Abstract

Rickets of any etiology is rarely encountered in modern clinical practice, and a primary presentation in an adolescent is even less common. Most cases of rickets are due to abnormalities in vitamin D intake, absorption, activity, or metabolism; others are related to phosphate deficiency from excessive renal excretion (e.g., X-linked dominant hypophosphatemic rickets). When a patient presents with no evidence of hereditary rickets and a standard workup fails to reveal the cause, unusual etiologies must be considered. Tumor-induced hypophosphatemia is a paraneoplastic condition that typically presents with osteomalacia in adults in their fifth decade of life1. We present a case of tumor-induced rickets in a previously healthy adolescent. The patient and his family were informed that data concerning the case would be submitted for publication, and they provided consent. A fourteen-year-old black adolescent presented to the pediatrician with the vague symptoms of bilateral knee and ankle pain, as well as generalized weakness. His mother was concerned that he “walked like a 70-year-old man.” He had no history of trauma or related family history. At the time of presentation, his height was at the 70th percentile and his weight was above the 90th percentile for age. He had no overt skeletal deformities. The pain was initially attributed to “growing pains.” He was prescribed nonsteroidal anti-inflammatory drugs, physical therapy, and shoe insoles. When the pain did not remit over the subsequent seven months, he was referred to a primary care sports medicine clinic where he was diagnosed with bilateral patellofemoral syndrome and bilateral pes planus. Radiographs of the knees obtained at that time demonstrated notable physeal widening and generalized demineralization of the cortices bilaterally (Fig. 1). Laboratory assessment was initiated (Table I). He was diagnosed with vitamin D deficiency and hypophosphatemic rickets and was prescribed calcitriol as well as sodium …

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