Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 16 P572

ECE2008 Poster Presentations Obesity (94 abstracts)

Activated protein C levels in obesity and weight loss influence

Eva Solá 1-6 , Francisco España 1-6 , Amparo Vayá 1-6 , Amparo Estellés 1-6 , Katherinne García 1-6 & Antonio Hernández-Mijares 1-6


1Doctor Peset University Hospital, Valencia, Spain; 2Research Center, La Fe University Hospital, Valencia, Spain; 3La Fe University Hospital, Valencia, Spain; 4Research Center, La Fe University Hospital, Valencia, Spain; 5Doctor Peset University Hospital, Valencia, Spain; 6Doctor Peset University Hospital, Valencia, Spain.

Introduction: Several haemostatic disturbances have been described in obese patients. Nevertheless, the state of coagulation inhibitors has been scarcely studied in these patients. Activated protein C (APC) is the anticoagulant enzyme formed upon activation of the protein C (PC) by the thrombin-thrombomodulin complex on the surface of endothelial cells. Morbid obesity is associated to endothelial dysfunction, which could cause a reduction in APC generation.

Methods: Sixty-seven severe or morbid obese patients (51 women, 16 men), aged 34 ± 11 years, were compared with 67 normal-weight controls (45 women, 22 men), aged 32 ± 10 years. After initial evaluation, the patients received treatment for 4 weeks with a very low-calorie diet (VLCD), followed by a low calorie diet (1200–1500 kcal/day) for 2 months. Exclusion criteria were organic, infectious or inflammatory disease, ischaemic heart disease or stroke, diabetes mellitus, hyperlipidaemia and hypertension. An anthropometric and analytical evaluation was performed before and after the diet, measuring APC, PC and prothrombin fragment F1+2 as a marker of hypercoagulability. Student t-test was used to compare the differences between groups. Pearson correlation coefficients were calculated to describe the association between variables.

Results: Obese patients showed significantly higher levels of APC, PC and F1+2 (P=0.001, P=0.015 and P=0.010 respectively). After adjusting for BMI, differences in APC remained statistically significant (P=0.047). After three months of diet, a significant decrease in APC (P=0.043) and F1+2 (P=0.025) and a non significant decrease in PC (P=0.067) was observed.

Conclusions: APC levels are increased in obese patients, in part because of greater thrombin generation and higher PC levels. After weight loss, we have found a decrease in APC levels, due in part to a thrombin generation reduction.

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