Potential presence of metals in patients treated with metal-metal coupling prostheses for hip arthroplasty at 7 and 10 years of follow-up.

BACKGROUND: Beginning in 2008, metal-on-metal prostheses have been in the spotlight owing to much higher revision rates than expected. Adverse local tissue reactions have been well described in the literature as potential complications. METHODS: Between 2012 and 2013, 13 patients with metal-on-metal total hip replacements were evaluated clinically and radiologically and with laboratory samples. The same tests were repeated between 2015 and 2016 on eight patients to assess any changes. In the laboratory assessment, we searched for chromium, cobalt, molybdenum, and nickel in blood and urine samples over 24 h. RESULTS: Clinical assessment has shown good score in all patients except one. On a second examination, between 2015 and 2016, all patients obtained results similar to those obtained in the first assessment, except a patient, who reported a recent fall. In the radiological assessment between 2012 and 2013, results were optimal, apart from a case of aseptic mobilization. The patients reassessed 3 years after the first examination showed radiological results similar to those previously obtained, apart from a patient, who showed signals of mobilization. Metal levels found in their blood decreased in most cases after 3 years. Urine levels of nickel increased in five subjects, and chromium levels increased in four, but levels of cobalt and molybdenum decreased in four patients. CONCLUSION: It could be hypothesized that the decreasing trend of metal ion levels is associated with a stable wear status. On the contrary, a progressive increase in metal ion levels must be considered as early proof of implant loosening.

Hypophosphatemic rickets: etiology, clinical features and treatment.

Hypophosphatemic rickets (HR) is a genetic disorder, which prevents sufficient reabsorption of phosphate in the proximal renal tubule, with increased phosphate excretion, resulting in rickets. The more common form of HR is an X-linked inherited trait, with a prevalence of 1/20,000. The defective gene is located on the X chromosome, but females may present with a wide variety of clinical manifestations. The less common form of HR is caused by autosomal-dominant transmission. Activating mutations of the fibroblast growth factor 23 (FGF-23) gene and inactivating mutations in the phosphate regulating gene (PHEX gene with homologies to endopeptidases on the X chromosome), involved in the regulation of FGF-23, have been identified and have been implicated in the pathogenesis of these disturbances. A review of etiopathogenesis and clinical, differential diagnostic and therapeutic aspects of HR, with a particular emphasis on bone impairment, is reported.