Abstract
Dermatoglyphic investigations which prove the existence of genetic predisposition to occupational fluorosis in workers of aluminum and criolite plants were carried out. Mathematical methods of pattern recognition were used for the multifactorial analysis. It was found that the complex analysis of ten the most informative dermatoglyphic parameters permits to prognosticate a genetically determined risk of this occupational disease.
-
-
Preliminary screening of fluorine-stained osteoblastic apoptosis-related microRNA.
This article has been accepted for publication and undergone full peer review but has not been through the copy editing, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1002/ar.24709. Endemic fluorosis is a chronic systemic
-
A case of bone fluorosis of undetermined origin
After predominant theories on the causes of fluorosis are described and remarks made about the metabolism of fluoride, an observation of bone fluorosis in a 64-year-old patient is reported. Because, despite painstaking research, none of the known causes of bone fluorosis could be found in our patient, a new pathomechanism is being offered for discussion, i.e.,
-
Prolactin rs1341239 T allele may have protective role against the brick tea type skeletal fluorosis
OBJECTIVE: Prolactin (PRL) has been reported to be associated with increased bone turnover, and increased bone turnover is also a feature of skeletal fluorosis (SF). Autocrine/paracrine production of PRL is regulated by the extrapituitary promoter and a polymorphism in the extrapituitary PRL promoter at -1149 (rs1341239) is associated with disturbances
-
[Genetic factors predisposing to occupational fluorosis].
Having analyzed a total amount of all systems, the authors specified the most important genetic markers predisposing to chronic flour intoxication: the patients demonstrated higher frequency of ACP1*A and PGM1*1-alleles, phenotypes of acid phosphatase AA, of phosphoglucomutase 1+1+ and 2+2+, of dry cerumen consistence--d. The results could help to improve
-
[Qualitative and quantitative variation of serum proteins in fluorosis patients].
Comparison between patients with occupational fluorosis, a group of healthy workers, and a sample from the general population revealed differences in concentrations of some polymorphic serum proteins. These differences depended on phenotypes of patients. TF 1-2, PI 1-2, and HP 2-1 patients exhibited a decreased concentration of transferrin (TF), a
Related Studies :
-
-
-
Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
-
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.
-
"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.
-
Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
-
Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
Related FAN Content :
-