Category: Calcium/Bone Disorders
Objective : Hypercalcemia has been well described in patients with disseminated coccidioidomycosis but the mechanism is not well understood. The mechanism is believed to be unrelated to excessive 1-alpha-hydroxylase activity which has been associated with other granulomatous processes, most notably sarcoidosis. We present a case of hypercalcemia in an immobile patient with disseminated coccidioidomycosis.
Case Presentation: A 43-year-old male with recent meningitis secondary to coccidioidomycosis on fluconazole therapy initially presented with generalized weakness. He developed fever, headache and left leg weakness. During this time, patient had significant immobility and was able to stand for only brief periods of time. Patient was hospitalized for four months and diagnosed with disseminated coccidioidomycosis complicated by CNS vasculitis. Patient was put on amphotericin, fluconazole and an extended course of glucocorticoids with a slow taper.
Upon discharge, he had a corrected calcium of 8.5 mg/dL. One month later, he developed hypercalcemia over the course of 7 days with an initial corrected calcium of 8.5 mg/dL and a peak corrected calcium of 12.0 mg/dL with an ionized calcium of 1.68 mmol/L. Patient had been asymptomatic denying any bone pain, abdominal pain or polyuria during this time. Patient also had no evidence of renal insufficiency or nephrolithiasis.
Patient had a low PTH (7.3 ng/L), normal 25-hydroxyvitamin D (57.0 ng/mL), low 1,25-dihydroxyvitamin D (9.8 ng/mL), normal urine calcium (251 mg/day) and normal PTHrP (14 pg/mL). Patient was given 1 dose of pamidronate 60 mg IV and the corrected calcium decreased from 11.8 to 9.8 mg/dL. Patient was also started on hydrocortisone 10 mg PO q 6:00 am and 5 mg PO q 3:00 pm.
Methods : n/a
Results : n/a
Discussion : Hypercalcemia is well described in disseminated coccidioidomycosis but not well understood. It is believed that the underlying process is independent of excessive 1-alpha-hydroxylase activity, PTH or PTHrP. This is supported by our patient’s low 1,25-dihydroxyvitamin D level, low PTH and normal PTHrP. Immobility likely contributed to the patient’s hypercalcemia, but it is interesting that the patient had normal calcium levels for almost 6 months before developing hypercalcemia rapidly over the course of one week. One possible explanation is that the hypercalcemia had been masked by glucocorticoids and uncovered during the steroid taper.
Conclusion : Hypercalcemia in disseminated coccidioidomycosis is not well understood and may work independently of 1-alpha-hydroxylase activity and PTH. It may also be associated with immobility. Glucocorticoids may help prevent this hypercalcemia though the exact mechanism is unknown.
Scripps Mercy Hospital
San Diego, California
I completed medical school at the University of Virginia in 2016. I am currently a third-year internal medicine resident at Scripps Mercy Hospital and I am very excited to be chief resident next year before pursuing a fellowship in endocrinology.
Endocrinology Attending and Associate Program Director, Internal Medicine
Scripps Mercy Hospitals San Diego and Chula Vista
I earned my MD degree at Jefferson Medical College in Philadelphia followed by Internal Medicine residency at Scripps Mercy San Diego. From there, I completed a 2-year Endocrinology fellowship at Scripps Green/Scripps Clinic also in San Diego. I worked in private practice in Phoenix for 2 years before returning to Scripps where I am an Endocrinology teaching attending and Associate Program Director of the Internal Medicine residency program. I have been an AACE member since 2011 and a fellow of AACE since 2016.