Ricket is a condition that produces weak or soft bones in children. Symptoms include swollen feet, dwarf growth, bone pain, large forehead, and difficulty sleeping. Complications may include fractures, muscle spasms, abnormally curved spine, or intellectual disabilities.
The most common cause is vitamin D deficiency. This can occur due to eating a diet without enough vitamin D, dark skin, too little sun exposure, exclusive breastfeeding without vitamin D supplements, celiac disease, and certain genetic conditions. Other factors may include not enough calcium or phosphorus. The underlying mechanism involves inadequate calcification of the growth plate. Diagnosis is generally based on blood tests finding low calcium, low phosphorus, and high alkaline phosphatase along with X-rays.
Prevention includes vitamin D supplements for exclusively breast-fed infants. Treatment depends on the underlying cause. If due to vitamin D deficiency, treatment is usually with vitamin D and calcium. This generally results in improvements in a few weeks. Bone deformity can also increase over time. Sometimes surgery can be done to improve bone deformity. Genetic form of this disease usually requires special care.
Rafts generally occur in the Middle East, Africa, and Asia. Generally not common in the United States and Europe, except among certain minority groups. It begins in childhood, usually between the ages of 3 and 18 months. The disease rate is the same in men and women. Cases that are believed to have become rickets have been described since the 1st century. This disease is common up to the 20th century. Initial treatment includes the use of cod liver oil.
Video Rickets
Signs and symptoms
Raft signs and symptoms may include bone pain, and susceptibility to fractures, especially greenstick fractures. Early bone damage may occur in infants such as soft and thin skull bones - a condition known as craniotabes which is the first sign of rickets; skull bossing can be present and delayed closure of the fontanel.
Young children may have lowered their legs and thickened their ankles and wrists; older kids may have knocking knees. The spine arch of kyphoscoliosis or lumbar lumbosis may be present. The pelvic bone may change shape. A condition known as rachary rachitis can occur as a thickening caused by the formation of nodules in the costochondral joint. It appears as a visible bump in the middle of each rib in a line on each side of the body. It somewhat resembles a rosary, giving rise to a name. Pigeon chest deformity can lead to the presence of the Harrison groove.
Hypocalcemia, low levels of calcium in the blood can lead to uncontrolled muscle spasms. Dental problems can also arise.
X-rays or advanced radiographs of rickets tend to be present in the classical way: bent legs (the outer curve of the long bones of the leg) and a deformed chest. Skull changes also occur causing the appearance of a typical "square head" known as "quadratum cap". This deformity persists in adult life if left untreated. Long-term consequences include permanent curvature or long bone damage, and a curved back.
Maps Rickets
Cause
Lack of mother can be a real cause of bone disease from before birth and decrease bone quality after birth. The main cause of congenital rickets is a vitamin D deficiency in the mother's blood, which babies share. Vitamin D ensures that serum phosphate and calcium levels are sufficient to facilitate bone mineralization. Congenital rickets can also be caused by other maternal diseases, including severe osteomalacia, untreated celiac disease, malabsorption, pre-eclampsia, and premature birth. Rakhets in children are similar to osteoporosis in the elderly, with brittle bones. Pre-natal care includes checking vitamin levels and ensuring that any deficiencies are given.
Also breast-fed baby exclusively may require the prevention of rickets with vitamin D supplementation or increased exposure to sunlight.
In bright countries like Nigeria, South Africa, and Bangladesh, there is enough endogenous vitamin D due to sun exposure. However, this disease occurs among older toddlers and children in these countries, which in this state is associated with low dietary calcium intake due to cereal based diet.
Those at higher risk for developing rickets include:
- Breastfed babies whose mothers are not exposed to sunlight
- Babies who are breastfed are not exposed to sunlight
- A breast-fed baby with little sunlight
- Teenagers, especially when undergoing accelerated growth of puberty
- Any child whose diet does not contain enough vitamin D or calcium
Sunlight
Sunlight, especially ultraviolet light, allows human skin cells to convert vitamin D from inactive to active. In the absence of vitamin D, the calcium diet is not well absorbed, resulting in hypocalcemia, which causes bone and tooth deformities and neuromuscular symptoms, for example. hyperexitability. Foods containing vitamin D include butter, eggs, fish liver oil, margarine, fortified milk and juice, portabella and shiitake mushrooms, and oily fish such as tuna, herring, and salmon. A rare X-linked dominant form is called vitamin D rickets that are resistant to vitamin D or X-linked hypophosphatemia.
Cases have been reported in the UK in recent years of rickets in children from many social backgrounds caused by insufficient production in the body of vitamin D because sun's ultraviolet rays do not reach the skin due to the use of strong sunscreen, too much "cover" in in the sun, or not out into the sun. Other cases have been reported among children of some ethnic groups where mothers avoid sun exposure for religious or cultural reasons, leading to maternal vitamin D deficiency; and people with darker skin need more sun to maintain vitamin D levels.
Rickets has historically been a problem in London, especially during the Industrial Revolution. The continuous thick fog and heavy industrial haze seeping into the city blocks large amounts of sunlight in such a way that up to 80 percent of children at one time have varying degrees of rickets in one form or another. Sometimes known in German as "the English Disease" (Die Englische Krankheit)
Diseases that cause soft bones in infants, such as hypophosphatasia or hypophosphatemia can also cause rickets.
Evolutionary considerations
Hypotheses of natural selection Vitamin D: Rickets are often a result of vitamin D3 deficiency. The natural selection hypothesis of vitamin D suggests that vitamin D production from sunlight is a selective force for human skin color variations. The correlation between human skin color and latitude is considered to be a positive selection result for different levels of solar ultraviolet radiation. North latitude has a selection for lighter skin that allows UV rays to produce vitamin D from 7-dehydrocholesterol. In contrast, the latitude near the equator has a selection for darker skin which can block most UV radiation to protect against toxic levels of vitamin D, as well as skin cancer.
An often cited anecdote to support this hypothesis is that relatively dark arctic populations for their latitudes, such as the Inuit, have a diet that is historically rich in vitamin D. Because these people are getting vitamin D through their diet, there is no positive selective force to synthesize vitamin D from sunlight.
Environmental mismatch: Ultimately, vitamin D deficiency arises from a mismatch between the evolutionary environment of the previous population and the current environment. The risk of this discrepancy increases with advances in transportation methods and the increasing size of urban populations at high latitudes.
Similar to environmental mismatches when dark-skinned people live in high latitudes, Rickets can also occur in religious communities that require long clothing with veils and veils. This veil and veil serves as a barrier to sunlight that prevents individuals from synthesizing vitamin D naturally from the sun.
In a study by Mithal et al., Vitamin D deficiency from various countries measured with lower 25-hydroxyvitamin D. 25 (OH) D was an easily measurable indicator of vitamin D insufficiency. This percentage should be considered a relative vitamin D level, and not as predicting evidence for rickets development.
Asian immigrants living in Europe have an increased risk of vitamin D deficiency. Vitamin D insufficiency is found in 40% of non-Western immigrants in the Netherlands, and over 80% of Turkish and Moroccan immigrants.
The Middle East, despite high levels of sun exposure, has the highest rates of rickets worldwide. This may be explained by limited exposure to sunlight due to cultural practices and lack of vitamin D supplementation for lactating women. Up to 70% and 80% of teenage girls in Iran and Saudi Arabia, respectively, have vitamin D deficiency. Socioeconomic factors that limit the diet rich in vitamin D also play a role. In the United States, vitamin D deficiency varies widely with ethnicity. Among men aged 70 years and older, the prevalence of low serum 25 (OH) D levels was 23% for non-Hispanic whites, 45% for Mexican Americans, and 58% for non-Hispanic blacks. Among women, the prevalence was 28.5%, 55%, and 68%, respectively.
A systematic review published in the Cochrane Library observed children up to three years in Turkey and China and found a negative relationship between vitamin D and rickets. In Turkey, children who received vitamin D had only 4% chance of developing rickets compared with children who did not receive medical intervention. In China, the combination of vitamin D, calcium, and nutritional counseling is associated with reduced risk of rickets.
With this evolutionary perspective, parents can supplement their nutritional intake with enhanced vitamin D drinks if they feel their child is at risk of vitamin D deficiency,
Diagnosis
Rickets can be diagnosed with the help of:
- Blood tests:
- Calcium serum may indicate low levels of calcium, serum phosphorus may be low, and serum alkaline phosphatase may be high from bone or changes in bone form or structure. It can show an enlarged leg and joint.
- Bone density scan is possible.
- Radiographs typically show a temporal calcification zone widening from secondary metaphysis to unmineralized osteoid. Cupping, fraying, and splaying metaphyses usually come with growth and continue to withstand loads. These changes are seen primarily in rapid growth sites, including the proximal humerus, the distal radius, the distal femur and both the proximal and the distal tibia. Therefore, a skeletal survey for rickets may be performed with anteroposterior radiography of the knee, wrist, and ankle.
Type
- Vitamin D related rinetset
- Vitamin D deficiency
- Vitamin D-dependent rickets
- Type 1 (25-Hydroxyvitamin D3 1-alpha-hydroxylase deficiency)
- Type 2 (calcitriol receptor mutation)
- Hypocalcemia-related rickets
- Hypocalcemia
- Chronic renal failure (CKD-BMD)
- Hypophosphatemia associated with rickets
- Default
- a vitamin D-resistant racquet
- Autosomal dominant hypophosphatemic rickets (ADHR)
- Autosomal hypophosphatemic (ARHR) research
- Hypophosphatemia (usually secondary to malabsorption)
- Fanconi's syndrome
- Default
- Secondary to other diseases
- tumor-induced osteomalacia
- McCune-Albright syndrome
- Epidermal nevus syndrome
- Dent's Disease
Differential diagnosis
Infants with rickets often experience fractures. This sometimes leads to child abuse allegations. This problem seems to be more common for breastfed infants solely of black mothers, in winters in temperate climates, suffering from malnutrition and no vitamin D supplements. The people with darker skin produce less vitamin D than the skin brighter, for the same amount of sunlight.
Treatment and prevention
The most common ricket treatment is the use of vitamin D. However, surgery may be necessary to eliminate severe bone disorders.
Diets and sunshine
Treatment involves an increase in dietary intake of calcium, phosphate and vitamin D. Exposure to ultraviolet B (most easily obtained when the sun is highest in the sky), cod liver oil, halibut-liver oil, and vitaminsol are all sources of vitamin D.
Insufficient amount of UV light in the sun every day and enough supply of calcium and phosphorus in the diet can prevent rickets. Dark-skinned people need to be exposed to ultraviolet light for longer. Vitamin D replacement has been shown to improve rickets using ultraviolet light therapy methods and drugs.
Recommendations for 400 international units (IU) of vitamin D daily for infants and children. Children who did not get adequate amounts of vitamin D had a higher risk of rickets. Vitamin D is essential to allow the body to absorb calcium for use in proper calcification and bone maintenance.
Supplementation
Adequate vitamin D levels can also be achieved through dietary supplementation and/or sun exposure. Vitamin D 3 (cholecalciferol) is the preferred form because it is more readily absorbed than vitamin D 2 . Most dermatologists recommend vitamin D supplements as an alternative to unprotected ultraviolet exposure due to an increased risk of skin cancer associated with exposure to sunlight. Endogenous production with full body exposure to sunlight is about 250 Ã,Âμg (10,000 IU) per day.
According to the American Academy of Pediatrics (AAP), all infants, including those exclusively breastfed, may need vitamin D supplements until they start drinking at least 17 ounces of US (500 ml) vitamin D fortified milk or formula. one day.
Epidemiology
In developed countries, rickets are a rare disease (incidence less than 1 in 200,000). More recently, cases of rickets have been reported among children who were fed plant-based substitutes and were not given vitamin D supplements.
In 2013/2014 there are less than 700 cases in the UK.
History
Greek physician Soranus of Ephesus, one of the Methodic vice principal principals who trained at Alexandria and later in Rome, reported bone deformation in infants as early as the first and second centuries AD. The raft was not defined as a special medical condition until 1645, when a British physician Daniel Whistler gave the earliest known disease description. In 1650 a treatise on rickets was published by Francis Glisson, a physician at Caius College, Cambridge, who said it first appeared about 30 years earlier in Dorset and Somerset counties. In 1857, John Snow suggested rickets, then widespread in England, caused by the forgery of bread bread with alum. German pediatrician Kurt Huldschinsky managed to show in the winter of 1918-1919 how rickets can be treated with ultraviolet lights. The role of diet in the development of rickets was determined by Edward Mellanby between 1918-1920. In 1923, American physician Harry Steenbock showed that ultraviolet light radiation increases the vitamin D content of food and other organic matter. Steenbock irradiation techniques are used for groceries, but are most remembered for milk. In 1945, rickets were removed in the United States; no cases were recorded in Cuba, but they were there since the Special Period.
Etymology
The word rickets may be derived from the Old English wrickken ('to twist'), although as it is suspected, some of the main dictionaries simply say "unknown origin". The name rickets is plural but usually single in construction. The Greek word "rachitis" (???????, meaning "in or from the spine") was then adopted as a scientific term for rickets, mainly because of the words' similarity in sound.
See also
- Hypervitaminosis D
References
External links
Source of the article : Wikipedia
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