Summary
Based on archaeological research, it can be concluded that skeletal changes caused by rickets already
existed in antiquity. The disease causing skeletal deformities was first described in 1645 by Daniel
Whistler. As he observed it occurring frequently in English city children, he called it “the English
disease”.
The cause of rickets is a vitamin D deficiency – caused by both a poor diet and insufficient sun
exposure.
Rickets causes changes in the skeletal system (bone softening and deformation, bone pain),
radiological symptoms (changes in the epiphyses, deformation of the pelvis, fragility of the limbs) and
extrosseous symptoms (hypocalcemic convulsions and tetany, heart failure, cardiac dysfunction and
arrest, impaired growth body weight and length, delayed motor development with muscle weakness,
increased intracranial pressure, agitation and irritability). Laboratory tests show decreased levels of
vitamin D3 and calcium.
Effective measures to prevent rickets are supplementation with vitamin D3, calcium, and being
outdoors (especially in warm seasons) and being exposed to sunlight. In cases of deficiencies,
supplementation with such preparations as Calcineff D3K2 or Calcineff Minerals is recommended.
Based on descriptions found in manuscripts and archaeological works, it can be assumed that skeletal
changes that could be caused by rickets already existed in antiquity. Medieval descriptions of the
symptoms of rickets date back to the 15th century, as is known from the information contained in
later written sources.
For the first time, a more extensive description of the disease causing skeletal deformities was given
by Daniel Whistler in 1645 in his scientific work presented at the University of Leyden entitled: De
morbo puerili Anglorum, quem patrio idiomate indigenae vocant “the rickets”. Five years later,
Francis Glisson’s book De Rachitide sive morbo puerili qui vulgo the Rickets dicitur was published, in
which he presented a complete clinical picture of this disease. In 1651, the book was translated into
English, indicating an interest in rickets in England during this period. The next two centuries did not
bring new discoveries and reports about this disease.
Rickets cases became epidemic in nineteenth-century England and some other northern European
countries, where little sunlight and living conditions in smoky, industrial cities were at the root of the
phenomenon. Hence the historical name of rickets – the English disease.
Deficiency rickets is a disorder of chondrocyte differentiation, growth plate mineralization and
osteoid mineralization due to vitamin D deficiency and / or low calcium intake in children. Deficiency
rickets is diagnosed on the basis of history, physical examination and biochemical tests, and
confirmed by X-ray examinations.
The most common cause of rickets is vitamin D deficiency – caused both by poor diet and insufficient
sun exposure (UV radiation is necessary to convert one of the cholesterol derivatives into vitamin D3).?
Bone mineralization requires the supply of adequate amounts of calcium and phosphate. Vitamin D
regulates their absorption from the intestine. Calcium deficiency causes the release of parathyroid
hormone (PTH), which eventually leads to the processes that cause rickets. It is a disease of the
growing bone, while osteomalacia (a metabolic disease of the bone consisting in insufficient
mineralization and reduction of bone density) refers to disturbances in bone mineralization after the
end of the bone growth process. Deficiency rickets also occurs in the course of fat malabsorption,
liver diseases, renal failure and diseases requiring total parenteral nutrition.
Infants and adolescents, due to their rapid growth, are at increased risk of rickets and osteomalacia
due to vitamin D deficiency. Rickets has a significant effect on the health of infants, children and
adolescents, and its effects persist into adulthood. The sequelae of rickets and osteomalacia may
include: hypocalcemic tetany, life-threatening hypocalcemic cardiomyopathy, bone pain and muscle
weakness, deformation of the bones of the extremities and pelvis, abnormal physical development,
developmental delay, and tooth developmental disorders.
Rickets is becoming more common not only in developing countries (with lower incomes), but also in
well-developed (wealthy) countries. Its incidence, for example, in Canada is 2.9 / 100,000, in Australia
– 4.9 / 100,000, in Great Britain – 7.5 / 100,000, and in the United States – 24 / 100,000. they mainly
affect immigrants, while the prevalence of rickets in white people is the same or is even decreasing.
The symptoms of rickets include:
1) bone and dental symptoms: bone softening, thickening of the cartilage-bone joints of the ribs,
widening of the wrists and ankle joints, delayed parietal atresia, delayed tooth eruption, deformation
of the lower limbs, prominent frontal tumors, bone pain;
2) radiological symptoms: changes within the epiphyses, pelvic deformities, including narrowing of
the pelvic canal (risk of death and difficulties in labor), permanent deformities, fractures due to
minimal injuries;
3) post-osteochondrosis symptoms: hypocalcemic convulsions and tetany, heart failure, cardiac
dysfunction and arrest, impaired weight gain and body length, delayed motor development with
muscle weakness, increased intracranial pressure, agitation and irritability;
4) biochemical symptoms: a decrease in the concentration of 25-hydroxyvitamin D [25 (OH) D],
phosphate and calcium, and an increase in PTH and serum alkaline phosphatase (AP) levels, as well as
a decrease in calcium and an increase in urine phosphate.
Prevention
In infants from birth to 12 months of age, irrespective of the feeding method, the recommended dose
of vitamin D for the prevention of rickets is 400 IU (10 ?g) per day. As recommended by the US
National Academy of Medicine, all older children and adults should receive 600 IU of vitamin D in
their diet and / or supplements per day.
A very good preparation for the prevention of rickets is Calcineff D3 K2, containing 1000 IU of vitamin
D3, 600 mg of calcium ions and 35 ?g of vitamin K2 in one tablet.
A similar preparation is Calcineff Minerals, containing 400 mg of calcium, 200 mg of magnesium, 10
mg of zinc and 2000 IU of vitamin D3 in 1 tablet.
Vitamin D and calcium dosage to treat deficiency rickets?
AUTHOR: Dr n. farm. Andrzej Tarasiuk