人类氟骨症:对该病认识的最新进展的综述。

Progress in food & nutrition science Pub Date : 1986-01-01
K A Krishnamachari
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引用次数: 0

摘要

地方性氟骨症是一种慢性代谢性骨关节疾病,在地方性氟骨症流行的地区,通过饮水或很少从食物中摄入大量氟化物而引起。氟化物是一种蓄积性毒素,可以改变骨组织的吸收和吸收。它还影响骨矿物质代谢的稳态。摄入氟化物的总量是决定该疾病临床病程的最重要因素,其特征是轴骨关节和四肢主要关节的固定。骨硬化、骨软化和不同程度的骨质疏松症以及外生骨骺形成的组合是骨病变的特征。在一定比例的病例中,观察到继发性甲状旁腺功能亢进伴有相关的特征性骨改变。与早期的想法相反,严重致残形式的氟骨症也见于儿科年龄组。骨代谢转换增加、骨胶原合成受损和对钙的渴求增加是氟化物中毒的特征。在钙摄入量明显正常的情况下,长期摄入小剂量氟化物,骨质疏松症在儿童年龄组和较高的身体负荷中很常见。与骨矿物质代谢有关的激素改变见于氟中毒。肾脏是氟化物的主要排泄器官。年龄、性别、饮食中的钙摄入量、氟摄入的剂量和持续时间以及处理氟的肾脏效率是影响结果的因素。血清参数很少有助于诊断。尿氟化物升高和骨氟化物含量增加是氟化物中毒的指标。氟中毒是一种可预防的致残疾病。目前还没有有效的治疗氟中毒的药物。工业氟中毒在全球范围内呈上升趋势。骨密度测量是早期诊断的工具。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Skeletal fluorosis in humans: a review of recent progress in the understanding of the disease.

Endemic skeletal fluorosis is a chronic metabolic bone and joint disease caused by ingesting large amounts of fluoride either through water or rarely from foods of endemic areas. Fluoride is a cumulative toxin which can alter accretion and resorption of bone tissue. It also affects the homeostasis of bone mineral metabolism. The total quantity of ingested fluoride is the single most important factor which determines the clinical course of the disease which is characterized by immobilization of joints of the axial skeleton and of the major joints of the extremities. A combination of osteosclerosis, osteomalacia and osteoporosis of varying degrees as well as exostosis formation characterizes the bone lesions. In a proportion of cases secondary hyperparathyroidism is observed with associated characteristic bone changes. Contrary to earlier thinking, severe crippling forms of skeletal fluorosis are seen in paediatric age group too. Increased metabolic turnover of the bone, impaired bone collagen synthesis and increased avidity for calcium are features in fluoride toxicity. Osteosclerotic picture is evident when small doses of fluoride are ingested over a long period of time during which calcium intakes are apparently normal while osteoporotic forms are common in paediatric age group and with higher body load of the element. Alterations in hormones concerned with bone mineral metabolism are seen in fluorosis. Kidney is the primary organ of excretion for fluorides. Age, sex, calcium intake in the diet, dose and duration of fluoride intake and renal efficiency in fluoride handling are the factors which influence the outcome. Serum parameters rarely help in the diagnosis. Elevated urinary fluoride and increased bone fluoride content are indicators of fluoride toxicity. Fluorosis is a preventable crippling disease. No effective therapeutic agent is available which can cure fluorosis. Industrial fluorosis is on the increase on a global basis. Bone density measurement is a tool for early diagnosis.

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