Rickets treatment

In 1919, Huldschinski (8) realized that uv light cured rickets and impacted on its etiology. The uv light and codHver oil were found to be usehil in the treatment of the disease, and irradiation of food produced the same effect as irradiation of the animal. The link between irradiation and plant materials led to the conclusion that ergosterol was an antirachitic substance, and an extensive effort was made to characterize the chemistry of irradiated ergosterol. 

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. 

Oral calcium may also be used in the treatment of osteoporosis, osteomalacia, rickets, and latent tetany. 

Calcium chloride and gluconate - A6 unct /e therapy in the treatment of insect bites or stings, such as Black Widow spider bites to relieve muscle cramping sensitivity reactions, particularly when characterized by urticaria depression due to overdosage of magnesium sulfate acute symptoms of lead colic rickets osteomalacia. 

Phototherapy is the generic term covering therapies which use light either with or without a sensitiser. Those that do not require a sensitiser use the natural chromophores within the tissue to perform this function e.g. treatment of vitamin D deficiency in rickets, and neonatal jaundice). Those that do use an added sensitiser include photochemotherapy (largely psoriasis and skin disorders) and photodynamic therapy (currently mainly cancer). Photodynamic therapy is differentiated from photochemotherapy by its additional requirement for the presence of oxygen at molecular or ambient levels.In this text we will deal only with photodynamic therapy since, at the present time, this is the main driving force in phototherapy. ° ... 

It is indicated in prophylaxis and treatment of rickets, postmenopausal osteoporosis, Fanconi syndrome and hypoparathyroidism. 

Phosphate is critical to normal bone mineralization when phosphate stores are deficient, a clinical and pathologic picture resembling vitamin D-deficient rickets develops. However, affected children fail to respond to the usual doses of vitamin D used in the treatment of nutritional rickets. A defect in l,25(OH)2D production by the kidney has also been noted,... 

Anecdotal observations suggest that excessive use of oral phosphates may be a risk factor for the development of tertiary hyperparathyroidism in patients with X-linked hypophosphatemic rickets. Of 13 patients with X-linked hypophosphatemic rickets two developed tertiary hyperparathyroidism and 11 secondary hyperparathyroidism during treatment (939). Patients with tertiary hyperparathyroidism had on average earlier and longer treatment and higher doses of phosphates (over lOOmg/kg/day) than the 11 patients with secondary hyperparathyroidism. Those who later developed tertiary hyperparathyroidism had very high serum parathormone concentrations (over 42 pmol/1). 

Makitie O, Kooh SW, Sochett E. Prolonged high-dose phosphate treatment a risk factor for tertiary hyperparathyroidism in X-linked hypophosphatemic rickets. Clin Endocrinol 2003 58 163-8. 

Treatments of diseases such as osteoporosis, rickets and osteomalacia, in which there is a disturbance of phosphate levels, is complicated by the interdependence of calcium metabolism. This topic has recently been discussed in relation to clinical medicine21. There is the further difficulty that absorption of phosphate from the bowel can be decreased in the presence of calcium or aluminium salts because of the formation of their insoluble phosphates. Uptake of phosphate by bone is exploited in the treatment of polycythaemia vera by intravenous injection of 32P as sodium phosphate. The resulting irradiation of the neighbouring red bone marrow diminishes the production of red cells. 

Phosphate is critical to normal bone mineralization when phosphate stores are deficient, a clinical and pathologic picture resembling vitamin D-deficient rickets develops. However, such children fail to respond to the usual doses of vitamin D employed in the treatment of nutritional rickets. A defect in l,25(OH)2D production by the kidney has also been noted, because the serum l,25(OH)2D levels tend to be low relative to the degree of hypophosphatemia observed. This combination of low serum phosphate and low or low-normal serum l,25(OH)2D provides the rationale for treating such patients with oral phosphate (1-3 g daily) and calcitriol (0.25-2 Mg daily). Reports of such combination therapy are encouraging in this otherwise debilitating disease. 

Type IE vitamin D-dependent rickets is caused by a target tissue defect in response to l,25(OH)2D. Studies have shown a number of point mutations in the gene for the l,25(OH)2D receptor, which disrupt the functions of this receptor and lead to this syndrome. The serum levels of l,25(OH)2D are very high in type II but not in type I. Treatment with large doses of calcitriol has been claimed to be effective in restoring normocalcemia. Such patients are totally refractory to vitamin D. One recent report indicates a reversal of resistance to calcitriol when 24,25(OH)2D was given. These diseases are rare. 

The symptoms of vitamin D deficiency disease has been documented in 16th century literature. A clear picture of the basis for the disease and methods of treatment were unclear until the experiments by Sir Edward Mellanby (3,4). In the early 1920 s, cod liver oil was known to cure rickets and xerophthalmia. The name vitamin D was given to... 

Several studies reporting intermediate oral exposure of children to white phosphorus were located. In most cases the white phosphorus was administered as a treatment for rickets, but in some cases white phosphorus was administered to healthy children to prevent the development of rickets. In studies reporting the effects of white phosphorus on bones in children, the doses of white phosphorus administered (0.026-0.158 mg/kg/day) were several orders of magnitude lower than those reported following intentional or accidental white phosphorus poisoning. 

An arachitic child was treated with 0.119 mg/kg/day white phosphorus for 82 days (Compere 1930b). Following treatment, the child had a "heavy phosphorus line" and increased density of cortices. Treatment with white phosphorus did not generally improve the condition of the bones in children with rickets. Because these children were sickly, the relevance of the observed effects to potential effects of white phosphorus in normal, healthy children could not be ascertained. 

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

Anticonvulsant treatment Fibrogenes imperfecta ossium Osteitis fibrosa cystica Osteomalacia Osteoporosis Osteopenia Osteosclerosis Renal osteodystrophy Rickets... 

Vitamin D deficiency remains the most common cause of rickets and osteomalacia in the world, with the exception of the United States and the Scandinavian countries where most dairy products are supplemented with this vitamin. This deficiency can be caused either by dietary habits or by insufficient exposure to ultraviolet light. The same type of symptoms can be observed when there is interruption of the normal vitamin D metabolic pathways due to a number of liver and/or kidney diseases. In addition, a number of inherited factors can lead to different types of vitamin D resistance which require massive supplements of vitamin D and/or minerals. Extensive reviews have been published depicting both the clinical features and their most likely causes, as well as the possible treatments of the different types of clinical disorders resulting from vitamin D deficiencies [113-117], The newly defined role for l,25(OH)2D3 upon the hematopoietic system could also have clinical relevance in bone disorders such as osteoporosis where patients have been shown to possess abnormal T-cell subsets [118]. 

Hypercalcemia persists for many months after the cessation of excessive intakes of vitamin D, because of the accumulation of the vitamin in adipose tissue and its slow release into the circulation. The introduction of calcitriol and 1 a -hydroxycalcidiol for the treatment of such conditions as hypoparathyroidism, renal osteodystrophy, hypophosphatemic osteomalacia, and vitamin D-dependent rickets has meant that hypercalcemia is less of a problem than when high doses of vitamin D were used in the treatment of these conditions. Because calcitriol has a short half-life in the circulation, the resultant hypercalcemia is of shorter duration than after cholecalciferol, and adjustment of the dose is easier. 

Greig F, Casas J, and Castells S (1989) Changes in plasma osteocalcin concentrations during treatment of rickets. Journal of Pediatrics 114, 820-3. 

Indications for vitamin D are the prevention and cure of rickets of all kinds and osteomalacia, and the symptomatic treatment of some cases of hypoparathyroidism also psoriasis. 

Rickets and ostec malacia can be treated with daily oral doses of ergocaiclfcnol (0-01 15-0 mg/day). Treatment is continued for 1 to 3 months and is coupled with adequate levels of dietary calcium and phosphate. Where the disease is due to a defect in 1-hydroxylase, treatment is wdth l,25-(OI... 

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