Résumé
Recent reports have been suggested the possible role of 3-hydroxy-3 methyl gluteryl Coenzyme A [HMG-C0A] reductase inhibitors to represent an entirely new approach in treating osteoporosis by stimulating the proliferation and differentiation of osteoblasts, the specialized cells that create new bone formation. Also, statins have been reported to prevent bone resorption through blocking an early step in mevalonate pathway and so preventing prenylation, a step that is required for osteoclasts function. The aim of the present work was to study the effect of HMG-CoA reductase inhibitors [statins]; simvastatin and pravastatin, on bone mineral density [BMD] of dyslipidemic postmenopausal females with type 2 diabetes mellitus and having osteoporosis. Thirty postmenopausal dyslipidemic type 2 diabetic females above 50 years with no history of any disease or drugs that affect bone metabolism were included in this study and classified into 2 groups; I] included 15 patients received 40mg daily of simvastatin and II] included 15 patients received 40mg daily of pravastatin both for 3 months. Each patient was subjected to full history taking, complete clinical examination, laboratory investigations including, fasting and post-prandial plasma glucose, glycosylated haemoglobin, alanine aminotransferase [ALT], serum cholesterol and triglycerides, serum calcium [total and ionized] and phosphorus. Serum osteocalcin, biochemical marker of bone formation, was measured by immunometric assay and urinary deoxypyridinoline [DPD], biochemical marker of bone resorption was measured by competitive immunoassays. Dual energy X-ray absorptiometry [DEXA] was used to assess BMD of forearm [peripheral site] and L2-L3 lumbar vertebrae [axial site]. The results of the present work can be summarized as follows; the serum levels of osteocalcin and the BMD revealed significant increase and the urinary levels of DPD revealed significant decrease after 3 months of simvastatin in group I. A mild change in osteocalcin, urinary DPD and BMD had been noticed after 3 months of pravastatin in group II, yet it did not reach a statistical significant level. Also, there was significant reduction of serum cholesterol and triglycerides levels after 3 months therapy of either simvastatin or pravastatin and none of the patients showed any abnormal change in ALT levels supporting the safety of these drugs regarding their effect on the liver. Our results suggest the beneficial unexpected role of lipophyllic statins, simvastatin, in prevention and treatment of osteoporosis. Further studies are needed to reach the best effective dose and mode of administration of statin in preventing and treating osteoporosis. Also, the possibility of using statins in combination with other currently used drugs in this domain