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1.
J Pediatr Hematol Oncol ; 41(2): e83-e89, 2019 03.
Article in English | MEDLINE | ID: mdl-30044347

ABSTRACT

OBJECTIVE: The aim of this study was to evaluate the vitamin D-PTH axis in thalassemia major (TM) in relation to hepatic siderosis liver iron content. DESIGN AND PARTICIPANTS: In this case-controlled observational study, vitamin D-PTH axis was studied in 158 TM and 84 age and ethnicity-matched healthy nonthalassemic controls attending University College Hospital, London. Patients were classified as 25-hydroxy vitamin D (25-OHD) insufficient and sufficient if the value was less than or greater than 50 nmol/L, respectively. 25-OHD data were evaluated in relation to markers of iron load in TM. RESULTS: In TM, 25-OHD insufficiency was 8-fold higher than the control group (odds ratio [OR], 8.1; 95% confidence interval [CI], 4.3-15.0; P<0.001). Similarly, serum PTH (P<0.001), calcium (P<0.001), and phosphate levels (P<0.05) were also significantly lower in TM compared with the controls. In TM, serum ferritin of >2500 µg/L (OR, 5.3; 95% CI, 2.3-12.3; P<0.01), liver iron of >7 mg/g dry weight (OR, 8.8; 95% CI, 3.5-10.3; P<0.001), and serum alanine aminotransferase of >50 IU/L (OR, 9.7; 95% CI, 4.0-23.5; P<0.001) were independent risk factors for low 25-OHD levels. CONCLUSIONS: Our results suggest that TM had a 8-fold higher risk of 25-OHD insufficiency compared with the controls. This was likely to be associated with hepatic hemosiderosis.


Subject(s)
Hemosiderosis/blood , Liver Diseases/blood , Parathyroid Hormone/blood , Vitamin D/analogs & derivatives , beta-Thalassemia/blood , Adult , Alanine Transaminase/blood , Case-Control Studies , Female , Ferritins/metabolism , Hemosiderosis/etiology , Humans , Liver Diseases/etiology , Male , Risk Factors , Vitamin D/blood , beta-Thalassemia/therapy
2.
Neurobiol Aging ; 33(10): 2382-9, 2012 Oct.
Article in English | MEDLINE | ID: mdl-22217419

ABSTRACT

Vitamin D(3) plays a key role in immune regulation and may protect against the aging process. A focal point for age-related changes is the outer retina of the eye where there is high metabolic demand resulting in a gradual increase in extracellular deposition, inflammation, and cell loss giving rise to visual decline. Here, we demonstrate that vitamin D(3) administration for only 6 weeks in aged mice significantly impacts on this aging process. Treated mice showed significant reductions in retinal inflammation and levels of amyloid beta (Aß) accumulation, which is a hallmark of aging. They also had significant reductions in retinal macrophage numbers and marked shifts in their morphology. These changes were reflected in a significant improvement in visual function, revealing that vitamin D(3) is a route to avoiding the pace of age-related visual decline. Excess amyloid beta deposition and inflammation are risk factors leading to age-related macular degeneration (AMD), the largest cause of blindness in those older than 50 years in developed countries. Recently, vitamin D(3) has been linked epidemiologically to protection against age-related macular degeneration. Hence, vitamin D(3) enrichment is likely to represent a beneficial route for those at risk.


Subject(s)
Aging/drug effects , Cholecalciferol/administration & dosage , Retinitis/drug therapy , Amyloid beta-Peptides/metabolism , Animals , Female , Macrophages/drug effects , Macular Degeneration/drug therapy , Mice , Mice, Inbred C57BL , Visual Perception/drug effects
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