![]() ![]() Hootsuite - Social Media Management. With Hootsuite, you can monitor keywords, manage multiple Twitter, Facebook, LinkedIn, Foursquare and WordPress profiles. Original Article. Cetuximab-Induced Anaphylaxis and IgE Specific for Galactose-. Christine H. Chung, M.D., Beloo Mirakhur, M.D., Ph.D., Emily Chan, M. Find patient medical information for MELATONIN on WebMD including its uses, effectiveness, side effects and safety, interactions, user ratings and products that have it. 9.1 HISTORICAL. The full-blown expression of hypothyroidism is known as myxedema. Adult myxedema escaped serious attention until Gull described it in 1874 1. Get the latest news and analysis in the stock market today, including national and world stock market news, business news, financial news and more. Micronutrient Information Center. Vitamin D is a fat- soluble vitamin that regulates calciumhomeostasis and is vital for bone health (1). The Linus Pauling Institute's Micronutrient Information Center is a source for scientifically accurate information regarding the roles of vitamins, minerals. Learn about acute myeloid leukemia and find information on how we support and care for people with AML before, during, and after treatment. Review Article. Mechanisms of Disease. Antiinflammatory Action of Glucocorticoids — New Mechanisms for Old Drugs. Turk Rhen, Ph.D., and John A. Cidlowski, Ph.D. While it can also be obtained from dietary sources or supplements, vitamin D3 (cholecalciferol) is synthesized in the human skin from 7- dehydrocholesterol upon exposure to ultraviolet- B (UVB) radiation from sunlight (see the article on Vitamin D and Skin Health). Vitamin D2 (ergocalciferol) is a vitamin D analog photosynthesized in plants, mushrooms, and yeasts; vitamin D2 is also sometimes used in vitamin D food fortification(2). When vitamin D3 in skin is inadequate due to insufficient exposure to UVB radiation, oral intake of vitamin D is necessary to meet vitamin D requirements. Cholecalciferol and ergocalciferol are biologically inactive precursors of vitamin D and must be converted to biologically active forms in the liver and kidneys. Indeed, following dietary intake or synthesis in the epidermis of skin after UVB exposure, both forms of vitamin D enter the circulation and are transported to the liver by the vitamin D- binding protein (and to a lesser extent by albumin). In hepatocytes (liver cells), vitamin D is hydroxylated to form 2. D (calcidiol; calcifediol). Exposure to sunlight or dietary intake of vitamin D increases serum levels of 2. D. 2. 5- hydroxyvitamin D constitutes the major circulating form of vitamin D, and the sum of 2. D2 and 2. 5- hydroxyvitamin D3 levels in serum is used as an indicator of vitamin D nutritional status (3). The renal 2. 5- hydroxyvitamin D- 1. The production of 1,2. D in the kidneys is regulated by several factors, including serum phosphorus, calcium, parathyroid hormone (PTH), fibroblast growth factor 2. FGF- 2. 3), and 1,2. D itself. While the kidney is the main source of 1. Most of the physiological effects of vitamin D in the body are related to the activity of 1,2. D (4). Various forms of vitamin D are listed in Figure 1. Most, if not all, actions of vitamin D are mediated through a nuclear transcription factor known as the vitamin D receptor (VDR) (5). Upon entering the nucleus of a cell, 1,2. D binds to the VDR and recruits another nuclear receptor known as retinoic acid X receptor (RXR). In the presence of 1,2. D, the VDR/RXR complex binds small sequences of DNA known as vitamin D response elements (VDREs) and initiates a cascade of molecular interactions that modulate the transcription of specific genes. Thousands of VDREs have been identified throughout the genome, and VDR activation by 1,2. D is thought to directly and/or indirectly regulate 1. Maintenance of serumcalcium levels within a narrow range is vital for normal functioning of the nervous system, as well as for bone growth and maintenance of bone density. Vitamin D is essential for the efficient utilization of calcium by the body (1). The parathyroid glands sense serum calcium levels and secrete parathyroid hormone (PTH) if calcium levels decrease below normal (Figure 2). Elevations in PTH stimulate the activity of the 2. D3- 1. Higher levels of 1,2. D result in VDR activation and changes in gene expression that normalize serum calcium by (1) increasing the intestinal absorption of dietary calcium, (2) increasing the reabsorption of calcium filtered by the kidneys, and (3) mobilizing calcium from bone when there is insufficient dietary calcium to maintain normal serum calcium levels (7). The regulations of calcium and phosphorushomeostasis are closely related, and the calciotropic hormones PTH and 1,2. D can also control serum phosphorus. Specifically, 1,2. D increases intestinal phosphorus absorption by stimulating the expression of a sodium- phosphate cotransporter in the small intestine. While PTH increases urinary excretion of phosphorus by reducing reabsorption in the kidney, it is not yet clear whether 1,2. D can directly regulate renal phosphorus transport. The phosphaturic hormone fibroblast growth factor 2. FGF- 2. 3), secreted by osteoblasts (bone- forming cells), limits the production of 1,2. D by inhibiting 2. D- 1. Differentiation results in the specialization of cells for specific functions. In general, differentiation of cells leads to a decrease in proliferation. While cellular proliferation is essential for growth and wound healing, uncontrolled proliferation of cells with certain mutations may lead to cancer. The active form of vitamin D, 1,2. D inhibits proliferation and stimulates the differentiation of cells through binding to the VDR (1). Acting through the VDR, 1,2. D is a potent immune system modulator. The VDR is expressed by most cells of the immune system, including regulatory T cells and antigen- presenting cells, such as dendritic cells and macrophages (9). Under specific circumstances, monocytes, macrophages, and T cells can express the 2. D3- 1. There is considerable scientific evidence that 1,2. D has a variety of effects on immune system function, which may enhance innate immunity and inhibit the development of autoimmunity(1. Conversely, vitamin D deficiency may compromise the integrity of the immune system and lead to inappropriate immune responses (see Autoimmune diseases). The VDR is expressed by insulin- secreting cells of the pancreas, and the results of animal studies suggest that 1,2. D plays a role in insulin secretion under conditions of increased insulin demand (1. Cross- sectional and prospective studies suggest that insufficient vitamin D levels may have an adverse effect on insulin secretion and glucose tolerance in type 2 diabetes (noninsulin- dependent diabetes mellitus) (reviewed in 1. The renin- angiotensin system plays an important role in the regulation of blood pressure (1. Renin is an enzyme that catalyzes the cleavage (splitting) of a small peptide (angiotensin I) from a larger protein (angiotensinogen) produced in the liver. Angiotensin- converting enzyme (ACE) catalyzes the cleavage of angiotensin I to form angiotensin II, a peptide that can increase blood pressure by inducing the constriction of small arteries and by increasing sodium and water retention. The rate of angiotensin II synthesis is dependent on renin (1. Research in mice lacking the gene encoding the VDR indicates that 1,2. D decreases the expression of the gene encoding renin through its interaction with the VDR (1. Since inappropriate activation of the renin- angiotensin system can contribute to the development of hypertension, achieving adequate vitamin D levels may be important for decreasing the risk of high blood pressure (see Hypertension). In vitamin D deficiency, calcium absorption cannot be increased enough to satisfy the body’s calcium needs (4). Consequently, PTH production by the parathyroid glands is increased and calcium is mobilized from the skeleton to maintain normal serum calcium levels — a condition known as secondary hyperparathyroidism. Although it has long been known that severe vitamin D deficiency has serious consequences for bone health, research suggests that less obvious states of vitamin D deficiency are common and increase the risk of osteoporosis and various other health problems (see Disease Prevention). In infants and children, severe vitamin D deficiency results in the failure of bone to mineralize. The process of mineralization, which involves the production of crystals of calcium phosphate by bone- forming cells, determines the hardness and strength of bones. Vitamin D deficiency severely affects rapidly growing bones. The growth plates of bones continue to enlarge, but in the absence of adequate mineralization, weight- bearing limbs (arms and legs) become bowed. In infants, rickets may result in delayed closure of the fontanels (soft spots) in the skull, and the rib cage may become deformed due to the pulling action of the diaphragm. In severe cases, low serum calcium levels (hypocalcemia) may cause seizures. Although fortification of food has led to complacency regarding vitamin D deficiency, nutritional rickets is still being reported throughout the world (1. Although adult bones are no longer growing, they are in a constant state of turnover, or . Muscle pain and weakness were prominent symptoms of vitamin D deficiency in a study of Arab and Danish Muslim women living in Denmark (2. In a cross- sectional study of 1. Minnesota for the evaluation of persistent, nonspecific musculoskeletal pain, 9. D levels equal to or below 2. L, with a mean concentration of 1. L, which is indicative of vitamin D insufficiency (2. Loss of muscle strength greatly contributes to increased risk of falling and bone fractures, especially in older people (2. In addition, long- term vitamin D insufficiency may be a contributing factor to osteoporosis in the elderly (see Osteoporosis). Both environmental factors and cultural practices result in variations in vitamin D status: The efficiency of vitamin D synthesis, absorption, and metabolism also depends on a variety of biological factors: Growing awareness that vitamin D insufficiency has serious health consequences beyond rickets and osteomalacia highlights the need for accurate assessment of vitamin D nutritional status. It is currently agreed that the measurement of total serum 2. D concentration (1 ng/m. L corresponding to 2. L) is the best indicator to evaluate vitamin D status. However, high- quality evidence is still needed to ensure that the current cutoff values are optimal to define states of insufficiency and deficiency (3. Although laboratory reference values for sufficient levels of vitamin D have been initially based on serum 2. D levels from cohorts of healthy individuals, additional studies have suggested that health- based cutoff values aimed at preventing secondary hyperparathyroidism and bone loss should be considerably higher. Indeed, while it is considered that serum 2. D concentrations less than 8- 1. L (2. 0- 2. 5 nmol/L) indicate severe deficiency associated with rickets and osteomalacia, several studies have observed that PTH levels (4. D levels below 3. L (8. 0 nmol/L). Yet, more recent studies have failed to find threshold values of serum 2.
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