Hipovitaminose D em Adultos: Entendendo Melhor a Apresentação de Uma Velha Doença

Autor: Melissa Orlandin Premaor e Tania Weber Furlanetto
Data: 29/04/2007 - 13:55 h
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A pré-vitamina D é produzida na pele, onde, através de foto-reação mediada pela luz solar, isomeriza-se em vitamina D. É metabolizada no fígado em 25-hidroxivitamina D. Esta é o substrato para a formação do verdadeiro hormônio, a 1,25-dihidroxivitamina D, que ocorre sob a influência do cálcio sérico e do hormônio da paratireóide. Receptores nucleares mediam suas funções principais. A doença causada pela deficiência de vitamina D em indivíduos adultos se estabelece de forma sutil, com hipocalcemia leve, hiperparatireoidismo reacional, gerando perda do osso trabecular e estreitamento do osso cortical, o que leva a um risco aumentado de fraturas. Essa doença é muito prevalente na Europa, África, América do Norte e alguns países da América do Sul,
como Chile e Argentina. O padrão-ouro para o diagnóstico de hipovitaminose D é a dosagem de 25-hidroxivitamina D no soro, e valores abaixo de 50 nmol/L seriam suficientes para causar aumento na concentração sérica do hormônio da paratireóide e perda óssea. Fatores de risco para esta doença são pouca exposição à luz solar, envelhecimento da pele e doenças que alteram o metabolismo da vitamina D. Seu tratamento é feito através da reposição oral de vitamina D, o que o torna fácil e barato. (Arq Bras Endocrinol Metab 2006;50/1:25-37)

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Zoledronic Acid and Clinical Fractures and Mortality after Hip Fracture
Published at www.nejm.org September 17, 2007 (10.1056/NEJMoa074941)

Kenneth W. Lyles, M.D., Cathleen S. Colón-Emeric, M.D., M.H.Sc., Jay S. Magaziner, Ph.D., Jonathan D. Adachi, M.D., Carl F. Pieper, D.P.H., Carlos Mautalen, M.D., Lars Hyldstrup, M.D., D.M.Sc., Chris Recknor, M.D., Lars Nordsletten, M.D., Ph.D., Kathy A. Moore, R.N., Catherine Lavecchia, M.S., Jie Zhang, Ph.D., Peter Mesenbrink, Ph.D., Patricia K. Hodgson, B.A., Ken Abrams, M.D., John J. Orloff, M.D., Zebulun Horowitz, M.D., Erik Fink Eriksen, M.D., D.M.Sc., Steven Boonen, M.D., Ph.D., for the HORIZON Recurrent Fracture Trial

ABSTRACT :
Background Mortality is increased after a hip fracture, and strategies that improve outcomes are needed.

Methods In this randomized, double-blind, placebo-controlled trial, 1065 patients were assigned to receive yearly intravenous zoledronic acid (at a dose of 5 mg), and 1062 patients were assigned to receive placebo. The infusions were first administered within 90 days after surgical repair of a hip fracture. All patients (mean age, 74.5 years) received supplemental vitamin D and calcium. The median follow-up was 1.9 years. The primary end point was a new clinical fracture.

Results The rates of any new clinical fracture were 8.6% in the zoledronic acid group and 13.9% in the placebo group, a 35% risk reduction with zoledronic acid (P=0.001); the respective rates of a new clinical vertebral fracture were 1.7% and 3.8% (P=0.02), and the respective rates of new nonvertebral fractures were 7.6% and 10.7% (P=0.03). In the safety analysis, 101 of 1054 patients in the zoledronic acid group (9.6%) and 141 of 1057 patients in the placebo group (13.3%) died, a reduction of 28% in deaths from any cause in the zoledronic acid group (P=0.01). The most frequent adverse events in patients receiving zoledronic acid were pyrexia, myalgia, and bone and musculoskeletal pain. No cases of osteonecrosis of the jaw were reported, and no adverse effects on the healing of fractures were noted. The rates of renal and cardiovascular adverse events, including atrial fibrillation and stroke, were similar in the two groups.

Conclusions An annual infusion of zoledronic acid within 90 days after repair of a low-trauma hip fracture was associated with a reduction in the rate of new clinical fractures and improved survival. (ClinicalTrials.gov number, NCT00046254)

Full text FREE: http://content.nejm.org/cgi/content/full/NEJMoa074941v2