ESPE Yearbook of Paediatric Endocrinology

Brief Summary: This review describes the widespread global issue of childhood rickets, focusing on how disparities in health, nutrition, and environmental factors contribute to its prevalence.

Nutritional rickets is primarily caused by deficiencies in vitamin D or calcium, often due to inadequate nutrition or lack of sunlight exposure. This leads to impaired bone development in children, with potential lifelong consequences. Rickets has historically been more prevalent in marginalized populations, particularly in industrialized cities with high pollution and poor access to nutrition.

Rickets disproportionately affects vulnerable populations, particularly those in low-income countries, immigrant communities in higher-latitude regions, and groups experiencing poor nutrition or limited sunlight due to cultural practices or environmental factors. High rates of rickets are observed in various parts of the world, including Southeast Asia, the Middle East, Africa, and immigrant communities in Europe and North America. Factors such as migration, urbanization, and climate also contribute to these disparities.

The authors emphasize the importance of addressing rickets through global public health policies, such as vitamin D supplementation, dietary fortification, and education about proper nutrition for infants, children, and pregnant women. Additionally, they discuss the need for more randomized clinical trials to establish the best treatment regimens.

There is the critical need for global policies and investments to address the root causes of rickets, particularly in underprivileged and marginalized populations, to prevent long-term health impacts like osteoporosis in adulthood.

References: 1. Kajakumar K, Thomas SB. Reemerging Nutritional Rickets: A Historical Perspective. Arch Pediatr Adolesc Med. 2005;159(4):335–341. doi: 10.1001/archpedi.159.4.335a.2. Munns CF, Shaw N, Kiely M, et al. Global Consensus Recommendations on Prevention and Management of Nutritional Rickets. J Clin Endocrinol Metab 2016; 101(2):394–415.