Inadequate stay in sunlight predisposes a vitamin D deficiency. In order for the bone mineralization is impaired children suffer from rickets, osteomalacia in adults and may be easier to osteoporosis. The diagnosis is made (D2 + D3) in the measurement of the serum 25 (OH) D. For therapy, vitamin D, calcium and phosphate are given orally. Often, prevention is possible. Rare hereditary diseases lead to a disturbed vitamin D metabolism (dependency).
Vitamin D has two main forms:
(. See also overview of vitamins) Vitamin D has two main forms: D2 (ergocalciferol) D3 (cholecalciferol): The naturally occurring form is also used for the low-dose supplements of vitamin D3 is the form in the skin (by sunlight UV radiation) comes synthesized and v in the diet. a. in cod liver oil and saltwater fish (see table: sources, functions and effects of vitamins). In some industrialized countries, milk and other foods with vitamin D enriched. Breast milk contains little vitamin D, on average, only 10% of existing in enriched cow’s milk quantity. The vitamin D levels may decrease with age, since the synthesis is reduced in the skin. decoding reduce use of sunscreen and a dark pigmentation of the skin also the synthesis of vitamin D in the skin. Vitamin D is a prohormone with active metabolites that act as hormones. The liver metabolizes Vitamin D to 25 (OH) D, which then by the kidneys in 1,25 (OH) 2D (dihydroxycholecalciferol 1.25, calcitriol or active vitamin D hormone) is converted. 25 (OH) D, the main form in the bloodstream, has metabolic activity, but is 1,25 (OH) 2D in the metabolism of most active. The conversion of 25 (OH) D to 1,25 (OH) 2D is regulated by its own concentration, parathyroid hormone and serum concentrations of calcium and phosphate. Vitamin D affects many organ systems (see Table: Effects of vitamin D and its metabolites), but increased it especially calcium and Phosphorresorption from the intestine and promotes bone formation and mineralization. Vitamin D and related analogs can be used to treat psoriasis, hypoparathyroidism and renal osteodystrophy. The benefits of vitamin D for Vobeugung of leukemia and breast, prostate and colon cancer is not proven any more than its benefits in preventing falls (1,2,3) for seniors D .. effects of vitamin and its metabolites Organ Effect bone promotes bone formation by maintaining appropriate calcium and phosphate concentrations immune system Stimulates immunogenic activity and tumor reduction, reduced risk of autoimmune diseases Intestinal Enhances calcium and phosphate transport (absorption) kidney Enhances Kalziumrückresorption through the tubules parathyroid Inhibits the secretion of parathyroid hormone pancreas stimulates insulin production notes 1. Cummings SR, Kiel DP, Black DM: Vitamin D supplementation and Increased risk of falling: A cautionary tale of vitamin supplements retold. JAMA Intern Med 176 (2): 171-172, 2016. 2. Uusi-Rasi K, R Patil, Karinkanta S, Kannus P, et al: Exercise and vitamin D in case prevention among older women: A randomized clinical trial. JAMA Intern Med 75 (5): 703-711, 2015. 3. LeBlanc ES, Chou R: vitamin D and falls – adaptation of new data with current guidelines. JAMA Intern Med 175 (5): 712-713, 2015. Vitamin D deficiency and dependence Inadequate stay in sunlight predisposes a vitamin D deficiency. In order for the bone mineralization is impaired children suffer from rickets, osteomalacia in adults and may be easier to osteoporosis. The diagnosis is made (D2 + D3) in the measurement of the serum 25 (OH) D. For therapy, vitamin D, calcium and phosphate are given orally. Often, prevention is possible. Rare hereditary diseases lead to a disturbed vitamin D metabolism (dependency). Vitamin D deficiency is prevalent worldwide. He is a frequent cause of rickets and osteomalacia, but this may cause problems such by other medical conditions. As by renal tubular dysfunction, hypophosphatemic (vitamin D resistant) rickets, chronic metabolic acidosis, hyperparathyroidism, hypoparathyroidism, inadequate calcium consumption and diseases or drugs that inhibit the mineralization of the substantia compacta. Vitamin D deficiency causes hypocalcemia, which stimulates the production of parathyroid hormone and leads to a hyperparathyroidism. This increases the absorption of calcium, mobilization of calcium from the bones and the retention of calcium in the kidneys, but increases phosphate excretion. As a result, the serum calcium levels may be normal, but because of hypophosphatemia bone mineralization is impaired. Etiology A vitamin D deficiency arises from the following reasons: Insufficient stay in the sunlight an inadequate intake of vitamin D. Reduced absorption of vitamin D Abnormal metabolism of vitamin D resistance to the action of vitamin D Inadequate Sonnenlichexposition or supply Insufficient direct sunlight or stay in the use of sunscreens and inadequate supply are given in a clinically significant deficiency usually simultaneously. Among the patients at risk include the elderly, who are often malnourished and do not stay long enough in the sun, groups such as women and children, who usually remain in the house or wear clothing that covers the entire body and face. The vitamin D depots older people are often insufficient when they no longer leave the house, living in institutions, to stay in the hospital or have suffered a hip fracture. The direct exposure to sunlight is recommended 5-15 min (suberythemale dose) on the arms and legs or face, arms and hands, at least 3 times a week. However, many dermatologists advise of increased sunlight off because the risk of skin cancer increases absorption ist.Reduzierte A malabsorption can deprive the body of vitamin D, only a small amount of 25 (OH) D is in the enterohepatic circulation zurückgeführt.Stoffwechselanomalien Vitamin D deficiency may be caused by the incorrect production of 25 (OH) D or 1,25 (OH) 2D. People with chronic kidney disease developing rickets or osteomalacia since the kidneys produce less 1,25 (OH) 2D, and the phosphate levels are elevated. Liver dysfunction may also affect the production of active vitamin D metabolites. In autosomal recessive vitamin D-dependent rickets (type I) runs out incorrectly or not from the conversion of 25 (OH) D to 1,25 (OH) 2D in the kidneys. An X-linked inherited familial hypophosphatemia reduces vitamin D synthesis in the kidneys. Many anti-epileptic drugs and the use of glucocorticoids increase the need for vitamin D-Supplementierung.Resistenz against the effects of vitamin D from type II hereditary vitamin D-dependent rickets, there are several forms which cause mutations in the 1,25 (OH) 2D receptor is located. This receptor affects the metabolism of the intestine, kidney, bone and other cells. In this disorder is 1,25 (OH) 2D is abundant, but it can not act as the receptor nonfunctional ist.Symptome and discomfort A vitamin D deficiency can be at any age cause of muscle pain, muscle weakness and body aches. Suffers from a pregnant woman from vitamin D deficiency, can occur in the fetus malformations. In rare cases, a severe deficiency of the mother, through which a osteomalacia developed leads, neonatal rickets with metaphyseal lesions. Rickets causes softening of the entire skull (craniotabes) in infants. At palpation the Okziput- and parietal bones are in the form of a table tennis ball. Older babies who are suffering from rickets begin until later, to sit and crawl, and the fontanelle closes later; the skull is wide and flat, the rib cartilage thicken. These protrusions of the ribs cartilage along the lateral rib cage may be spherical appearance (rachitic rosary). In children aged between one and four years, the epiphyseal larger at the lower ends of the radius, ulna, tibia and fibula; A kyphoscoliosis develops the child starts with a delay to run. Older children and adolescents indicate pain when walking; in extreme cases caused deformities such as O and X legs. The pelvic bone can flatten, leading to a narrowing of the birth canal in adolescent girls. Tetany is the result of hypocalcemia and can occur with vitamin D deficiency in childhood or adulthood. Tetany caused paresthesias of the lips, tongue and fingers, facial spasms and Karpopedal- and in severe cases, seizures. A deficiency of the mother can cause tetany in the newborn. Osteomalacia predisposes those affected to fractures. In older people, a minor trauma can lead to hip fracture führen.Diagnose 25 (OH) D (D2 + D3) levels support following criteria the presumption of vitamin D deficiency already: Inadequate sunlight exposure or dietary intake in the history of symptoms and signs of rickets, osteomalacia or Neugeborenentetanie Characteristic bone changes in the X-ray image X-ray images of the radius and ulna as well as serum levels of calcium, phosphate, alkaline phosphatase, parathyroid hormone and 25 (OH) D are required to vitamin D deficiency from other causes of bone demineralization to differentiate. Assessment of vitamin D status and serological tests for syphilis should be considered in infants with Schädelerweichung (craniotabes) based on history and physical examination, but most cases of Schädelerweichung heal spontaneously. Rickets can be distinguished from chondrodystrophia, as the latter is characterized by a large head, short extremities, thick bones and normal serum levels of calcium, phosphate and alkaline phosphatase. Tetany caused by infantile rickets can not be clinically distinguished from attacks by other causes. Blood tests and clinical studies provide support for the Differenzierung.Röntgenaufnahmen bone changes that can be seen on X-ray images that precede the clinical abnormalities. In rickets, the changes show most clearly at the lower ends of the radius and ulna. The ends of the diaphyseal lose their crisp, clear definition, they are cup-shaped and thin patchy or frayed out. Later, the distance between the diaphysis and the metacarpal bones seems increased, since the ends of the radius and ulna were decalcified and radiolucent. The cortex other bones is also radiolucent. Characteristic deformities arise because the bones bend at the cartilage-shaft connection, because the shaft is softened. With the beginning of healing is demonstrated by the pineal gland, a thin, white Kalzifikationslinie that is denser and thicker with progressive calcification. Is made later calcification of the cortical bone, which is radiopaque in subperiosteal area. In adults, the bone demineralization of the spine, pelvis and lower extremities can be seen on the X-ray image; the fibrous strips are also visible, and in the cortical bone incomplete, band-shaped demineralized areas appear (pseudo fractures, Looser transformation zones Milkman syndrome) .Labortests Since the 25 (OH) D levels reflect the body depots of vitamin D and better than symptoms of vitamin D deficiency can be described as other vitamin D metabolites, is considered the best way to determine a vitamin D deficiency in general, 25 (OH) D (D2 + D3) levels for maximum bone health, the 25 (OH) D should -Zielwerte> 20-24 ng / ml (ca. 50-60 nmol / l) amount; whether higher levels have more benefits, it is unclear also increases calcium absorption higher the risk of coronary heart disease. the diagnosis can not be clearly set, the serum levels of 1,25 (OH) 2D, and the calcium concentration of the urine can be determined. In severe deficiency of serum 1,25 (OH) 2D mirror is far below the standard value, it is usually no longer measurable. The urine contains little calcium in every occurrence of the defect, with the exception of deficiencies associated with an acidosis. Of vitamin D deficiency, serum calcium levels are low or normal due to secondary hyperparathyroidism. The serum phosphate level decreases, the serum levels of alkaline phosphatase rise. The serum parathyroid hormone levels may be normal or elevated. Type I hereditary vitamin D-dependent rickets leads to normal serum 25 (OH) D levels, a low serum 1,25 (OH) 2D and calcium levels and normal or low serum Phosphat.Therapie correction of calcium – and phosphate deficiency supplementation with vitamin D calcium Angel (common) and phosphate deficiency should be corrected. As long as the calcium and phosphate intake is adequate, adults can be treated with osteomalacia and rickets children with uncomplicated with the daily intake of 40 mcg 1600 I.E.Vitamin D3. The serum 25 (OH) D and -1.25 (OH) 2D increase values ??within 1-2 days. The serum calcium and get -phosphatspiegel, the values ??for alkaline phosphatase decline in 10 days. Until the third week of treatment, calcium and phosphate is incorporated into the bone sufficient, which is visible on X-ray. After about a month, the daily dose will be gradually to the normal level of 15 mcg (600 IU) is reduced to obtain a constant level in the control. If a tetany on vitamin D should be up to a week with calcium salt i.v. be supplemented (hypocalcemia: treatment). Some older patients require 25 to> 50 mcg (1000 to ? 2000 IU) of vitamin D3 daily to keep the 25 (OH) D levels> 20 ng / mL (> 50 nmol / l); this dose is higher than the recommended daily allowance (RDA) for men <70 years (600 IU) or> 70 years (800 IU). The upper intake limit for vitamin D is 4000 I.E./Tag. Sometimes higher doses of vitamin D2 (. Eg 25,000 to 50,000 IU every week or every month) prescribed; because vitamin D3 is more potent than vitamin D2, this is now preferred. Since rickets and osteomalacia, caused by defective production of vitamin D metabolites, are vitamin D-resistant, they have refused when the usual effective dose is administered to a deterioration caused by inadequate supply of rickets. Here is an endocrinological examination is necessary because the treatment of a specific defect depends. Running the 25 (OH) D synthesis from faulty, the administration increased from 50 micrograms / day (2,000 IU) of vitamin D3 serum levels and leads to a clinical improvement of the condition. Patients with kidney disease often need a 1,25 (OH) 2D (calcitriol) supplementation. The hereditary vitamin D-dependent rickets type I therapy can be 1,25 (OH) 2D with the once-daily intake of 1-2 mcg. In some patients with type II hereditary vitamin D-dependent rickets treatment with a high dose of such strikes. B. 10-24 mcg / day of 1,25 (OH) 2D to; others require a longer period Kalziuminfusionen.Prävention A diet advice is for groups of importance for which there is the risk of vitamin D deficiency. The enrichment of flour for unleavened flat bread (chapati) with vitamin D (125 mcg / kg) was successfully performed for Indian immigrants in Britain. The benefits of sun exposure for vitamin D status must be weighed against the increased risks of skin damage and skin cancer. All children should still receive up to 6 months of once-daily supplemental vitamin D dose of 10 mcg of birth (400 IU); from 6 months to get a more versatile food. advantages of a higher dosage, as provided for by the RDA requirements are not nachgewiesen.Wichtige points A vitamin D deficiency is common and results from insufficient exposure to sunlight and inadequate supply (usually together occurring) and / or from chronic kidney disease. A deficiency can be at any age cause of muscle pain and weakness, body aches and osteomalacia. Patients suspected of having a deficiency of vitamin D, which show little sunlight and a low dietary intake, show typical symptoms and complaints (z. B. rickets, muscle pain, bone pain) or a bone demineralization in the radiograph. In order to confirm the diagnosis, the value of 25 (OH) D (D2 + D3) is determined. For the treatment of vitamin D deficiency existing deficiencies in calcium and phosphate are balanced, and it is given D supplemental vitamin. Vitamin D intoxication hypervitaminosis D resulting from the ingestion of the vitamin in excess. When vitamin D toxicity, bone resorption and the intestinal absorption of calcium is increased, resulting in hypercalcemia. In case of manifest hypercalcemia, symptoms show. The diagnosis is based on increased blood levels of 25 (OH) D. As part of the therapy, the vitamin D intake is interrupted, calcium intake restricted and, applied in cases of severe intoxication, corticosteroids or bisphosphonate. Since the synthesis of 1,25 (OH) 2D (the most active vitamin D metabolites) accurately controlled, results in a vitamin D hypervitaminosis only if patients are taking an extremely high dose which was prescribed or in an over-dose vitamin supplement is included. In infants, the supply of 1000 mcg leads (40,000 IU) of vitamin D per day within 1-4 months of intoxication. Adults who carry out over several months in 1250 mcg / day (50,000 IU) may cause a toxic effect. A vitamin D intoxication can be iatrogenic triggered when a hypoparathyroidism is treated too aggressively). Symptoms and complaints The main symptoms of vitamin D toxicity are due to the hypercalcemia. Anorexia, nausea and vomiting are typical, often follow polyuria, polydipsia, weakness, nervousness, pruritus, and ultimately kidney failure. Proteinuria, urinary casts, azotemia, and metastatic calcification, particularly in the kidneys, can auftreten.Diagnose hypercalcemia and risk factors or increased 25 (OH) D levels in the serum, the reference to an overdose of vitamin D intake in the history may be the only way to distinguish a vitamin D intoxication from other causes of hypercalcemia. Elevated serum calcium levels of 12-16 mg / dl (3-4 mmol / l) provide a reliable finding in toxic symptoms constitute The serum levels of 25 (OH) D. Is typically to> 150 ng / ml (> 375 nmol / l ) elevated. 1,25 (OH) 2D, which need not be determined to confirm the diagnosis, is located in the standard. The serum calcium levels of patients high doses of vitamin D, v. a. the reactive 1,25 (OH) 2D obtained should be monitored frequently, first week, then monatlich.Therapie intravenous fluid as well as corticosteroids or bisphosphonates After termination of the vitamin D intake reduce hydration (normal saline iv), corticosteroids or bisphosphonates, which preventing absorption in the bone calcium levels. Existing kidney damage or metastatic calcifications are sometimes irreversible.