Recommendations for preventionand treatment of glucocorticoid-induced osteoporosis in patients with rheumatic disorders
O. Růžičková; M. Bayer 1; K. Pavelka; V. Palička 2; Společnost Pro Metabolickáonemocnění Skeletu Čls Jep; Česká Revmatologická Společnost Čls Jep
Revmatologický ústav, Praha 1Klinika dětí a dorostového lékařství 1. LF UK, Praha 2Ústav klinické biochemie a diagnostiky, FN Hradec Králové
Čes. Revmatol., , 2004, No. 4, p. 163-174.
An association between increased levels of endogenous glucocorticoids and osteoporosis wasalready described in 1932. Hench had administrated glucocorticoids to rheumatoid arthritis patientsfor the first time in 1948 and Nordin described increased prevalence of vertebral fractures inpatients taking glucocorticoids in 1960. Glucocorticoids, for their antiinflammatory and immunosupressiveeffect, represent indispensable and widely used medicaments in rheumatology at thepresent time, but simultaneously the most frequent cause of secondary osteoporosis. Chronicinflammatory disorders, which we treat with glucocorticoids, might start in the childhood or in theyoung adulthood when glucocorticoids have negative effect on the reached peak bone density andlater participate in an accelerated bone loss. The fastest drop in bone mineral density (BMD) valuesin association with glucocorticoid treatment occurs during the first 6–12 months of treatment, when it can reach even 5%per month. The majority of patients treated with glucocorticoids have low valueof bone density and their prevalence of fractures is between 30–50%. Decreased value of bone densityis the main risk factor of fractures. Their risk progressively increase in relation to decreasing valuesof BMD. An exponential increase of risk of fractures when T-score in BMD decreases under –2.5 SDis observed in patients with primary osteoporosis. That was the reason to declare this value asa diagnostic criterion for osteoporosis. Treatment with glucocorticoids shifts this threshold for thedevelopment of fractures higher, probably to the value of –1.5 SD in T-score, it means out ofdetermination of osteoporosis. 1 SD decrease of BMD within the patients treated with glucocorticoidsis followed by increased risk of vertebral body fractures compared with untreated individuals.This fact is due to the change of bone quality during the glucocorticoid treatment, which is notdetectable by absorptiometry. The safe dose of glucocorticoids does not exist, that is why it is alwaysnecessary to use the lowest, but still effective dose, for as short time as possible. Everyadministrationof prednisolon in a dose of 5 mg and more (or equivalent) for a period of 3 months should becomplemented with preventive antiosteoporotic regimen. It should start together with the glucocorticoidtreatment and last for the same period of time of its administration. In considering topossible GIOP development, every patient has to be carefully examined in the beginning of thetreatment. Calcium and vitamin D supplementation, besides non-pharmacological interventions,are basic for the glucocorticoid induced osteoporosis (GIOP) prevention and treatment. Othermedicaments are bisphosphonates, hormone replacement therapy, calcitonin and anabolic agentswhich have been approved to be effective in prevention and treatment of GIOP. The prevention ofGIOP is essential, but when it is already present, the treatment is imperative. It is necessary to dealwith all the risk factors. Calcium and vitamin D supplementation are basic for the treatment.Bisphosphonates are pharmacological agents of the first choice in the prevention and treatment ofGIOP.Themost often discussed issue at the present time ishormone replacement therapy. Calcitoninis a drug of second choice whereas parathormon is a medicament of the future.
glucocorticoid-induced osteoporosis, bone mineral density, calcium, vitamin D, bisphosphonates,hormone replacement therapy, calcitonin, parathormon
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