Rationale: Prevalence and pathophysiology of HPN-associated metabolic bone disease (MBD) xe patially unknown. Therefore, we began a systematic review of 0ur patients in order to increase our knowledge in this paticular field. Here, we report two cases of skeletal fluorosis, an unusual HPN-related bone abnormality.
Method: Until now, 12 patients (6 men, 6 women), aged 55 + 16 (MfSD), on HPN for 42 + 27 months (12-144) have been assessed. Clinical symptoms were recorded and laboratory pxameters including makers of bone metabolism, hormonal and nutritional status, radiologic studies and measurement of bone mineral density (BMD) by dual absorptiometry were performed. If needed bone biopsy was done.
Results: Ten patients had low BMD (median cortical T-score: -2.3, range: -5.4 to -1.6) ; median trabecular T-score: -2.8, range: -3 to -0.8). In 2 men aged 80 and 68 (HPN since 12 and 7 years), with a history of back pain, diffuse bone condensation on radiologic studies and high bone tunover on biochemical analysis, trabecular BMD was increased at +4.06 and +4X9. Biopsy confilms osteomalacia and revealed an increased fluoride content (1.04 and 0.49%, N: O.lf0.07%). Aluminium content was normal. In one patient fluoride was not only provided by trace elements solutions but also by an important consumption of mineral water containing high fluoride levels (78 g over 12 years).
Conclusions: Most HPN patients exhibit MBD, more often osteopenia or osteoporosis than osteomalacia. Fluoride deficiency has been suggested to be responsible for decreased BMD in HPN patients. By contrast, the present work gives evidence for possible fluoride toxicity in other HPN patients. In these patients IV trace elements may not be the sole source of fluoride, and therefore, clinicians should be cxefull about their patients oral fluoride intake.