PubMed Health⌕ Search

Biomedical subjects

M Luque-Ramírez

Publications and source records attributed to M Luque-Ramírez.

2 recordsLinked to original sources

Adiponectin and resistin in PCOS: a clinical, biochemical and molecular genetic study.

BACKGROUND: We conducted a cross-sectional case-control study to evaluate the possible involvement of adiponectin and resistin in the pathogenesis of polycystic ovary syndrome (PCOS). METHODS: Seventy-six PCOS patients and 40 non-hyperandrogenic women matched for BMI and degree of obesity were included. Serum adiponectin and resistin levels, anthropometrical and hormonal variables, the 45 T-->G and 276 G-->T polymorphisms in the adiponectin gene, and the -420 C-->G variant in the resistin gene, were analysed. RESULTS: Serum adiponectin concentrations were reduced in PCOS patients compared with controls (P = 0.038) irrespective of the degree of obesity, whereas serum resistin levels were increased in overweight and obese women compared with lean subjects (P = 0.016), irrespective of their PCOS or controls status. The adiponectin and resistin polymorphisms were not associated with PCOS and did not influence serum levels of adiponectin, resistin and other clinical and hormonal variables. In a multiple regression model, the waist-to-hip ratio, free testosterone levels and age, but not insulin resistance, were the major determinants of hypoadiponectinaemia. CONCLUSIONS: PCOS patients present with hypoadiponectinaemia, in relation with abdominal adiposity and hyperandrogenism. Our present results suggest that hyperandrogenism and abdominal obesity, by reducing the serum levels of the insulin sensitizer adipokine adiponectin, might contribute to the insulin resistance of PCOS.

Adiponectin↗

[Hungry bone syndrome related to hyperthyroidism].

Hungry bone syndrome is a common clinical entity which is accompanying of hypocalcemia, hypomagnesemia, and hipophosphatemia, results from an increase in bone formation. It is related to a pathological scenario which causes an imbalance between osteoclast-mediated bone resorption and osteoblast-mediates bone formation, favouring the latter. Its classic presentation occurs after parathyroidectomy in hyperparathyroydism's patients. Its clinical features are largely due to plasmatic calcium levels reduction. Hungry bone syndrome is frequent in hyperparathyroid's patients who have development bone disease before surgery. Even less frequent, it has also been described after thyroydectomy in patients with hyperthyroidism. We hereby report a case of hungry bone syndrome in one patient who suffers a Graves' disease. Then, we will provide a brief review of pathogenesis and therapeutic features.

Adult↗