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English Abstract
Journal Article
[Progressive course of hypophosphatemic osteomalacia during 25-year follow up].
Medicinski Pregled 2010 May
INTRODUCTION: Hypophosphatemic osteomalacia is defined as mineralization of the newly formed bone matrix (osteoids) in adults as a consequence of the phosphate deficiency.
CASE REPORT: A female from Belgrade, aged 62 years fell ill in 1982. when she was 36. She first felt pains in bones associated with chronic fatigue. In 1986. during her hospitalization the presence of neoplastic hematologic, endocrinologic, urogenital and gastroenterologic system deseases was excluded. Hypophosphatemic osteomalacia was diagnosed on the basis of the history, clinical presentation, physical examination, radiologic finding and laboratory analyses (lower serum phosphorus level). The initial therapy included a mixture of phosphates, vitamin D and calcium. The doses were several times corrected over the following four years. In 1990 she had a mild clinical deterioration requiring recorrection of the mentioned therapy. In 1993 bilateral femoral neck fractures occurred and subsequent osetosynthe as was performed. The disease had a progressive character in spite of the administered drug therapy so that multiple fractures occurred in 2000. During the last hospitalization in 2008. neither new pseudo fractures nor fractures were found although biochemical profile of the hypophosphatemic osteomalacia was still present.
CONCLUSION: The aim of this study was to emphasize the complexity in both diagnostic and therapeutic approach in the case of hypophosphatemic osteomalacia. In the presented case the patient showed a complicated and progressive course. In our opinion such course was a consequence of impossible etiologic treatment and discontinued therapy
CASE REPORT: A female from Belgrade, aged 62 years fell ill in 1982. when she was 36. She first felt pains in bones associated with chronic fatigue. In 1986. during her hospitalization the presence of neoplastic hematologic, endocrinologic, urogenital and gastroenterologic system deseases was excluded. Hypophosphatemic osteomalacia was diagnosed on the basis of the history, clinical presentation, physical examination, radiologic finding and laboratory analyses (lower serum phosphorus level). The initial therapy included a mixture of phosphates, vitamin D and calcium. The doses were several times corrected over the following four years. In 1990 she had a mild clinical deterioration requiring recorrection of the mentioned therapy. In 1993 bilateral femoral neck fractures occurred and subsequent osetosynthe as was performed. The disease had a progressive character in spite of the administered drug therapy so that multiple fractures occurred in 2000. During the last hospitalization in 2008. neither new pseudo fractures nor fractures were found although biochemical profile of the hypophosphatemic osteomalacia was still present.
CONCLUSION: The aim of this study was to emphasize the complexity in both diagnostic and therapeutic approach in the case of hypophosphatemic osteomalacia. In the presented case the patient showed a complicated and progressive course. In our opinion such course was a consequence of impossible etiologic treatment and discontinued therapy
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