Paper
Nonalimental Scurvy With Relapse Symptoms After Stopping Oral Vitamin C Supplementation
Published Jul 31, 2018 · Nina Vaezipour, K. Leibundgut
Pediatrics
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Abstract
On the basis of a history of a child with scurvy showing relapse symptoms after stopping treatment, we capture possible individual differences of vitamin C homeostasis. Historically linked to sea voyagers in the 18th century, scurvy has become extremely rare during the last century in developed countries. However, it is still present in some at-risk populations and often overlooked in pediatric patients with restricted diets due to behavioral, neurodevelopmental, or psychiatric problems. So far, the only known etiology of developing scurvy is nutritional deficiency of vitamin C. In this report, we describe the case of a 3-year-old previously healthy Swiss girl without any history of previous poor dietary intake, who presented a picture of systemic inflammation including persisting fever, palpable purpura located on the extensor sides of the extremities, refusal to bear weight, and gingival bleeding. Blood tests revealed a significant increase of inflammatory markers and hypoalbuminemia. Full-body MRI revealed symmetrical bone marrow edema consistent with findings in previously reported cases of children with scurvy. After starting a high-dose oral vitamin C supplementation, the patient showed rapid clinical, laboratory, and radiologic improvement, but after stopping the treatment 4 months later, the patient developed relapse symptoms with pronounced fatigue, refusing to walk, and hair loss. These symptoms led us to restart the oral supplementation, which resulted in secondary normalization of her condition. The cause of her symptoms still remains unclear and presents the first case to our knowledge describing scurvy symptoms that are not directly linked to deficient dietary intake.
A 3-year-old Swiss girl with scurvy symptoms showed relapse symptoms after stopping oral vitamin C supplementation, suggesting a possible individual difference in vitamin C homeostasis.
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