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Rickets-vitamin D deficiency and dependency.

Sahay M, Sahay R - Indian J Endocrinol Metab (2012)

Bottom Line: In addition, some varieties are due to inherited defects in vitamin D metabolism and are called vitamin D dependent rickets.This chapter highlights rickets/osteomalacia related to vitamin D deficiency or to inherited defects in vitamin D metabolism.Hypophosphatemic rickets and rickets due to renal tubular acidosis are discussed in other sections of the journal.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Osmania Medical College and General Hospital, Hyderabad, Andhra Pradesh, India.

ABSTRACT
Rickets is an important problem even in countries with adequate sun exposure. The causes of rickets/osteomalacia are varied and include nutritional deficiency, especially poor dietary intake of vitamin D and calcium. Non-nutritional causes include hypophosphatemic rickets primarily due to renal phosphate losses and rickets due to renal tubular acidosis. In addition, some varieties are due to inherited defects in vitamin D metabolism and are called vitamin D dependent rickets. This chapter highlights rickets/osteomalacia related to vitamin D deficiency or to inherited defects in vitamin D metabolism. Hypophosphatemic rickets and rickets due to renal tubular acidosis are discussed in other sections of the journal.

No MeSH data available.


Related in: MedlinePlus

Bony deformities in rickets
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Figure 1: Bony deformities in rickets

Mentions: The skeletal changes are similar in calcipenic and phosphopenic rickets.[40] The anterior fontanelle closes by 18 months and posterior by 3 months normally. However, in rickets, there is a delay in the closure of the fontanelles. There is parietal and frontal bossing, craniotabes (soft skull bones) with ping pong bones in infants, enlargement of the costochondral junction of ribs (the “rachitic rosary”), Harrison sulcus due to the muscular pull of the diaphragm on the lower ribs, widening of the wrist and bowing of the distal radius and ulna, and progressive lateral bowing of the femur and tibia. Widening of ankle (double malleoli) can be seen. The age of the child and weight bearing determine the type and the site of deformities. In infants, the deformities are seen in forearm bones and the tibia. In toddlers, there is exaggeration of normal physiological bowing of the legs (genu varum). Older children have either genu valgum [Figure 1] or windswept deformity of the lower limbs (genu varum on one side and valgum on the other). There may be kyphosis or scoliosis. In adults, the bony deformities are unusual; however, in females there may be triradiate pelvis which makes normal vaginal delivery difficult.


Rickets-vitamin D deficiency and dependency.

Sahay M, Sahay R - Indian J Endocrinol Metab (2012)

Bony deformities in rickets
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3313732&req=5

Figure 1: Bony deformities in rickets
Mentions: The skeletal changes are similar in calcipenic and phosphopenic rickets.[40] The anterior fontanelle closes by 18 months and posterior by 3 months normally. However, in rickets, there is a delay in the closure of the fontanelles. There is parietal and frontal bossing, craniotabes (soft skull bones) with ping pong bones in infants, enlargement of the costochondral junction of ribs (the “rachitic rosary”), Harrison sulcus due to the muscular pull of the diaphragm on the lower ribs, widening of the wrist and bowing of the distal radius and ulna, and progressive lateral bowing of the femur and tibia. Widening of ankle (double malleoli) can be seen. The age of the child and weight bearing determine the type and the site of deformities. In infants, the deformities are seen in forearm bones and the tibia. In toddlers, there is exaggeration of normal physiological bowing of the legs (genu varum). Older children have either genu valgum [Figure 1] or windswept deformity of the lower limbs (genu varum on one side and valgum on the other). There may be kyphosis or scoliosis. In adults, the bony deformities are unusual; however, in females there may be triradiate pelvis which makes normal vaginal delivery difficult.

Bottom Line: In addition, some varieties are due to inherited defects in vitamin D metabolism and are called vitamin D dependent rickets.This chapter highlights rickets/osteomalacia related to vitamin D deficiency or to inherited defects in vitamin D metabolism.Hypophosphatemic rickets and rickets due to renal tubular acidosis are discussed in other sections of the journal.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Osmania Medical College and General Hospital, Hyderabad, Andhra Pradesh, India.

ABSTRACT
Rickets is an important problem even in countries with adequate sun exposure. The causes of rickets/osteomalacia are varied and include nutritional deficiency, especially poor dietary intake of vitamin D and calcium. Non-nutritional causes include hypophosphatemic rickets primarily due to renal phosphate losses and rickets due to renal tubular acidosis. In addition, some varieties are due to inherited defects in vitamin D metabolism and are called vitamin D dependent rickets. This chapter highlights rickets/osteomalacia related to vitamin D deficiency or to inherited defects in vitamin D metabolism. Hypophosphatemic rickets and rickets due to renal tubular acidosis are discussed in other sections of the journal.

No MeSH data available.


Related in: MedlinePlus