A Not So Clear Case of Hypercalcemia
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports
November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders
- 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical
- Carvalho, Andrei Felipe S., University of Miami Health System, Miami, Florida, United States
- Alonso, Shawn, University of Miami Health System, Miami, Florida, United States
- Alcegueire, Kara, University of Miami Health System, Miami, Florida, United States
- Waheed, Ahmed A., University of Miami Health System, Miami, Florida, United States
Hypercalcemia is a frequent finding in clinical practice and is most commonly due to primary hyperparathyroidism or an underlying malignancy.1 Therefore, it is generally recommended that the initial workup begin with determining whether the cause is either parathyroid hormone (PTH)-dependent or independent.1,2 Although this approach is helpful in most cases, here we present a case where the cause is not quite so clear.
A 67-year-old woman with a history of hypertension and chronic kidney disease stage 3a, presented with one week of abdominal pain and constipation. On arrival, her vitals were normal, and her exam was notable for mild abdominal tenderness. Initial labs revealed hypercalcemia with a calcium 12.6mg/dL, albumin 3.9g/dL, phosphorous 2.4mg/dL, hemoglobin 9.7g/dL and an elevated creatinine of 2.8mg/dL, with a baseline 1.8mg/dL. Serum PTH was elevated at 677pg/mL, and 25-oH vitamin D was low-normal at 31ng/mL. Imaging showed an 11mm parathyroid mass suspicious for an adenoma, which was presumed to be the cause of the hypercalcemia. However, despite adequate intravenous fluids, the patient’s kidney function did not improve as excepted, which in addition to the patient’s age and the anemia, prompted further workup. The patient was then found to have an IgG-kappa monoclonal gammopathy, which led to a bone marrow biopsy revealing 20% plasma cells. The patient was diagnosed with multiple myeloma.
Although the hypercalcemia was likely driven by the parathyroid adenoma given the degree of PTH elevation, we suspect that the multiple myeloma was also likely contributing. Interestingly, although the exact mechanism remains unknown, there are numerous case reports, dating back decades, and even a small prospective study describing an association between monoclonal gammopathies, including multiple myeloma, and primary hyperparathyroidism.3,4,5 Given the prevalence of reported cases, some authors suggest ruling out a coexisting monoclonal gammopathy at the time of diagnosis of primary hyperparathyroidism, particularly in the elderly and those with difficult to control hypercalcemia.5,6,7 As seen in this case, had it not been for the additional lab abnormalities the diagnosis of myeloma would have likely been delayed. Thus, this case gives us an opportunity to highlight a clinically important association between primary hyperparathyroidism and monoclonal gammopathies.