Rickets – bowed legs was not the primary feature – Jan 2018

Vitamin D deficiency causes rickets in an urban informal settlement in Kenya and is associated with malnutrition

Matern Child Nutr. 2018 Jan; 14(1): online 2017 May 3. doi: 10.1111/mcn.12452
PMCID: PMC5763407, PMID: 28470840
Kelsey D. J. Jones, 1 , 2 C. Ulrich Hachmeister, † Maureen Khasira, 1 Lorna Cox, 4 Inez Schoenmakers, 4 , 5 Caroline Munyi, 3 H. Samira Nassir, 3 Barbara Hünten‐Kirsch, 3 Ann Prentice, 4 , 6 and James A. Berkley 1 , 7

VitaminDWiki

Subset of table

%
Wrist widening 100 %
Rachitic rosary90 %
Swollen knees19 %
Bowed legs 14 %
Bone pain on walking5 %
Minor feature – Open Fontanelle90 %
Minor feature – Double malleoli52 %
Minor feature – Harrison's groove48 %
Minor feature – Developmental delay52 %
Comorbidity – URTI 62 %

Wrist widening images from the web

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Rachitic rosary images from the web

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See also VitaminDWiki

Overview of Rickets and vitamin D contains the following summary

Rate of rickets is usually < 0.1% of births, unless dark skin or breastfed
Rate of rickets has greatly increased with the drop in vitamin D levels during the past 40 years
400 IU can prevent/treat most rickets Turkey gave vitamin D to EVERY child and eliminated Rickets
A low serum level of vitamin D does not indicate rickets
Sometimes rickets is also associated with a poor vitamin D receptor
Giving enough Vitamin D to the mother PREVENTS Rickets
Rate of rickets in some countries varies from 10% to 70% (typically poor health overall)
Rickets has been more than doubling in many countries
Rickets is strongly associated with severe breathing problems (weak ribs)
Bowed legs is not the primary indication of rickets    (3 other indications of rickets are seen more often)
Some Rickets is due to poor genes - Vitamin D needed lifelong – June 2020
Vitamin D and Rickets consensus took 80 years

Rickets category has 127 items

 Download the PDF from VitaminDWiki

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.

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