We present the case of a 63 year old male with a chronic medical illness presents complaining of left shoulder pain.
Radiographs of the clavicles (Fig. 1-2, right and left respectively), demonstrate expansile, centrally lucent lesions peripherally, but separate from the acromioclavicular joint.
CT thorax (Fig. 3-4) demonstrates the left sided clavicular lesion to be expansile and centrally lytic (Fig. 3), and also shows a further similar lesion anteriorly in a left sided rib (Fig. 4).
Radiographs of the forelegs (Fig. 5-6, right and left respectively) demonstrate further, similar lesions throughout each tibia, which, when compared with previous radiographs had remained stable over a period of five years. (Additional information to be gleaned from Fig. 5 is the presence of vascular calcifications and vascular clips, providing a clue to the underlying Diabetes and consequent vasculopathy, eventually leading to renal failure, and ultimately renal osteodystrophy).
Patients with renal failure often undergo hypertrophy of the hyperparathyroid glands induced by hyperphosphataemia due to decreased renal excretion. Consequently increased Parathyroid hormone (PTH) alters bone metabolism leading to a promotion of osteoclasts, osteoblasts and osteocytes, giving rise to bone resorption, periosteal reactions and Brown tumors.
The changes associated with renal osteodystrophy are in many cases reversible following renal transplantation; however, this may take years.
Hyperparathyroidism:
• Subperiosteal resorption of bone produces lace-like irregularity of the cortical margin progressing to scalloping and spiculation. Seen in the tufts of the distal phalanges and also seen at other sites e.g. diametaphyses of the middle phalanges (radial aspects), inferior surface of ribs and calcaneus, medial proximal tibia, humerus and femur, and the inferior clavicles, particularly distally [1, 2, 3].
• Juxtaarticular erosions, particularly likely to be manifested in the hands and feet, as well as resorption of the lamina dura around the teeth [4].
• Manifestations of osteoporosis: intracortical resorption and a tunneling appearance secondary to intra-haversian osteoclasis.
• Endosteal bone resorption seen in the upper extremities, particularly the hands, as scalloped areas along the cortex. When multiple in the skull, they give rise to the classic “salt and pepper” appearance.
• Subtendinous and subligamentous resorption: surface scalloping at entheses which may be either smooth or irregular, most frequent on the inferior calcaneus, the greater/lesser trochanters and the anterior inferior iliac spine. Resorption of adjacent ligaments and tendons may occur [5].
Brown tumors:
• Also referred to as osteoclastomas, represent accumulations of giant cells and fibromatous material which produce destructive, often expansile lesions in bone. These are particularly frequent with primary hyperparathyroidism; however, most are seen in relation to secondary hyperparathyroidism as this is far more common. While Brown tumours can be painful, this is usually only a feature when bone expansion and/or pressure on local neurovascular structures occurs.
• Often solitary but may be multiple. Frequently eccentric or cortical in the long bones, giving rise to endosteal scalloping and expansion. Most frequently seen in the ribs, pelvis, facial bones and femora. They may heal following correction of the underlying condition, demonstrating calcification, sclerosis and eventual disappearance. Rarely, when an autonomous adenoma develops (Tertiary Hyperparathyroidism), surgical excision of the adenoma may be required to effect healing.
Osteosclerosis:
• Trabeculae often appear coarsened in patients with renal osteodystrophy due to resorption of secondary trabeculae. Often diffuse, affecting the entire skeleton, in its initial stages manifested as increased density along the vertebral end-plates producing a so-called “rugger-jersey” spine appearance.
Multiple Brown tumours in a patient with Renal osteodystrophy (Secondary hyperparathyroidism).
1. On the left shoulder X-ray, localized bone destruction and cystic expansile lesions are observed at the distal end of the clavicle. Part of the cortical bone is discontinuous, indicating a clear destructive change.
2. In the proximal humeral cortex, localized cortical thinning suggests potential bone resorption or destruction.
3. On the CT scans, an area resembling a “cavity” or low-density lesion is visible along the border of the clavicle and surrounding soft tissue; there is no significant soft tissue expansion, but the bone cortex shows erosion and marked scalloping.
4. On the forearm X-ray, alterations in bone density are present, including focal cortical thinning and evidence of cortical resorption along the medial cortex.
5. Overall, multiple areas of abnormal bone density and localized bone destruction are evident, suggesting progressive bone changes.
1. Secondary Hyperparathyroidism with Bone Changes:
Given the patient’s history of chronic disease (suspected chronic renal insufficiency), the imaging findings (typical subperiosteal resorption and multiple bone lesions suggestive of Brown tumors) align with the characteristics of renal osteodystrophy.
2. Multiple Myeloma:
Although multiple myeloma may also present with bone destruction and lytic lesions, it is often accompanied by other systemic features (such as anemia and hyperproteinemia). Its destructive pattern is typically more diffuse. Considering the characteristic signs of renal-related bone abnormalities, secondary hyperparathyroidism should be the primary consideration.
3. Other Bone Tumors or Metastases:
Bone metastases or primary bone tumors can also produce lytic lesions. However, given the history of chronic renal insufficiency leading to secondary metabolic imbalances, plus the typical subperiosteal bone resorption on imaging, secondary hyperparathyroidism-induced bone changes should be prioritized.
Combining the patient’s age, chronic disease history (suggesting chronic kidney failure), and imaging findings (multiple subperiosteal resorption areas, bone destruction, and suspected Brown tumors), the most likely diagnosis is: Secondary Hyperparathyroidism (Secondary HPT) with Brown Tumors.
If further confirmation is needed, assessments of parathyroid hormone (PTH), serum calcium, serum phosphate, and vitamin D levels, as well as parathyroid ultrasound or radioisotope scans, are recommended. A biopsy of suspicious lesions may help exclude other tumors if necessary.
1. Treatment Overview:
• Conservative Medical Management: For secondary hyperparathyroidism, the first step is to manage the underlying chronic kidney disease and improve electrolyte balance. If a kidney transplant is feasible, an evaluation should be conducted, as transplant can correct the metabolic disturbances at their source.
• Pharmacological Therapy: This includes phosphate binders, calcitriol (active vitamin D), calcium supplements, etc., to reduce PTH levels. Medications that suppress parathyroid function may also be considered if needed.
• Surgical Intervention: If the parathyroid glands exhibit substantial hyperplasia (e.g., adenoma or marked enlargement) and medical therapy fails to effectively control PTH, parathyroidectomy may be considered to limit progression of bone disease.
• Local Management of Bone Lesions: In cases of severe bone pain or instability, internal fixation or lesion curettage combined with bone grafting may be performed to prevent pathological fractures and relieve pain.
2. Rehabilitation/Exercise Prescription (FITT-VP Principle):
• Frequency: 3-5 times per week, maintaining consistency with moderate-intensity sessions.
• Intensity: Begin with low-intensity activities based on the patient’s bone condition and cardiorespiratory readiness, such as mild resistance training and low-impact aerobic exercises (e.g., walking or elliptical training).
• Time: Start with 15-30 minutes per session. Increase gradually according to tolerance.
• Type: Prioritize low-impact aerobic exercises and gentle range-of-motion plus muscle-strengthening exercises, such as seated cycling, level walking, or upper limb training with resistance bands or light dumbbells.
• Volume & Progression: Adjust exercise duration and resistance slightly every 2-4 weeks, provided there is no significant pain or worsening bone discomfort. If pain, fatigue, or fracture risk factors arise, reduce or pause exercise and seek medical review.
• Precautions: Owing to bone fragility and potential calcium/phosphorus metabolism abnormalities, it is essential to prevent falls and avoid overexertion. Using braces or supports is advisable, and high-impact, twisting, or excessive weight-bearing actions should be avoided.
Disclaimer:
This report is based on the available data for reference only and cannot replace in-person consultation or professional medical advice. For specific diagnosis and treatment plans, please consult relevant specialists and follow up closely.
Multiple Brown tumours in a patient with Renal osteodystrophy (Secondary hyperparathyroidism).
