Page 78 - Slipped Capital Femoral Epiphysis Pathogenetic and Clinical aspects

Chapter 4
There are few reports on the abnormalities of the physis in children with CRF. One case report [47] described an 8-year old girl who died of long-standing uraemia where an absent columnar cartilage and an irregular zone of calcification were found in the physis. Several authors claim that the columnar cartilage of the physis is irregularly formed in children with CRF [43-45, 47, 48], resembling the abnormalities of the physis that are observed in SCFE [3-7].
The development of renal osteodystrophy (ROD) is one of the most severe clinical problems complicating CRF. ROD represents a range of disorders, ranging from high-turnover bone disease as a result of hyperparathyroidism to low-turnover osteomalacia and adynamic bone. Secondary hyperparathyroidism may cause growth failure by modulating genes involved in enchondral bone formation and alternating the architecture of the physis [15, 44, 49].
The risk of SCFE and/or avascular necrosis in children with CRF as a result of rhGH treatment and ROD remains equivocal. However, it is advisable to obtain radiographs of the osseous structures before GH therapy in children with CRF and growth retardation has commenced [49].
In conclusion, chronic diseases in children cause growth impairment via different mechanisms acting on the GH-IGF-1 axis. Mainly in children with CRF, where ROD can become a severe complication, physis abnormalities can look like the same abnormalities that are observed in SCFE.
Diagnostic endocrine measurements in SCFE
Endocrine evaluation of patients with SCFE is often inconclusive. Many studies have reported on hormonal measurements in patients with SCFE, including measurements of triiodothyronine (T3), thyroxine (T4), testosterone, 17B-oestradiol, thyroid-stimulating hormone (TSH), insulin-like growth factor-1 (IGF-1), insulin- like growth factor binding protein 3 (IGFB3), growth hormone (GH), PTH, 1,25 dihydroxyvitamin D and cortisol levels. All plasma and urinary hormone levels in patients with SCFE were similar to controls. Also, pubertal development was normal and comparable to the controls [50-53].
One retrospective study, published in 1988, reported decreased T3, testosterone and GH levels [51]. Papavasiliou et al. [54] investigated seven boys and seven girls suffering with SCFE [54] and found that the levels of FSH, LH and testosterone were lower than expected. The investigators claimed a possible temporary hormonal dis-order, which may play a role in the development in SCFE. The results
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