ABSTRACT
Nutritional rickets, caused by vitamin D and/or calcium deficiency is by far the most common cause of rickets. In resource-limited settings, it is therefore not uncommon to treat rickets with vitamin D and calcium. If rickets fails to heal and/or if there is a family history of rickets, then refractory rickets should be considered as a differential diagnosis. Chronic low serum phosphate is the pathological hallmark of all forms of rickets as its low concentration in extracellular space leads to the failure of apoptosis of hypertrophic chondrocytes leading to defective mineralisation of the growth plate. Parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) control serum phosphate concentration by facilitating the excretion of phosphate in the urine through their action on the proximal renal tubules. An increase in PTH, as seen in nutritional rickets and genetic disorders of vitamin D-dependent rickets (VDDRs), leads to chronic low serum phosphate, causing rickets. Genetic conditions leading to an increase in FGF23 concentration cause chronic low serum phosphate concentration and rickets. Genetic conditions and syndromes associated with proximal renal tubulopathies can also lead to chronic low serum phosphate concentration by excess phosphate leak in urine, causing rickets. In this review, authors discuss an approach to the differential diagnosis and management of refractory rickets
ABSTRACT
he present study was conducted to evaluate the neurobehaviour of term appropriate for gestational aland small for gestational age babies during the first two weeks of life in a tertiary care hospital. Forty eight appropriate and thirty small for gestation age babies were evaluated using Brazelton Neurobehavioural Assessment Scale on 3rd, 7th and 14th day of life. The behaviour of AGA babies is characterized by optimal performance in habituation, range of state, regulation of state and autonomic stability. The behavior is at low to mid-range in orientation and in motor clusters. All the behavior clusters showed improvement over first 14 days except for regulation of state which showed a lower performance on day 7 and 14. The behavior performance of SGA babies on day 3, compared to AGA babies, was lower in all the clusters except orientation where they performed much better. The percentage improvement of scores in SGA babies is higher than in AGA babies and by day 14 SGA babies are scoring higher than AGA babies in orientation, autonomic stability and regulation of state. The difference in the neurobehavior pattern of babies in relation to their intrauterine growth suggests need for appropriate care.