ICCBH2015 Poster Presentations (1) (201 abstracts)
1Fundation clinic Infantil Club Noel - University Libre, Corserinsa, Cali-Valle del Cauca, Colombia; 2Institut of Orthopedic Rosselvet, Bogota, Colombia; 3Universiry Libre-Fundation CLinic Infantil Club Noel, Cali-Valle del Cauca, Colombia.
The Rickets is a disease which disturbs normal bone formation through different methods, like vitamin D deficiency, malabsorption, chronic renal disease, metaphisary dysplasia, low phosphorus and resistant rickets.
The peak age at which rickets is most prevalent is usually 318 months, and the characteristic clinical features of this metabolic bone disease include enlargement of the epiphyses of the long bones and rib cage, bowing of the legs, bending of the spine, and weak and toneless muscles. In the past, severe rickets entailed severe deforming and debilitating bone disease.
To describe two patients pediatrics with rickets entailed severe deforming and debilitating bone disease, and the biochemical characteristics are table 1.
Age | Sex | Calcio (mg/dl) | fosforo | PTH (pg/ml) | Alkalin fosfatasa (UL) | 25OHVITAMINA D (ng/ml) | 1.25OHVITA D | Densitometry L4 | Type |
6 | Boys | 5.37 | 5.4 | 212 | 2049 | 12.8 | 15 | −4.2 DE | Carencial |
9 | Girls | 7.3 | 5 | 163 | 1311 | 20.2 | 295 | −6 DE | type II rickets |
Exogenous vitamin D deficiency is the most frequent cause of rickets. It is linked to two fundamental facts that can act independently or simultaneously: limited sun exposure and vitamin D deficiency in the nutrition. Besides the vitamin D deficiency, calcium deficiency and acquired and inherited disorders in vitamin D, calcium and phosphorus metabolism are also causes of rickets.
Disclosure: The authors declared no competing interests.