Abstract
A description of the fluoride overfeed in Hooper Bay, Alaska, that resulted in the first reported death due to fluoride toxicity caused by drinking water from a community water system.
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Pharmacokinetic aspects of topical fluorides
Pharmacokinetic studies have revealed quantitative information about the bioavailability, rate of absorption, distribution, and clearance of fluoride following the use of fluoride-containing dentifrices, gels, varnishes, and solutions. It is concluded that following the use of topical fluoride products, variable amounts of fluoride are swallowed and absorbed into the systemic circulation--amounts which may be sufficient to produce acute
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An outbreak of fatal fluoride intoxication in a long-term hemodialysis unit
OBJECTIVE: To determine the cause of an outbreak of acute illness and death in a long-term hemodialysis unit. DESIGN: A retrospective cohort and case-control study of patients receiving hemodialysis and a laboratory study of a model deionization system to purify water for hemodialysis. SETTING: An outpatient hemodialysis unit of a university hospital. PATIENTS:
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[Analysis on clinical characteristics of 316 patients with hydrofluoric acid burns].
Objective: To investigate the clinical characteristics of patients with hydrofluoric acid (HF) burns. Methods: Clinical data of 316 patients with HF burns admitted to Zhejiang Quhua Hospital from January 2004 to December 2016 were retrospectively analyzed. Patients were divided into non and mild poisoning group (NMP, n=157), moderate poisoning group (MP,
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Acute fluoride toxicity. Pathophysiology and management.
Acute intoxication with inorganic fluoride disrupts numerous physiological systems. As a potent acid it acts corrosively on the skin and mucous membranes, producing severe burns. As the most electronegative element it tightly binds many cations essential to homeostasis, producing, for example, profound hypocalcaemia and resultant inhibition of normal blood coagulation.
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Sodium fluoride produces a K+ efflux by increasing intracellular Ca2+ through Na+-Ca2+ exchange.
Acute fluoride intoxication increases intracellular calcium (Cai), manifested by increased twitch tension in cardiac muscle, and by potassium efflux (mediated by Ca2+-dependent K+ channels) in fluoridated erythrocytes. Fluoride, like isoproterenol, stimulates adenylate cyclase, and could increase Cai via the effects of cAMP on Ca2+ channels. However, while the inotropic effects
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