Abstract:
The commonest cause of rickets worldwide is vitamin D deficiency, but studies from
sub-Saharan Africa describe an endemic vitamin D-independent form that responds to
dietary calcium enrichment. The extent to which calcium-deficiency rickets is the
dominant form across sub-Saharan Africa and in other low-latitude areas is unknown.
We aimed to characterise the clinical and biochemical features of young children with
rickets in a densely populated urban informal settlement in Kenya. Because malnutrition
may mask the clinical features of rickets, we also looked for biochemical indices of risk
in children with varying degrees of acute malnutrition. Twenty one children with rickets,
aged 3 to 24 months, were identified on the basis of clinical and radiologic features,
along with 22 community controls, and 41 children with either severe or moderate acute
malnutrition. Most children with rickets had wrist widening (100%) and rachitic rosary
(90%), as opposed to lower limb features (19%). Developmental delay (52%), acute
malnutrition (71%), and stunting (62%) were common. Compared to controls, there were
no differences in calcium intake, but most (71%) had serum 25-hydroxyvitamin D levels
below 30 nmol/L. These results suggest that rickets in young children in urban Kenya is
usually driven by vitamin D deficiency, and vitamin D supplementation is likely to be
required for full recovery. Wasting was associated with lower calcium (p = .001),
phosphate (p < .001), 25-hydroxyvitamin D (p = .049), and 1,25-dihydroxyvitamin D (p
= 0.022) levels, the clinical significance of which remain unclear.