Showing posts with label vitamin D. Show all posts
Showing posts with label vitamin D. Show all posts

Osteomalacia treatment - Vitamin D deficiency

Home > Osteomalacia > Osteomalacia treatment

Successful treatment of osteomalacia is accomplished by mineralization of the soft bones matrix with light, dietary advice and supplements of vitamin D and calcium.
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Sunlight (ultraviolet B light) in the treatment of osteomalacia (soft bones)

The sunlight apart from containing visible light composes a broad band of invisible light and ultraviolet (UV) light is one of them.
Ultraviolet light is again divided into three types depending upon the wave length like UV-A, UV-B and UV-C.
The UV-A spectrum causes sun tan and sunburn. Long exposure to UV-C can cause skin cancer. UV-B is involved in the production of vitamin D in the skin and strengthening the soft bones.
The presence of UV-B is relative to the slant of the light. Greater the slant lesser are the UV-B rays present.
Exposure between 10am-2pm gives the maximum benefit of vitamin D synthesis and helps in osteomalacia treatment.
In places like north America, Canada, northern Europe, northern Asia and southern Australia the slant of the sunlight is greater especially in their winter.
People who are confined to homes or have indoor jobs and those with darker skin are very high risk groups in these areas and may become deficient in vitamin D and develop osteomalacia resulting in soft bones.
They should make every possible attempt to go out in the sun to prevent osteomalacia.
The exposure of face, arms and hands to 15-20 minutes of sunlight is sufficient to produce required vitamin D in fair skinned people and will help in prevention of osteomalacia.
For people with darker skin require more exposure as the dark pigment melanin in their skin filters the sunlight.

Light-therapy (phototherapy) for osteomalacia 

The light treatment is given using lamps which give light near equal to sunlight for a specific period. Special bulbs and lamps are available in the market.
Alternatively UV-B radiating devices are also available with the sole purpose of vitamin D production in the skin.
Please take medical advice before using them in osteomalacia care due to the side-effects of the over-exposure.

Nutrition in osteomalacia

Food rich in cholecalciferol like fortified milk and cereals, egg, canned tuna and sardines, herring, mackerel and salmon are given during recuberation. Cod and its liver oil and liver are good sources of vitamin D. However it is doubtful whether adequacy levels of the nutrient can be reached through food sources only.

Vitamin D (cholecalciferol) supplements for Osteomalacia

Depending upon the condition, osteomalacia treatment includes oral or intra-muscular supplements of cholecalciferol and calcium. Phosphorus supplements may also be given.
During this period, supplements of cholecalciferol of strength 800-4000 IU/per day are given for 6 - 8 weeks.
Serum levels of calcium rises within 48 hours of the start of the treatment with cholecalciferol.
There will be marked improvement of the condition of the osteomalacia affected within a few days of starting of the treatment for soft bones (osteomalacia).
After 8 weeks the cholecalciferol dose may be reduced to the normal maintenance level of 400 IU/day and the condition of osteomalacia resolves.
If there is any absorption problem in osteomalacia affected, intra-muscular injections are given and excess vitamin D is stored by the body for future utilization. Sufficient calcium should be given during treatment.
During treatment regular blood tests may be done to keep track of the cholecalciferol in serum. Cholecalciferol in excess can cause hypercalcaemia, a condition in which the presence of excess calcium in the blood causing problems.

For the treatment of osteomalacia, efforts must be taken to prevent it by sufficient exposure of the body to sunlight and the inclusion of vitamin D rich food in our daily diet.
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Vitamin D deficiency causes rickets in children

Home > Vitamin D deficiency causes rickets

Deficiency of vitamin D or/and calcium and phosphorus are the causes of the nutritional disorders and rickets disease in children.

A number of factors including lack of sunlight exposure and nutritional vitamin D deficiency cause rickets. Certain metabolic disorders, digestive disorders and genetic factors can also lead to rickets.

Lack of sufficient exposure to sunlight (ultraviolet B light) causes rickets

Most of the vertebrate animals including man produce vitamin D in their skin photochemically, with the exception of cats, dogs and a few other animals.
The ultraviolet B light (UVB) from the sun reacts with 7-dehydrocholesterol in the stratum basale and stratum spinosum of the epidermis layer (upper layer of skin) and by a chemical process cholecalciferol is synthesized.
The melanin pigment deposits in the skin function as UVB filter and the dark-skinned people have to be exposed to, more sunlight than the light colored people to produce the same quantity of cholecalciferol.
Children and people who always live and work indoors and are rarely exposed to sunlight are high risk group for developing deficiency of vitamin D.
The intensity of sunlight decreases with higher latitudes and in children living there deficiency of cholecalciferol arises in winter especially if they are dark skinned.

Nutritional deficiency of calcium and phosphorus causes rickets

Calcium and phosphorus are very important for the formation and growth of bone tissue and bones. Any insufficiency of these minerals lead to bone deformities and rickets disease.

Maternal deficiency of cholecalciferol, calcium and phosphorus causes rickets in the newborns

The deficiency in pregnant women reduces the availability of these to the fetus.
Bone formation in the fetus may be affected and the density of the bones is reduced and results low birth weight.
Further if the shortfall is not cured by supplements, birth deformities occur in the newborn children.
Nursing mother's nutritional deficiency causes rickets disease in the infant.
The human milk has just sufficient quantities of cholecalciferol in a healthy woman.
If the lactating mother is not having sufficient reserves of it and is poorly nourished having little exposure to sunlight, the milk becomes poor in this nutrient.

Lactose intolerance and food habits causes rickets disease

Milk and milk products which are rich in calcium are not tolerated by some people and they have problem digesting them.
Unless they eat other sources of calcium they develop vitamin D deficiency.
Vegans who do not include milk and milk products are among the high risk groups to get vitamin D deficiency.

Malabsorption of fats from intestine causes rickets disease

Vitamin D is fat-soluble and requires dietary fat in the intestine for absorption.
In various conditions and ailments like Crohn's disease, cystic fibrosis and in certain liver disorders fat and vitamin D absorption from the intestine is affected and results in its deficiency.

Certain medication causes rickets disease

Phenobarbital and phenytoin are used for preventing and controlling epileptic seizures.
These drugs convert vitamin D into inactive compounds by increasing the hepatic metabolism. This leads to reduction in calcium absorption. Orlistat (weight-loss drug) and cholestyramine (cholesterol-lowering drug) reduces absorption of fat soluble vitamin D.
Corticosteroids like prednisone can affect cholecalciferol metabolism and decrease calcium absorption and result in rickets.

Hereditary predisposition for rickets disease

Vitamin D resistant rickets is hereditary. Here the rickets disease is inherited as a sex-linked genetic disorder. In this condition kidney is impaired from retaining phosphate.
Excessive use of sunscreen and spending more time in-doors causes this ailment.
Understanding the causes and proper preventive measures and treatment can resolve rickets disease.

Related topics:
Rickets disease overview
Symptoms
Diagnosis
Treatment
Prevention
Osteomalacia (in adults)
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Vitamin D deficiency causes rickets
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Osteomalacia causes - soft bones - adults - vitamin D deficiency


Among many factors, severe vitamin D deficiency causes osteomalacia resulting in soft bones by their hypomineralisation in adults.
Adult skeletal structures after attaining growth, due to many factors connected with vitamin D deficiency, lose the calcium and phosphorus in them during bones turnover and become soft. The causes of osteomalacia are numerous.

Insufficient exposure to sunlight is one of the prime causes of osteomalacia (soft bones)

People living in higher latitudes face shorter days, especially in winter. They are also compelled to be home bound due to adverse weather conditions and soft bones result. In darker skinned people the soft bones problem is compounded due to their reduced vitamin D synthesis ability. This is due to high melanin pigment deposits in their skin which cut off UV-B rays from reaching the vitamin D producing region of the skin and causes vitamin D deficiency and osteomalacia (soft bones).

Deficiency of vitamin D in diet is one of the causes of osteomalacia

The plant sources of vitamin D are very limited. Animal fats especially fish oils and fats are rich in vitamin D. Eggs and animal liver also contains vitamin D. Fortified milk and fortified cereal flours also can be good sources. Vegans who do not even drink milk are in the risk of getting osteomalacia and soft bones. Economically weaker sections of the people are prone to get affected by both calcium and vitamin D deficiency. This causes osteomalacia and soft bones.

Living in places continuously affected by fog and smog causes osteomalacia

Residents of the cities continuously covered by fog and smog may be affected or get into presymptomatic stage of this ailment and soft bones.

Medicine used in the treatment of epilepsy and seizures causes osteomalacia

Epileptics may suffer from soft bones. Epileptic seizures are prevented and controlled by phenobarbital and phenytoin. These drugs increase the hepatic metabolism. By this reaction the vitamin D is converted into inactive forms and the calcium absorption is affected leading to soft bones.

Orlistat (weight-loss drug) and cholestyramine (cholesterol-lowering drug) reduce absorption of fat soluble vitamins like vitamin D. Corticosteroids like prednisone may decrease calcium absorption and causes osteomalacia (soft bones) by affecting cholecalciferol metabolism.

Malnutrition during pregnancy causes osteomalacia

Pregnant women transfer lots of vitamin D, calcium and phosphorus to the growing fetus. The vitamin D and calcium reserves in the pregnant woman's body are tapped to maintain uninterrupted supply to the growing fetus. If the supplies are not replenished by diet, supplements and sunlight exposure deficiency results and causes osteomalacia and soft bones.

Celiac disease causes osteomalacia

Celiac disease (coeliac disease) is a disorder of the small intestine which is autoimmune in nature with genetic predisposition. In this disease there is a reaction of the body to gluten protein present in wheat. There is inflammation of the small intestine and atrophy of the villi which are responsible for nutrient absorption.

Hence there no nutrient absorption and along with many deficiency induced ailments, severe deficiency of vitamin D also occurs and causes osteomalacia and soft bones. Certain types of cancers, hereditary disorders in the metabolism , renal diseases like renal tubular acidosis and disease of the liver can be the causes of osteomalacia and soft bones.
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Osteomalacia prevention- Soft bones - - Vitamin D

Home > Osteomalacia prevention -Vitamin D - Soft bones

Prevention of osteomalacia (soft bones) is by exposure to sufficient sunlight (ultraviolet B light), exposure to UV-B lamps, dietary intake of balanced foods and use of supplements of vitamin D, calcium and phosphorus.

Prevention of osteomalacia in pregnant women and nursing mothers

Pregnant women are among the high risk group for osteomalacia.
During pregnancy there is increased fetal demand of vitamin D and calcium.
As the pregnancy progresses there is greater demand of calcium for the growth of soft bones of fetus. Pregnant women if they continue with their normal diet during their late pregnancy their calcium and vitamin D reserves get depleted and osteomalacia occurs.
To protect from osteomalacia, pregnant women should have sufficient exposure of sunlight, eat food high in vitamin D and take calcium and calcitriol supplements.
Lactating mothers lose calcium and vitamin D through the milk.
Hence nursing mothers are also prone to deficiency disease of osteomalacia in them is by following the prevention methods as in the case of pregnant women.

Prevention of osteomalacia in vegans and vegetarians

Vegans and vegetarians may be eating calcium sources of vegetarian food.
However for the absorption of calcium in the gut they must have sufficient calcitriol (vitamin D).
If they are deficient, they may also develop osteomalacia.
The prevention is by resorting to exposure to sunlight, balanced food and supplements.

Prevention of soft bones in adults living in higher latitudes

People living in higher latitudes are highly prone to develop osteomalacia as the incidence of sunlight is at a greater angle in higher latitudes, especially in winter.
The slant of sunlight greatly reduces the availability of the UV-B rays required for calcitriol production in the skin.
In winter the available time of the sunlight itself is reduced.
For the prevention of osteomalacia they must take dietary supplements of vitamin D and UV-B light exposure under medical guidance.

Soft bones in dark skinned adults

The darker color of the skin is due the presence of melanosomes (bundles of melanin pigment). Greater number of melanosomes contribute to darker skin. The melanin deposits function as sunlight filters.
In dark skin very less amount of UV-B rays reach the synthesis areas compared to lighter skin for the same time of exposure leading to deficiency and soft bones.
For protection deficiency and soft bones the dark skinned people should get more exposure to sunlight and if necessary take dietary supplements.
Prevention of osteomalacia (soft bones) in elderly persons, persons affected by gastrointestinal disorders, renal disorders and certain types of cancers is a vast subject by itself.
These are the very high risk adults groups for soft bones and constant monitoring of their blood serum levels for calcium is necessary for preventing of osteomalacia, apart from constant efforts to shore up their calcium and vitamin D levels.

Related posts:
Osteomalacia.
Causes.
Symptoms.
Diagnosis.
Treatment.
Rickets in children.

Current topic:
Vitamin D for prevention of osteomalacia and soft bones.

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Osteomalacia - vitamin D deficiency - adults

Home > Osteomalacia - Vitamin D deficiency in adults

Osteomalacia is a condition in adults where in the bones get softened due to deficiency of vitamin D or the inability of body to absorb/utilise cholecalciferol.
The essential problem in this metabolic disease of adults is the non-availability of phosphorus and/or calcium for mineralisation of freshly formed osteoid usually in adults.
This disease in children is called rickets. The basic cause of this mineral insufficiency is the deficiency of vitamin D (cholecalciferol).

Unlike the severity of the symptoms in children this insufficiency in adults shows signs like body pains, muscle pains and soft fragile bony structures.
Osteomalacia is hypomineralization of the osteoid after the cessation of its growth.
In contrast, in rickets, hypomineralization of the growing bones takes place affecting growth plates.

Normal mineralisation depends on many interdependent factors, which supply sufficient phosphorus and calcium to the skeletal tissues.
By its action on the gastrointestinal tract, parathyroid glands, kidneys and the bones, vitamin D maintains a balance of calcium and phosphorus.
Hydroxylation of cholecalciferol is necessary for the maintenance of the above balance. Hydroxylation takes place in liver and kidneys.
Osteomalacia occurs when any of the above metabolic processes dysfunctions and soft bones result.

Though both osteomalacia and osteoporosis result in soft and fragile bones in adults the processes of the making of this condition are very different.
In osteoporosis, porosity of the skeletal tissue results due to faster breaking down of them than their reformation.
However in osteomalacia though the two activities are balanced, the bones which are formed do not get mineralised to become hard and dense.

There are a number of causes for the occurrence of osteomalacia, the most important being the deficiency of cholecalciferol in adults.
The signs of osteomalacia are general weakness, myalgia, lack of appetite, loss of weight and fragile and soft bones.
This malady of deficiency is diagnosed with blood tests, biopsy and radiography.
Osteomalacia is treated by giving large doses of vitamin D to replenish it in adults.

Related topics:
Causes of the ailment in adults.
Osteomalacia symptoms.
Diagnosis.
Treatment.
Prevention of vitamin deficiency in adults.
Rickets in children.
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Rickets diagnosis - vitamin D deficiency - children

Home > Diagnosis of rickets - Vitamin D deficiency in children

Visual observations supported by analytical, radiographic and differential methods confirm the diagnosis of rickets and deficiency of vitamin D in children.
Diagnosis of rickets by visual observations
Sleep pattern of the patient is observed. Affected children sleep poorly and are restless in the night. Their constant movements in the bed, may even cause the hair on their head to wear off. This is a clear sign of vitamin D deficiency and on set of rickets. There is every possibility of wrong interpretation of this sign of rickets as psychosis.
The growth pattern of the children are observed. The growth in the affected is slow and often retarded.
The affected persons will be slow in sitting up, crawling and walking.
The bones of the affected children may bend due to weight of the body and the joints may deform giving deformities like bowed leg and pigeon-breast; a clear diagnosis of vitamin D deficiency.
The muscles of the affected children will be weak and the patients will have pain and distress while moving.
Due to leaching of phosphorus and calcium the bone will be weakened and there can be a history of fractured bones indicating the deficiency of vitamin D.
The broadening and thickening of wrists and ankles is a clear sign of vitamin D deficiency.
The patients show frontal bossing and the forehead becomes prominent and square.
During dental examination, the affected children show delay in emergence of teeth, abnormal tooth structure and cavities.
Diagnosis of rickets by laboratory studies
Serum test and measurements of phosphorus, calcium, parathyroid hormone and alkaline phosphatase are taken for diagnosis of rickets.
In early disease the ionised fraction of calcium will be low, but may be within the reference range.
Serum phosphate will be lower than the reference range.
Parathyroid hormone will show increased values.
Serum calcidiol will show decreased values.
Serum alkaline phosphatase will be more than the reference values.
Levels of serum citrates will be less than 2.5 mg/dl.
Urine calcium will show decrease in levels.
Urine phosphates will show increase in levels.
Diagnosis of rickets by radiography
Radiographic study of long bones, ankles, wrist and knees is made.
In rickets affected children who are able to walk, the defective bone growth give a clear image of bent limbs.
Typical appearance of growth plates with lack of normalcy in mineralisation of the cartilages is seen.
Fraying (irregularity and widening) of the growth plate is seen in radiography.
The metaphysis show concavity (cupping) and the metaphyseal end of bone shows splaying (widening).
Differential diagnosis
Excluding the related signs help. Severe deficiency of calcium and phosphorus can show the symptoms.
Diagnosis to be done to exclude Hypophosphatasia, a rare metabolic bone disease, with confusing symptoms similar to rickets.
A form of short limbed dwarfism, Jansen syndrome may also show metaphyseal chondroplasia.
Hereditary vitamin D -resistant rickets has to be differentiated.

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Diagnosis of rickets - Vitamin D deficiency in children.
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Rickets disease -Lack of vitamin D - Prevention

› › Lack of vitamin D and rickets disease prevention

Prevention of rickets disease involves sufficient exposure to sunlight (ultraviolet B light) and dietary intake of sufficient human growth hormone (HGH), calcium, phosphorus and vitamin D (Cholecalciferol).
Measures for prevention of rickets disease are to be started right during pregnancy.
Pregnant woman must have adequate intake of balanced diet with additional supplements of vitamin D and minerals and lack of these can affect the growing fetus.
Human milk is just sufficient in vitamin D depending on the nutritional status of the lactating mother.

As the growing infant has great demand for calcium and Cholecalciferol the nursing mother should not lack in exposure to sunlight.
The nursing mother should consume diet rich in calcium and Cholecalciferol and also take supplements if required for the warding off lack of vitamin D.
The infant who is solely dependent on mother's milk should be given sufficient exposure to sunlight daily for prevention of low levels of vitamin D and occurrence of this disease.

rachitis disease rickets children
Children are affected by rickets disease (enlarge)(courtesy: Dr. Tom and Rosie Thacher)
Further as the daily demand of nutrients increases many fold in infants, vitamin D and other supplements may be started early for prevention of rickets arising due lack of them.
Light skinned infants may require about twenty minutes of ultraviolet light exposure per day for protection from developing rickets.
Dark skinned infants require more exposure for warding off this vitamin D deficiency, as the skin pigment interferes in the Cholecalciferol synthesis by cutting off the light.

Vegans who do not consume even milk have low levels of both calcium and vitamin D (Cholecalciferol).
Vegans and their infants are highly prone to develop rickets disease; their nutritional status regarding both calcium and Calcitriol must be monitored. They must take vitamin D supplements as protection.

Premature infants and underweight infants have greater demand for vitamin D, calcium and phosphorus and may develop rickets, if they are insufficient in them.
People living in higher latitudes are at the risk of developing rickets especially in the winter months due to lack of sufficient sun exposure in short days .

Dark skinned children living in higher latitudes are highly prone to rickets and they must be supplemented with cholecalciferol as prevention.
For prevention of rickets disease people living in higher latitudes must take food rich in Calcitriol and also take supplements.

People suffering from gastrointestinal disorders and prolonged illness may lack vitamin D must take supplements  to ward off deficiency.
Renal disease cause lack of Calcitriol absorption and calcitriol supplements must be taken for
prevention of rickets.The deficiency can be checked. For prevention of rickets disease sufficient exposure to sunlight, taking food rich in vitamin D and taking supplements is necessary.

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Prevention of rickets disease in children - Lack of vitamin D.
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