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العنوان
Role of Vitamin D and Its Deficiency in Pediatric Critical Illness /
المؤلف
Gohar, Mohamed Abd El Monem Mohamed Abd El Monem.
هيئة الاعداد
باحث / محمد عبد المنعم محمد عبد المنعم جوهر
مشرف / أحمد أنور خطاب
مناقش / نجوان يسري كامل صالح
مناقش / أحمد أنور خطاب
الموضوع
Pediatrics. Pediatric emergencies. Pediatric intensive care.
تاريخ النشر
2016.
عدد الصفحات
119 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
جراحة العظام والطب الرياضي
تاريخ الإجازة
4/12/2016
مكان الإجازة
جامعة المنوفية - كلية الطب - العظام
الفهرس
Only 14 pages are availabe for public view

from 136

from 136

Abstract

Vitamin D3 (Cholecalciferol) and Vitamin D2 (Ergocalciferol) are the most important forms of Vitamin D in human. They are fat soluble vitamins. Skin exposure to UV of the sun is considered the main source of Vitamin D in addition to very few foods that contain it such as salmon, tuna, mackerel, fish liver oils, beef liver, cheese, and egg yolks. Recommended Dietary Allowance (RDA) for Vitamin D for infants below one year is 400 IU and for children more than one year is 600 IU.Vitamin D deficiency is common and has been estimated to affect about one billion people worldwide. While the primary role of this pleiotropic hormone is regulation of calcium metabolism, it also plays a key role in several pathways of the innate immune response system, controlling cell growth, differentiation and apoptosis. Over the last years, several groups have reported on an inverse association between vitamin D levels in critically ill patients and severity of disease including length of ICU stay and mortality. Moreover, Vitamin D levels decline further during ICU stay which is explained by insufficient replacement of vitamin D via enteral or parenteral nutrition in the absence of UV-B exposure. Calcitriol, through VDR receptors, has significant impact on the morphology, proliferation, and growth of cardiac cells.
Calcitriol is known to be one of the negative endocrine regulators of the renin-angiotensin-aldosterone system (RAAS). Calcitriol supplementation was shown to reduce plasma renin activity, angiotensin II levels, blood pressure, and myocardial hypertrophy. Vitamin D deficiency is linked to various mechanisms that play a significant role in the pathogenesis of CHF. These mechanisms include the activation of RAAS, the presence of oxidative stress in different tissues including the skin, skeletal muscles, heart, and peripheral blood mononuclear cells, and activation of pro-inflammatory cytokines as interleukin (IL)-8 and tumor necrosis factor (TNF)-alpha. Cells of the innate and adaptive immune system were shown to express the Vitamin D receptor (VDR). Vitamin D enables macrophages to respond to and kill bacterial and viral organisms and exerts an influence on epidermal keratinocytes to fulfill their barrier function. Monocytes cultured in severely vitamin D-deficient plasma express less cathelicidines and improve their function with 25(OH)D as well as 1,25(OH)2D. Cathelicidines are important antimicrobial peptides that are of great interest in critically ill patients because they constitute part of the initial defense line against pathogens. They are expressed in epithelia of airways, the bladder and gastrointestinal tract, which are all considered important entry sites of nosocomial infections.
Vitamin D deficiency has been shown to increase the risk of viral respiratory tract infections and RSV-associated bronchiolitis. The Vitamin D receptor is present in bronchial smooth muscle cells which are associated with active protein synthesis. It has been demonstrated that Vitamin D inhibits bronchial smooth muscle proliferation induced by platelet-derived growth factor. This finding suggests a role of Vitamin D in cell growth and survival and morphogenesis and airway remodeling, which may be important in asthma patho-physiology and treatment.
Low serum vitamin D levels are a risk factor for pneumonia. The risk of contracting pneumonia was more than 2.5 times greater in subjects with the lowest vitamin D levels than in subjects with high Vitamin D levels. Vitamin D deficiency is common in renal critically ill patients and associated with increased mortality, as well as an increased risk of acute kidney injury. Potential mechanisms of how a deficiency in vitamin D could predispose individuals to increased risk of acute renal failure include dys-regulation of the immune system, predisposing patients to sepsis, endothelial dysfunction and prevention of healing of renal ischemia-reperfusion injury. The non-classical effects of Vitamin D may play a relevant role in the mortality and morbidity of patients with CKD, specifically affecting the possible progression of their renal disease and co-existing cardiovascular disease, which is the major cause of death in this population.
Hypocalcemia is one of the electrolyte disturbances that can cause seizures. Having a stable extracellular ionized calcium concentration is critical for normal brain cell function, and Vitamin D and parathyroid hormone (PTH) play a central role in maintaining a stable extracellular ionized calcium concentration.