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Common Deficiency Rickets – Causes, Symptoms, Treatment

Common Deficiency Rickets (vitamin D sensitive rickets) is a metabolic disorder of calcium and phosphorus deposit in matrix and growth cartilage of the bone due to activation deficiency of pro-vitamin in the skin or vitamin D deficiency in the diet.

The process of collection, concentration and delivery of calcium and phosphorus necessary for calcification is under the influence of vitamin D.

The origin of vitamin D is endogenous (vitamin D3 synthesized in the skin under the influence of ultraviolet light) and exogenous (from food).

The main causes of rickets are multiple:

Age – the onset of disease is generally after the age of 3-6 months to 2 years;


Sunlight regime – winter period, temperate climate does not allow efficient transformation of pro-vitamins D in the skin in vitamin D;

Rapid growth – favors the appearance of rickets by increased need for vitamin D and minerals;

Skin pigmentation – rickets is a disease that occurs more frequently in blacks, since their skin does not allow adequate penetration of ultraviolet rays;

Disorders of intestinal absorption (which may occur in celiac disease, pancreatitis, cystic fibrosis)

Extrahepatic biliary atresia (absence of extrahepatic biliary) – is responsible for the inability of vitamin D absorption due to lack of bile salts;

Chronic kidney disease – disturbing activity of enzymes that induce the formation of active metabolites of vitamin D of renal origin;

Prolonged corticosteroid therapy – alter the matrix protein of bone and the intestinal absorption of calcium;

Children with epilepsy – which are taking phenobarbital or phenytoin, make rickety bone demineralization;

Poor diet, excess flour, artificial feeding with cow’s milk;

Inadequate living conditions, poor housing, poor hygiene, overcrowding.

The clinical picture of the disease is polymorphic.

At the onset, rickety infants are pale, nervous and restless sleep. Can develop a strong perspiration of the scalp, leading by pruritus (itching)  produced to alopecia (hair loss) typicaly of occipital area.

Subsequently is installing a hypotonic (low tone) muscle and a weight delayed development.

The  state period of the disease is characterized by a series of bone signs that become evident after several months of vitamin deficiencies, are symmetrical, painless spontaneous at infant and prevalent in areas of rapid growth.

In the skull can be seen the following changes:

– Craniotabesul occipital and parietal (skull bone softening) – appears in the first months;

– Plagiocephalia – crushing of parietal and occipital bone  plate with the back asymmetry of the skull;

– Excessive expansion and closure after the age of 2 years of anterior fontanelle;

– Frontal and parietal bose – are prominent;

– Teeth appear anarchic, are less developed, fragile, with early caries.

Thorax is deformed, flattened laterally, flared at the base and presents “rachitic condrocostal rosary ” that appear as nodules (tangible and visible) caused by the swollen of the area costal cartilage-calcified portion of the ribs.

At the extremities, changes occur after the age of 6 months:

– “Rickety bracelets” – are thickening of distal extremity of the radius;

The backbone presents various mild or moderate modifications (scoliosis = appreciable lateral deviation of the spine from the vertical normal line, lumbar spine kyphosis or lumbar lordosis).

Basin is deformed concomitant with the spine

Leg deformities become evident with orthostatic position and walking and consists in the appearance of genu valgum (standing in the “x”) and of genu varum (legs in “brackets”).

Muscles are weak, hypotonic. This weakness leads to great, relaxed belly (“the batracian”).

Laboratory changes that occur in rickets are:

– Serum calcium – is normal or low;

– Urinary calcium (urinary excretion of calcium) – is greatly reduced;

– Phosphorus levels (blood concentration) – low;

– Phosphaturia (urine excretion) – increased;

– Alkaline phosphatase is increased in serum ;

– Parathyroid hormone – increased.

Another very important test for the diagnosis of rickets is the X-ray (radiography of wrist, lower leg, skull, spine, chest) that highlights a number of changes characteristic of this condition.

Treatment of rickets is prophylactic and curative

Prophylactic treatment is recommended at pregnant women to start by taking calcium and vitamin D  especially in the last months of pregnancy and avoiding premature births. Postnatal prophylaxis is done by  exposure of children at the sun in sunny weather, promoting natural food and especially by taking vitamin D supplements.

With regard to curative treatment, vitamin D should be administered orally or by injection, according to regimens.

Calcium intake is indicated in all forms of rickets.

After healing rickets, prophylaxis will be done until the age of 7-8 years and even 15 years.

It also recommends a lifestyle  hygienic-dietary rational and the  treatment of associated deficiencies.

Untreated, rickets can have severe consequences. During development of the disease it may occur a number of non-infectious complications (rickets tetany, bone deformities with functional sequelae, statural growth retardation) and infectious complications (rachitic lung, pulmonary atelectasis).

Proper prevention is the best prognostic factor.

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