When Sunshine Is Not Enough: A Case Report of Vitamin D-Deficiency Rickets Causing Secondary Hyperparathyroidism in Florida

Rickets is a pediatric metabolic bone disorder caused by impaired growth plate mineralization, most commonly due to vitamin D deficiency.While classic manifestations include growth delay and bone deformities, acute presentations due to severe hypocalcemia are less common and may obscure the diagnosis.We describe a 13-month-old African-American girl who presented with bilateral hand stiffness and persistent thumb flexion secondary to profound hypocalcemia caused by severe vitamin D deficiency, highlighting an atypical neuromuscular presentation of nutritional rickets.The patient had no significant medical history and presented to the emergency department with a three-day history of subjective fever and a one-day history of bilateral finger stiffness and persistent thumb flexion.She was unable to walk and exhibited a downward trend in weight-for-age.Laboratory investigations revealed hypocalcemia (total calcium, 4.4 mg/dL; ionized calcium, 2.47 mg/dL), hypomagnesemia (1.3 mg/dL), elevated parathyroid hormone (210.1 pg/mL), and severe 25-hydroxyvitamin D deficiency (9.5 ng/mL).EKG demonstrated QT prolongation, and wrist radiographs showed metaphyseal fraying, widening, and cupping.Following calcium gluconate and magnesium infusions, the patient was admitted for further management of electrolyte abnormalities and underwent pediatric subspecialty evaluation for suspected nutritional rickets.This case highlights the diagnostic challenge of atypical nutritional rickets when acute metabolic derangements overshadow skeletal findings.Severe hypocalcemia can manifest as carpopedal spasm and cardiac conduction abnormalities, requiring prompt recognition.While inflammatory, infectious, and endocrine etiologies must be excluded, targeted laboratory and radiographic evaluation remains essential.Multidisciplinary management with calcium, vitamin D, and magnesium supplementation improved clinical and biochemical status.However, early readmission for recurrent hypocalcemia after initial discharge underscored the need for close outpatient follow-up.This case of vitamin D-deficiency rickets with secondary hyperparathyroidism and failure to thrive in South Florida underscores that adequate regional UV exposure does not preclude nutritional deficiency.Proper nutritional education, early recognition, and timely follow-up are essential for recovery and prevention of long-term sequelae.At approximately 14 months after presentation, she remained asymptomatic with a normalized 25-hydroxyvitamin D level of 44 ng/mL.

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Journal
Cureus
Published
2026-10-27
DOI
https://doi.org/10.7759/cureus.118677
Primary Topic
Vitamin D Research Studies
Type
article
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article

When Sunshine Is Not Enough: A Case Report of Vitamin D-Deficiency Rickets Causing Secondary Hyperparathyroidism in Florida

Judith Cornely, Jossias Genao Cruz, Kyle Colvin, Jorge Lima Gallardo et al.
Cureus
Vitamin D Research Studies
article

When Sunshine Is Not Enough: A Case Report of Vitamin D-Deficiency Rickets Causing Secondary Hyperparathyroidism in Florida

Judith Cornely, Jossias Genao Cruz, Kyle Colvin, Jorge Lima Gallardo, Ernesto Tejeda Gomez, Ryan Chierico, Gabriella E Kovalcik
article en

Abstract

Rickets is a pediatric metabolic bone disorder caused by impaired growth plate mineralization, most commonly due to vitamin D deficiency.While classic manifestations include growth delay and bone deformities, acute presentations due to severe hypocalcemia are less common and may obscure the diagnosis.We describe a 13-month-old African-American girl who presented with bilateral hand stiffness and persistent thumb flexion secondary to profound hypocalcemia caused by severe vitamin D deficiency, highlighting an atypical neuromuscular presentation of nutritional rickets.The patient had no significant medical history and presented to the emergency department with a three-day history of subjective fever and a one-day history of bilateral finger stiffness and persistent thumb flexion.She was unable to walk and exhibited a downward trend in weight-for-age.Laboratory investigations revealed hypocalcemia (total calcium, 4.4 mg/dL; ionized calcium, 2.47 mg/dL), hypomagnesemia (1.3 mg/dL), elevated parathyroid hormone (210.1 pg/mL), and severe 25-hydroxyvitamin D deficiency (9.5 ng/mL).EKG demonstrated QT prolongation, and wrist radiographs showed metaphyseal fraying, widening, and cupping.Following calcium gluconate and magnesium infusions, the patient was admitted for further management of electrolyte abnormalities and underwent pediatric subspecialty evaluation for suspected nutritional rickets.This case highlights the diagnostic challenge of atypical nutritional rickets when acute metabolic derangements overshadow skeletal findings.Severe hypocalcemia can manifest as carpopedal spasm and cardiac conduction abnormalities, requiring prompt recognition.While inflammatory, infectious, and endocrine etiologies must be excluded, targeted laboratory and radiographic evaluation remains essential.Multidisciplinary management with calcium, vitamin D, and magnesium supplementation improved clinical and biochemical status.However, early readmission for recurrent hypocalcemia after initial discharge underscored the need for close outpatient follow-up.This case of vitamin D-deficiency rickets with secondary hyperparathyroidism and failure to thrive in South Florida underscores that adequate regional UV exposure does not preclude nutritional deficiency.Proper nutritional education, early recognition, and timely follow-up are essential for recovery and prevention of long-term sequelae.At approximately 14 months after presentation, she remained asymptomatic with a normalized 25-hydroxyvitamin D level of 44 ng/mL.

Cureus
Nova Southeastern University (US), Broward Health Medical Center (US)
Good health and well-being
Openalex Percentile: Top 12%
Vitamin D Research Studies
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