ACTA ENDOCRINOLOGICA (BUC)

Introduction. Hypogonadotropic hypogonadism is an endocrine disease with a major effect on bone tissue turnover leading to bone demineralization and secondary osteoporosis. Case report. A 42 year old man underwent a total left hip joint arthroplasty for a left aseptic femoral head necrosis with an unsatisfactory evolution because of pain, marked functional deficit, limping and instability sensation in the operated lower limb. Five years before the patient was diagnosed with hypogonadotropic hypogonadism presenting gynecomastia, gynoid fat distribution, eunuchoidal skeletal proportions, reduced facial hair, a Tanner III stage of the external genital development, without erectile dysfunction. The unsatisfactory post-operative result was secondary to an aseptic mechanical degradation due to bone mineral loss (secondary osteoporosis) and also application of undersized non-cemented implant. Standard biological analyses did not show modification, the inflammatory tests were negative. The DXA examination, after a period of 2 years without treatment, showed a decrease of bone mineral density and confirms the diagnosis of secondary osteopenia. It was made the decision of surgical intervention and replacement of the uncemented femoral component with a cemented one. After the surgery, the therapy with bisphosphonates, calcium, vitamin D3 and testosterone is reinitiated. Discussion. The clinical outcome of biointegration of a non-cemented prosthesis depends in first of all of the biological status of the patient, with normal BMD, normal calcium and D vitamin levels. The secondary osteoporosis with local aseptic inflammation on the surface of the prosthesis and bone contact led to mechanical failure which maked necessary the revision surgery, in order to replace the prosthesis with a cemented one. Conclusions. In our case the presence of hypogonadotropic hypogonadism with secondary osteoporosis, represents a contraindication for non-cemented total hip joint arthroplasty, due to major risk of loosening.

Context. Adipokines secreted by fat cells are vital to the control of energy metabolism, communicating the nutrient status with the tissues responsible for controlling both energy intake and expenditure and insulin sensitivity. Objective. We aimed to prove in an experimental animal study that maternal obesity has long term adverse fetal metabolic consequences, which pass on even to the next generation of descendants. Design. The effects of maternal obesity have been studied on animal model using 50 obese female Wistar rats, in which we induced obesity by high-calorie high-fat diet administered by gavage. Subjects and Methods. Obese rat females were sacrificed at gestation term and we analyzed the secretion of adipokines from maternal venous blood: leptin and adiponectin, placental, pancreatic, liver and brain homogenates lipid peroxidation levels estimated by: MDA (malonyl-dialdehyde), total thiols and GSH – as antioxidant factors and routine biochemistry. Results. Low levels of adiponectin and increased levels of leptin positively correlated with the value of placental and fetal tissue lipid peroxidation (from the liver, pancreas and brain) measured by elevated MDA and total thiols and low levels of GSH. The lipid peroxidation in the organs examined generated consistent results, showing high levels of peroxidation expressed through high values of MDA in the groups with Omega 6 supplements respectively no supplementation, and low levels of antioxidants expressed through glutathione and thiols. Conclusions. Endocrine secretion of adipokines from the adipocytes and the recruited macrophages of obese mothers is positively correlated with placental and tissue lipid peroxidation level and routine biochemical parameters.