Abstract
Chronic fluoride toxicosis caused lameness, dental lesions and illthrift in an extensive beef cattle herd in northern Australia. Up to 15% of the herd was lame and the disease forced the culling of large numbers of cows. The source of fluoride was fertiliser-grade monoammonium and diammonium phosphate fed as part of a mineral supplement. Large quantities of mineral supplement were provided to the cattle because lameness was attributed to phosphorus deficiency, which is endemic in the area. Most lameness developed in the late dry season in the post-lactation phase. Severe lameness was caused by fractured pedal bones.
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Fluorosis and periostitis deformans as complications of prolonged voriconazole treatment
We describe a case of development of painful periostitis deformans in a 39-year-old woman who was receiving long-term voriconazole treatment for Aspergillus infection as a complication of orthotopic liver transplant. Measurement of fluoride levels strongly supports fluorosis to be the mechanism of the voriconazole-induced periostitis deformans and supports the concept
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Reducing the off-target endocrinologic adverse effects of azole antifungals—can it be done?
Highlights Azole antifungals are associated with off-target endocrinologic adverse events. Skeletal fluorosis, pseudohyperaldosteronism, adrenal insufficiency, hyponatraemia and hypogonadism are reported. Clinical and biochemical monitoring may play a role in prevention and progression. Novel azoles offer therapeutic advantages due to greater selectivity of binding to fungal CYP51. Integration of pharmacogenomics
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Voriconazole
A 57-year-old man, who was receiving immunosuppressive therapy after liver transplantation, began receiving broad-spectrum antibiotics and antifungals (including amphotericin B liposomal) for a suspected fungal infection of the brain. Four days later, brain biopsy and subsequent culture led to identification of Scedosporium boydii/apiosperumum as the causative pathogen, and voriconazole [dosage
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Skeletal fluorosis due to inhalation abuse of a difluoroethane-containing computer cleaner
Skeletal fluorosis (SF) is endemic in many countries and millions of people are affected worldwide, whereas in the United States SF is rare with occasional descriptions of unique cases. We report a 28-year-old American man who was healthy until two years earlier when he gradually experienced difficulty walking and an abnormal gait,
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Periostitis deformans due to wine fluorosis.
On the basis of 29 cases observed during 1948 to 1968, the author reports a disease termed periostitis deformans which was caused in alcoholics by sodium fluoride added to wine in concentrations of the order of 8 to 72 ppm. Four difference phases of the disease are described which are
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Fluoride & Osteoarthritis
While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.
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"Pre-Skeletal" Fluorosis
As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.
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Skeletal Fluorosis: The Misdiagnosis Problem
It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.
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