Vitamin d deficiencyE55.9

Vitamin deficiency caused by malassimilation syndromes or, more rarely, by greatly reduced exposure to UV light or a lack of dietary vitamin D supply, with hypocalcemia and hypophosphatemia (rickets) being the main causes. A reduced vitamin D activity (e.g. due to vitamin D receptor polymorphisms) is apparently associated with an increased risk of melanoma.

Photoprotective agents and vitamin D: in principle, an efficient UVB filter lowers vitamin D levels. To what extent this has a clinical relevance in the summer months is completely unclear.

• Treatment of the underlying disease. For vitamin D metabolic disorders, substitution of the metabolically active metabolite, e.g. 1,25 (OH)2-D3 such as cholecalciferol (e.g. vigantoletten, decristol). Dosage varies according to the severity of the clinical picture.
• Prophylaxis in case of a recognizable risk of vitamin D deficiency: 500-1000 IU Vit. D/day p.o. Prophylaxis in case of malabsorption: 3000-5000 IU Vit. D/day p.o. or 50.000-100.000 IU Vit. D as ED in individual intervals (usually every three months).
• Therapy of rickets and osteomalacia: 1000-5000 IU Vit. D/day p.o. over 1 year, for introduction 200.000 IU Vit. D can be administered once.
• Supporting therapy for osteoporosis: 1000-3000 IU Vit. D/day p.o. Therapy control by monitoring serum calcium and urinary calcium excretion. Cave! Hypercalcemia.
• Infants: Recommended rickets prophylaxis from the 5th day of life starting with a 2-year substitution treatment with 500 IU/day of vitamin D (e.g. Vigantol oil) p.o.

1. Macbeth AE et al.(2011) What's new in skin cancer? An analysis of guidelines and systematic reviews published in 2008-2009 Clin Exp Dermatol 36:453-458.