pituitary gland and pancreas (see Images 19-22). Hyperparathyroidism develops in 95%
of patients with MEN 1, and hypercalcemia occurs in those aged 10-30 years.
In multiple endocrine neoplasia type 2a syndrome (MEN-2a), parathyroid disease is infrequent and occurs in conjunction with medullary cancer of the thyroid and pheochromocytoma. Two rare hereditary syndromes include an
inherited form of primary hyperparathyroidism that is not associated with other endocrine tumors and a hyperparathyroidism–jaw tumor syndrome. In patients with the latter, fibrous jaw tumors are seen with parathyroid adenomas
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and potentially with thyroid cancer, renal cysts, and Wilms tumors.

Cystic Diseases of the Kidney
Multiple Endocrine Neoplasia, Type 2

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Resource Center Renal Cell Carcinoma
Resource Center Thyroid Disease
Familial Isolated Primary Hyperparathyroidism Caused by Mutations of the MEN1 Gene
Preferred Examination
Parathyroid imaging
To image the parathyroid glands before a repeat operation for recurrent or persistent disease, technetium-99m sestamibi (99m Tc MIBI) scanning or magnetic resonance imaging (MRI) are the preferred imaging modalities because
[22,23,24,25,26,27 ]
of their high sensitivities in depicting ectopic or mediastinal glands.
99m
Tc MIBI imaging has a sensitivity of 70-95% in depicting parathyroid tumors, and this modality allows 3-dimensional (3-D) imaging with anterior-to-posterior localization of the tumor. Studies reveal equal sensitivities of99m Tc MIBI
imaging and MRI in the localization of abnormal glands before a repeat surgery, with sensitivities of 82-85%. By combining the 2 modalities, the sensitivity increases to 94%.
Ultrasonography may be preferred for initial preoperative tumor localization, if desired by the surgeon, because of this technique's low risk, low cost, and high sensitivity in depicting parathyroid glands that are not ectopic or in the
mediastinum.[28,29 ]However, many surgeons believe that the initial 4-gland exploration enables a 95% cure rate with little morbidity and that initial preoperative localization provides no improvement in the outcome. Some surgeons
advocate initial localization to guide directed dissection, obviating bilateral exploration. Opponents argue that the sensitivities of imaging modalities are not sufficient and that parathyroid glands can be missed in an unacceptable
number of patients.
Musculoskeletal imaging
The diagnosis of primary hyperparathyroidism is made by means of the laboratory confirmation of an elevated PTH level in the setting of hypercalcemia.
Radiologically, radiographs may yield the most specific findings that are consistent with the disorder, and radiography is the preferred examination when the clinical findings suggest primary hyperparathyroidism. Radiographs of the
hands may yield the diagnostic finding of subperiosteal resorption, which is virtually pathognomonic for the disease (See Images 2-4 and 23). If radiographs of the hands reveal no abnormalities, other sites are unlikely to
demonstrate abnormal findings. Dual-energy x-ray absorptiometry (DXA) and quantitative CT (QCT) scanning may provide evidence of osteoporosis that is consistent with the diagnosis; however, the finding is nonspecific for
primary hyperparathyroidism.
Limitations of Techniques
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Radiographs of the hand may yield the pathognomonic finding of subperiosteal resorption, which is consistent with a diagnosis of primary hyperparathyroidism. However, other findings on radiographs are not specific for this
disorder. In addition, DXA and QCT scanning are the preferred diagnostic modalities for the evaluation of osteoporosis, which is one of the most common findings in patients with primary hyperparathyroidism. However,
osteoporosis may be associated with a host of other diagnoses; therefore, the specificity of this condition may be limited. Currently, the diagnosis of primary hyperparathyroidism is primarily based on the laboratory confirmation of
elevated PTH concentrations in the setting of an increased calcium level.
Differential Diagnoses
Adamantinoma Osteoblastoma
Ankylosing Spondylitis Osteomalacia and Renal Osteodystrophy
Bone Metastases Osteomyelitis, Acute Pyogenic
Calcium Pyrophosphate Deposition Disease Osteomyelitis, Chronic
Chondroblastoma Osteoporosis, Involutional
Crohn Disease Psoriatic Arthritis
Eosinophilic Granuloma, Skeletal Rheumatoid Arthritis, Hands
Ewing Sarcoma Rheumatoid Arthritis, Spine
Fibrous Dysplasia Rickets
Gout Ulcerative Colitis
Hyperparathyroidism, Secondary
Other Problems to Be Considered
Osteoarthritis, Secondary
Reiter Syndrome, Musculoskeletal
The differential diagnosis depends on which of the many possible findings of primary hyperparathyroidism are being considered and the imaging modality used.
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.
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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.
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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.
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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
99m
In parathyroid imaging, localization of the parathyroid glands may be accomplished with 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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Intervention
Ultrasonography-guided fine-needle aspiration and biopsy are infrequently performed in the setting of recurrent or persistent disease and equivocal imaging findings. The procedure may be used in conjunction with ethanol
ablation as a therapeutic modality, but this is rarely indicated.
Medicolegal Pitfalls
Related Medscape topic:
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Special Concerns
[30 ]
Hyperparathyroidism in pregnancy is associated with increased perinatal morbidity and mortality rates related to hypocalcemic tetany in the newborn.
Hyperparathyroidism is uncommon in women of childbearing age, but in patients who are affected, 15% are associated with neonatal tetany. The incidence of stillbirths and neonatal death is 2%.

Pediatrics/Neonatal Care Nursing
Multimedia
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Media file 1: Radiograph of the proximal tibia and fibula. Diffuse demineralization attributed to trabecular resorption is the most common
plain radiographic sign of primary hyperparathyroidism.
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Media file 2: Bilateral anteroposterior (AP) radiographic views of the hands in a patient with multiple endocrine neoplasia syndrome type 1
(MEN 1) and primary hyperparathyroidism. These images show subperiosteal bone resorption along the radial aspects of the middle
phalanges.
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Media file 3: Anteroposterior radiographic view of the right hand in a patient with multiple endocrine neoplasia syndrome type 1 (MEN 1) and
primary hyperparathyroidism (same patient as in Image 2). This image shows subperiosteal bone resorption along the radial aspects of the
middle phalanges (arrows).
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Media file 4: Radiograph of the middle phalanges in a patient with primary hyperparathyroidism. This image demonstrates subperiosteal
resorption that has resulted in severe tuftal resorption (white arrows). Also, note the subperiosteal and intracortical resorption of the middle
phalanges (black arrows).
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Media file 5: Anteroposterior radiographic view of the left shoulder in external rotation in a patient with primary hyperparathyroidism. This
image shows the healing stage of marked subperiosteal resorption (arrow) of the medial aspect of the proximal humerus.
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Media file 6: Radiograph of the proximal humerus in a patient with primary hyperparathyroidism (same patient as in Image 5). This image
shows the healing stage of marked subperiosteal resorption of the medial aspect of the proximal humerus. A subsequent fracture through
the surgical neck of the humerus is also depicted.
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Media file 7: Radiograph of the shoulder in a patient with primary hyperparathyroidism. This image depicts subperiosteal distal clavicular
resorption (arrows).
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Media file 8: Radiograph of the shoulder in a patient with primary hyperparathyroidism. This image demonstrates distal clavicular resorption.
Media file 9: Anteroposterior radiographic view of the top of the calvarium in a patient with primary hyperparathyroidism. This image shows
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trabecular bone resorption that has resulted in the salt-and-pepper appearance of the calvarium.
Media file 10: Radiograph of the distal femur in a patient with primary hyperparathyroidism. This image shows scalloped defects along the
inner margin of the cortex, which denote endosteal resorption.
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Media file 11: Radiograph of the femur in primary hyperparathyroidism (same patient as in Image 10). This image shows scalloped defects
along the inner margin of the femoral cortex (arrows), which denote endosteal resorption.
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Media file 12: Anteroposterior radiographic view of the clavicles. This image shows symmetric subchondral bone resorption of the
acromioclavicular joints. Distal clavicular resorption can be subperiosteal or subchondral, but this finding is not specific for primary
hyperparathyroidism.
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Media file 13: Radiograph of the humerus in a patient with primary hyperparathyroidism. This image depicts a brown tumor. Note the
osseous expansion and lucency of the proximal humerus. Brown tumors can have varied appearances.
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Media file 14: Radiograph of the mid femoral diaphysis in a patient with primary hyperparathyroidism. This image depicts brown tumors.
Note the eccentric (arrowheads) and central positions (arrow) of the lesions.
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Media file 15: Radiograph of the pelvis in a patient with primary hyperparathyroidism. Note the presence of brown tumors in the pelvis.
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Media file 16: Radiograph of brown tumors of the pelvis in a patient with primary hyperparathyroidism (same patient as in Image 15).
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Media file 17: Sonogram of the kidney in a patient with primary hyperparathyroidism. This image shows medullary nephrocalcinosis.
Media file 18: Technetium-99m sestamibi (99mTc MIBI) images in a patient with primary hyperparathyroidism. The initial (A) and 3.5-hour
delayed (B) images demonstrate a 6-cm parathyroid adenoma (arrows).
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Media file 19: Technetium-99m sestamibi scan (99mTc MIBI) in a patient with multiple endocrine neoplasia syndrome type 1 (MEN 1) (same
patient in Images 19-22). These images demonstrate persistent abnormal activity of the inferior right parathyroid gland that is consistent
with an adenoma.
Media file 20: Sagittal (left image) and coronal (right image) T1-weighted magnetic resonance images of the brain in a patient with multiple
endocrine neoplasia syndrome type 1 (MEN 1) (same patient in Images 19-22). These images show a pituitary macroadenoma (arrows).
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Media file 21: Computed tomography (CT) scan of the pancreas in a patient with multiple endocrine neoplasia syndrome type 1 (MEN 1) and a
gastrinoma (same patient in Images 19-22). This image shows a pancreatic head mass (large white arrow), as well as a low-attenuating
lesion in the liver (small black arrowhead) that indicates metastases. Note the calcifications of the right renal medullary pyramids (medullary
nephrocalcinosis; black arrows) in this nonenhanced CT scan.
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Media file 22: Indium-111 (111In) octreotide scan in a patient with multiple endocrine neoplasia syndrome type 1 (MEN 1) (same patient in
Images 19-22). These nuclear images demonstrate abnormal activity in the pituitary macroadenoma (curved arrow), parathyroid adenoma
(straight arrow), and gastrinoma metastases throughout the abdomen (arrowheads).
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Media file 23: Radiograph of the phalanges in a patient with primary hyperparathyroidism. This image demonstrates subperiosteal resorption
that has resulted in severe tuftal resorption (arrows).
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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
Contributor Information and Disclosures
Author
Bonnie Freitas, M D, Assistant Professor, Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland
Bonnie Freitas, MD is a member of the following medical societies: Alpha Omega Alpha and American College of Physicians-American Society of Internal Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Alex Freitas, MD, Assistant Professor, UCLA Department of Radiology, Assistant Chief of Musculoskeletal Radiology, Renaissance Imaging Medical Associates
Alex Freitas, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Radiology, Radiological Society of North America, and Society of Skeletal Radiology
Medical Editor
Leon Lenchik, MD, Director, Densitometry Minifellowship, Assistant Professor, Department of Radiology, Wake Forest University Medical Center
Leon Lenchik, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, and Radiological Society of North America
31 sur 32 17/03/2011 16:05

Pharmacy Editor
Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Managing Editor
Wilfred CG Peh, MD, MBBS, FRCP(Glasg), FRCP(Edin), FRCR, MHSM, Clinical Professor, Faculty of Medicine, National University of Singapore; Senior Consultant Radiologist, Programme Office, Singapore Health Services
Wilfred CG Peh, MD, MBBS, FRCP(Glasg), FRCP(Edin), FRCR, MHSM is a member of the following medical societies: American Roentgen Ray Society, British Institute of Radiology, International Skeletal Society, Radiological
Society of North America, Royal College of Physicians, and Royal College of Radiologists
CME Editor
Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Chief Editor
Felix S Chew, MD, M BA, EdM, Professor, Department of Radiology, Vice Chairman for Radiology Informatics, Section Head of Musculoskeletal Radiology, University of Washington
Felix S Chew, MD, MBA, EdM is a member of the following medical societies: American Roentgen Ray Society, Association of University Radiologists, and Radiological Society of North America
Further Reading
© 1994-2011 by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)
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Hyperparathyroidism, Primary: [Print] - eMedicine Radiology http://emedicine.medscape.

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The incidence peaks in those aged 40-70 years.

The disease is rare in children.

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