The fall and rise of rickets

The near-disappearance of vitamin D-deficient rickets from much of the world's population is a story of sequential victories for keen powers of observation, and for major initiatives in science and public health. In the early 20th century, rickets was one of the most disabling disorders of childhood, causing severe skeletal deformities of the spine and extremities, and growth failure. Pelvic involvement could cause dystocia, leading to neonatal and infant mortality. The conquest of rickets resulted from a remarkable sequence of lessons learned. In 1890, Palm (1) observed that the geographical incidence of rickets was inversely related to the amount of exposure to sunshine. Almost 20 years later, Huldschinsky (2) recognized that the protective effect of sunlight was attributable to its ultraviolet (UV) spectrum and that rickets could be cured by exposure to the UV radiation of a mercury vapour quartz lamp. (I still remember being placed under such a lamp for that purpose as a very young boy – my eyes protected by heavily smoked goggles!). During the same era, Mellanby (3) in the United Kingdom showed that cod liver oil contained an antirachitic factor, which McCollum (4) at Johns Hopkins Hospital, Baltimore, Maryland, found to be a fat-soluble substance that he called vitamin D. The accepted prophylactic dose of vitamin D was 400 IU/day, the amount contained in one teaspoon of cod liver oil. Following these discoveries, the widespread supplementation of cow's milk and infant formulas with vitamin D, legally mandated in many jurisdictions, resulted in the virtual disappearance of rickets from the clinical experience of most paediatricians. Despite this extraordinary triumph of preventive health care, rickets has resurfaced in two contexts – in exclusively breastfed infants and in infants and children who, for geographical or other reasons, have received inadequate exposure to UV light, or whose mothers lacked such exposure. In the latter part of the 20th century, rickets reappeared among infants in population groups where women wore heavy robes, and often veils, virtually precluding exposure to sunshine. In northern Canada, where UV exposure is limited for much of the year, rickets continues to occur in aboriginal populations, as documented by Innes et al (pages 455–458). Finally, Rucker and associates (5) recently documented marked seasonal variations in serum 25-hydroxyvitamin D levels in a community-dwelling sample of healthy Canadians living in Calgary, with some values falling below the accepted lower limits of normal. The clinical significance of these observations is not yet clear. It is clear that while rickets is no longer endemic, certain populations and individuals are vulnerable to vitamin D insufficiency, regardless of whether the insufficiency progresses to clinical rickets. Whether the current wave of heliophobia to prevent skin cancer may deprive some individuals of sufficient UV exposure to maintain vitamin D sufficiency is an interesting matter for speculation.

Récupéré en direct depuis OpenAlex et désinversé. Les résumés ne sont pas conservés dans cette base de données : les index inversés représentent 8,6 Go des 9,3 Go de texte de la base, et le serveur dispose de 13 Go libres.