Deficiency of a parathyroid hormone fragment containing the midportion and 1,25-dihydroxyvitamin D in serum of patients with slipped capital femoral epiphysis.

The endocrine abnormality that causes slipped capital femoral epiphysis (SCFE) has not been revealed. Recent studies have shown that parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] are involved in growth-plate chondrogenesis and matrix mineralization. Thus we examined in 13 patients with SCFE the serum levels of three immunoreactive forms of PTH (iPTH): the whole peptide [(1-84)PTH], the fragment containing the COOH-terminal portion (C-PTH), and the midportion (M-PTH). Additionally, serum levels of 25-hydroxyvitamin D [25-(OH)D] and 1,25-(OH)2D were measured. We found that the levels of M-PTH were significantly lower than those of controls, whereas levels of C-PTH and (1-84)PTH were not significantly different from those of controls. Similarly, levels of 1,25-(OH)2D were also significantly lower than control levels. In patients with initially low levels of M-PTH and 1,25-(OH)2D in whom the levels were monitored over a period, all levels returned to normal within a year after the onset of disease. The deficiency of M-PTH or 1,25-(OH)2D during the growth spurt could result in SCFE, although in this study, we cannot deny the possibility that the slippage may cause the deficiency.