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Classification according to ICD-10
E55.0 Florid rickets
E64.3 Consequences of rickets
E83.30 Familial hypophosphatemic rickets
E83.31 Vitamin D dependent rickets
N25.0 Renal rickets
ICD-10 online (WHO version 2019)
Child who also has rickets due to malnutrition. Note the bent legs and the distended wrists. (1970)

The rickets (from the Greek ῥάχις rháchis, back, backbone), synonymous English disease , English rickets , in older texts also (etymologically correct) rickets , describes a disease of the growing bones with impaired mineralization of the bones and usually associated with vitamin D deficiency Disorganization of the growth plates in children. The clinical picture corresponding to rickets in adulthood is osteomalacia .

Rickets is due to an insufficient concentration of the calcium - phosphate product in the blood and the hormonal counter-regulation mechanisms that this causes . The frequent calcium deficiency rickets is usually caused by an acquired vitamin D metabolic disorder or insufficient calcium intake with food. It is differentiated from the rare phosphate deficiency rickets , which is caused by a mostly inherited excessive loss of phosphate through the kidneys. In addition to growth disorders with deformation of the bones, the symptoms include in particular swelling of the cartilage-bone boundaries at the growth plates. Treatment depends on the cause. It consists of supplementing with vitamin D, if necessary also with calcium or phosphate. For prophylaxis , it is common practice to give infants a single daily dose of vitamin D during the first year of life.


Since rickets is not a reportable disease, there are hardly any figures on the incidence of the disease. A panel of experts from the American Center for Disease Control has determined the frequency of hospital treatment for rickets in nine children in one million. Outpatient rickets therapy was given in the same report with a frequency of between 23 and 32 per million children. In this collective, African-American children were by far the most frequently affected with three quarters of inpatient and 100% of outpatient cases. Subclinical vitamin D deficiency without clinical symptoms of rickets is found much more frequently even in highly developed countries. In American studies, 80% of the newborns and at the end of winter almost half of the girls between the ages of nine and eleven years had decreased vitamin D concentrations in their blood. Vitamin D deficiency is epidemic even in countries with high levels of sun exposure. B. when women wear a burqa for religious reasons . In Europe, rickets is more common in infants and young children on a macrobiotic diet. Among these children, more than half developed symptoms of rickets.


Basically, the frequent calcium deficiency rickets , which is caused by a vitamin D deficiency, is differentiated from the rare phosphate deficiency rickets , in which the symptoms arise from increased loss of phosphate in the urine by the kidneys.

Calcium Phosphate Metabolism

The balance of the calcium-phosphate metabolism is regulated within narrow limits by the hormones parathyroid hormone , calcitriol (vitamin D) and calcitonin . The concentration of the two substances is closely linked by a constant solubility product . Most of the calcium and phosphate supply is stored in the bones in the form of hydroxyapatite . If there is an imbalance for one of the two minerals between absorption via the intestine and excretion via the kidneys, fluctuations in concentration are compensated for by rapid storage in or depletion from the bone. Vitamin D is not only necessary for the incorporation of calcium and phosphate into the bones (mineralization), but also promotes their absorption from the intestines and their recovery from the fore-urine in the kidneys. If there is a vitamin D deficiency, calcium can only be insufficiently absorbed from the intestine. The resulting calcium deficiency leads to insufficient incorporation of hydroxyapatite in the growing bones. This becomes increasingly softer and deforms. At the same time, the non-calcified basic bone substance ( osteoid ) increases, which causes the bones to develop in the area of ​​the growth plates. Humans produce vitamin D mainly from an intermediate product of cholesterol biosynthesis , 7-dehydrocholesterol . This is converted into vitamin D 3 in the skin under the action of ultraviolet radiation from sunlight , in the liver to 25-hydroxy-cholecalciferol and then in the kidneys by 1α-hydroxylase to the actually active hormone 1,25-dihydroxy-cholecalciferol (calcitriol ) activated. Only a small proportion of the vitamin D requirement is absorbed from food (for more details see under vitamin D ).

Calcium deficiency rickets

The most common cause of calcium deficiency rickets is an inadequate vitamin D supply with reduced sun exposure combined with an inadequate vitamin D supply. Much less often, the production of the active form of vitamin D 3 is disrupted by a congenital enzyme defect (vitamin -D-dependent rickets type I and II). Rickets can also be a symptom of a disease of the intestine in which insufficient calcium can be absorbed ( celiac disease , cystic fibrosis ) or of the kidneys, in which the activation of the vitamin D precursors is impaired. Certain drugs for the treatment of epilepsy ( phenytoin , phenobarbital ) can cause rickets due to reduced calcium absorption in the intestine and an increased breakdown of vitamin D 3 .

Phosphate deficiency rickets

A phosphate deficiency rickets is usually caused by an increased loss of phosphate through the kidneys. The only exception are premature infants , who may be based on an insufficient phosphate intake in relation to the rapid catching-up growth. In addition to hereditary familial hypophosphatemic rickets ( phosphate diabetes ), damage to the kidney tubules ( De Toni Fanconi syndrome ) - usually as a symptom of congenital cystinosis or acquired through poisoning - leads to phosphopenic rickets.

A distinction is made between several hereditary forms of phosphate-deficient rickets. X-linked dominant inherited hypophosphatemic rickets is the most common form of inherited rickets. It occurs around once in every 20,000 live births. 70% of the patients have mutations in the phosphate regulator gene PHEX on the X chromosome. PHEX codes for a protease that cleaves small peptide hormones. The protease is expressed in teeth, bones and the parathyroid glands and leads to the downregulation of fibroblast growth factor 23 (FGF-23) via an unexplained mechanism. An autosomal dominant form of hypophosphatemic rickets is caused by a mutation in FGF-23. A hereditary form with increased calcium excretion has also been described.


Open bite in deciduous teeth
Deformity of the wrist
X-ray of the wrist in a child with florid rickets

In the second to third month of life, the first symptoms appear in the form of restlessness, nervousness , increased sweating and the resulting itchy rash ( miliaria ). About a month later, there is muscle weakness with a frog belly , a tendency to constipation ( constipation ) and the first softening of the bones on the skull (craniotabes). Now the calcium deficiency can also lead to increased muscle excitability ( tetany ) and even cramps. About a month later, the flattening of the back of the head and expansion of the cranial sutures (epiphyte formation) create the image of a square skull. The swellings of the cartilage-bone borders on the growth plates of the ribs on the chest are also called the rosary . Wrists and ankles are also increasingly widening due to the expansion of the epiphyses ( Marfan's sign , “double limbs”). Later, a delayed tooth eruption, defects in the tooth enamel , a delayed mineralization of the jawbone up to an open bite appear . Because the rib cage is unusually soft, the muscle pull at the base of the diaphragm leads to a retraction, the Harrison groove. Other typical bone deformations include curvature of the legs (bow legs, genua vara ), whereby the long tubular bones are varically bent (inward), and the deformities are less in the joint itself. In adults, the growth plates are already closed and a vitamin D deficiency only results in osteomalacia without the bone deformations so typical in childhood.


X-ray of a child with rickets

The diagnosis is made by the typical symptoms, the changes in the bones visible in the X-ray and by an increased activity of alkaline phosphatase in the blood. Since the X-ray examination does not show any specific distinguishing features between calcium deficiency and phosphate deficiency rickets, further laboratory tests must be used to differentiate between these forms. This is done by determining the parathyroid hormone , which is increased in calcipenic rickets and normal in the phosphopenic form. Furthermore, the concentration of the individual vitamin D precursors is determined to avoid classic vitamin D deficiency rickets (with reduced 25 (OH) vitamin D 3 , but low normal dihydroxy-cholecalciferol values) from the vitamin D dependent forms (with normal 25 (OH) vitamin D 3 - and abnormally low dihydroxy-cholecalciferol concentration in VDAR I or normal vitamin D 3 - and excessively high dihydroxy-cholecalciferol concentration in VDAR II).

Differential diagnosis

Different forms of metaphyseal chondrodysplasia are to be distinguished, e.g. B. Jansen's metaphyseal chondrodysplasia .


Treatment is basically based on the cause.

Baby Jesus in Dürer painting Maria with the pear slices (1512 KHM in Vienna ) has characteristic features of a vitamin D deficiency on protrusion of forehead and crown bumps with Hinterhauptabflachung (Caput quadratum), flaccid abdominal wall, thorax deformation and swelling of the epiphyses of Wrists and ankles.

In classic vitamin D deficiency rickets, children first receive vitamin D and calcium in high doses for three weeks, then in significantly reduced doses for another three weeks. Subsequently, a switch to a calcium-rich diet with appropriate sun exposure is sufficient. However, if there is vitamin D-dependent type I rickets with impaired conversion of vitamin D 3 into the active dihydroxy-cholecalciferol, calcitriol must be administered in addition to high-dose calcium substitution. As soon as the soft bone is saturated with calcium, a lifelong substitution of calcitriol is sufficient. Type II vitamin D-dependent rickets, on the other hand, is often difficult. A sole supply of calcium and dihydroxy-cholecalciferol in the form of tablets may not be sufficient here. In such cases, additional calcium infusions are necessary to adequately saturate the bone. Then calcium must continue to be consumed in extremely high amounts in order to maintain normal calcium levels in the blood.

In the case of the phosphopenic form, in addition to treatment with calcitriol, phosphate must also be substituted. See also the separate article on phosphate diabetes .

In children with classic rickets, malpositions of bones usually heal independently after vitamin D substitution, but thigh-length splints are recommended for severe deformities of the legs ( orthoses ). In the phosphate-deficient forms and in adolescents are more likely to significantly change operations necessary is where offset by a wedge removal of the axis error.


According to the recommendations of the German Society for Social Pediatrics, infants in the first year of life are given preventive vitamin D 3 from the second week of life , there in tablet form. The Nutrition Commission of the Swiss Society for Pediatrics and the Swiss Society for Neonatology recommend a daily intake of 300–500 IU from the first days of life, the maximum daily dose should not exceed 1000 IU. It is administered there in a drop solution.

With 300–600 IU (in Germany 500 IU) the dosage is well above the assumed daily requirement of 100 to 200 IU, but natural fluctuations are to be compensated just as well as occasionally forgotten doses. This substitution is recommended for breastfed and bottle-fed infants alike during the entire first year of life and, if necessary, through the second winter of life. The suggested dosage is considered to be sufficiently safe even if the industrially manufactured bottled milk is additionally fortified with vitamin D, since symptoms of overdose in the form of increased thirst, increased urination, persistent loss of appetite, constipation and failure to thrive have in rare cases only been described at dosages above 2,000 I.U.


Title page of the work De Rachitide sive morbo puerili ... , Leiden 1672, by Francis Glisson

As bone finds and studies of Egyptian mummies show, rickets has existed from prehistory at all times and in all parts of the world. The first descriptions as an independent clinical picture come from Hieronymus Reusner from the 16th century. The disease was known to be treated with cod liver oil as early as the 16th century. About a hundred years later, the name Morbus Anglorum ("English disease") is coined by Whistler. It would last into the 19th century. The disease was observed to emerge in the English counties of Somerset and Dorset around 1620. In 1650, Francis Glisson first described the disease in detail. In the eighteenth century there was a pile of papers on rickets. In Europe, rickets reappeared after the world wars due to malnutrition . Even today it is prevalent in the poor countries of the world. The foundations for treating this disease were not laid in England until the early 20th century. At that time , the smog caused by environmental pollution from industry and private wood firing often settled over cities in valley and basin areas in certain weather conditions, so that the UV radiation from the sun was partially shielded, which in the skin increased the reduction of 7-dehydrocholesterol Cholecalciferol causes. The result was that many children showed the typical symptoms. Interestingly, the disease also hit the English upper class. Only a small amount of UV light could get through their glazed winter gardens, which means that rickets can occur even with a high standard of living. Regular administration of cod liver oil helps to prevent the disease, as cod liver oil is particularly rich in vitamin D. Being outdoors too is a good prevention. The Polish pediatrician and researcher, Jan Rudolf Raczyński (1865–1918), who suspected a connection between rickets and a lack of sunlight, sent rachitic children to the Carpathians in 1912 for healing. Edward Mellanby and Elmer McCollum artificially produced rickets in dogs and rats through specially prepared food, which in all cases was curable by cod liver oil. This led to the assumption that cod liver oil contains an "anti-rachitic vitamin". In 1918/19 the German pediatrician Kurt Huldschinsky cured young rickets patients completely with UV radiation. Since then, the disease has only occurred rarely in Central Europe. The Americans Harry Steenbock and Alfred Fabian Heß (1875–1933) and LF Unger then found out that there is a substance (provitamin) in the skin of mammals that turns into an anti-rachitic vitamin when exposed to radiation. As a result, food, such as milk for children, was irradiated.

The autosomal dominant phosphate deficiency rickets was first described in 1939.

Rickets in animals

Rickets occurs in captive animals or pets primarily in growing birds , reptiles, and amphibians . In addition to an absolute calcium or vitamin D deficiency and artificial light without a UV component, the triggering factors are often too low a calcium: phosphorus ratio in the diet. This should be around 1.5–2: 1. In the event of excessive phosphorus intake, the formation of activated vitamin D (1,25-hydroxy-vitamins D 2 and D 3 ) in the kidneys is reduced, so that the absorption of calcium from the intestine is reduced.

In birds, rickets occurs mainly in songbirds , parrots and hens that are raised on one side with mixtures of grains. The calcium: phosphorus ratio of many seeds is very low (corn 1:17, millet and sunflower seeds about 1: 6). In affected young birds, the sternum , thighbone and tibiotarsus are curved . Therapy is carried out by changing the food and adding calcium and vitamin D. Crooked bones can only be corrected by a corrective osteotomy and subsequent osteosynthesis ; in severe cases, the bird must be euthanized.

In reptiles, an inadequate calcium: phosphorus ratio (high proportion of meat or insects low in calcium) as well as vitamin D, calcium and / or UV light deficiencies are the main causes of rickets, but an excess of vitamin D can also be a trigger be. In turtles , the back armor ( plastron ) in particular is insufficiently mineralized, so that it appears soft and crooked (saddle-shaped). In snakes and lizards , the spine is curved, and broken bones can occur mainly in the lumbar spine ("hump"). The "rosary formation" on the ribs is rarely seen. Therapy is the same as for birds. As a prophylactic measure, 200 IU / kg and day of vitamin D 3 can be used, and a vitamin-mineral mixture can be added for meat feed .

In amphibians, one-sided feeding of chitin-rich insects (calcium and vitamin D deficiency) is the main cause of rickets. Typical for them is a shortening and softening of the lower jaw. Therapy is carried out by changing the diet and adding calcium and vitamin D.

Rickets is very rare in domestic mammals. Rickets can be provoked experimentally in dogs, but practically never occurs. Vitamin D prophylaxis, as in children, is not recommended for dogs, since an excess of calcium can lead to disorders of the enchondral ossification .


  • K. Kruse: Current Aspects of Vitamin D Deficiency Rickets. In: Monthly Pediatrics. (6/2000) 148, pp. 588-595.
  • MJ Lentze ao: Pediatrics - Basics and Practice. 2nd Edition. Springer 2002.
  • K. Gabrisch, P. Zwart: Diseases of pets. 6th edition. Schlütersche, Hannover 2005, ISBN 3-89993-010-X .
  • JE Scherberich: Calcium-phosphate and bone metabolism. In: The Nephrologist. 3 (2008), pp. 507-517.
  • Irmtraut Sahmland: rickets (English disease, double limbs). In: Werner E. Gerabek , Bernhard D. Haage, Gundolf Keil , Wolfgang Wegner (eds.): Enzyklopädie Medizingeschichte. De Gruyter, Berlin / New York 2005, ISBN 3-11-015714-4 , p. 1211.

Web links

Commons : Rickets  - collection of pictures, videos and audio files

Individual evidence

  1. KS Scanlon (Ed.): Vitamin D expert panel meeting October 11-12, 2001, Atlanta, Ga. Final report. PDF (English; 391 kB), accessed on April 20, 2006.
  2. ^ MF Holick: Resurrection of vitamin D deficiency and rickets. In: The Journal of Clinical Investigation. 2006, 116, pp. 2062-2072 PMID 16886050 full text (English)
  3. PC Dagnelie, FJ Vergote, WA van Staveren, H. van den Berg, PG Dingjan, JG Hautvast: High prevalence of rickets in infants on macrobiotic diets. In: Am J Clin Nutr. 51 (1990), pp. 202-208. PMID 2154918
  4. a b c d R. Schnabel, D. Haffner: Diagnosis and therapy of rickets. In: Monthly Pediatrics. 2005, 153, pp. 77-90.
  5. a b V. S. Jagtap, V. Sarathi, AR Lila, T. Bandgar, P. Menon, NS Shah: Hypophosphatemic rickets. In: Indian Journal of Endocrinology and Metabolism. Volume 16, No. 2, 2012, pp. 177-182. doi : 10.4103 / 2230-8210.93733 .
  6. Albert Gossauer: Structure and reactivity of biomolecules. Verlag Helvetica Chimica Acta, Zurich 2006, ISBN 3-906390-29-2 , p. 152.
  7. Paediratica Vol. 22, No. 1, 2011, p. 7: Recommendations for feeding healthy newborns during the first days of life , accessed on April 17, 2015
  8. a b J.-Ch. Sournia, J. Poulet, M. Martiny (Ed.): Illustrated history of medicine. Directmedia, Berlin 2004.
  9. JFL Cappel: Attempt a complete treatise on the so-called English disease. Berlin et al. 1787.
  10. ^ Otto Westphal , Theodor Wieland , Heinrich Huebschmann: life regulator. Of hormones, vitamins, ferments and other active ingredients. Societäts-Verlag, Frankfurt am Main 1941 (= Frankfurter Bücher. Research and Life. Volume 1), pp. 52–54 ( The English disease ), here: p. 52.
  11. F. Glisson: De Rachitide sive Morbo puerili, qui vulgo dicitur the Rickets, tractatus. London 1650.
  12. Irmtraut Sahmland: Rickets. 2005, p. 1210.
  13. ^ Austrian Biographical Lexicon: Raczyński, Jan Rudolf .
  14. ^ Otto Westphal, Theodor Wieland, Heinrich Huebschmann: life regulator. Of hormones, vitamins, ferments and other active ingredients. 1941, p. 52.
  15. ^ Otto Westphal, Theodor Wieland, Heinrich Huebschmann: life regulator. Of hormones, vitamins, ferments and other active ingredients. 1941, p. 52 f.
  16. Philipp Osten: Rickets can be cured with ultraviolet light. In: Berliner Zeitung . April 14, 2007, accessed June 19, 2019 .
  17. Christian Floto: Office hours; X, O or unequal legs. Deuschlandfunk, June 18, 2019, accessed on June 19, 2019 .
  18. ^ Otto Westphal, Theodor Wieland, Heinrich Huebschmann: life regulator. Of hormones, vitamins, ferments and other active ingredients. 1941, p. 53.
  19. Stalking rickets .
This version was added to the list of articles worth reading on June 5, 2007 .