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J Clin Endocrinol Metab. 2002 Jul;87(7):3074-7.
Intraoperative testosterone assay for virilizing ovarian tumor topographic assessment: report of a Leydig cell tumor of the ovary in a premenopausal woman with an adrenal incidentaloma.

Regnier C, Bennet A, Malet D, Guez T, Plantavid M, Rochaix P, Monrozies X, Louvet JP, Caron P.

Department of Endocrinology, Centre Hospitalier Universitaire (CHU) Rangueil, avenue Jean Poulhes, 31403 Toulouse Cedex, France.

Ovarian virilizing tumors are rare and can lead to assessment difficulties because of their small size. A 41-yr-old female was referred for evaluation of hirsutism that had increased within the previous 3 yr. Menstrual cycle length was normal. Plasma testosterone was 3.9 ng/ml (normal range, 0.2-0.8 ng/ml), was not suppressible by 2 mg dexamethasone (4.3 ng/ml), and was increased (6.3 ng/ml) after three daily injections of hCG (5000 IU). Abdominal computed tomography scan showed an adrenal nodule (13 x 6 mm) that remained unchanged after 3 months. Ultrasound examination of the pelvis was normal. Ovarian and adrenal venous catheterization did not yield additional information. Topographic assessment was made by intraoperative measurement of testosterone in the samples taken from each ovarian vein (competitive chemiluminescent immunoassay ADVIA Centaur; right ovarian vein, 105 ng/ml; left ovarian vein, 5 ng/ml; peripheral blood, 7 ng/ml). Right annexectomy resulted in normalization of testosterone levels (0.22 ng/ml). Histopathological examination found a Leydig cell tumor of hilar type (1.5 cm). This observation illustrates the usefulness of intraoperative measurement of testosterone by a rapid automated technique for topographic assessment of ovarian virilizing tumor in premenopausal women.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12107203&dopt=Abstract

J Clin Endocrinol Metab. 2002 Jul;87(7):3287-90.
A specific elevation in tissue plasminogen activator antigen in women with polycystic ovarian syndrome.

Kelly CJ, Lyall H, Petrie JR, Gould GW, Connell JM, Rumley A, Lowe GD, Sattar N.

Department of Medicine and Therapeutics, University of Glasgow, Glasgow G31 2ER, Scotland, UK.

There is increasing evidence that elevated plasma levels of hemostatic factors [fibrinogen, factor VII, von Willebrand factor, fibrin D-dimer, and tissue plasminogen activator (t-PA) antigen] are independently linked to risk for coronary heart disease (CHD). Women with polycystic ovary syndrome (PCOS) are insulin-resistant and have increased risk for CHD and type 2 diabetes, but there are few data on hemostatic markers in women with PCOS. Seventeen women with PCOS (defined on the basis of elevated testosterone and oligomenorrhea) and 15 healthy women matched as a group for body mass index (BMI) were recruited. Insulin sensitivity was assessed using the hyperinsulinemic euglycemic clamp technique. Factor VIIc was determined by a clotting assay; fibrinogen was determined by nephelometry; and t-PA, D-dimer, and von Willebrand factor antigens were measured by ELISA techniques. Of these hemostatic markers, only t-PA concentration was significantly (P = 0.013) elevated in women with PCOS relative to controls. t-PA correlated with BMI in both PCOS and controls (r = 0.428, P < 0.1; and r = 0.686, P < 0.01) and inversely with the insulin sensitivity index (r = -0.590, P < 0.05; and r = -0.620, P < 0.05, respectively). After further adjustment for BMI and insulin sensitivity, there remained a significant difference in t-PA between cases and controls (P = 0.017). Together, age and insulin sensitivity explained 39% of the variance in t-PA in women with PCOS (P < 0.05). Total testosterone did not correlate significantly with t-PA in either group. We conclude that women with PCOS have significantly increased t-PA concentrations relative to women with normal menstrual rhythm and normal androgens. We suggest that elevated t-PA and dysfibrinolysis may be a factor in the increased cardiovascular morbidity seen in PCOS.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12107238&dopt=Abstract

J Clin Endocrinol Metab. 2002 Jul;87(7):3394-8.
Decreased pituitary-gonadal secretion in men with obstructive sleep apnea.

Luboshitzky R, Aviv A, Hefetz A, Herer P, Shen-Orr Z, Lavie L, Lavie P.

Endocrine Institute, Haemek Medical Center, Afula 18101, Israel. luboshitzky-lalit.org

Decreased libido is frequently reported in male patients with obstructive sleep apnea (OSA). The decline in morning serum testosterone levels previously reported in these patients was within the normal adult male range and does not explain the frequent association of OSA and sexual dysfunction. We determined serum LH and testosterone levels every 20 min between 2200-0700 h with simultaneous sleep recordings in 10 men with sleep apnea and in 5 normal men free of any breathing disorder in sleep. The mean levels and area under the curve of LH and testosterone were significantly lower in OSA patients compared with controls [LH, 24.9 +/- 10.2 IU/liter.h vs. 43.4 +/- 9.5 (P < 0.005); testosterone, 67.2 +/- 11.5 nmol/liter.h vs. 113.3 +/- 26.8 (P < 0.003)]. Four of 10 patients had hypogonadal morning (0700 h) serum testosterone levels. Analysis of covariance (ANCOVA) revealed that the 2 groups differed significantly in the amount of LH and testosterone secreted at night independent of age or degree of obesity. After partialing out body mass index, there was a significant negative correlation between the amounts of LH and testosterone secreted at night and the respiratory distress index, but not with degree of hypoxia. Our findings suggest that OSA in men is associated with dysfunction of the pituitary-gonadal axis. The relation between LH-testosterone profiles and the severity of OSA suggests that sleep fragmentation and, to a lesser extent, hypoxia in addition to the degree of obesity and aging may be responsible for the central suppression of testosterone in these patients.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12107256&dopt=Abstract

J Endocrinol. 1999 Apr;161(1):33-40.
Involvement of gonadal steroid hormone disturbance in altered prolactin receptor gene expression in the liver of diabetic mice.

Yasui T, Murakami T, Maeda T, Oka T.

Laboratory of Genetics and Physiology, National Institutes of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, 20892, USA.

The levels of mRNA for long and three short forms of prolactin receptor (PRLR) were examined in the livers of normal (db+/db-) and insulin-resistant diabetic (db+/db+) mice to assess the role of gonadal steroid hormones in the regulation of PRLR gene expression in diabetes mellitus. In females, plasma levels of testosterone in diabetic mice were higher, and those of 17beta-estradiol were lower when compared with levels in normal mice. By contrast, diabetic male mice had lower plasma levels of testosterone than normal males and showed no significant difference in the low circulating level of 17beta-estradiol compared with normal males. The short 3 form of PRLR (PRLR3) mRNA was the most abundant in the liver of both normal and diabetic mice. In addition, the level of PRLR3 mRNA in normal females was 8-fold higher than in normal males. The level of PRLR3 mRNA in diabetic females was approximately a quarter lower than in normal females, whereas the level of PRLR3 mRNA in diabetic males was approximately 2-fold higher than in normal males. During postnatal development, the level of PRLR3 mRNA increased during puberty in normal females, while the level in diabetic females decreased to a nadir at 7 weeks of age followed by a progressive rise. On the other hand, the levels of PRLR3 mRNA in both normal and diabetic males decreased gradually during 5 to 14 weeks of age. Testosterone treatment of diabetic males and females resulted in a 49.1 and 49.8% decrease of PRLR3 mRNA respectively. 17beta-Estradiol treatment slightly (18%) increased levels of PRLR3 mRNA in diabetic males. These results suggest that the hepatic level of PRLR mRNA is regulated by the inhibitory effect of testosterone and the stimulatory effect of estrogen in both normal and diabetic mice.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10194526&dopt=Abstract

Hair loss is a problem in modern soceity. Examining the factors of hair growth may shed light on how hair loss might occur. How long can hair grow before it stops growing eventually if it does? Given that the hair growth rate is quite uniform and constant, somewhere between 0.3-0.5 millimeters per day, it's believed that the length of anagen, the growth phase, differs among individuals, and this is the major determinant to the maximum hair length. For some individuals, anagen may last ten years. Of course the length of the anagen is governed by genes, and the genetic background of the individuals. Non-genetic factors such as nutritional condition, weather, seasonal changes (hair may grow a bit faster during winter), taking medications, health condition may of course influence the rate of hair growth as well as hair loss. The shape of the hair, straight or curly, is dependent on the shape of the follicle. A circular or round hair follicle would generate straight hair, while the follicle with oval or elliptical shapes (in its cross-section) would produce a curly hair.

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