Displaying publications 1 - 20 of 41 in total

Abstract:
Sort:
  1. Norazlina M, Chua CW, Ima-Nirwana S
    Med J Malaysia, 2004 Dec;59(5):623-30.
    PMID: 15889565
    Vitamin E deficiency has been found to impair bone calcification. This study was done to determine the effects of vitamin E deficiency and supplementation on parathyroid hormone, i.e. the hormone involved in bone regulation. Female Sprague-Dawley rats were divided into 4 groups: 1) normal rat chow (RC), 2) vitamin E deficiency (VED), vitamin E deficient rats supplemented with 3) 60 mg/kg alpha-tocotrienol (ATT) and 4) 60 mg/kg (alpha-tocopherol (ATF). Treatment was carried out for 3 months. Vitamin E deficiency caused hypocalcaemia during the first month of the treatment period, increased the parathyroid hormone level in the second month and decreased the bone calcium content in the 4th lumbar bone at the end of the treatment. Vitamin E supplementation (ATT and ATF) failed to improve these conditions. The bone formation marker, osteocalcin, and the bone resorption marker, deoxypyridinoline did not change throughout the study period. In conclusion vitamin E deficiency impaired bone calcium homeostasis with subsequent secondary hyperparathyroidism and vertebral bone loss. Replacing the vitamin E with pure ATF or pure ATT alone failed to correct the changes seen.
    Matched MeSH terms: Parathyroid Hormone/blood
  2. Chin KY, Ima-Nirwana S, Ibrahim S, Mohamed IN, Wan Ngah WZ
    Nutrients, 2014 Nov 26;6(12):5419-33.
    PMID: 25431881 DOI: 10.3390/nu6125419
    Vitamin D insufficiency is a global health problem. The data on vitamin D status in Malaysian men is insufficient. This study aimed to investigate vitamin D status among Chinese and Malay men in Malaysia and its associating factors. A cross-sectional study was conducted on 383 men aged 20 years and above, residing in Klang Valley, Malaysia. Their age, ethnicity, body anthropometry and calcaneal speed of sound (SOS) were recorded. Their fasting blood was collected for serum 25-hydroxyvitamin D (25(OH)D), intact parathyroid (PTH), total calcium and inorganic phosphate assays. Vitamin D deficiency was defined as a serum 25(OH)D level <30 nmol/L and insufficiency as a serum 25(OH)D level between 30 and 50 nmol/L. The overall prevalence of vitamin D deficiency was 0.5%, and insufficiency was 22.7%. Vitamin D deficiency and insufficiency were more prevalent in the Malays compared to the Chinese. Being Chinese, older in age, having lower body mass index (BMI) and a high physical activity status were associated significantly with a higher serum 25(OH)D level (p < 0.05). The serum PTH level was inversely associated with the serum 25(OH)D level (p < 0.05). As a conclusion, a significant proportion of Malaysian men have vitamin D insufficiency, although deficiency is uncommon. Steps should be taken to correct the vitamin D status of these men.
    Matched MeSH terms: Parathyroid Hormone/blood
  3. Green TJ, Skeaff CM, Rockell JE, Venn BJ, Lambert A, Todd J, et al.
    Eur J Clin Nutr, 2008 Mar;62(3):373-8.
    PMID: 17342165
    OBJECTIVE: To describe the vitamin D status of women living in two Asian cities,--Jakarta (6 degrees S) and Kuala-Lumpur (2 degrees N), to examine the association between plasma 25-hydroxyvitamin D and parathyroid hormone (PTH) concentrations, and to determine a threshold for plasma 25-hydroxyvitamin D above which there is no further suppression of PTH. Also, to determine whether dietary calcium intake influences the relationship between PTH and 25-hydroxyvitamin D.

    DESIGN: Cross-sectional.

    SETTING: Jakarta, Indonesia and Kuala Lumpur, Malaysia.

    PARTICIPANTS: A convenience sample of 504 non-pregnant women 18-40 years.

    MAIN MEASURES: Plasma 25-hydroxyvitamin D and PTH.

    RESULTS: The mean 25-hydroxyvitamin D concentration was 48 nmol/l. Less than 1% of women had a 25-hydroxyvitamin D concentration indicative of vitamin D deficiency (<17.5 nmol/l); whereas, over 60% of women had a 25-hydroxyvitamin D concentration indicative of insufficiency (<50 nmol/l). We estimate that 52 nmol/l was the threshold concentration for plasma 25-hydroxyvitamin D above which no further suppression of PTH occurred. Below and above this concentration the slopes of the regression lines were -0.18 (different from 0; P=0.003) and -0.01 (P=0.775), respectively. The relation between vitamin D status and parathyroid hormone concentration did not differ between women with low, medium or high calcium intakes (P=0.611); however, even in the highest tertile of calcium intake, mean calcium intake was only 657 mg/d.

    CONCLUSION: On the basis of maximal suppression of PTH we estimate an optimal 25-hydroxyvitamin D concentration of approximately 50 nmol/l. Many women had a 25-hydroxyvitamin D below this concentration and may benefit from improved vitamin D status.

    Matched MeSH terms: Parathyroid Hormone/blood*
  4. Ngai M, Lin V, Wong HC, Vathsala A, How P
    Clin. Nephrol., 2014 Oct;82(4):231-9.
    PMID: 25161115 DOI: 10.5414/CN108182
    BACKGROUND: Vitamin D deficiency is associated with secondary hyperparathyroidism and mineral and bone disorder (MBD) in chronic kidney disease (CKD). This study aimed to determine the prevalence of vitamin D insufficiency/deficiency, and the association between vitamin D status and MBD in a multi-ethnic CKD population in Southeast Asia.

    METHODS: Predialysis CKD patients were included in this cross-sectional study. Patient demographics, medical/medication histories, and laboratory parameters (serum 25-hydroxyvitamin D (25(OH)D), creatinine, phosphate (P), calcium, albumin, and intact-PTH (i-PTH)) were collected and compared among patients with various CKD stages. The association between 25(OH)D and these parameters was determined by multiple linear regression.

    RESULTS: A total of 196 patients with mean ± SD eGFR of 26.4 ± 11.2 mL/min/1.73 m2 was included. Vitamin D deficiency (25(OH)D concentration < 15 ng/mL) and insufficiency (25(OH)D concentration 16 - 30 ng/mL) was found in 29.1% and 57.7% of the patients, respectively. Mean ± SD serum 25(OH)D was 20.8 ± 9.3 ng/mL. Female patients had lower vitamin D concentrations than males (16.9 ng/mL vs. 23.9 ng/mL; p < 0.001). Vitamin D levels were also higher in Chinese (22.3 ng/mL) than Malay (17.3 ng/mL) and Indian (13.1 ng/mL) patients (p < 0.05). Nonadjusted analyses showed higher i-PTH concentration in vitamin D deficient patients (p < 0.05).

    CONCLUSION: Despite being a sun-rich country all year round, the majority (86.8%) of predialysis CKD patients in Singapore have suboptimal vitamin D status. Lower vitamin D concentrations were found in females and in those with darker skin tone. Vitamin D deficient patients also tended to have higher i-PTH levels.

    Matched MeSH terms: Parathyroid Hormone/blood
  5. Rahman SA, Chee WS, Yassin Z, Chan SP
    Asia Pac J Clin Nutr, 2004;13(3):255-60.
    PMID: 15331337
    Serum levels of 25-hydroxyvitamin D (25 (OH) D) were determined in 276 (103 Malays and 173 Chinese) postmenopausal women, aged 50 to 65 years. The level of 25 (OH) D was significantly lower in the postmenopausal Malay women (44.4 +/-10.6 nmol/L) compared to the Chinese women (68.8 +/- 15.7 nmol/L) (P<0.05). There were 27% Malay women with serum 25 (OH) D in the range of 50 - 100 nmol/L (defined as lowered vitamin D status, or hypovitaminosis D) and 71% with levels in the range of 25 - 50 nmol/L (defined as vitamin D insufficiency) compared to 87% and 11% Chinese women respectively. Serum 25 (OH) D was found to significantly correlate with BMI, fat mass and PTH level. Multivariate analyses showed that race has a strong association with vitamin D status. The high prevalence of inadequate levels of serum vitamin D found in our study may have important public health consequences and warrants the development of a strategy to correct this problem in the older adult Malaysian population.
    Matched MeSH terms: Parathyroid Hormone/blood
  6. Tan KM, Saw S, Sethi SK
    J Clin Lab Anal, 2013 Jul;27(4):301-4.
    PMID: 23852789 DOI: 10.1002/jcla.21602
    BACKGROUND: In this study, we aimed to determine the normal ranges of 25-hydroxy-vitamin D(3) (25-OHD(3)), parathyroid hormone (PTH), and the markers of bone turnover, procollagen type 1 N propeptide (P1NP) and C-terminal cross-linked telopeptide of type 1 collagen (CTX), in normal healthy women in Singapore, and to explore the relationship between vitamin D, PTH, and these markers of bone turnover in the women.

    METHODS: One hundred and ninety-seven healthy women, aged 25 to 60, were selected from a hospital staff health screening program; 68% were Chinese, 18% Malay, and 14% Indian. P1NP, CTX, and 25-OHD(3) were measured using the Roche Cobas® electrochemiluminescence immunoassay. Serum PTH was measured using the Siemens ADVIA Centaur® immunoassay.

    RESULTS: Sixty-five percent had 25-OHD(3) concentrations <50 nmol/l. Vitamin D insufficiency (25-OHD(3) < 50 nmol/l) was more prevalent in Malays (89%) and Indians (82%) compared to Chinese (56%). There was no correlation between vitamin D and age. PTH positively correlated with age, and Malays and Indians had higher PTH concentrations than Chinese. There was an inverse correlation between PTH and 25-OHD(3), but no threshold of 25-OHD(3) concentrations at which PTH plateaued. The bone turnover markers P1NP and CTX inversely correlated with age but were not different between ethnic groups. CTX and P1NP exhibited good correlation, however, there was no significant correlation between 25-OHD(3) or PTH concentrations and the bone turnover markers P1NP and CTX.

    CONCLUSIONS: Healthy women in Singapore have a high prevalence of vitamin D insufficiency. Vitamin D insufficiency was more prevalent in Malays and Indians compared to Chinese.

    Matched MeSH terms: Parathyroid Hormone/blood
  7. Ralph AP, Rashid Ali MRS, William T, Piera K, Parameswaran U, Bird E, et al.
    BMC Infect Dis, 2017 04 27;17(1):312.
    PMID: 28449659 DOI: 10.1186/s12879-017-2314-z
    BACKGROUND: Vitamin D deficiency (low plasma 25-hydroxyvitamin D [25D] concentration) is often reported in tuberculosis. Adjunctive vitamin D has been tested for its potential to improve treatment outcomes, but has proven largely ineffective. To better understand vitamin D in tuberculosis, we investigated determinants of 25D and its immunologically active form, 1,25-dihydroxyvitamin D (1,25D), their inter-relationship in tuberculosis, longitudinal changes and association with outcome.
    METHODS: In a prospective observational study of adults with smear-positive pulmonary tuberculosis in Sabah, Malaysia, we measured serial 25D, 1,25D, vitamin D-binding protein (VDBP), albumin, calcium, parathyroid hormone, chest x-ray, week 8 sputum smear/culture and end-of-treatment outcome. Healthy control subjects were enrolled for comparison.
    RESULTS: 1,25D was elevated in 172 adults with tuberculosis (mean 229.0 pmol/L, 95% confidence interval: 215.4 - 242.6) compared with 95 controls (153.9, 138.4-169.4, p 
    Matched MeSH terms: Parathyroid Hormone/blood
  8. Md Dom S, Abdul Razak HR, Ahmad Zaiki FW, Saat NH, Abd Manan K, Che Isa IN, et al.
    Quant Imaging Med Surg, 2013 Feb;3(1):49-53.
    PMID: 23483040 DOI: 10.3978/j.issn.2223-4292.2013.02.06
    The aim of this study was to investigate the changes in parathyroid hormone (PTH) level of rabbit foetal bodies exposed to ultrasound at different gestational stages. A total of 9 pregnant rabbits (Oryctolagus cuniculus) were insonated for 60 minutes at the middle of 1(st), 2(nd) and 3(rd) gestational stages for group A (n=14 newborns), group B (n=7 newborns) and group C (n=24 newborns) respectively. Seven pregnant rabbits with 41 newborns severed as negative control group. Blood samples were withdrawn from each newborn rabbits for Parathyroid Hormone-Intact (PTH-I) test. Results of the independent samples t-test implied statistically significant differences (P<0.05) between the control group and the 1(st) stage (P=0.001), the 2(nd) stage (P<0.001) and the 3(rd) stage group (P<0.001). This in-vivo study revealed diagnostic ultrasound heating has the potential of affecting foetal PTH level. This study observed significantly low PTH level for all the treated groups. A further study should be instituted to determine whether this finding in rabbit may also occur in human by means of clinical trials.
    Matched MeSH terms: Parathyroid Hormone
  9. Ismail NA, Kamaruddin NA, Azhar Shah S, Sukor N
    Clin Endocrinol (Oxf), 2020 06;92(6):509-517.
    PMID: 32073675 DOI: 10.1111/cen.14177
    INTRODUCTION: Primary aldosteronism (PA) contributed to the cardiovascular disease and metabolic alterations independent of the blood pressure level. Evidence exists that aldosterone excess also affects calcium and mineral homeostasis. PA subjects have been shown to have greater prevalence of vitamin D deficiency. However, the impact of vitamin D treatment in this population has never been assessed.

    OBJECTIVE: This study aimed to evaluate the effect of vitamin D treatment on clinical and biochemical outcomes of PA patients.

    METHODS: Two hundred forty hypertensive subjects were screened, 31 had positive ARR, and 17 patients with newly confirmed PA following positive confirmatory test that has not been subjected for definitive treatment were enrolled. Clinical parameter (blood pressure) and biochemical parameters (renal profile, plasma aldosterone concentration, plasma renin activity, serum calcium, vitamin D, intact parathyroid hormone, 24-hour urinary calcium) were measured at baseline and 3 months of treatment with Bio-D3 capsule. Primary outcomes were the changes in the blood pressure and biochemical parameters.

    RESULTS: About 70% of our PA subjects have low vitamin D levels at baseline. Three months following treatment, there were significant: (a) improvement in 25(OH)D levels; (b) reduction in systolic blood pressure and plasma aldosterone concentration; and (c) improvement in the eGFR. The vitamin D deficient subgroup has the greatest magnitude of the systolic blood pressure reduction following treatment.

    CONCLUSIONS: This study demonstrated significant proportion of PA patients has vitamin D insufficiency. Vitamin D treatment improves these interrelated parameters possibly suggesting interplay between vitamin D, aldosterone, renal function and the blood pressure.

    Matched MeSH terms: Parathyroid Hormone
  10. Chee WS, Suriah AR, Chan SP, Zaitun Y, Chan YM
    Osteoporos Int, 2003 Oct;14(10):828-34.
    PMID: 12915959
    Dietary studies often report low calcium intake amongst post-menopausal Malaysian women and calcium deficiency has been implicated as part of the etiology of age-related bone loss leading to osteoporosis. Therefore, the objective of this study was to examine the effectiveness of high calcium skimmed milk (Anlene Gold, New Zealand Milk, Wellington, New Zealand) to reduce bone loss in Chinese postmenopausal women. Two hundred subjects aged 55-65 years and who were more than 5 years postmenopausal were randomized to a milk group and control group. The milk group consumed 50 g of high calcium skimmed milk powder daily, which contained 1200 mg calcium (taken as two glasses of milk a day). The control group continued with their usual diet. Using repeated measures ANCOVA, the milk supplement was found to significantly reduce the percentage of bone loss at the total body compared to the control group at 24 months (control -1.04%, milk -0.13%; P<0.001). At the lumbar spine, the percentage of bone loss in the control group was significantly higher (-0.90%) when compared to the milk (-0.13%) supplemented group at 24 months (P<0.05). Similarly, milk supplementation reduced the percentage of bone loss at the femoral neck (control -1.21%, milk 0.51%) (P<0.01) and total hip (control -2.17%, milk -0.50%) (P<0.01). The supplemented group did not experience any significant weight gain over the 24 months. The serum 25-hydroxy vitamin D level improved significantly (P<0.01) from 69.1 +/- 16.1 nmol/l at baseline to 86.4 +/- 22.0 nmol/l at 24 months in the milk group. In conclusion, ingestion of high calcium skimmed milk was effective in reducing the rate of bone loss at clinically important lumbar spine and hip sites in postmenopausal Chinese women in Malaysia. Supplementing with milk had additional benefits of improving the serum 25-hydroxy vitamin D status of the subjects.
    Matched MeSH terms: Parathyroid Hormone/blood
  11. Wong SK, Chin KY, Ima-Nirwana S
    PMID: 31505801 DOI: 10.3390/ijerph16183313
    A positive association between metabolic syndrome (MetS) and osteoporosis has been demonstrated in previous animal studies. The mechanisms of MetS in orchestrating the bone remodelling process have traditionally focused on the interactions between mature osteoblasts and osteoclasts, while the role of osteocytes is unexplored. Our earlier studies demonstrated the bone-promoting effects of tocotrienol using a rat model of osteoporosis induced by MetS. This study aimed to investigate the expression of osteocyte-derived peptides in the bone of rats with MetS-induced osteoporosis treated with tocotrienol. Age-matched male Wistar rats (12-week-old; n = 42) were divided into seven experimental groups. Two groups served as the baseline and normal group, respectively. The other five groups were fed with a high-carbohydrate high-fat (HCHF) diet to induce MetS. The five groups of HCHF animals were treated with tocopherol-stripped corn oil (vehicle), annatto tocotrienol (60 and 100 mg/kg), and palm tocotrienol (60 and 100 mg/kg) starting from week 8. At the end of the study, the rats were sacrificed and their right tibias were harvested. Protein was extracted from the metaphyseal region of the proximal right tibia and levels of bone peptides, including osteoprotegerin (OPG), soluble receptor activator of nuclear factor-kappa B ligand (sRANKL), sclerostin (SOST), Dickkopf-related protein 1 (DKK-1), fibroblast growth factor-23 (FGF-23), and parathyroid hormone (PTH), were measured. The vehicle-treated animals displayed higher levels of sRANKL, SOST, DKK-1, FGF-23, and PTH as compared to the normal animals. Oral supplementation of annatto and palm tocotrienol (60 and 100 mg/kg) reduced the levels of sRANKL and FGF-23 in the HCHF animals. Only 100 mg/kg annatto and palm tocotrienol lowered SOST and DKK-1 levels in the HCHF animals. In conclusion, tocotrienol exerts potential skeletal-promoting benefit by modulating the levels of osteocytes-derived bone-related peptides.
    Matched MeSH terms: Parathyroid Hormone/metabolism
  12. Chin KY, Nirwana SI, Ngah WZ
    Clin Interv Aging, 2015;10:1377-80.
    PMID: 26346636 DOI: 10.2147/CIA.S90233
    Previous reports of patients undergoing parathyroidectomy and of patients receiving teriparatide as antiosteoporotic treatment have suggested a plausible relationship between parathyroid hormone (PTH) and uric acid. However, similar data at population level were lacking. The current study aimed to determine the relationship between PTH and uric acid in a group of apparently healthy Malaysian men.
    Matched MeSH terms: Parathyroid Hormone/blood*
  13. Singh HJ, Mohammad NH, Nila A
    J Matern Fetal Med, 1999 May-Jun;8(3):95-100.
    PMID: 10338062
    To ascertain the calcium status in normal pregnant Malay women.
    Matched MeSH terms: Parathyroid Hormone/blood*
  14. Ong LM, Narayanan P, Goh HK, Manocha AB, Ghazali A, Omar M, et al.
    Nephrology (Carlton), 2013 Mar;18(3):194-200.
    PMID: 23311404 DOI: 10.1111/nep.12029
    The objective of the study was to compare the efficacy and safety of oral paricalcitol with oral calcitriol for treating secondary hyperparathyroidism.
    Matched MeSH terms: Parathyroid Hormone/blood
  15. Lim KP, Yong SL
    Malays Fam Physician, 2019;14(1):31-34.
    PMID: 31289630
    We describe a 29-year-old Para 1 post-Emergency Lower Segment Caesarean Section (EMLSCS) for fetal distress and Preterm Rupture of the Membrane (PROM) referred by the Obstetric team for persistent bradycardia. She had the typical features of Albright's Hereditary Osteodystrophy (AHO). The laboratory investigation revealed hypocalcemia, hyperphosphatemia with a high Parathyroid hormone (PTH) level and low free Thyroxine 4 (fT4) with high Thyroid Stimulating Hormone (TSH). The patient was diagnosed with Pseudohypoparathyroidism (PHP) Type 1A associated with TSH resistance based on the somatic features of AHO present as well as biochemical and radiological abnormalities.
    Matched MeSH terms: Parathyroid Hormone
  16. Wong SK, Mohamad NV, Giaze TR, Chin KY, Mohamed N, Ima-Nirwana S
    Int J Mol Sci, 2019 May 27;20(10).
    PMID: 31137764 DOI: 10.3390/ijms20102587
    Patients with advanced prostate cancer often develop bone metastases, leading to bone pain, skeletal fracture, and increased mortality. Bone provides a hospitable microenvironment to tumor cells. The disease manifestation is driven by the interaction between invading tumor cells, bone-forming osteoblasts, and bone-resorbing osteoclasts. The increased level of osteoclast-activating factor (parathyroid hormone-related peptide, PTHrP) is believed to induce bone resorption by upregulating receptor activator of nuclear factor-kappa B ligand (RANKL) and the release of various growth factors into the bone microenvironment to enhance cancer cell growth. However, the underlying molecular mechanisms remain poorly understood. This review outlines the possible molecular mechanisms involved in governing bone metastases driven by prostate cancer, which further provide the basis in searching for new molecular targets for the development of potential therapy.
    Matched MeSH terms: Parathyroid Hormone-Related Protein/metabolism
  17. Norazmi, K., Khairul, A.J.
    MyJurnal
    Primary hyperparathyroidism with severe bone disease as a result of excessive parathyroid hormone ( PTH ) release and severe hypercalcaemia can lead to 'hungry bone syndrome' (HBS) post operatively. This is due to sudden cessation of PTH and drop in serum calcium. We reported a case a young man with primary hyperparathyriodism due to a single parathyroid adenoma with severe bone disease and post operatively developed hungry bone syndrome.
    Matched MeSH terms: Parathyroid Hormone
  18. Ng JS, Chin KY
    Int J Med Sci, 2021;18(3):604-614.
    PMID: 33437195 DOI: 10.7150/ijms.50680
    Chronic psychological stress affects many body systems, including the skeleton, through various mechanisms. This review aims to provide an overview of the factors mediating the relationship between psychological stress and bone health. These factors can be divided into physiological and behavioural changes induced by psychological stress. The physiological factors involve endocrinological changes, such as increased glucocorticoids, prolactin, leptin and parathyroid hormone levels and reduced gonadal hormones. Low-grade inflammation and hyperactivation of the sympathetic nervous system during psychological stress are also physiological changes detrimental to bone health. The behavioural changes during mental stress, such as altered dietary pattern, cigarette smoking, alcoholism and physical inactivity, also threaten the skeletal system. Psychological stress may be partly responsible for epigenetic regulation of skeletal development. It may also mediate the relationship between socioeconomic status and bone health. However, more direct evidence is required to prove these hypotheses. In conclusion, chronic psychological stress should be recognised as a risk factor of osteoporosis and stress-coping methods should be incorporated as part of the comprehensive osteoporosis-preventing strategy.
    Matched MeSH terms: Parathyroid Hormone/metabolism
  19. Campion KL, McCormick WD, Warwicker J, Khayat ME, Atkinson-Dell R, Steward MC, et al.
    J Am Soc Nephrol, 2015 Sep;26(9):2163-71.
    PMID: 25556167 DOI: 10.1681/ASN.2014070653
    The calcium-sensing receptor (CaR) modulates renal calcium reabsorption and parathyroid hormone (PTH) secretion and is involved in the etiology of secondary hyperparathyroidism in CKD. Supraphysiologic changes in extracellular pH (pHo) modulate CaR responsiveness in HEK-293 (CaR-HEK) cells. Therefore, because acidosis and alkalosis are associated with altered PTH secretion in vivo, we examined whether pathophysiologic changes in pHo can significantly alter CaR responsiveness in both heterologous and endogenous expression systems and whether this affects PTH secretion. In both CaR-HEK and isolated bovine parathyroid cells, decreasing pHo from 7.4 to 7.2 rapidly inhibited CaR-induced intracellular calcium (Ca(2+)i) mobilization, whereas raising pHo to 7.6 potentiated responsiveness to extracellular calcium (Ca(2+)o). Similar pHo effects were observed for Ca(2+)o-induced extracellular signal-regulated kinase phosphorylation and actin polymerization and for L-Phe-induced Ca(2+)i mobilization. Intracellular pH was unaffected by acute 0.4-unit pHo changes, and the presence of physiologic albumin concentrations failed to attenuate the pHo-mediated effects. None of the individual point mutations created at histidine or cysteine residues in the extracellular domain of CaR attenuated pHo sensitivity. Finally, pathophysiologic pHo elevation reversibly suppressed PTH secretion from perifused human parathyroid cells, and acidosis transiently increased PTH secretion. Therefore, pathophysiologic pHo changes can modulate CaR responsiveness in HEK-293 and parathyroid cells independently of extracellular histidine residues. Specifically, pathophysiologic acidification inhibits CaR activity, thus permitting PTH secretion, whereas alkalinization potentiates CaR activity to suppress PTH secretion. These findings suggest that acid-base disturbances may affect the CaR-mediated control of parathyroid function and calcium metabolism in vivo.
    Matched MeSH terms: Parathyroid Hormone/secretion*
  20. Abukhadir SS, Mohamed N, Mohamed N
    Curr Drug Targets, 2013 Dec;14(13):1601-10.
    PMID: 24138635
    Osteoporosis is the most common bone disease in humans; it represents a major public health problem. This chronic disease is characterized by increase in bone fracture due to: reduced bone mass, deterioration of micro architectural and decreased bone strength, bone fragility; and bone mineral density 2.5 or more standard deviations below the normal mean. Secondary osteoporosis is a common cause of osteoporosis, and there are many underlying risk factors for osteoporosis. Chronic alcohol abuse is one of the modifiable risk factors in osteoporosis. There is evidence of correlation between chronic alcohol abuse and low bone mass. Alcohol is directly toxic to the bone; with increased incidence of fractures and complications. Although there is a paucity of studies regarding alcohol induced osteoporosis therapy, it can be classified into antiresorptive therapy and anabolic therapy. Bisphosphonates have been demonstrated to be clinically relevant to prevent bone damage associated with alcohol use while parathyroid hormone increased bone mineralization as well as bone formation in alcohol treated rats. Vitamin D supplementation could prevent bone toxicity in chronic drinkers. This review discussed the pathogenesis of alcohol-induced osteoporosis and the agents available for its treatment. Other potential therapies are also discussed.
    Matched MeSH terms: Parathyroid Hormone/pharmacology; Parathyroid Hormone/therapeutic use
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links