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Osseous Manifestations of Primary Hyperparathyroidism: Imaging Findings

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Osseous Manifestations of Primary Hyperparathyroidism: Imaging Findings Hindawi International Journal of Endocrinology Volume 2020, Article ID 3146535, 10 pages https://doi.org/10.1155/2020/3146535 Review Article Osseous Manifestations of Primary Hyperparathyroidism: Imaging Findings Jackson Bennett ,1 James W. Suliburk ,2 and Fanny E. Moro´n 3 1School of Medicine, Baylor College of Medicine, Houston, TX, USA 2Department of Surgery, Baylor College of Medicine, Houston, TX, USA 3Department of Radiology, Baylor College of Medicine, Houston, TX, USA Correspondence should be addressed to Fanny E. Mor´on; [email protected] Received 13 September 2019; Revised 10 December 2019; Accepted 8 January 2020; Published 21 February 2020 Academic Editor: Giorgio Borretta Copyright © 2020 Jackson Bennett et al. -is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Primary hyperparathyroidism is a systemic endocrine disease that has significant effects on bone remodeling through the action of parathyroid hormone on the musculoskeletal system. -ese findings are important as they can aid in distinguishing primary hyperparathyroidism from other forms of metabolic bone diseases and inform physicians regarding disease severity and complications. -is pictorial essay compiles bone-imaging features with the aim of improving the diagnosis of skeletal in- volvement of primary hyperthyroidism. 1. Introduction the symptomatic classical variant in some individuals [2, 4]. Other HPT disease subtypes include secondary and tertiary Hyperparathyroidism (HPT) is an endocrine disorder de- disease, which are primarily seen in patients with chronic fined by a state of inappropriately increased levels of renal disease and posttransplant patients [7]. parathyroid hormone (PTH) activity from one or more Bone is a major target organ of PTH, and inappro- parathyroid glands [1]. Primary hyperparathyroidism priately elevated PTH levels in PHPTcan lead to changes in (PHPT) is a main disease subtype with classical and nor- the appearances of bones on a variety of diagnostic imaging mocalcemic variants. Hypercalcemia is evident in patients evaluations. Metabolic bone disease is an established with classical PHPT, while the normocalcemic variant clinical manifestation of PHPT as PTH is a major regulator demonstrates normal total and ionized calcium levels after of osteoclast activity and bone remodeling [8]. In addition, correcting for albumin [2–4]. Classical PHPT is most the biomechanical properties of bone as seen in PHPT’s commonly asymptomatic and due to autonomous secretion variants, including fracture risk and protective bone of parathyroid hormone from a benign parathyroid ade- treatment, are an area of ongoing scientific interest [3]. noma in 80% of patients with lack of feedback inhibition of However, the clinical and physical symptoms as well as calcium [1, 4, 5]. Multigland disease (double adenoma, triple imaging findings that have been historically taught are adenoma, and spontaneous four-gland hyperplasia), para- considered relatively rare today in clinical presentation and thyroid carcinoma, and syndromic forms of PHPT typically context. -is is thought to be due to earlier diagnosis and comprise the remaining 20% of cases [5–7]. -e normo- regular evaluations of calcium. From an epidemiological calcemic variant is characterized by secondary elevations in disease perspective of PHPT, the prevalence in the United PTH without an exact known etiology. -is variant may States of the classical hypercalcemia form has been esti- represent a subclinical, asymptomatic early stage of PHPT, mated to be 0.86% overall with a certain degree of vari- and it has the potential to progress to hypercalcemic status in ability [9, 10]. Many cases of Western PHPT are now 20% of cases and cause the target end organ damage seen in initially identified in otherwise asymptomatic patients 2 International Journal of Endocrinology through routine biochemical screening in up to 2% of patients over the age of 55 [1, 4, 11], while more severe, overt radiographical bone disease is rarer with potential to carry complications [1, 6, 12]. Widened prevalence esti- mates also exist for other disease phenotypes such as the normocalcemic form of PHPT (0.4–11%). Additionally, the modern incidence and prevalence estimates of PHPT have increased regionally in the USA, Europe, and China, which is thought to be attributed to a worldwide increase in routine biochemical disease screening. -is is contrasted with developing countries in which PHPT presents with higher serum calcium levels and more symptomatic disease compared to the asymptomatic hypercalcemia seen in the USA, Europe, and China [9, 10]. -ere is an overlap regarding the bone imaging findings of primary and secondary HPT. While secondary HPT is not specifically discussed in depth here, it has a unique osteo- sclerotic effect on the axial skeleton that produces a classic “rugger-jersey spine” [13]. In this pictorial essay, we mainly focus on the skeletal findings of PHPT bone disease as seen on multiple imaging modalities. We present an organized discussion on subperiosteal bone resorption-acroosteolysis, subchondral bone resorption, brown tumors of the body, Figure 1: Subperiosteal resorption of the radial aspect of the salt-and-pepper skull, and osteopenia associated with PHPT. middle phalanges of the second and third fingers (white arrows); -e overall aim of this pictorial essay is to review this wide feathery appearance and early tufts resorption-acroosteolysis (red range of musculoskeletal imaging findings associated with arrows). PHPT in addition to common differential conditions to aid in diagnosing and enhancing our knowledge of this enig- if osseous involvement is a concern [16]. In addition to the matic disease. hand, subperiosteal resorption, cortical thinning, and acroosteolysis can also be seen in the long bones (Figures 2–4), the lamina dura of teeth and spine [5, 17]. 1.1. Subperiosteal Bone Resorption. Subperiosteal bone re- Intracortical resorption can also occur and it appears on sorption corresponds to destruction of the bone underneath radiographs as cigar/oval-shaped or tunnel-shaped radio- the cortical periosteum of long bones; it is due to increased lucency within the cortex (Figure 3). In combination, bone turnover. -e mechanism of heightened levels of bone subperiosteal bone resorption and the brown tumors of turnover is due to the unregulated effects of parathyroid osteitis fibrosis cystica (OFC) contribute to 2% of symp- hormone on bone calcium homeostasis as seen in PHPT [5]. tomatic HPT manifestations on bone [18]. -e radiographic Elevated PTH levels lead to upregulation of nuclear factor- differential diagnosis for subperiosteal arthritis, like changes κβ ligand (RANKL), which interacts with its respective in the hand, includes rheumatoid arthritis. RANK receptor on osteoclast progenitor cells, leading to Acroosteolysis is a type of subperiosteal bone resorption resorption via the indirect growth of bone-remodeling os- pattern seen in PHPT and renal osteodystrophy that is lo- teoclasts [8, 14]. -ese findings in the phalanges are defining, cated at the distal phalangeal tufts. Diffuse or “band-like” pathognomonic musculoskeletal imaging features of pri- radiolucent patterns of resorption may occur, characteris- mary HPT [15]. tically at the midshaft and distal phalanx of a single or -e osseous changes most commonly occur at the multiple digits. Key radiological findings to note entail tuft proximal and middle phalanges located on the radial destruction (Figure 1), soft tissue tapering and shortening at margins of the second and third fingers, and they are best distal phalanx, a lucent line crossing the middle phalanx, viewed on radiographs [13]. On radiographs, subperiosteal calcifications, and arthritic changes. Other etiologies of this bone resorption appears as lace-like subperiosteal/intra- osseous finding include scleroderma, vascular, infectious, cortical irregular margin of phalangeal cortical bone [5, 12] inflammatory, thermal injury, and traumatic and congenital with thinned and feathery cortical bone (Figure 1). While causes of distal phalangeal shortening. Since acroosteolysis elevated serum calcium levels in the setting of high PTH of the phalanges can occur in various other conditions, it is activity ensure a probable diagnosis of PHPT, a majority of important to correlate these findings with other associated patients who have skeletal changes associated with PHPT clinical and imaging features of HPT [5, 15]. (up to 95% of patients) are best assessed radiographically at the hand, highlighting this location as a very specific osseous finding of the disease [5, 16]. -us, when clinical findings 1.2. Subchondral Resorption around Specific Joints. suggest PHPT, radiography is the preferred imaging study, Subchondral resorption is an osseous abnormality with specifically at the hand, to look for subperiosteal resorption trabecular destruction underneath cartilage surfaces of International Journal of Endocrinology 3 (a) (b) Figure 2: Clavicular subchondral resorption (arrows), widening of the articular space and irregular-feathery articular surface bilaterally. (a) (b) (c) Figure 3: Additional cases of brown tumors (black arrows) in the ulna, fibula, and humerus. Prominent forearm demineralization with subperiosteal (red arrows), intracortical, and trabecular resorption in the forearm bones and humerus with resultant appearance of coarse internal trabeculation.
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