Vitamin Rickets

Chronic renal disease Hypophosphatemic vitamin D-resistant rickets Vitamin D-dependent rickets... 

Early 1900s Treatment of histamine shock, pellagra (niacin deficiency) and rickets (vitamin D deficiency) Electrocardiography and cardiac catheterization... 

The fourth section deals with various aspects Digestion, Absorption, and Nutritional Biochemistry. The chapter Obesity considers current problems with respect to the ever-increasing incidence of imbalance between energy intake and utilization. Key problems of undemutrition are discussed in the chapters Protein-Energy Malnutrition and Vitamin A Deficiency in Children. The chapters Lactose Intolerance, Pancreatic Insufficiency, and Abetalipoproteinemia focus on the biochemical processes underlying food digestion and absorption. Calcium Deficiency Rickets, Vitamin B12 Deficiency, and Hemochromatosis provide discussions of absorption and utilization of vitamin D, vitamin B12, and iron, respectively. 

In the early part of this century many vitamin deficiency diseases were identified and cured. Vitamin D cured rickets. Vitamin C (ascorbic... 

Vitamin D deficiency can result in an increased excretion of calcium and phosphate and, consequently, impairs bone formation through inadequate calcification of cartilage and bones (childhood rickets). Vitamin D deficiency in adults leads to osteomalacia, a softening and weakening of bones. Hypercalcemia is a result of excessive intake of vitamin D (>50 pg/day), causing calcium carbonate and calcium phosphate deposition disorders involving various organs. 

A disease resulting from a deficiency of one or more vitamins is hypovitaminosis (if vitamin is supplied in insufficient quantity) or avitaminosis (complete lack of vitamin manifested by some biochemical processes disorder). Deficiency of vitamins was formerly one of the main causes of many diseases and deaths. Pellagra (deficiency of some B-complex vitamins), scurvy (vitamin C), beriberi (thiamine), rickets (vitamin D), pernicious anaemia associated with reduced ability to absorb vitamin Bj2 (corrinoids) and xerophthalmia (vitamin A) are now well-known diseases caused by vitamin deficiency. Excessive intake of one or more vitamins (especially of lipophilic vitamins A and D) also causes an abnormal state resulting from disturbances of biochemical processes and can lead to severe diseases known as hypervitaminosis. 

Vitamin Dj has m.p. 115-117°C and D, m.p. 82 83 "C. Both vitamins, which have almost identical actions, are used for the prevention and cure of infantile rickets they are essential for the normal development of teeth, and are used for treating osteomalacia and dental caries. They are necessary for the absorption of Ca and P from the gut. 

Our word vitamin was coined m 1912 m the belief that the substances present m the diet that prevented scurvy pellagra beriberi rickets and other diseases were vital amines In many cases that belief was confirmed certain vitamins did prove to be amines In many other cases however vitamins were not amines Nevertheless the name vitamin entered our language and stands as a reminder that early chemists recognized the crucial place occupied by amines m biological processes... 

Vitamin D3 is a key compound m the process by which Ca " is absorbed from the mtes tine Low levels of vitamin D3 lead to Ca " concentrations m the body that are msuffi cient to support proper bone growth resulting m the bone disease called rickets... 

Phosphorus Disorders. Phosphoms nutrient deficiency can lead to rickets, osteomalacia, and osteoporosis, whereas an excess can produce hypocalcemia. Faulty utilisation of phosphoms results in rickets, osteomalacia, osteoporosis, and Paget s disease, and renal or vitamin D-resistant rickets. 

Vitamin D [1406-12-2] is a material that is formed ia the skin of animals upon kradiation by sunlight and serves as a precursor for metaboUtes that control the animal s calcium homeostasis and act ki other hormonal functions. A deficiency of vitamin D can cause rickets, as weU as other disease states. This tendency can be a problem wherever animals, including humans, especially kifants and children, receive an kiadequate amount of sunshine. The latter phenomenon became prevalent with the advent of the kidustrial revolution, and efforts to cute rickets resulted ki the development of commercial sources of vitamin D for supplementation of the diet of Hvestock, pets, and humans. 

Historically, rickets prevention or cure was used to evaluate adequate vitamin nutrient levels. More recendy, in the absence of uv light, Edwards (216) found different vitamin levels were required for the optimisa tion of the various effects of vitamin in poultry, ie, 275 lU/kg for growth, 503... 

Disease States. Rickets is the most common disease associated with vitamin D deficiency. Many other disease states have been shown to be related to vitamin D. These can iavolve a lack of the vitamin, deficient synthesis of the metaboUtes from the vitamin, deficient control mechanisms, or defective organ receptors. The control of calcium and phosphoms is essential ia the maintenance of normal cellular biochemistry, eg, muscle contraction, nerve conduction, and enzyme function. The vitamin D metaboUtes also have a function ia cell proliferation. They iateract with other factors and receptors to regulate gene transcription. 

Vitamin D is a family of closely related molecules that prevent rickets, a childhood disease characterized by inadequate intestinal absorption and kidney reabsorption of calcium and phosphate. These inadequacies eventually lead to the demineralization of bones. The symptoms of rickets include bowlegs,... 

One of the triumphs of the science of nutrition is the careful investigation that linked childhood rickets with vitamin D deficiency. This work, which led to methods for treating the disease, is too familiar to need repetition. A direct consequence of these efforts was the elucidation of the pivotal role played by vitamin D in calcium metabolism, as well as the structural studies that revealed that this compound (102) is in fact a steroid derivative. The past... 

Vitamin D is not strictly a vitamin since it can be synthesized in the skin, and under most conditions that is its major source. Only when sunlight is inadequate is a dietary source required. The main function of vitamin D is in the regulation of calcium absorption and homeostasis most of its actions are mediated by way of nuclear receptors that regulate gene expression. Deficiency—leading to rickets in children and osteomalacia in adults—continues to be a problem in northern latitudes, where sunlight exposure is poor. 

In the vitamin D deficiency disease rickets, the bones of children are undermineralized as a result of poor absorption of calcium. Similar problems occur in adolescents who are deficient during their growth spurt. Osteomalacia in adults results from demineralization of bone in women who have little exposure to sunlight, often after several pregnancies. Although vitamin D is essential for prevention and treatment of osteomalacia in the elderly, there is little evidence that it is beneficial in treating osteoporosis. 

Vitamin A (retinol), present in carnivorous diets, and the provitamin (P-carotene), found in plants, form retinaldehyde, utilized in vision, and retinoic acid, which acts in the control of gene expression. Vitamin D is a steroid prohormone yielding the active hormone derivative calcitriol, which regulates calcium and phosphate metaboUsm. Vitamin D deficiency leads to rickets and osteomalacia. 

Vitamin D receptor (VDR) 1,25 dihydroxyvitamin-D3 Vitamin D response in patients affected with rickets (96) Susceptibility to osteoporosis (97) and autosomal dominant rickets disease (96)... 

Malloy PJ, Eccleshall TR, Gross C, Van Maldergem L, Bouillon R, Feldman D. Hereditary vitamin D resistant rickets caused by a novel mutation in the vitamin D receptor that results in decreased affinity for hormone and cellular hyporesponsiveness. J Clin Invest 1997 99[2] 297-304. 

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