Serum Parathyroid Hormone Levels in Chronic Endemic Fluorosis

Köroğlu, Banu Kale; Ersoy, Ismail Hakki; Köroğlu, Mert; Balkarlı, Ayşe; Ersoy, Siddika; Varol, Simge; Tamer, Mehmet Numan

doi:10.1007/s12011-010-8847-2

Cited by 27 publications

(21 citation statements)

References 24 publications

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“…It has also been reported that chronic exposure to F may disturb Ca homeostasis by producing hypocalcaemia due to its stimulating effect on osteoblastic cell proliferation ( 10 – 12 ) , resulting in an increase in bone formation ( 13 – 15 ) , which needs extra Ca. This alteration of extracellular Ca level is sensed by Ca-sensing receptor (CASR) ( 16 ) and the parathyroid glands are triggered to secrete more parathyroid hormone to combat the Ca imbalance in the body, producing secondary hyperparathyroidism ( 14 , 17 ) . Parathyroid hormone triggers the conversion of 25-hydroxy-vitamin D 3 (25(OH) vitamin D 3 ) to 1,25-dihydroxy-vitamin D 3 (1,25(OH) 2 vitamin D 3 ) in the proximal convoluted tubule of the kidneys ( 18 ) to maintain plasma ionised Ca concentrations within narrow physiological limits by acting on the intestine, kidneys and bone ( 18 ) through its receptor – vitamin D receptor (VDR) ( 19 ) .…”

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confidence: 99%

Amelioration of chronic fluoride toxicity by calcium and fluoride-free water in rats

et al. 2012

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The study was undertaken to explore the amelioration of chronic fluoride (F) toxicity (with low and normal Ca) in rats. The study was conducted in two phases. In phase I (6 months), seventy-six Wistar, weanling male rats were assigned to four treatment groups: normal-Ca (0·5 %) diet (NCD), Caþ F2 ; low-Ca (0·25 %) diet (LCD), Ca2 F2; NCD þ100 parts per million (ppm) F water, CaþFþ ; LCD þ 100 ppm F water, Ca2Fþ. In phase II (reversal experiment, 3 months), LCD was replaced with the NCD. Treatment groups Caþ Fþ and Ca2Fþ were divided into two subgroups to compare the effect of continuation v. discontinuation along with Ca supplementation on reversal of chronic F toxicity. In phase I, significantly reduced food efficiency ratio (FER), body weight gain (BWG), faecal F excretion, serum Ca and increased bone F deposition were observed in the treatment group Ca2Fþ. Reduced serum 25-hydroxy-vitamin D 3 , increased 1,25-dihydroxy-vitamin D 3 and up-regulation of Ca-sensing receptor, vitamin D receptor and S100 Ca-binding protein G (S100G) were observed in treatment groups Ca2 F2 and Ca2Fþ. In phase II (reversal phase), FER, BWG and serum Ca in treatment groups Ca2 Fþ/Caþ F2 and Ca2Fþ /Caþ Fþ were still lower, as compared with other groups. However, other variables were comparable. Down-regulation of S100G was observed in F-fed groups (Caþ Fþ/Caþ Fþ and Ca2Fþ /Caþ Fþ ) in phase II. It is concluded that low Ca aggravates F toxicity, which can be ameliorated after providing adequate Ca and F-free water. However, chronic F toxicity can interfere with Ca absorption by down-regulating S100G expression irrespective of Ca nutrition.Key words: Chronic fluoride toxicity: Rats: Low calcium: Calcium homeostasis Chronic fluoride (F) toxicity is caused due to exposure to excess F . 1·5 parts per million (ppm) (1) , mainly through water and is endemic in twenty-five countries across the globe. In India, F endemicity has been reported in 196 districts of nineteen states and is considered as a public health problem (2) . Chronic F toxicity is categorised as dental, skeletal and non-skeletal fluorosis, based on the tissue affected. The very first sign of chronic F toxicity is exhibited by teeth, i.e. dental mottling, called dental fluorosis (3) . Skeletal fluorosis progresses in a slow manner and, therefore, is not clinically visible in its initial phase. Clinical symptoms of skeletal fluorosis include restricted movements of joints, stiffness and deformities of the spine such as kyphosis, bony exostoses and paraplegia due to spinal compression (4) . Non-skeletal fluorosis affects tissues other than the dental and skeletal system such as the gastrointestinal tract, brain, muscle, etc. Any kind of manifestation in these organs of inhabitants of fluorotic areas may indicate non-skeletal fluorosis (3) . Apart from these well-defined clinical symptoms, reduced food intake and body weight gain (BWG) have been observed in F-fed animals (5 -8) . However, other studies did not show any difference in BWG (9) in F-fed animals. The rea...

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Amelioration of chronic fluoride toxicity by calcium and fluoride-free water in rats

et al. 2012

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“…Osteosclerosis on imaging and bone biopsy are consistent with the disease. Secondary hyperparathyroidism is also frequently noted [3,4]. While elevated serum, urine, and bone fluoride levels are usually seen, urinary fluoride levels can remain elevated despite normal serum levels following cessation of inhalant abuse, as occurred in our case (the patient had refrained for two months prior to presentation due to psychiatric hospitalization) [5][6][7].…”

Section: Discussionmentioning

confidence: 50%

Skeletal Fluorosis: An Unusual Manifestation of Computer Cleaner Inhalant Abuse

Liane

Chow

Kline

2020

Cureus

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Skeletal fluorosis is a metabolic bone disease caused by accumulation of fluoride and is generally associated with chronic exposure to fluoride-contaminated groundwater, a phenomenon endemic to developing countries. Whereas elevated water fluoride concentrations do not constitute a public health issue in the United States, emergence of skeletal fluorosis as a sequela of chronic recreational exposures has been described. In this case report, our 33-yearold male patient with a history of major depressive disorder and substance abuse was hospitalized for hyperkalemia and acute kidney injury discovered on routine bloodwork due to concomitant nonsteroidal anti-inflammatory drugs (NSAID) and antihypertensive use. Upon hospital admission, he was found to be anemic with a significantly elevated alkaline phosphatase. Given a history of low back pain in the setting of these laboratory abnormalities, lower spine and pelvic imaging revealed diffusely increased bone density and sclerosis. Hematologic evaluation ensued to include a peripheral smear and bone marrow biopsy. Given the patient's history of computer cleaner inhalant abuse, serum and urinary fluoride levels were obtained. Serum fluoride returned within normal limits though urinary fluoride was increased. Bone marrow histopathology revealed prominent diffuse sclerosis which in conjunction with urinary fluoride levels and computer cleaner inhalant abuse history supported the diagnosis of skeletal fluorosis. Skeletal fluorosis in the United States is rare and presents with non-specific findings requiring a high index of suspicion based on a detailed patient history for expedient diagnosis.

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“…Although, clinical cases of skeletal fluorosis are rare in the United States [Kurland et al, 2007; Whyte et al, 2008] in other parts of the world where skeletal fluorosis is more common, patients often demonstrate pseudo-hyperparathyroidism [Teotia and Teotia, 1973; Teotia et al, 1998; Gupta et al, 2001; Xu et al, 2010; Koroglu et al, 2011]. Epidemiologic studies show that individuals of the population exposed to similar fluoride levels demonstrate variable skeletal features ranging from excessive bone formation to bone resorption [Teotia et al, 1998; Harinarayan et al, 2006].…”

Section: Discussionmentioning

confidence: 99%

Fluoride Modulates Parathyroid Hormone Secretion in vivo and in vitro

Puranik¹,

Ryan

Yin³

et al. 2014

Cells Tissues Organs

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The study objective was to investigate the effects of fluoride on intact parathyroid hormone (iPTH) secretion. Thyro-parathyroid complexes (TPC) from C3H (n = 18) and B6 (n = 18) mice were cultured in Ca²⁺-optimized medium. TPC were treated with 0, 250, or 500 µM NaF for 24 h and secreted iPTH assayed by ELISA. C3H (n = 78) and B6 (n = 78) mice were gavaged once with distilled or fluoride (0.001 mg [F^-]/g of body weight) water. At serial time points (0.5-96 h) serum iPTH, fluoride, total calcium, phosphorus, and magnesium levels were determined. Expression of genes involved in mineral regulation via the bone-parathyroid-kidney (BPK) axis, such as parathyroid hormone (Pth), calcium-sensing receptor (Casr), vitamin D receptor (Vdr), parathyroid hormone-like hormone (Pthlh), fibroblast growth factor 23 (Fgf23), α-Klotho (αKlotho), fibroblast growth factor receptor 1c (Fgf1rc), tumor necrosis factor 11 (Tnfs11), parathyroid hormone receptor 1 (Pth1r), solute carrier family 34 member 1 (Slc34a1), solute carrier 9 member 3 regulator 1 (Slc9a3r1), chloride channel 5 (Clcn5), and PDZ domain-containing 1 (Pdzk1), was determined in TPC, humeri, and kidneys at 24 h. An in vitro decrease in iPTH was seen in C3H and B6 TPC at 500 µM (p < 0.001). In vivo levels of serum fluoride peaked at 0.5 h in both C3H (p = 0.002) and B6 (p = 0.01). In C3H, iPTH decreased at 24 h (p < 0.0001), returning to baseline at 48 h. In B6, iPTH increased at 12 h (p < 0.001), returning to baseline at 24 h. Serum total calcium, phosphorus, and magnesium levels did not change significantly. Pth, Casr,αKlotho,Fgf1rc,Vdr, and Pthlh were significantly upregulated in C3H TPC compared to B6. In conclusion, the effects of fluoride on TPC in vitro were equivalent between the 2 mouse strains. However, fluoride demonstrated an early strain-dependent effect on iPTH secretion in vivo. Both strains demonstrated differences in the expression of genes involved in the BPK axis, suggesting a possible role in the physiologic handling of fluoride.

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Serum Parathyroid Hormone Levels in Chronic Endemic Fluorosis

Cited by 27 publications

References 24 publications

Amelioration of chronic fluoride toxicity by calcium and fluoride-free water in rats

Amelioration of chronic fluoride toxicity by calcium and fluoride-free water in rats

Skeletal Fluorosis: An Unusual Manifestation of Computer Cleaner Inhalant Abuse

Fluoride Modulates Parathyroid Hormone Secretion in vivo and in vitro

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