Introduction: Vitamin D, calcium, and/or phosphate deficiency can lead to metabolic bone disease and increased risk of fracture. Children and adolescents with dark skin pigmentation and those who lack exposure to sunlight are at greater risk for vitamin D deficiency. Myopathy due to vitamin D deficiency is common and often missed or masked by other diagnoses.

Severe vitamin D deficiency typically results in hypocalcemia with hypophosphatemia, rarely with rhabdomyolysis and unexpected hyperphosphatemia. Here, we present an unusual case of hypocalcemic myopathy resulting in hyperphosphatemia and hungry bone syndrome secondary to severe vitamin D deficiency in a young wrestler.

Case Presentation: A 16-year-old previously healthy African American male presented with 3-month history of numbness and tingling throughout his body. He was on his high school wrestling team and was on a very restricted diet trying to stay in his weight class. He was found to have calcium of 5.4 mg/dL, phosphorous of 6.1 mg/dL, ionized calcium of 0.77 mmol/L, vitamin D 25 OH of 4.9 ng/ml, parathyroid hormone of 239.8 pg/ml, and creatinine kinase of 978 U/L. Skeletal survey showed severe rickets. He was started on calcitriol and required multiple IV calcium boluses to maintain normal calcium levels. This was suggestive of a component of hungry bones syndrome. Levels of calcium normalized and he was discharged on a regimen of elemental calcium, vitamin D, and calcitriol. We discuss a case of severe hypocalcemia secondary to severe vitamin D deficiency and hyperphosphatemia secondary to rhabdomyolysis as evidenced by elevated CK levels.

Working Diagnosis Hypocalcemic myopathy and hungry bone syndrome secondary to severe vitamin D deficiency

Discussion: Vitamin D, calcium, and or phosphate deficiency can result in undermineralized bone and excess osteoid, leading to metabolic bone disease and increased risk for fractures. Vitamin D is converted to calcitriol which binds to vitamin D receptors, controlling calcium and phosphate homeostasis, critical for normal bone remodeling. Acute hypocalcemia presentation can vary from perioral or acroparesthesias, myopathy, seizures, and arrhythmias. Our patient had severe hypocalcemia and vitamin D deficiency with hyperphosphatemia, likely due to the elevated CK from skeletal muscle cell lysis.

Vitamin D deficiency is common in athletes, especially if training indoors, such as wrestlers. Wrestlers may also follow restrictive diets to maintain their weight class. This can have detrimental effects on their health, such as kidney failure, rhabdomyolysis, arrhythmias, or death.

Conclusion: Severe and prolonged vitamin D deficiency results in rickets and hypocalcemia with hypophosphatemia. Seldomly severe hypocalcemia results in hypocalcemic myopathy which can lead to rhabdomyolysis and hyperphosphatemia. To our knowledge, there are no previously reported cases of hypocalcemic myopathy with hyperphosphatemia and hungry bone syndrome resulting from severe vitamin D deficiency. Pediatric providers should screen student athletes for restrictive diets and be aware of the potentially severe outcomes of these radical diets.