Antioxid Redox Signal. 2006 Mar-Apr;8(3-4):572-81

Chung HY, Sung B, Jung KJ, Zou Y, Yu BP.

Emerging pathological evidence indicates that major chronic aging-related diseases such as atherosclerosis, arthritis, dementia, osteoporosis, and cardiovascular diseases, are inflammation-related. In this review, inflammation is examined as a possible underlying basis for the molecular alterations that link aging and agerelated pathological processes. A proposal for the molecular inflammation hypothesis of the aging views the redox derangement that occurs during aging as the major factor for increased risk for age-related inflammation. Accumulated data strongly indicate the activation of redox-sensitive transcription factors and dysregulated gene expression under the age-related oxidative stress seems to be the major culprits. Key players involved in the inflammatory process are the age-related upregulation of NF-kappaB, IL-1beta, IL-6, TNFalpha, cyclooxygenase-2, adhesion molecules, and inducible NO synthase. Furthermore, data are presented on the molecular events involved in age-related NF-kappaB activation and phosphorylation by IkappaB kinase/NIK and MAPKs. Experimental data on antiaging calorie restriction (CR) for its antiinflammatory efficacy by suppressing the upregulated proinflammatory mediators will be reviewed. Also, the involvement of another super family of transcription factors, PPARs (PPARalpha, gamma) as regulators of proinflammatory responses and NF-kappaB signaling pathway is described as well as a discussion on the physiological significance of a well-maintained balance between NF-kappaB and PPARs.

Clin J Pain. 2006 May;22(4):325-331

Dugan SA, Powell LH, Kravitz HM, Everson Rose SA, Karavolos K, Luborsky J.

OBJECTIVES: The authors examined whether self-reported menopausal status is associated with musculoskeletal pain in a multiethnic population of community-dwelling middle-aged women after considering sociodemographics, medical factors, smoking, depression, and body mass index using a cross-sectional study design. METHODS: Participants were 2218 women from the Study of Women's Health Across the Nation assessed at the time of their third annual follow-up exam. Two dependent variables were derived from a factor analysis of survey questions about pain. These 2 outcomes were Aches and Pains, derived from 5 of 6 pain symptom questions and Consultation for Low Back Pain, derived from 1 question. RESULTS: Prevalence of aches and pains was high, with 1 in 6 women reporting daily symptoms. Compared with premenopausal women, those who were early perimenopausal (P=0.002), late perimenopausal (P=0.002), or postmenopausal (P<0.0001) reported significantly more aches and pains in age-adjusted analysis. With complete risk factor adjustment, postmenopausal women still reported significantly greater pain symptoms (P=0.03) than did premenopausal women. Menopausal status was marginally related to consulting a healthcare provider for back pain. DISCUSSION: This study demonstrates an association between pain and self-reported menopausal status, with postmenopausal women experiencing greater pain symptoms than premenopausal women.

       

Endocr Pract. 2006 Mar-Apr;12(2):174-8

Orrego JJ, Bair J.

Objective: To describe a 48-year-old woman with presumed idiopathic hyperprolactinemia, who was found to have a macroprolactinoma after receiving hormone replacement therapy for almost 3 years. Methods: We present a detailed case report, including a chronologic summary of clinical and laboratory findings as well as the drug history of our patient. The related literature is also reviewed. Results: Premenopausal women with idiopathic hyperprolactinemia or microprolactinomas (<1 cm) are treated with dopamine agonists if fertility is desired or galactorrhea is bothersome. Otherwise, estrogens and progestational agents may be prescribed to regularize menses and prevent osteoporosis. Several case reports of prolactinoma formation or enlargement after exposure to exogenous estrogens have been published. In our patient, a perimenopausal woman with presumably idiopathic long-standing hyperprolactinemia, a macroprolactinoma developed within 3 years after initiation of hormone replacement therapy for management of perimenopausal symptoms. The only clue for ordering a pituitary imaging study in this case was a substantial increase in the level of the serum prolactin. Treatment with cabergoline normalized the patient's serum prolactin level and considerably decreased the size of her pituitary adenoma. Conclusion: It is postulated that exogenous estrogens could have an important role in tumor development or growth in some patients with idiopathic hyperprolactinemia. Therefore, it is recommended that women with idiopathic hyperprolactinemia or microprolactinomas treated with estrogens be considered for concomitant therapy with dopamine agonists. In all cases, serum prolactin levels should be diligently monitored.

Eur J Endocrinol. 2006 Jun;154(6):907-16

Lambrinoudaki I, Christodoulakos G, Rizos D, Economou E, Argeitis J, Vlachou S, Creatsa M, Kouskouni E, Botsis D.

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: 225.2 +/- 41.3 vs Q4: 246.2 +/- 38.4 mg/dl, P < 0.01), low-density lipoprotein (LDL)-cholesterol (Q1: 146.9 +/- 37.2 vs Q4: 171.8 +/- 35.3 mg/dl, P < 0.001), atherogenic index of plasma (AIP) (Q1: -0.224 +/- 0.238 vs Q4: -0.087 +/- 0.254, P < 0.01), apolipoprotein B (ApoB) (Q1: 100.7 +/- 23.1 vs Q4: 113.9 +/- 23.8 mg/dl, P < 0.001) and higher high-density lipoprotein (HDL)-cholesterol (Q1: 60.7 +/- 14.5 vs Q4: 52.9 +/- 13.0 mg/dl, P < 0.01). Accordingly, women in the highest free androgen index (FAI) quartile had higher AIP (Q1: -0.232 +/- 0.254 vs Q4: -0.078 +/- 0.243, P < 0.001) and ApoB (Q1: 102.4 +/- 25.5 vs Q4: 114.2 +/- 25.8 mg/dl, P < 0.01) and lower HDL-cholesterol (Q1: 62.0 +/- 15.7 vs Q4: 51.9 +/- 11.6 mg/dl, P < 0.001) and apolipoprotein A (Q1: 159.6 +/- 25.6 vs Q4: 147.9 +/- 24.1 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: 2.00 +/- 1.36 vs Q4: 2.66 +/- 1.60, P < 0.01), FAI (Q1: 1.70 +/- 1.12 vs Q4: 3.04 +/- 1.66, P < 0.001) and FEI (Q1: 1.70 +/- 0.91 vs Q4: 3.08 +/- 1.77, 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.

Gynecol Endocrinol. 2006 Apr;22(4):207-12

Serum leptin concentrations in pre- and postmenopausal women on sex hormone therapy.

Bednarek-Tupikowska G, Filus A, Kuliczkowska-Plaksej J, Tupikowski K, Bohdanowicz-Pawlak A, Milewicz A.

Department of Endocrinology, Diabetology and Isotope Treatment, Wroclaw Medical University, Wroclaw, Poland.

Aim. The aim of the present study was to investigate the influence of endogenous estradiol and estrogen and estrogen-progestin therapies on concentration in pre- and postmenopausal women.Materials and methods. The study groups consisted of 26 women with surgical menopause (mean+/-standard deviation (SD): age 51.8+/-2.6 years, body mass index (BMI) 26.45+/-4.56 kg/m(2)), 54 with natural menopause (mean+/-SD: age 50.5+/-3.0 years, BMI 25.75+/-4.09 kg/m(2)) and 40 premenopausal controls (mean+/-SD: age 48.3+/-2.3 years, BMI 26.23+/-4.12 kg/m(2)). The group with surgical menopause received estradiol transdermally (50 mug/day) and those with natural menopause received additionally medroxyprogesterone acetate (5 mg/day) for the last 12 days of the cycle. Before and after 4 months of therapy, body weight, waist and hip circumferences and blood pressure were measured, and BMI and waist-to-hip ratio (WHR) were calculated. Serum leptin, follicle-stimulating hormone (FSH), estradiol (E(2)), testosterone, prolactin and dehydroepiandrosterone sulfate (DHEAS) were measured prior to and after treatment.Results. Leptin concentrations did not differ statistically among the groups. No correlations between leptin and E(2), FSH, prolactin, testosterone and DHEAS concentrations were found in any of the groups before and after treatment. Leptin level correlated positively with body mass, BMI and hip and waist circumferences in all groups. There were no correlations between leptin and WHR in the pre- and postmenopausal groups. In the premenopausal group and in some postmenopausal groups, serum leptin level correlated with blood pressure.Conclusions. Endogenous E(2) and androgens in premenopausal women and estrogen and estrogen-progestin therapies in postmenopausal subjects do not influence serum leptin concentrations. Leptin level is related to body mass and BMI, but not to sex hormone status. The distribution of adipose tissue and the type of obesity (android or gynoid) have no influence on serum leptin concentration. The correlation between serum leptin level and blood pressure requires further investigation.