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Volume 79, Issue 2, Pages 111-116 (February 2009)


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Insulin sensitivity and lipid metabolism with oral contraceptives containing chlormadinone acetate or desogestrel: a randomized trial☆☆

Angelo CagnacciCorresponding Author Informationemail address, Serena Ferrari, Alessandra Tirelli, Renata Zanin, Annibale Volpe

Received 1 August 2008; received in revised form 2 September 2008; accepted 2 September 2008. published online 17 October 2008.

Abstract 

Background

Second-generation and third-generation oral contraceptives containing 30 mcg or more of ethinylestradiol (EE) decrease insulin sensitivity (SI). In this study, we investigated whether SI is decreased by contraceptives containing lower doses EE or by progestins with antiandrogenic properties.

Study Design

Twenty-eight young healthy women were randomly allocated to receive 20 mcg of EE and 150 mcg of desogestrel (DSG) (n=14) or 30 mcg of EE and 2 mg of chlormadinone acetate (CMA) (n=14) for 6 months. SI and glucose utilization independent of insulin (Sg) were investigated by the minimal model method. Lipid modifications were also analyzed.

Results

SI decreased with EE/DSG (7.09±1.4 vs. 4.30±0.91; p=.04; n=12), but not with EE/CMA (5.79±0.93 vs. 6.79±1.1; p=.48; n=12). SI modifications observed in the two groups were significantly different (−2.79±1.15 vs. 1.0±1.38; p=.05). Sg did not vary with either treatment. The response of C-peptide to glucose increased, but significantly so only with EE/CMA (p=.01). The C-peptide/insulin response increased with both EE/DSG (p=.05) and EE/CMA (p=.04). High-density lipoprotein (HDL) cholesterol (p=.02) and triglycerides (p=.02 and p=.01) increased in both groups, but HDL/low-density lipoprotein cholesterol (p=.02), apoprotein A1 (Apo-A1) (p=.04) and Apo-A1/apoprotein B (p=.048) increased significantly only with EE/CMA.

Conclusions

The present study confirms that DSG, even when associated with low EE dose, decreases SI. By contrast, EE/CMA does not deteriorate SI and induces a favorable lipid profile.

Department of Obstetrics, Gynecology and Pediatrics, Gynecology and Obstetrics Unit, University of Modena, Policlinico of Modena, Via del Pozzo 71, 41100 Modena, Italy

Corresponding Author InformationCorresponding author. Dipartimento Materno Infantile, Ginecologia e Ostetricia, Policlinico di Modena, Via del Pozzo 71, 41100 Modena, Italy. Tel.: +39 59 4224511; fax: +39 59 4224394.

 This study received unrestricted funds from the Department of Obstetrics and Gynecology, University of Modena.

☆☆ The present trial was registered with the European Clinical Trial Database (no. 2007-007931-25).

PII: S0010-7824(08)00452-6

doi:10.1016/j.contraception.2008.09.002


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