Bilateral Simultaneous Avulsion Fractures of the Proximal Tibia in a 14-Year-Old Athlete with Vitamin-D Deficiency

Fractures involving the proximal tibial epiphysis are rare and form 0.5% of all epiphyseal injuries. The specific anatomical and developmental features of the proximal tibial epiphysis make it vulnerable to unique patterns of fractures. Vitamin-D plays a vital role in bone homeostasis and its deficiency has an impact on fracture risk and healing. We present the first ever reported case of simultaneous bilateral proximal tibial physeal fractures in an athlete with vitamin-D deficiency. Treatment consisted of plaster immobilisation, and the patient made a full recovery and returned to preinjury level of activities. We report this case for its uniqueness and as an educational review of the importance of the developmental anatomy of the proximal tibia. We review the literature and discuss how the stages of the growing physis determine the type of fracture sustained.

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Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice

Endocrine Reviews ◽

10.1210/er.2008-0004 ◽

2008 ◽

Vol 29 (6) ◽

pp. 726-776 ◽

Cited By ~ 984

Author(s):

Roger Bouillon ◽

Geert Carmeliet ◽

Lieve Verlinden ◽

Evelyne van Etten ◽

Annemieke Verstuyf ◽

...

Keyword(s):

Vitamin D ◽

Vitamin D Deficiency ◽

Growth Plate ◽

Vitamin D Receptor ◽

Endocrine System ◽

Bone Homeostasis ◽

High Calcium Intake ◽

Full Spectrum ◽

High Calcium ◽

Deficient Mice

Abstract The vitamin D endocrine system is essential for calcium and bone homeostasis. The precise mode of action and the full spectrum of activities of the vitamin D hormone, 1,25-dihydroxyvitamin D [1,25-(OH)2D], can now be better evaluated by critical analysis of mice with engineered deletion of the vitamin D receptor (VDR). Absence of a functional VDR or the key activating enzyme, 25-OHD-1α-hydroxylase (CYP27B1), in mice creates a bone and growth plate phenotype that mimics humans with the same congenital disease or severe vitamin D deficiency. The intestine is the key target for the VDR because high calcium intake, or selective VDR rescue in the intestine, restores a normal bone and growth plate phenotype. The VDR is nearly ubiquitously expressed, and almost all cells respond to 1,25-(OH)2D exposure; about 3% of the mouse or human genome is regulated, directly and/or indirectly, by the vitamin D endocrine system, suggesting a more widespread function. VDR-deficient mice, but not vitamin D- or 1α-hydroxylase-deficient mice, and man develop total alopecia, indicating that the function of the VDR and its ligand is not fully overlapping. The immune system of VDR- or vitamin D-deficient mice is grossly normal but shows increased sensitivity to autoimmune diseases such as inflammatory bowel disease or type 1 diabetes after exposure to predisposing factors. VDR-deficient mice do not have a spontaneous increase in cancer but are more prone to oncogene- or chemocarcinogen-induced tumors. They also develop high renin hypertension, cardiac hypertrophy, and increased thrombogenicity. Vitamin D deficiency in humans is associated with increased prevalence of diseases, as predicted by the VDR null phenotype. Prospective vitamin D supplementation studies with multiple noncalcemic endpoints are needed to define the benefits of an optimal vitamin D status.

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Effect of Vitamin D3 on Untreated Graves' Disease with Vitamin D Deficiency

Clinical Medicine Insights Case Reports ◽

10.4137/ccrep.s13157 ◽

2014 ◽

Vol 7 ◽

pp. CCRep.S13157 ◽

Cited By ~ 4

Author(s):

Omar N. Alhuzaim ◽

Naji Aljohani

Keyword(s):

Vitamin D ◽

Thyroid Gland ◽

Vitamin D Deficiency ◽

Vitamin D3 ◽

Graves Disease ◽

Bone Homeostasis ◽

Heterogeneous Distribution ◽

Satisfactory Outcome ◽

Vitamin D Levels ◽

History Of

Objective Besides its classical role in calcium and bone homeostasis, vitamin D is considered a potent immunomodulator that can affect the pathogenesis of several autoimmune diseases. Our aim is to evaluate the effect of vitamin D correction to a patient with new onset Graves' disease (GD) with an underlying vitamin D deficiency. Method We describe the effect of vitamin D3 on untreated Graves' disease with vitamin D deficiency. Results A healthy Saudi woman in her 40s sought consultation with a three-month history of palpitation. She denied any history of heat intolerance, weight loss, menstrual irregularity or sweating. She has a history of chronic muscle aches and pains. Physical examination revealed a mild diffusely enlarged and non-tender thyroid gland with no bruit. She had no signs of Graves' ophthalmopathy. In laboratory examinations, the initial thyroid function test, which was done in an outside hospital, revealed a TSH, 0.01 mIU/L; FT4, 22.5 pmol/L and FT3, 6.5 pmol/L. Vitamin D 25-OH level was done in our hospital and showed a result of 26.0 nmol/L with a TSH, 0.013 mIU/L; FT4, 16.7 pmol/L; and FT3, 3.8 pmol/L. TSH receptor antibody was positive. TC-99 m thyroid scintigraphy demonstrated an enlarged thyroid gland with increased radiotracer trapping and heterogeneous distribution. The patient was given only oral cholecalciferol 4000 IU per day since November 2012 (prescribed by an outside hospital) then from May 2013 onwards she was given 50,000 IU per month. Follow-up laboratory exams revealed improved vitamin D levels as well as TSH and FT4. She eventually improved both clinically and biochemically with a satisfactory outcome. Conclusion Vitamin D deficiency may exacerbate the onset and/or development of GD and correction of the deficiency may be able to reverse it. However, further prospective clinical studies will be needed to define the role of vitamin D treatment in GD.

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Vitamin D Deficiency and Possible Role in Multiple Sclerosis

European Neurological Review ◽

10.17925/enr.2015.10.02.131 ◽

2015 ◽

Vol 10 (2) ◽

pp. 131 ◽

Cited By ~ 3

Author(s):

Michael F Holick ◽

Stuart Cook ◽

Gustavo Suarez ◽

Mark Rametta ◽

◽

...

Keyword(s):

Multiple Sclerosis ◽

Vitamin D ◽

General Population ◽

Serum Level ◽

Vitamin D Deficiency ◽

Sun Exposure ◽

Vitamin D Supplementation ◽

Protective Effects ◽

Bone Homeostasis ◽

Vitamin D Metabolism

Vitamin D is not only an essential nutrient for bone homeostasis but has also been implicated in many other disorders including cardiovascular disease (CVD) and autoimmune diseases. Here we review the problem of vitamin D deficiency and guidelines to help achieve adequate levels in both the general population and in multiple sclerosis (MS) patients and its role in MS and impact on treatment. Although there is a lack of consensus on vitamin D deficiency and insufficiency, they have been defined as a serum level of 25(OH)D <50 nmol/L or 52.5–72.5 nmol/L, respectively. Deficiency is common in all age groups. Vitamin D is probably involved in the prevention of a number of disease states and 25(OH)D is thought to regulate at least 2,000 genes. Vitamin D toxicity is very rare, with none seen at doses up to 20,000 IU/day. However, the majority of primary care clinicians are not aware of the recommended dose for vitamin D supplementation and optimum serum level in terms of patients with MS. Several organisations have concluded that vitamin D screening cannot be recommended in the general population. Guidelines have been published on treatment and prevention of vitamin D deficiency, particularly for at-risk groups and during pregnancy. There is much evidence for the protective effects of vitamin D in MS. A higher level of sun exposure and intake of vitamin D as well as of serum 25 (OH)D, are associated with a lower risk of MS. It also has a beneficial effect on the clinical course of MS, such as lowering the risk of relapses. Growing evidence indicates that the effects of interferon-beta are additively enhanced by 25(OH)D in MS and this may be due to its modulating vitamin D metabolism.

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Vitamin D deficiency and the course of SARS-CoV-2 infection

Pediatria i Medycyna Rodzinna ◽

10.15557/pimr.2021.0002 ◽

2021 ◽

Vol 17 (1) ◽

pp. 17-21

Author(s):

Agnieszka Lipińska-Opałka ◽

◽

Joanna Milart ◽

Jacek Z. Kubiak ◽

Bolesław Kalicki ◽

...

Keyword(s):

Vitamin D ◽

Immune Response ◽

Vitamin D Deficiency ◽

Serum Vitamin ◽

Main Role ◽

Bone Homeostasis ◽

Strong Argument ◽

Serum Vitamin D ◽

Vitamin D Levels ◽

Anti Inflammatory

Vitamin D is a fat-soluble steroid hormone. Its main role is to regulate calcium and phosphate levels, which are strictly associated with ossification and bone homeostasis. However, due to the presence of a nuclear vitamin D receptor (VDR) in the majority of cells of the human body, vitamin D also displays multiple effects beyond the bones. Calcitriol (1,25(OH)2D) not only affects cell growth and differentiation, but also stimulates the immune system by, for example, modulating the production of IL-4 and IL-5 anti-inflammatory cytokines. High numbers of VDRs have been found on macrophages, dendritic cells and lymphocytes, among other cells, which can be considered a very strong argument for the participation of vitamin D in autoimmune and anti-inflammatory processes. In recent months we have been witnessing the development of the COVID-19 pandemic. One of the most dangerous consequences of SARS-CoV-2 infection is acute respiratory distress syndrome caused by the activation of lung macrophages and the so-called cytokine storm. A recent study on COVID-19 patients suggests that vitamin D activates the innate immune response and suppresses the acquired immune response; the resultant decreased cytokine expression can reduce the severity of inflammation associated with COVID-19. Among older children and adults, vitamin D deficiency is widespread and observed worldwide, including in the Polish population. Based on numerous studies, normal serum vitamin D levels were established. Vitamin D concentration below 20 ng/mL is considered deficient and a level between 20 and 30 ng/mL is regarded as suboptimal. An optimal vitamin D concentration is 30–50 ng/mL.

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