Patient 2 is a 66-year-old woman with a history of Crohn's disease and an ileostomy. She presented to the emergency department with profound, debilitating weakness 22 days following her regularly scheduled dose of denosumab. She had received biannual treatments for 5 years at this point. Neurological exam revealed 5-/5 strength in all extremities. She exhibited mild psychomotor slowing. Chvostek sign was absent. Serum chemistries demonstrated a serum total calcium of 4.5 mg/dL, magnesium 1.6 mg/dL, phosphorous of <1.0 mg/dL, ionized calcium 0.89 mmol/L and intact PTH 2,356 pg/mL. 25-hydroxy vitamin D was 4 ng/mL. The last prior vitamin D measurement in our records was 2 years prior and measured <4.0 ng/mL. This measurement was drawn 2 weeks after a dose of denosumab was administered, and the importance of supplementation was reinforced to the patient at that time. This patient had no evidence of CKD with an eGFR of 101 mL/min/1.72m2 and a serum creatinine of 0.7 mg/dL. It should be noted that patient 2 had a history of mild, asymptomatic hypocalcemia (with values ranging from 6.0 to 10.4 mg/dL) in the year prior to admission with an intact PTH ranging between 300 and 500 pg/mL and mildly low serum phosphorous levels. Vitamin D deficiency limiting intestinal phosphorous absorption and denosumab-induced elevated PTH levels causing phosphaturia would account for hypophosphatemia. Patients with vitamin D deficiency in the absence of denosumab treatment typically have mildly elevated PTH levels, though generally no higher than 110 pg/mL []. The laboratory findings upon admission of both patients are presented in Table .
A 74-year-old male with a past medical history of severe osteoporosis, chronic obstructive pulmonary disease (COPD), marginal gastric ulcers status-post sleeve gastrectomy, and Crohn’s disease status-post small bowel resection presented to the emergency department due to an acute onset of right shoulder pain. Vital signs revealed a temperature of 37.2°C, blood pressure of 112/61 mmHg, heart rate of 78, respiratory rate of 16 and oxygen saturation of 92% on 1.5 L by nasal cannula, which he used at baseline. Initial laboratory workup revealed severe hypocalcemia at 4.8 mg/dL and hypophosphatemia at 0.8 mg/dL. Upon further history taking, the patient stated that he receives denosumab injections for his severe osteoporosis. The patient denied muscle cramps, spasms, weakness, seizures, facial twitching, lightheadedness, and psychiatric changes. Of note, he had a history of chronic hypocalcemia with a baseline of 7 mg/dL and reported taking daily calcium and vitamin D supplements. His physical examination was unremarkable except for shoulder pain on passive range of motion. Chvostek and Trousseau signs were both negative. Additional laboratory workup (Table ) was significant for hyperparathyroidism and normal levels of magnesium, albumin, and vitamin D. His arterial blood gas results (Table ) revealed respiratory acidosis presumed to be due to COPD.\nThe patient was admitted to the intensive care unit, monitored on cardiac telemetry, and started on IV calcium carbonate in addition to his home calcium and vitamin D oral supplements. Endocrinology was consulted and calcium levels were trended until normalization. The patient was ultimately discharged on calcium carbonate 1,250 mg by mouth three times per day, calcium-vitamin D gummies by mouth three times per day, cholecalciferol 1,000 international units by mouth two times per day, and calcitriol 0.5 mcg oral capsule four times per day. His serum calcium level at eight months post-discharge has been maintained at roughly 9.5 mg/dL on this regimen and he has remained asymptomatic throughout.