Bone pain vitamin

Primary hyperparathyroidism occurs as a result of hyperplasia or the occurrence of adenoma. Secondary hyperparathyroidism may result from renal failure because of the associated phosphate retention, resistance to the metabolic actions of PTH, or impaired vitamin D metabolism. The last-mentioned factor is primarily responsible for the development of osteomalacia. Muscle symptoms are much more common in patients with osteomalacia than in primary hyperparathyroidism. Muscle biopsy has revealed disseminated atrophy, sometimes confined to type 2 fibers, but in other cases involving both fiber types. Clinical features of osteomalacic myopathy are proximal limb weakness and associated bone pain the condition responds well to treatment with vitamin D. 

For women whose breast cancer has metastasized to bone, bisphosphonates are recommended, in addition to chemotherapy or endocrine therapy, to reduce bone pain and fractures.28,64 Pamidronate (90 mg) and zoledronate (4 mg) can be given intravenously once each month. These bisphosphonates are given in combination with calcium and vitamin D. 

The nutritional experiments with carotene and fish oils led to the conclusion that a second fat-soluble compound was essential for normal rat growth. Rickets, the condition caused by vitamin D deficiency, is a disease afflicting children where, because of impaired calcification, bone formation is disturbed and the bones become bowed and otherwise deformed. In adults, especially multiparous women, vitamin D deficiency produced osteomalacia—demineralization of bone, leading to tenderness over the bones, pain, and muscle weakness. Rickets was particularly prevalent in slum areas. Glasgow, Vienna, and Lahore were notorious for the high incidence of the disease. 

Vitamin D deficiency after epiphyseal fusion causes osteomalacia, which produces less deformity than rickets. Osteomalacia may present as bone pain and muscle weakness. 

A clear lack of adequate vitamin D in childhood results in the disease rickets, characterized by deformed bones and stunted growth. Extracellular calcium levels are too low to permit normal bone mineralization. A related disease, osteomalacia, occurs in adults deficient in vitamin D. Osteomalacia is characterized by weakened bones and bone pain as a result of insufficient mineralization. 

High daily doses of retinoids can lead to hyper-vitaminosis A manifesting itself as dermal toxicity such as erythematous dermatitis, bone pains, neurological symptoms and hepatosplenomegaly. A recent study shows a correlation between low bone mineral density and too high intake of vitamin A. 

The choice of vitamin D preparation to be used in the setting of chronic renal failure in the dialysis patient depends on the type and extent of bone disease and hyperparathyroidism. No consensus has been reached regarding the advisability of using any vitamin D metabolite in the predialysis patient. l,25(OH)2D3 (calcitriol) will rapidly correct hypocalcemia and at least partially reverse the secondary hyperparathyroidism and osteitis fibrosa. Many patients with muscle weakness and bone pain gain an improved sense of well-being. 

Osteomalacia is the defective remineralization of bone during normal bone turnover in adults, so that there is a progressive demineralization, but with adequate bone matrix, leading to bone pain and skeletal deformities, with muscle weakness. Women with inadequate vitamin D status are especially at risk of osteomalacia after repeated pregnancies, as a result of the considerable drain on calcium reserves for fetal bone mineralization and lactation. 

Cholestasis-linked osteopathy (M. Loeper et al., 1939), which occurs much more frequently in the form of osteoporosis than osteomalacia, can be expected in up to 50% of cases. The pathogenesis is complex. Vitamin D status can be examined by determining 25-OH-cholecal-ciferol in the serum. Intestinal calcium loss and reduced calcium absorption due to vitamin D deficiency are key pathogenetic factors. It is still a matter of debate whether vitamin K deficiency (which can lead to reduced osteocalcin synthesis) and deficiencies in IGF I and II (which can cause dysfunction of the osteoblasts) are possible causes of this condition. Muscle and bone pain are frequent clinical symptoms, occurring mainly in the wrists and ankles. 

Vitamin D Calcium metabolism Fish-liver oil Bone pain and skeletal, deformities such as bowlegs. (Rickets) and knock-knee in children. Osteomalacia in adults. 

Vitamin D deficiency in adults cannot affect the epiphyseal plate, as it has disappeaced, but it can prevent normal mineralization of the osteoid layer in bone that turns over. In vitamin D deficiency the osteoclasts continue to create tunnels and pits in the bone. The osteoblasts continue to synthesize the protein matrix however, complete mineralization of the osteoid may not occur. The result is osteomalacia - This disease may present as bone pain about the hips. Osteomalacia can be diagnosed using a bone biopsy, A sample is taken from the iliac crest — the hip bone. An abnormally wide osteoid is indicative of the disease. X-rays can also be used to diagnose osteomalacia, which is characterized by arrays or zones of tiny fractures in sucli bones as the pelvis and femur. 

Isolated nutritional deficiencies. Iron, folate, or vitamin Bi2 deficiency may manifest as anemia, which may be mild vitamin K deficiency as a bleeding tendency and vitamin D deficiency as bone disease. They are reflected by a variety of signs and symptoms (glossitis, pallor, dermatitis, petechiae, bruising, hematuria, muscle or bone pain, or neurological abnormalities). 

Osteomalacia is a deficiency disease. Insufficient vitamin D leads to low plasma calcium levels. This stimulates the secretion of PTH, which causes release of calcium from bone and failure to mineralize new bone. Characteristic bone deformities result in children and bone pain and tenderness in affected adults. Treatment is by vitamin D replacement. 

In adults, vitamin D deficiency results in osteomalacia, a disease characterized by generahzed accumulation of undermineralized bone matrix. Severe osteomalacia may be associated with extreme bone pain and tenderness and proximal muscle weakness. A low serum level of 25-OHD is diagnostic. 

Endocrine A rare case of hypoparathyroidism in a 12-year-old child receiving (11.1 mCi) therapy for Graves disease was reported [26 ]. Symptoms of shortness of breath, paraesthesias in extremities, muscle spasms, bone pains, dysphagia, diarrhoea, restlessness, hypocalcemia, hyperphosphatemia and PTH (low-normal range) occurred post RAI. Compounding factors in this case were use of steroids to treat asthma and deliberate vitamin D deficiency. 

Vitamin C is essential for the formation of collagen, the principal structural protein in skin, bone, tendons, and ligaments, being a cofactor in the hydroxylation of the amino acids proline to 4-hydroxyproline, and of lysine to 5-hydroxylysine. These hydroxyamino acids account for up to 25% of the collagen structure. Vitamin C is also associated with some other hydroxylation reactions, e.g. the hydroxylation of tyrosine to dopa (dihydroxyphenylalanine) in the pathway to catecholamines (see Box 15.3). Deficiency leads to scurvy, a condition characterized by muscular pain, skin lesions, fragile blood vessels, bleeding gums, and tooth loss. Vitamin C also has valuable antioxidant properties (see Box 9.2), and these are exploited commercially in the food industries. 

Deficiency symptoms In vitamin C deficiency scurvy develops. It is characterized by ecchymosis, petechiae, swollen and bleeding gums, subperiosteal haemorrhage, bones are painful to touch, impaired wound healing, anaemia, loosening of teeth and gingivitis. 

Chronic nitrous oxide abuse can remove a lot of vitamin B12 from the bloodstream. B12 (cobalamin) is necessary for the creation of blood cells and neurotransmitters, as well as the protective layers that cover nerves. This results in nerve damage and pain balancing, walking, and concentration difficulties mental impairment mood disturbances (such as depression) and other physical problems. Chronic nitrous oxide use may also interfere with the production in bone marrow of white blood cells and red blood cells. Treatment with intramuscular injections of B12 may reverse these symptoms. 

Vitamin A (in excessive doses) produces toxicity such as nausea, vomiting, erythema, dermatitis, hair loss, bone and joint pains, loss of appetite, bleeding, and chronic liver diseases. Excess vitamin A is teratogenic in animals and humans daily intake should not exceed 20,000 IU. 

Bones joint pains, thickening of the long bones, hypercalcemia, and calcification of soft tissues, but with reduced bone mineral density. High intakes of vitamin A are associated with an increased rate of loss of bone mineral density with age, and some studies have shown that intakes above 1,500 /xg per day are associated with increased incidence of osteoporosis and hip fracture, although other studies have not shown any relationship between vitamin A intake and osteoporosis (Institute of Medicine, 2001). At high levels of intake, vitamin A both stimulates bone... 

An adult version of rickets caused by a deficiency of vitamin D, calcium, and phosphorous is called osteomalacia. The bones become soft and deformed and there is rheumatic pain. The disease is observed in the Middle East and Asia more so than in western countries. The way to prevent rickets and other bone diseases such as osteoporosis is a combination of calcium, phosphorous, and vitamin D. 

Musculoskeletal. Proximal myopathy and tendon rupture may occur. Osteoporosis develops insidiously leading to fractures of vertebrae, ribs, femora and feet. Pain and restriction of movement may occur months in advance of radiographic changes. A biphosphonate, with or without vitamin D, is useful for prevention and treatment. Growth in children is impaired. A vascular necrosis of bone (femoral heads) is a serious complication (at higher doses) it appears to be due to restriction of blood flow through bone capillaries. 

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