Rickets

Abstract

Rickets, once thought vanquished, is reappearing. In some less developed countries it hardly went away. This seminar reviews the effects of genes, stage of development, and environment on clinical expression of the disease. Rickets can be secondary to disorders of the gut, pancreas, liver, kidney, or metabolism; however, it is mostly due to nutrient deficiency and we concentrate on this form. Although calcium deficiency contributes in communities where little cows' milk is consumed, deficiency of vitamin D is the main cause. There are three major problems: the promotion of exclusive breastfeeding for long periods without vitamin D supplementation, particularly for babies whose mothers are vitamin D deficient; reduced opportunities for production of the vitamin in the skin because of female modesty and fear of skin cancer; and the high prevalence of rickets in immigrant groups in more temperate regions. A safety net of extra dietary vitamin D should be re-emphasised, not only for children but also for pregnant women. The reason why many immigrant children in temperate zones have vitamin D deficiency is unclear. We speculate that in addition to differences in genetic factors, sun exposure, and skin pigmentation, iron deficiency may affect vitamin D handling in the skin or gut or its intermediary metabolism.

Prevalence and predictors of vitamin D deficiency based on maternal mid-gestation and neonatal cord bloods: The Generation R Study

“…The concern about vitamin D deficiency during pregnancy reflects the robust evidence linking this exposure to higher risk of rickets in the offspring (Wharton and Bishop, 2003) and an increased risk of obstetric complications (Aghajafari et al, 2013, Nassar et al, 2011, Wei et al, 2013. There is also preliminary evidence to suggest that vitamin D deficiency may be linked to a range of later adverse health outcomes in the offspring (Boucher, 1998, McGrath, 2001, Brannon and Picciano, 2011, Christesen et al, 2012, Thorne-Lyman and Fawzi, 2012, Zipitis and Akobeng, 2008, Ponsonby et al, 2010.…”

Vitamin D Dependent Rickets Type I: Two Cases Report

“…Tam kan sayımı, böbrek fonksiyon testleri, transaminaz düzeyleri, tiroid fonksiyon testleri ve tam idrar tetkiki normaldi. Serum kalsiyum 8,5 mg/dL (8,(8)(9)(10)8) …”

“…Süt çocuklarında en erken bulgu distal ulna bölgesinde belirgindir. 9 Boy kısalığı ve yürüyememe şikâyeti ile başvuran her iki olgunun el bilek filmlerinde osteopenik gö-rünüm, radius ve ulna distal uçlarında çanaklaşma, fırçalaşma ve genişleme gözlendi (Resim 1a ve Resim 2).…”

Vitamin D Receptor Polymorphism among Rickets Children in Mongolia

“…[3][4][5] With regard to genetic factors, vitamin D receptor (VDR) polymorphism is considered to have an association with rickets, although few studies have examined the association. Point mutations in the VDR gene are identified in hereditary 1, 25-dihydroxyvitamin D3-resistant rickets, a rare but severe form of rickets.…”