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人类骨骼氟中毒:对该疾病认识的近期进展综述

Skeletal fluorosis in humans: a review of recent progress in the understanding of the disease.

作者信息

Krishnamachari K A

出版信息

Prog Food Nutr Sci. 1986;10(3-4):279-314.

PMID:3295994
Abstract

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.

摘要

地方性骨氟病是一种慢性代谢性骨与关节疾病,由通过饮水或极少情况下从地方性病区食物中摄入大量氟化物所致。氟化物是一种蓄积性毒素,可改变骨组织的增生和吸收。它还会影响骨矿物质代谢的稳态。摄入氟化物的总量是决定该病临床进程的唯一最重要因素,该病的特征是中轴骨骼关节和四肢主要关节固定。骨病变的特征是不同程度的骨硬化、骨软化和骨质疏松以及骨赘形成。在部分病例中,可观察到继发性甲状旁腺功能亢进及相关的特征性骨改变。与早期观点相反,严重致残型骨氟病在儿童年龄组中也可见到。骨代谢转换增加、骨胶原合成受损以及对钙的亲和力增加是氟中毒的特征。当长期摄入小剂量氟化物且钙摄入量明显正常时,骨硬化表现明显,而骨质疏松型在儿童年龄组及该元素体内负荷较高时较为常见。氟中毒时可见与骨矿物质代谢有关的激素改变。肾脏是氟化物的主要排泄器官。年龄、性别、饮食中钙的摄入量、氟化物摄入的剂量和持续时间以及肾脏处理氟化物的效率是影响结果的因素。血清参数很少有助于诊断。尿氟升高和骨氟含量增加是氟中毒的指标。氟病是一种可预防的致残性疾病。目前尚无有效的治疗药物可治愈氟病。全球范围内,工业性氟病呈上升趋势。骨密度测量是早期诊断的一种手段。

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