Children and adolescents of normal stature may develop osteoporosis, defined as having a lumbar bone mineral density (BMD) < z = -1.5 by dual-energy absorptiometry (DXA), and often accompanied by fractures, from a variety of genetic or acquired diseases. There are no FDA-approved pharmacotherapeutic agents in children for treatment of osteoporosis, as defined. We report our single-center, long-term experience in 129 children and adolescents (68 girls; 61 ♂) with oral alendronate for the treatment of osteoporosis. Patients ranged in age from infancy through late adolescence when the diagnosis of osteoporosis was made, and comprised a wide variety of disease entities: the most frequent was idiopathic osteoporosis (n = 61), followed by corticosteroid-induced osteoporosis (n = 19). No patients reported were growth-hormone or vitamin D-deficient. At the time of initiation of oral alendronate, the median (25th and 75th percentiles) lumbar z-score BMD = -2.1 (-2.7;-1.4) and most patients had suffered at least one atraumatic fracture prior to institution of alendronate. Since our report is experiential in nature, patients were divided into two groups for analysis: those who had finished a course of alendronate, and those that remain on oral alendronate, to account for the time element. The oral dose was either 10 mg daily or 70 mg once weekly in patients with initial weights > 30 kg, and was 5 mg daily or 35 mg once weekly with weights ≤ 30 kg in all patients. Forty-five patients (“stopped”) had an initial median lumbar BMD z-score = -1.8 (-2.4; -1.3), and were treated for 672 (513; 959) days with oral alendronate. At the time of discontinuation, the lumbar BMD delta (Δ) z-score achieved was +1.7 (+1; +2.2). The lumbar BMD z-score at the time of discontinuation of oral alendronate differed significantly (p < 0.001) from initial z-score. In 40 patients with sufficient follow-up data (six months), the lumbar BMD z-score = - 0.2 (-0.9; +0.33), 410 (353; 797) days after discontinuation of oral alendronate. The Δ score from initiation of oral alendronate therapy did not differ between the z-score at the time of discontinuation or most recent value (p = ns). All patients who were treated with oral alendronate, and subsequently had therapy "stopped", had cessation of their fractures within the first six months of initiation of therapy. No patients have resumed fracturing after discontinuation of oral alendronate. Five patients discontinued oral alendronate after a few months; one was due to esophageal symptoms. Eighty-three patients (“active”) with an initial median lumbar BMD z-score = -2.2 ((-2.8; -1.5) are being treated in similar manner with oral alendronate for 685 (351; 1022) days, as of 1st November 2004. The initial lumbar BMD z-score in this group was lower (p = 0.038) than in the “stopped” group. At most recent follow-up in the “active” group, BMD z-score was 0.94 (0.7; 1.03), a value significantly different than at initiation of oral alendronate. The lumbar BMD Δ z-score achieved = +3 (2.3; 3.7) is greater (p < 0.001) than the lumbar BMD Δ z-score at the time of discontinuation of oral alendronate in the “stopped” group. In conclusion, a wide range of children and adolescents were diagnosed with osteoporosis in the absence of linear growth failure or vitamin D deficiency. They generally had suffered atraumatic fractures prior to presentation. Oral alendronate led to a significant, relatively quick increase in lumbar BMD z-score and cessation of fractures. Patients taken off of oral alendronate have maintained lumbar BMD z-score for over one year. Short-courses of alendronate appear safe and efficacious in normalizing lumbar BMD z-score, stopping fractures, and maintaining bone density values once stopped.
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Faculty Member's Name: Craig B. Langman, MD
Consultant: Merck
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