Case study indicates potential link between chronic tophaceous gout and hypercalcemia
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PHILADELPHIA — Although rare, hypercalcemia should be treated as a potential threat for patients with from severe tophaceous gout, according to a case study presented at the ASN Kidney Week.
The case study presented the unusual case of a 40-year-old man with a history of severe tophaceous gout who developed severe hypercalcemia, as a result of granulomatous inflammation, and an increased calcitriol production caused by his chronic gout.
The patient was treated with a regimen of calcitonin, intravenous hydration and 40 mg of prednisone. According to investigators, his calcium levels recovered.
“The interesting point about this is the mechanism of action, the different pathophysiological mechanisms involved in hypercalcemia patients, and also because it changes the management. Not everybody just needs the classic hypercalcemia management with IV fluids, calcitonin and bisphosphonates,” Sirisha Gudlawar, MD, a nephrology fellow at the Medical College of Wisconsin and author of the study, told Healio.
“But I think these patients definitely need prednisone or other options for controlling the 1,25 dihydroxy production,” she said. “So, I think the pathophysiological mechanisms and the treatment that it is related to these will be helpful for the physicians, and I wanted to bring it up to the community to see that,” she added.
Gudlawar said that the exact mechanism for how the patient developed hypercalcemia, with no apparent history of the condition or genetic predisposition, was rare and pointed to granulomatous inflammation caused by his gout.
“We were wondering if there was any genetic predisposition to his hyperuricemia. He’s never had any hypercalcemia issues before [and] now comes in with symptomatic hypercalcemia. And we did work him up, including his malignancy and all the 25-hydroxy [and] 1,25 [dihydroxy],” Gudlawar said.
“But interestingly, his 1,25 dihydroxy calcitriol was elevated. There are only a few case reports that are published so far, indicating that there is increased production of calcitriol in patients with chronic tophaceous gout similar to the mechanism that happens in granulomatous diseases, where there is activation of macrophages causing the conversion.”
Despite the uncommon set of circumstances that led to the patient’s hypercalcemia, Gudlawar said that the case is important to clinicians as a reminder to keep watch for hypercalcemia in patients with tophaceous gout.
“Even though the skin biopsy that we did from the tophi [showed] there wasn’t any macrophage infiltration and there wasn’t any evidence of inflammation – despite that, he had the increased 1,25 [dihydroxy]. And though that number wasn’t that significantly elevated, his hypercalcemia improved with the steroid treatment,” Gudlawar said.
“I wanted to bring it out to the community to see that this can be a potential cause. Treatment with steroids would be beneficial in some patients. And despite some negative testing, I think this still should be on the physician’s radar.”
Reference:
- Gudlawar, S. Hypercalcemia associated with severe tophaceous gout. Presented at: ASN Kidney Week; Nov. 2-5, 2023; Philadelphia.
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