Displaying all 4 publications

  1. Chong HC, Chee SS, Goh EM, Chow SK, Yeap SS
    Clin Rheumatol, 2007 Feb;26(2):182-5.
    PMID: 16565892 DOI: 10.1007/s10067-006-0258-6
    The primary objective of this study was to determine the relationship between dietary calcium intake and bone mineral density (BMD) in premenopausal women with systemic lupus erythematosus (SLE) on corticosteroids (CS). The secondary aim was to identify other risk factors for osteoporosis in these patients. A cross-sectional sample of patients attending the SLE Clinic at a teaching hospital was recruited. BMD was measured using dual-energy X-ray absorptiometry. Daily dietary calcium intake was assessed using a structured validated food frequency questionnaire, in which patients were asked to estimate their food intake based on their recent 2-month dietary habits. Sixty subjects were recruited with a mean age of 33.70+/-8.46 years. The median duration of CS use was 5.5 years (range 0.08-24). The median cumulative dose of steroids was 17.21 g (range 0.16-91.37). The median daily dietary calcium intake was 483 mg (range 78-2101). There was no significant correlation between calcium intake and BMD, even after correcting for CS use. There were also no correlations between BMD and the duration of SLE, cumulative CS use, duration of CS use, smoking, alcohol intake, and SLE disease activity index score. Twenty-eight (46.7%) patients had normal BMD, 28 (46.7%) had osteopenia, and four (6.6%) had osteoporosis. Duration of SLE significantly correlated with cumulative CS dosage. In conclusion, 6.7% of these Asian premenopausal SLE women had osteoporosis and only 46.7% had normal BMD. Daily dietary calcium intake did not correlate with BMD.
    Study site: SLE clinic, University Malaya Medical Centre (UMMC), Kuala Lumpur, Malaysia
    Matched MeSH terms: Lumbar Vertebrae/metabolism
  2. Fong CY, Kong AN, Noordin M, Poh BK, Ong LC, Ng CC
    Eur. J. Paediatr. Neurol., 2018 Jan;22(1):155-163.
    PMID: 29122496 DOI: 10.1016/j.ejpn.2017.10.007
    INTRODUCTION: Children with epilepsy on long-term antiepileptic drugs (AEDs) are at risk of low bone mineral density (BMD). The aims of our study were to evaluate the prevalence and determinants of low BMD among Malaysian children with epilepsy.

    METHOD: Cross-sectional study of ambulant children with epilepsy on long-term AEDs for >1 year seen in a tertiary hospital in Malaysia from 2014 to 2015. Detailed assessment of anthropometric measurements; environmental lifestyle risk factors; serum vitamin D, calcium and parathyroid hormone levels; genotyping of single nucleotide polymorphisms of genes in vitamin D and calcium metabolism; and lumbar spine BMD were obtained. Low BMD was defined as BMD Z-score ≤ -2.0 SD.

    RESULTS: Eighty-seven children with mean age of 11.9 years (56 males) participated in the study. The prevalence of low lumbar BMD was 21.8% (19 patients). Multivariate logistic regression analysis identified polytherapy >2 AEDs (OR: 7.86; 95% CI 1.03-59.96), small frame size with wrist breadth of <15th centile (OR 14.73; 95% CI 2.21-98.40), and body mass index Z-score 2 AEDs, underweight or with small frame size as they are at higher risk of having low BMD.

    Matched MeSH terms: Lumbar Vertebrae/metabolism*
  3. 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: Lumbar Vertebrae/metabolism*
  4. Tan TT, Lau IS, Kong NC, Zainal AG
    Malays J Pathol, 1997 Jun;19(1):27-33.
    PMID: 10879239
    Matched MeSH terms: Lumbar Vertebrae/metabolism
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