June 02, 2000
Subject: Prozac and Fluoride(fluoxetine) death/abstract
Below is an abstract on the death of a child due to Prozac (fluoxetine).
Andreas Schuld provides us with updates on fluoride's impact on thyroid function. If you have not yet visited his web site nor read his review on teas, you may want to go to http://www.bruha.com/fluoride/html/virtual_library.htm
Specific Url's for previous reviews:
GREEN TEA, FLUORIDE AND THE THYROID(Open Letter)
COMPARISON OF SYMPTOMS:FLUORIDE POISONING/HYPOTHYROIDISM
Sallee FR, DeVane CL, Ferrell RE - "Fluoxetine-related death in a child with cytochrome P-450 2D6 genetic deficiency" J Child Adolesc Psychopharmacol 10(1):27-34 (2000)
The clinical course of a 9-year-old diagnosed with attention-deficit hyperactivity disorder, obsessive-compulsive disorder, and Tourette's
disorder and treated with a combination of methylphenidate, clonidine, and fluoxetine is described. The patient experienced over a 10-month period, signs and symptoms suggestive of metabolic toxicity marked by bouts of gastrointestinal distress, low-grade fever, incordination, and disorientation. Generalized seizures were observed, and the patient lapsed into status epilepticus followed by cardiac arrest and subsequently expired. At autopsy, blood, brain, and other tissue concentrations of fluoxetine and norfluoxetine were several-fold higher than expected based on literature reports for overdose situations. The medical examiner's report indicated death caused by fluoxetine toxicity. As the child's adoptive parents controlled medication access, they were investigated by social welfare agencies. Further genetic testing of autopsy tissue revealed the presence of a gene defect at the cytochrome P450 CYP2D locus, which
results in poor metabolism of fluoxetine. As a result of this and other evidence, the investigation of the adoptive parents was terminated. This is the first report of a fluoxetine-related death in a child with a confirmed genetic polymorphism of the CYP2D6 gene that results in impaired drug metabolism. Issues relevant to child and adolescent psychopharmacology arising from this case are discussed.
Fluoxetine normally inhibits cytochrome P450. Prolonged inhibition of P450
leads to thyroid hormone reduction. Thyroid hormones modulate the levels of
P450 in the liver, where the majority of thyroid hormone synthesis occurs.(T4 ->T3) .
A recent Canadian study by Urichuk et al (2000) of the University of Alberta in Edmonton showed that levels of p-trifluoromethylphenol (a metabolite of fluoxetine) was 10-fold higher in the liver of rats than in brain.
Further, studies by David Thompson [Monsanto...published in "Chemico-Biological Interactions" 126(1):1-14 (2000)] on 4-trifluoromethylphenol in rat liver slices showed intracellular glutathione levels decreased and fluoride ion levels increased in a time and concentration-dependent manner.
Glutathione is important as a co-factor for the enzyme glutathione peroxidase which is a selenium-containing enzyme ESSENTIAL for T4 to T3 synthesis in the liver.
In 1991, Guan in China found glutathione peroxidase to be useful as diagnostic function discriminant of mild and severe chronic fluorosis in blood biochemistry.
Best to all, Andreas Schuld
Parents of Fluoride Poisoned Children
Vancouver, BC, Canada
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