Child who is due to nutritional deficiency rickets also is ill. Notice the curved legs and wrists raised.

Because rickets is not a noticeable disease, there are few figures on disease incidence. An expert panel of the U.S. Center for Disease Control, the incidence of hospital treatment for rickets with nine out of a million children identified. Outpatient therapy rickets was in the same report with a frequency of 23 to 32 per one million children indicated. There are African-American children with three-quarters of inpatient and outpatient 100% of cases by far the most frequently affected. A sub clinical vitamin D deficiency without clinical symptoms of rickets, even in highly developed countries much more often found. In American studies had 80% of the newborns and at the end of winter, almost half of girl’s aged nine to eleven years of low vitamin D concentrations in the blood. In Europe, a rachitis increased in infants and young children, macrobiotic diets receive before. Among these children developed more than half the symptoms of rickets.

Basically, the frequent calcium-deficiency rickets caused by a vitamin D deficiency is caused by the rare phosphate-deficiency rickets distinguish where the symptoms by an increased loss of phosphate excreted in the urine by the kidneys arise.

The balance of the calcium-phosphate metabolism is due to the parathyroid hormone, Calcitriol (vitamin D) and calcitonin regulated within narrow limits. The concentration of both substances is characterized by a constant solubility are closely linked. The largest part of the stock of calcium and phosphate is in the form of hydroxyapatite in the bones stored. If it is one of the two minerals to an imbalance between absorption through the gut and excretion by the kidneys, the concentration fluctuations due to a rapid entry into or from the bone Entspeicherung balanced. Vitamin D is not just for one installation of calcium and phosphate in the bone (mineralization) is needed, but also promotes their uptake from the intestine and the recovery from the Vorharn in the kidneys. The resulting calcium deficiency leads to a lack of incorporation of hydroxyapatite into the growing bone. This becomes increasingly softer and deforms. At the same time reproduces the non-calcified bone matrix (Osteoid), whereby the Knochenauftreibungen growth in the joints arises. The human vitamin D is mainly from an intermediate product of Cholesterinbiosynthese, the 7-dehydrocholesterol, her. This is under the influence of ultraviolet radiation from sunlight in the skin to vitamin D3 is converted in the liver to 25-hydroxy-cholecalciferol and then in the kidneys by the 1α-hydroxylase to actually effective hormone 1,25-dihydroxy-cholecalciferol (Calcitriol) activated. Only a small proportion of the vitamin D requirement is derived from the diet (see more accurate vitamin D).

The most common cause of calcium deficiency rickets is a lack of vitamin D supply with reduced sun exposure combined with inadequate intake of vitamin D. Much rarer is the production of active form of vitamin D3 by a hereditary enzyme defect disrupted (vitamin D-dependent rickets type II and I). A rickets may also symptom of a disease of the intestines, when not enough calcium can be added (celiac disease, cystic fibrosis), or the kidneys, where the activation of vitamin D precursors affected his. Certain medications for the treatment of epilepsy (phenytoin, phenobarbital) may have rachitis by reduced calcium uptake in the intestine as well as increased degradation of vitamin D3 cause.

Phosphate-deficiency rickets is usually propagated by a loss of phosphate via the kidneys caused. The only exception is that premature baby, where there is a relatively fast catch-up to the relative lack of phosphate intake may underlie. Besides the hereditary familial congenital hypophosphatämischen rickets (phosphate diabetes) result in damage to the Nierentubuli (De Toni-Fanconi syndrome) – mostly as a symptom of a congenital Cystinose, or acquired by poisoning – a phosphopenischen rickets.

Deformity of the wrist

In the second to third month of life are the first symptoms in the form of restlessness, Schreckhaftigkeit, increased sweating and subsequent itchy rash (Miliaria). About a month later with a muscle weakness frog abdomen, constipation tendency (constipation) and the first metabolic bone disease at skull (Kraniotabes) were added. Now the calcium deficiency in addition to increased Muskelerregbarkeit (tetany) to lead cramps. Again about a month later is caused by flattening of the occiput and the Reamers cranial sutures (Epiphytenbildung) the image of a square skull. The perlschnurartig strung Reamers the cartilage-bone boundaries in the growth of the rib joints on the thorax are also called Rosary. Also hand and ankle are becoming increasingly common. Later, show a delayed tooth eruption and defects in tooth enamel. Because the chest is unusually soft, the diaphragm Muskelzug on approach to a recovery, the Harrison grooves. Among other typical bone deformities include Beinverkrümmungen (O-legs, Genoa Vara), where the long bones varsity (inwards) are bent, and the less in joint deformities itself. In adults, the growth has sealed joints, and it comes with a vitamin D deficiency osteomalacia simply without childhood typical bone deformities.

The diagnosis is confirmed by the typical symptoms that are visible on the X-ray changes in bones, and by an increased activity of alkaline phosphates in the blood. Since the X-ray examination no specific distinguishing features between a calcium deficiency and a phosphate-deficiency rickets showing must be made between these forms by further laboratory tests to be distinguished. This is a determination of parathyroid hormone, which increases calcipenischer rickets and in the form phosphopenischen normal. Furthermore, the concentration of each vitamin D precursors provides a classic vitamin D deficiency rickets (with low 25 (OH) vitamin D3. But low normal dihydroxy-cholecalciferol-values) of the vitamin D-dependent forms (with normal 25 (OH) vitamin D3 and abnormally low-dihydroxy cholecalciferol concentration in the VDAR I and normal vitamin D3 and excessively high-dihydroxy-cholecalciferol Konzentrantion in VDAR II) enclosed.

The treatment is based on the cause. In the classic vitamin D deficiency rickets get the children first three weeks of vitamin D and calcium in high doses. This will be followed for a further three weeks significantly reduced. Following is a switch to a calcium-rich diet with adequate sun exposure is sufficient. However, a vitamin D-dependent rickets type I disturbed with the conversion of vitamin D3 in the active dihydroxy-cholecalciferol in front, in addition to a high-calcium substitution Calcitriol administration. Once the soft bones with calcium aufgesättigt is simply a life-long substitution of Calcitriol. The vitamin D dependent rickets type II turn is often difficult. Single calcium and dihydroxy-cholecalciferol-in tablet intake ranges may be insufficient. In such cases, additional infusions of calcium needed to activate the bone according aufzusättigen. Calcium must then remain in extremely high volumes take normal calcium level in blood to maintain.

The form must be phosphopenischen addition to treatment with Calcitriol phosphate with a substitution made. See also the separate article on phosphate diabetes.

Heal bone deformities in children with classic rickets after substitution of vitamin D mostly independently, with serious deformations of the legs, however, long thigh rail recommended (braces). In the phosphate-deficiency in adolescents and forms are much more frequently needed conversion operations in which a Keilentnahme of Achsfehler balanced.

Following the recommendations of the German Society for Social Pediatrics infants received in the first year of life by the second week in a preventive dose of vitamin D3 in tablet form. With 500 IU dosage is well above the accepted daily needs of 100-200 IU, however, so that natural fluctuations should be the same as occasional missed doses. This substitution is fed infants and flaschenernährte equally throughout the first year and, where appropriate, also by the second winter of life is recommended. The proposed dosage is also valid for additional enrichment of industrially produced bottles of milk with vitamin D safe enough. Since overdose symptoms in the form of increased thirst, increased urination, persistent loss of appetite, constipation and failure to thrive, in rare cases only at doses over 2,000 IU were described.

Cover the work Rachitide sive de morbo puerili, Leiden 1672, by Francis Glisson

As bone discoveries of mummies and studies show it has the rickets from prehistory to at all time and in all parts of the Earth. The first description as a separate disease picture comes from Jerome Reusner from the 16th Century. A hundred years later the name morbus Anglorum, English disease, characterized by Whistler. He should be back to the 19th Century keep. Around the same time Francis Glisson also described the disease in detail. In the 18th Century accumulate finally Treatises of rickets. In Europe came after the two world wars rickets caused by malnutrition on again. She is still in the poor countries of the world is very widespread. The foundations for the cure of the disease were only the beginning of the 20th Century in England created. By the pollution caused by industrial smog then lay on the housing of workers, so that the sun could not penetrate the skin in vitamin D is activated. The result was that many children showed the typical symptoms. Interestingly, the disease arrived in the English upper class. With their glazed winter gardens could also not get UV light, resulting in rickets also a high standard of living may occur. Regular liver-gifts helped to prevent the disease, since liver oil particularly rich in vitamin D is.

Rickets occurs in captive animals or pets especially for growing birds, reptiles and amphibians before. Triggering factors, in addition to an absolute calcium or vitamin D deficiency and without artificial UVB often too low calcium: phosphorus ratio in the diet. This should amount to approximately 1,5-2:1. When an excessive intake of phosphorus is the formation of activated vitamin D (1.25-Hydroxy-vitamin D2 and D3) in the kidneys is reduced, so that the absorption of calcium from the intestine is reduced.

In birds comes rickets especially in singing, parrots, chickens and birds, which sided with grains which are mixtures. The calcium: phosphorus ratio of many seeds is very low (1:17 maize, millet and sunflower seeds approximately 1:6). For the young birds, it is mainly to curvature of the sternum, the thighbone and the Tibiotarsus. Feed conversion and additional administration of calcium do the therapy and vitamin D. crooked bones can only be by a Korrekturosteotomie and subsequent osteosynthesis corrected, in severe cases, the bird wills eingeschläfert.

When reptiles are also a poor calcium: phosphorus ratio (high proportion of meat or calcium-poor insects) as well as vitamin D, calcium and / or UV light, the main deficiency Rachitisursachen, but also a surplus of vitamin D may be triggered. When turtles is primarily the back tank (Plastron) inadequately mineralized, so that these soft and crooked (sattelförmig) appears. In snakes and lizards, it is mainly to curvature of the spine, where fractures especially in the lumbar spine (“hump formation”) can occur. The “Rosary education” to the ribs is rarely observed. The therapy is carried out as in birds. Prophylaxis can be 200 IU / kg / day of vitamin D3, with the addition of meat feeding a vitamin-mineral mixture used.

In amphibians is mainly the unilateral chitinreicher feeding insects (calcium and vitamin D deficiency) rickets-trigger. Typically, they have a softening and shortening of the mandible. Feed conversion and additional administration of calcium and vitamin D do the therapy.

In mammals house rickets is very rare. For dogs, there is a rachitis Although experimental trigger, but almost never before. From a vitamin D as prophylaxis in children is not recommended in dogs because it is by an excess of calcium to prevent disturbances of the ossification enchondralen coming.