SFEBES2023 Poster Presentations Bone and Calcium (41 abstracts)
Paradoxical severe hypercalcemia in a male bodybuilder with rhabdomyolysis: A case report
Quazi Islam 1 , Eleni Armeni 1,2 , Randa Eltayeb 1 , Ashley Grossman 1 , Bernard Khoo 1 , Irina Mladenova 1 , Dipesh Patel 1 , Saroj Sahoo 1 , Kalyan Shekhda 1 , Ahmed Yousseif 1 & Efthimia Karra 1
1Royal Free Hospital, London, United Kingdom. 2National and Kapodistrian University of Athens, 2nd Department of Obstetrics and Gynaecology, Aretaieio Hospital, Athens, Greece
Paradoxical severe hypercalcemia is a rare phenomenon observed in some patients in delayed phase following rhabdomyolysis. We present a case of 33-year-old male who developed severe hypercalcemia following successful treatment of rhabdomyolysis. Patient was admitted with agitation and disinhibition, was intubated in A&E due to metabolic acidosis (pH 6.7), hyperkalemia (K+ 7.3 mmol/l), lactic acidosis (23 mmol/l), and pyrexia (40°C). Toxicology screening shown presence of cocaine, levamisole (cocaine adulterant), and cotinine. Acute liver injury, sympathetomimetic cardiac overdrive, acute kidney injury (AKI) with reduced consciousness were also noted. Filtration was initiated for AKI, and the initial biochemistry indicated severe rhabdomyolysis (creatinine kinase [CK] 76,122 U/l) with adjusted calcium (Ca) levels of 2.06 mmol/l. Following filtration and aggressive intravenous fluid administration, CK level normalized to 108 U/l. However, the patient unexpectedly developed severe hypercalcemia (Ca 4.03 mmol/l) with low levels of vitamin D (<8 nmol/l), 1,25-dihydroxyvitamin D3 (14 pmol/l), and PTH-independent hypercalcemia (PTH <0.7).
Management: Initial consideration of hypercalcemia-of-immobilization led to bisphosphonate treatment; however, after renal team’s advice for improved RANKL inhibition, the patient was switched to denosumab. Subsequent management included rehydration, avoidance of calcium supplementation, and continuing calcium free filtration for AKI. With denosumab, the patient’s hypercalcemia gradually resolved, and vitamin D supplementation was initiated to correct the deficiency. Once stable, he was discharged from ITU with plan of local endocrine and renal team follow up.
Conclusion: This case highlights the rare occurrence of paradoxical hypercalcemia, in delayed phase of rhabdomyolysis, due to release of excessive calcium from sarcoplasmic reticulum. Awareness of this phenomenon is crucial for clinicians managing similar cases to ensure appropriate diagnosis and consideration of denosumab for RANKL inhibition in PTH-independent hypercalcemia associated with rhabdomyolysis. Further research is warranted to elucidate the underlying mechanisms for such complex cases.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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