Excerpt:
Summary
These data show that:
1. During a 2 year period, the chronic use of fluoridated water in patients undergoing maintenance hemodialysis was associated with a rise in serum phosphatase in 10 of 20 patients studied and an increased radiographic incidence of osteodystrophy.
2. Eight long-term hemodialysis patients manifested no radiographic evidence of osteodystrophy during their first 2 to 6 years of hemodialysis, and one of these patients currently has a negative bone survey, 9 years after starting hemodialysis. This may indicate that fluoridation is not universally associated with the development of osteodystrophy and/or that if osteodystrophy does develop in response to fluoridation, it may take years before it is radiographically appreciated.
3. The rates of bone uptake of dialysate fluoride and bone clearance of intravenously administered fluoride were both single exponential curves with similar slopes.
4. Rectilinear bone scans with F18 showed that, within the limits of the sensitivity of the technique, there is exclusive bone uptake of fluoride in uremic patients.
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Pattern of renal osteodystrophy in haemodialysis patients in Saudi Arabia
In order to know the pattern of renal osteodystrophy in haemodialysis patients in Saudi Arabia we conducted a multicentre study involving 209 patients. The mean age of the patients was 39.4 +/- 14 (18-70) years, 128 were males and 81 females. All patients were on acetate dialysate and their mean
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Renal osteodystrophy in patients on long-term hemodialysis with fluoridated water
Serum and bone fluoride concentrations of ten patients maintained on long-term hemodialysis with fluoridated water (1 ppm, i.e., 50uM) were correlated with duration of treatment and the occurrence of clinical, radiological, and histological manifestations of bone disease. Two patients had symptomatic renal osteodystrophy when accepted on the program, whereas six
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Comparison of renal osteodystrophy in patients dialyzed with deionized and non-deionized water
Discussion There are 2 major types of osteodystrophy which occur in various combinations in dialysis patients. The first and most commonly predominant is secondary hyperparathyroidism. This appears to be preventable, or at least controllable, with a bath calcium concentration above 6 mg%. The second type is osteomalacia. In certain centers it
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Fluoride metabolism and renal osteodystrophy in regular dialysis treatment
Fluoride in plasma, urine and bone tissue ash were estimated using a fluoride-ion electrode in 20 control persons (CP), 32 patients with compensated chronic renal failure (CRFP) and 59 patients in RDT (RDTP). The increase in plasma fluoride (CP: 2.4 +/- 1.4, CRFP: 6.5 +/- 2.2, RDTP: 12.3 +/- 4.5
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Bone disease in hemodialysis patients with particular reference to the effect of fluoride
Forty-one patients on our chronic hemodialysis program were assessed for the degree of progression of bone disease over an average period of 46 months. Seven patients were using a fluoridated dialysate. Four of these seven patients developed a marked increase in osteoid as judged by bone biopsy, while in the
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Fluoride & Osteomalacia
One of fluoride's most well-defined effects on bone tissue is it's ability to increase the osteoid content of bone. Osteoid is unmineralized bone tissue. When bones have too much of it, they become soft and prone to fracture -- a condition known as osteomalacia. As shown below, fluoride has repeatedly been
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Fluoridation, Dialysis & Osteomalacia
In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on
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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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Annapolis: Water Fluoridation Linked to Death of Dialysis Patient
EVENING CAPITAL (Annapolis, Maryland) November 29, 1979 Fluoride Linked to Death by Mary Ann Kryzankowicz Staff Writer Fluoride poisoning has been definitely linked to the death of a 65-year-old kidney dialysis patient who became ill during a blood cleaning process Nov 11. State Medical Examiner Dr. (illegible) Guard has ruled that Lawrence Blake, 65, of Arundel
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Skeletal Fluorosis in the U.S.
Although there has been a notable absence of systematic studies on skeletal fluorosis in the U.S., the available evidence indicates that the consumption of artificially fluoridated water is likely to cause skeletal fluorosis and other forms of bone disease in people with kidney disease and other vulnerable populations.
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