Endocrine Abstracts

Introduction: Hyperparathyroidism is a pathological condition characterized by the excessive secretion of parathyroid hormone (PTH), resulting from the hyperactivity of one or more parathyroid glands. This condition can manifest as primary, secondary, or tertiary hyperparathyroidism. However, determining the primary or tertiary origin of hyperparathyroidism can pose challenges in certain complex situations. In this report, we present a clinical case where identifying the primary or tertiary origin of hyperparathyroidism remains intricate.

Case Report: A 50-year-old patient with a three-year history of multiple myeloma complicated by end-stage renal failure requiring hemodialysis was diagnosed with hyperparathyroidism during routine medical follow-up. Despite maintaining a normal phosphocalcic balance, the patient reported diffuse bone pain and a general decline in health, with no other associated symptoms observed during the clinical examination. Sestamibi-Tc99 scintigraphy revealed three focal retentions of MIBI-Tc99m: one behind the upper right pole measuring 5.7×4.6 mm, one behind the lower right pole measuring 5.9×4.3 mm, and one behind the lower left pole measuring 5.6×4.8 mm. These findings suggested the presence of pathological parathyroid tissues, without any identified ectopic focus. Subsequently, the patient was referred for subtotal parathyroidectomy.

Discussion: Multiple myeloma is a hematologic malignancy characterized by osteolytic bone destruction resulting from increased osteoclastic resorption without a corresponding increase in bone formation. This process contributes significantly to the morbidity and mortality in multiple myeloma patients, leading to symptoms such as bone pain, diffuse osteopenia, focal lytic lesions, pathologic fractures, spinal cord compression, and hypercalcemia. Kidney failure, a common complication of multiple myeloma, can give rise to secondary and tertiary hyperparathyroidism. While both multiple myeloma (MM) and primary hyperparathyroidism (PHPT) are common causes of hypercalcemia, the simultaneous occurrence of these two pathologic processes in a single patient is exceedingly rare. Literature suggests that monoclonal gammopathies are more prevalent in patients with PHPT than in the general population, highlighting the importance of screening for monoclonal gammopathy in patients with PHPT. In the presented case, the patient had a history of kidney failure secondary to MM and presented with hyperparathyroidism. Sestamibi scintigraphy revealed hyperplasia of the parathyroid glands, consistent with both tertiary and primary hyperparathyroidism.

Conclusion: In cases where the origin of hyperparathyroidism remains challenging to determine, particularly when associated with multiple myeloma, careful consideration and further investigation are warranted. The coexistence of primary hyperparathyroidism with multiple myeloma represents a rare presentation, emphasizing the need for a thorough examination and comprehensive assessment.