Endometriosis is defined as the presence of endometrial glands and stroma outside the uterine cavity and is usually confined to the pelvis. Thoracic endometriosis syndrome (TES) is a rare disorder characterized by the presence of functioning endometrial tissue in the pleura, the lung parenchyma and the airways. TES may present with hemoptysis, due to the shedding of endometrial tissue in the bronchial tree, or spontaneous pneumothorax or hemothorax if the endometrial tissue is localized peripherally. Patients are of reproductive age, often nulliparous, with long-standing symptoms. The crucial issue for establishing the diagnosis is the cyclicity of the symptoms which occur along with the menstrual cycle. TES is virtually a diagnosis of exclusion, established on clinical grounds, since neither CT nor endoscopy are specific for TES. Treatment consists of gonadotropin-releasing hormone analogues, aiming to suppress the hypophyseal-gonadal axis, so as to ensure a regression of the endometrial implants. If medical treatment fails, surgical resection of the endometriomas is suggested, although relapse rate may be high.

Objective: To assess the association between endogenous sex hormones and risk factors for atherosclerosis in healthy postmenopausal women. Design: Cross-sectional study in a university menopause clinic. Methods: Serum sex hormones and lipid-lipoprotein profile, arterial pressure, homocysteine and insulin resistance, measured by the homeostasis model assessment of insulin resistance (HOMA-IR), were assessed in 598 healthy postmenopausal women not on hormone therapy. Results: Compared with women in the lowest testosterone quartile (Q), women in the highest testosterone quartile had higher total cholesterol (Q1: 225.2G41.3 vs Q4: 246.2G38.4 mg/dl, P!0.01), low-density lipoprotein (LDL)-cholesterol (Q1: 146.9G37.2 vs Q4: 171.8G35.3 mg/dl, P!0.001), atherogenic index of plasma (AIP) (Q1: -0.224G0.238 vs Q4: -0.087G0.254, P!0.01), apolipoprotein B (ApoB) (Q1: 100.7G23.1 vs Q4: 113.9G23.8 mg/dl, P!0.001) and higher highdensity lipoprotein (HDL)-cholesterol (Q1: 60.7G14.5 vs Q4: 52.9G13.0 mg/dl, P!0.01). Accordingly, women in the highest free androgen index (FAI) quartile had higher AIP (Q1: -0.232G0.254 vs Q4: -0.078G0.243, P!0.001) and ApoB (Q1: 102.4G25.5 vs Q4: 114.2G 25.8 mg/dl, P!0.01) and lower HDL-cholesterol (Q1: 62.0G15.7 vs Q4: 51.9G11.6 mg/dl, P!0.001) and apolipoprotein A (Q1: 159.6G25.6 vs Q4: 147.9G24.1 mg/dl, P!0.01) compared with women in the lowest FAI quartile. These differences remained significant after adjustment for age, body mass index (BMI), insulin resistance and social habits. The free estrogen index (FEI) exhibited similar associations to the FAI. HOMA-IR showed an independent positive association with total testosterone (Q1: 2.00G1.36 vs Q4: 2.66G1.60, P!0.01), FAI (Q1: 1.70G1.12 vs Q4: 3.04G1.66, P!0.001) and FEI (Q1: 1.70G0.91 vs Q4: 3.08G1.77, P!0.001). Conclusions: Increased androgenicity in healthy postmenopausal women is associated with an unfavorable cardiovascular risk profile. High endogenous estradiol is related to a pro-atherogenic lipid profile, an association which may, in part, be mediated by insulin resistance. 154 907-916 European Journal of Endocrinology

Abstract-Hyperprolactinemia has been associated with endothelial dysfunction and an adverse cardiovascular risk profile, possibly as a result of the vasoconstrictive properties of prolactin. In this cross-sectional study, we examined the hypothesis that prolactin contributes to the increased cardiovascular risk occurring in early menopause by studying apparently healthy women without hyperprolactinemia.

Endometriosis is a common gynecological disorder of the reproductive age characterised by pelvic pain, dysmenorrhea and infertility. Classic theories have failed to propose a precise pathogenetic mechanism. Recent studies have investigated the role of the immune system and oxidative stress in the development of endometriosis as well as the identification of biomarkers for a non-invasive diagnosis of the disease. At endometriotic sites, inflammatory cells including eosinophils, neutrophils and macrophages generate reactive oxygen species that contribute to the development of oxidative stress in the peritoneal cavity. Oxidative stress further augments immune response in affected sites. The oxidants exacerbate the development of endometriosis by inducing chemoattractants and endometrial cell growth-promoting activity. The oxidative proinflammatory state of the peritoneal fluid is an important mediator of endometriosis. Many studies investigate the correlation of endometriosis and oxidative stress but the results are discrepant. Furthermore, oxidative stress has been implicated in unexplained infertility and has been associated with some of its causative factors. Oxidative stress influences women's reproductive capacity. The association between endometriosis and infertility is described in several studies and still remains debated.

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