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      NSAIDs/corticosteroids--primum non nocere.

      Advances in experimental medicine and biology

      Adrenal Cortex Hormones, adverse effects, Anti-Inflammatory Agents, Non-Steroidal, therapeutic use, Cyclooxygenase 1, Cyclooxygenase 2, Cyclooxygenase 2 Inhibitors, Cyclooxygenase Inhibitors, Diuretics, Gastrointestinal Diseases, chemically induced, Humans, Isoenzymes, antagonists & inhibitors, pharmacology, Membrane Proteins, Osteoporosis, prevention & control, Prostaglandin-Endoperoxide Synthases, Vitamin D

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          NSAIDs/Corticosteroids are the most used and maybe misused drugs against "aches and pains of the musculoskeletal system". Their effectiveness to reduce (not cure) inflammation and related pain is without doubt. The problem is that of their side effects in particular of the GI-tract and other body systems. It is clear that these side effects occur more often and more seriously in a number of patients, the so-called high risk group: elderly women, patients with previous history of gastro-intestinal ulcer and corticosteroid users. The discovery that there are two pathways to influence cyclooxygenase activity and prostaglandin production and that some NSAIDs have a more marked COX-2 and COX-1 inhibition opens new perspectives. COX-1 is present in normal tissues and is responsible for the production of protective prostaglandins in the gastric mucosa and other tissues. COX-2 is induced by inflammatory cytokines and plays a role in the inflammatory cascade. Therefore more specific COX-2 antagonists should be safer for the gastro-intestinal mucosa and kidney function. The risk of hip fracture is 50% higher in patients receiving long-term corticosteroid therapy, and 30-35% of corticosteroid patients have vertebral fractures. The renewed interest in osteoporosis and increased number of papers on bone loss in RA reflect on the one hand the advances in technology to measure bone mineral density (BMD) accurately and precisely, and on the other hand the availability of effective drugs to stop bone loss and reverse the process. The possible deleterious effect of low dose corticosteroids continues to be a subject of concern, particularly in rheumatology where serum levels of free cortisone may be higher because of low albumen and other protein changes. Recently, several editorials and conflicting data obtained from cross-sectional and longitudinal studies in RA on steroid-induced osteoporosis have been published. Because the pathogenesis of steroid osteoporosis is distinct from that of entities such as postmenopausal osteoporosis, each therapy requires specific assessment in steroid treated patients. In recent years a wide variety of therapies, for example hormone replacement therapy, calcium supplements administered with vitamin D metabolites, thiazides, diuretics, anabolic steroids, tibolone, calcitonin and bisphosphonates, have been proposed to prevent osteoporosis in patients receiving longterm corticosteroid therapy, but there have been few carefully controlled trials, except for vitamin D and bisphosphonates.

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