Why are the high altitude inhabitants like the Tibetans shorter and lighter?

High altitude inhabitants (HAI) are generally smaller than low altitude inhabitants (LAI). This anthropological observation has recently been confirmed in the Tibetan refugees who have settled in India since 1950s. Those settled at lower altitudes (970 m) are taller and muscular than compatriots settled at higher altitudes (3500 m). While lower socioeconomic status is implicated in growth retardation at higher altitudes, the smaller stature in adults in well-off communities says otherwise. Hypobaric hypoxia (HH) is the main challenge at high altitudes, which the long established HAI have overcome via biological adaptations, including larger chests, raised blood hemoglobin, and producing more nitric oxide (NO), which deliver similar levels of oxygen to tissues, as LAI. The Tibetans produce 10-fold more NO than LAI. NO is a potent inhibitor of steroidogenesis. Therefore I hypothesize that the short stature and lower musculature in HAI results from steroid deficiency precipitated by NO, which HAI produce to cope with HH.

What caused lymphopenia in SARS and how reliable is the lymphokine status in glucocorticoid-treated patients?

Severe Acute Respiratory Syndrome (SARS) outbreak in 2002-03 caused morbidity in over 8000 individuals and mortality in 744 in 29 countries. Lymphopenia along with neutrophilia was a feature of SARS, as it is in respiratory syncytial virus (RSV) and Ebola infections, to name a few. Direct infestation of lymphocytes, neutrophils and macrophages by SARS coronavirus (CoV) has been debated as a cause of lymphopenia, but there is no convincing data. Lymphopenia can be caused by glucocorticoids, and thus any debilitating condition has the potential to induce lymphopenia via stress mechanism involving the hypothalamic-pituitary-adrenal axis. Cortisol levels are elevated in patients with RSV and Ebola, and cortisol was higher in SARS patients with lymphopenia before any steroid therapy. Glucocorticoids also down-regulate the production of proinflammatory lymphokines. Because of the insidious presentation, SARS was treated with antibacterial, antiviral and supra-physiological doses of glucocorticoids. Treatment with glucocorticoids complicated the issue regarding lymphopenia, and certainly calls into question the status of lymphokines and their prognostic implications in SARS.

Status of anti-thyroid peroxidase during normal pregnancy and in patients with hyperemesis gravidarum.

Autoimmune thyroid diseases (AITD) comprising Hashimoto's thyroiditis, primary myxedema, and Graves' disease are associated with autoantibodies directed against thyroglobulin and thyroid peroxidase (anti-TPO). Anti-TPO occur in 10% of pregnant women, half of whom reportedly develop postpartum thyroid dysfunction. We recently published data on the thyroid function reference ranges in pregnant Chinese but the AITD status of our cohort was unknown. In view of this missing information we have measured anti-TPO in specimens from our cohort stored at -80 degrees C, and compared these to those of patients with hyperemesis gravidarum (HG) and nonpregnant controls. After eliminating 3 outliers from 47 nonpregnant controls, the anti-TPO concentration range was 2.2-14.7 kIU/L (n = 44). In 282 pregnant control subjects, the anti-TPO levels were less than 14.7 kIU/L (upper limit of nonpregnant controls) in 189 (67%); between 14.7-55 kIU/L in 82 (29.1%); and greater than 55 kIU/L in 11 (3.9%). The percentage of women with anti-TPO greater than 14.7 kIU/L during the first, second, and third trimesters were 47% (30/64), 39% (49/126), and 16% (15/92), respectively. Anti-TPO level was significantly higher in pregnant controls compared to nonpregnant controls and patients with HG. With reference to other studies in which anti-TPO levels greater than 60 kIU/L were considered pathologic, we conclude that more than 96% of our pregnant controls were without AITD and the data on thyroid function reference ranges we previously reported remain valid.

Evidence for nitrite reductase activity in intact mouse Leydig tumor cells.

Nitric oxide (NO) supposedly derived via L-arginine-NO synthase (NOS) pathway has been implicated in inhibiting steroidogenesis by binding the heme moiety of steroidogenic enzymes. Previously, nitrite, and to a lesser extent nitrate ions inhibited steroidogenesis via NO by hitherto unknown reduction mechanism. Recently, a putative mammalian nitrite reductase activity ascribed to complex III of mitochondrial respiratory chain complexes (MRCC) has been reported, where MRCC inhibitors reduced NO production from nitrite variably. We thus studied the effects of MRCC inhibitors on testosterone production in mouse Leydig tumor cells (MLTC-1) without (basal) or with human chorionic gonadotropin (hCG) stimulation. In stimulated MLTC-1, MRCC inhibitors decreased testosterone production, order being: complex III (antimycin A and myxothiazol) > complex I (rotenone) > complex II (thenoyltrifluoroacetone), while cAMP production increased inversely. In unstimulated MLTC-1, MRCC inhibitors in same order, increased basal testosterone production, which correlated inversely with the percentage inhibition of NO production, with one exception; while antimycin A did not inhibit NO production in the nitrite reductase study mentioned above, it increased basal testosterone production in the present study. While MLTC-1 expressed mRNA for endothelial and neuronal, but not inducible NOS, various stimulators and inhibitors of L-arginine-NOS pathway had no effect on basal testosterone production in MLTC-1 or fresh Balb/c Leydig cells. Moreover, hCG increased nitrate uptake into MLTC-1, which suggests the gonadotropin aids nitrite and nitrate ions in their steroidogenesis inhibitory activity. In conclusion, this study supports the existence of a surrogate mammalian nitrite reductase and the dormancy of L-arginine-NOS pathway in MLTC-1.

Blocking BRE expression in Leydig cells inhibits steroidogenesis by down-regulating 3beta-hydroxysteroid dehydrogenase.

Conversion of cholesterol to biologically active steroids is a multi-step enzymatic process. Along with some important enzymes, like cholesterol side-chain cleavage enzyme (P450scc) and 3beta-hydroxysteroid dehydrogenase/isomerase (3beta-HSD), several proteins play key role in steroidogenesis. The role of steroidogenic acute regulatory (StAR) protein is well established. A novel protein, BRE, found mainly in brain, adrenals and gonads, was highly expressed in hyperplastic rat adrenals with impaired steroidogenesis, suggesting its regulation by pituitary hormones. To further elucidate its role in steroidogenic tissues, mouse Leydig tumor cells (mLTC-1) were transfected with BRE antisense probes. Morphologically the BRE antisense cells exhibited large cytoplasmic lipid droplets and failed to shrink in response to human chorionic gonadotropin. Although cAMP production, along with StAR and P450scc mRNA expression, was unaffected in BRE antisense clones, progesterone and testosterone yields were significantly decreased, while pregnenolone was increased in response to human chorionic gonadotropin stimulation or in the presence of 22(R)OH-cholesterol. Furthermore, whereas exogenous progesterone was readily converted to testosterone, pregnenolone was not, suggesting impairment of pregnenolone-to-progesterone conversion, a step metabolized by 3beta-HSD. That steroidogenesis was compromised at the 3beta-HSD step was further confirmed by the reduced expression of 3beta-HSD type I (3ss-HSDI) mRNA in BRE antisense cells compared with controls. Our results suggest that BRE influences steroidogenesis through its effects on 3beta-HSD action, probably affecting its transcription.

The effect of percutaneous oestradiol on atheroma formation in ovariectomized cholesterol-fed rabbits.

OBJECTIVE: The aim of this study was to examine the effect of percutaneous oestradiol on the lipid profile and on atheroma formation using an animal model. METHODS: The study was of 12 weeks duration. Fifty sexually mature female New Zealand White rabbits were divided into five groups of equal size. Two groups acted as controls and received normal rabbit chow. Rabbits in one of these groups were ovariectomized. The remaining three groups were ovariectomized but received 1% cholesterol enriched rabbit chow. One of these cholesterol-fed groups received 0.3 mg/kg percutaneous oestradiol daily whilst another received 0.1 mg/kg oral oestradiol daily. Measurements of concentrations of total cholesterol (TC), high density lipoprotein cholesterol (HDL-C) and triglycerides (TG) were made at the beginning and end of the study. Aortic atheroma formation was measured using computerized image analysis of uptake of Sudan III staining. RESULTS: After 12 weeks there were significant increases in the mean concentrations of TC in the three cholesterol-fed groups compared with controls (P < 0.001). Changes in HDL-C and TG concentrations were less consistent. The mean area of aortic atheroma formation was significantly less in both the percutaneous oestradiol group (4.9%) and the oral oestradiol group (8.6%) compared with the non-oestrogen-treated cholesterol-fed group (19.5%) (P < 0.001, < 0.01 respectively). CONCLUSION: These results suggest that percutaneous oestradiol has a direct protective effect on atheroma formation independent of serum concentrations of total cholesterol.

Differential expression of a stress-modulating gene, BRE, in the adrenal gland, in adrenal neoplasia, and in abnormal adrenal tissues.

Genes that modulate the action of hormones and cytokines play a critical role in stress response, survival, and in growth and differentiation of cells. Many of these biological response modifiers are responsible for various pathological conditions, including inflammation, infection, cachexia, aging, genetic disorders, and cancer. We have previously identified a new gene, BRE, that is responsive to DNA damage and retinoic acid. Using multiple-tissue dot-blotting and Northern blotting, BRE was recently found to be strongly expressed in adrenal cortex and medulla, in testis, and in pancreas, whereas low expression was found in the thyroid, thymus, small intestine and stomach. In situ hybridization and immunohistochemical staining indicated that BRE was strongly expressed in the zona glomerulosa of the adrenal cortex, which synthesizes and secretes the mineralocorticoid hormones. It is also highly expressed in the glial and neuronal cells of the brain and in the round spermatids, Sertoli cells, and Leydig cells of the testis, all of which are associated with steroid hormones and/or TNF synthesis. However, BRE expression was downregulated in human adrenal adenoma and pheochromocytoma, whereas its expression was enhanced in abnormal adrenal tissues of rats chronically treated with nitrate or nitrite. These data, taken together, indicate that the expression of BRE is apparently associated with steroids and/or TNF production and the regulation of endocrine functions. BRE may play an important role in the endocrine and immune system, such as the cytokine-endocrine interaction of the adrenal gland.

Effects of cyproterone and cyproterone acetate on the adrenal gland in the rat: studies in vivo and in vitro.

Male Wistar rats were treated for three weeks with cyproterone (1.7 or 5.1 mg/day) or cyproterone acetate (2 or 6 mg/day). The adrenal weights of animals treated with either dose of cyproterone acetate were significantly less (P less than 0.001) than those of untreated animals. In contrast, the adrenal weights of animals treated with cyproterone did not differ from those of the controls. The concentrations of corticosterone in the plasma were significantly less (P less than 0.001) in both groups treated with cyproterone acetate compared with those of the controls; only the higher dose of cyproterone reduced the plasma concentration of corticosterone (P less than 0.001). Cyproterone acetate inhibited the rat adrenal 3beta-hydroxysteroid dehydrogenase-5-ene,4-ene-isomerase complex in vitro, with both pregnenolone and dehydroepiandrosterone as substrates. Analysis of the reaction rates suggested an uncompetitive mode of inhibition. These results suggest that in rats the antiandrogens cyproterone and cyproterone acetate may provoke adrenal insufficiency by inhibition of steroid biosynthesis. Furthermore, indirect evidence from the mass and morphology of the adrenal suggests that cyproterone acetate may also suppress production or secretion of ACTH by the pituitary gland.

Role of chloride and inhibitory action of inorganic nitrate on gonadotropin-stimulated steroidogenesis in mouse Leydig tumor cells.

The involvement of adenylate cyclase-cyclic adenosine monophosphate (AC-cAMP) in gonadotropin-stimulated testicular steroidogenesis is well known. Little is known about the role of guanylate cyclase-cyclic guanosine monophosphate (GC-cGMP) or early chloride conductance stimulated by gonadotropins in steroidogenesis. Human chorionic gonadotropin (hCG) 1 IU/L caused significant androgen secretion without a discernible effect on cAMP production. Despite negligible intracellular cAMP, the protein kinase A inhibitor H89 blocked basal and hCG-stimulated steroidogenesis. The GC inhibitors methylene blue (MB) and LY83583 decreased androgen secretion, but hCG did not stimulate cGMP production and there was not a steroidogenic response to exogenous cGMP. A chloride-channel inhibitor, diphenylamine-2-carboxylate (DPC), at concentrations up to 0.6 mmol/L stimulated basal steroid secretion and hCG 10 IU/L stimulated cAMP production, but higher concentrations had an inhibitory effect. Substitution of chloride by gluconate enhanced basal steroid secretion, but nitrate completely abolished the effect of 1 IU/L hCG on androgen secretion, which could be partially overcome by increasing the gonadotropin concentration. In conclusion, chloride, perhaps by activating AC-cAMP, mediates the steroidogenic action of gonadotropins in mouse Leydig tumor cells (MLTC-1). Inorganic nitrate probably inhibited steroidogenesis via conversion to nitric oxide (NO) without involving the GC-cGMP pathway. Nevertheless, the results obtained with GC inhibitors suggest a role for the GC-cGMP pathway in Leydig cell steroidogenesis.

Low temperature blocks the stimulatory effect of human chorionic gonadotropin on steroidogenic acute regulatory protein mRNA and testosterone production but not cyclic adenosine monophosphate in mouse Leydig tumor cells.

Low temperatures slow down metabolism, partly because the kinetic energy of molecules is reduced and enzymes may be structurally impaired. We now report that relative to its maximal activity at 37 degrees C, adenylate cyclase (AC) still retained 25% functionality (determined as cyclic adenosine monophosphate [cAMP] production) at 4 degrees C in mouse Leydig tumor cells (MLTC-1) in response to 50 IU/L human chorionic gonadotropin (hCG), whereas steroidogenic acute regulatory (StAR) protein mRNA and testosterone production were completely impaired. The incubation of MLTC-1 with the phosphodiesterase inhibitor (3-isobutyl-1-methylxanthine; IBMX) resulted in significantly increased intracellular cAMP concentration at all 3 temperatures, but this had no impact on testosterone production. AC, cAMP, and phosphodiesterase form an important intracellular second-messenger mechanism in many organisms, some that inhabit very low temperature niches. The cold-resistance of AC and phosphodiesterase may thus have evolved to cope with adverse conditions. Although hibernation may lead to decreased steroid hormone production, it is also likely that cold-mediated decreased steroid hormone production induces hibernation.

Urinary excretion of testosterone and estradiol in Chinese men and relationships with serum lipoprotein concentrations.

Urinary excretion of total and free testosterone and estradiol was measured in 46 healthy Chinese men, along with serum concentrations of total testosterone and estradiol and the calculated free (unbound) concentrations. Associations with serum concentrations of total, low-density lipoprotein (LDL), high-density lipoprotein-2 (HDL2), and HDL3 cholesterol, apolipoproteins (apos) A-I and B, lipoprotein(a) [Lp(a)] were studied. Serum total and free testosterone concentrations were positively correlated with HDL and HDL2 cholesterol and apo A-I. Serum total and free estradiol levels showed borderline-significant negative associations with total and LDL cholesterol levels. Among urinary variables, total estradiol excretion was negatively associated with apo B levels and showed borderline-significant associations with total and LDL cholesterol. Adjustment for potential confounders, including age, body mass index (BMI), and waist to hip ratio (WHR), strengthened the associations between urinary total estradiol and serum total cholesterol, LDL cholesterol, and apo B. Urinary free estradiol showed a significant correlation with HDL3 cholesterol. Urinary excretion of total testosterone was significantly negatively associated with serum cholesterol and LDL cholesterol levels only after controlling for confounding variables. There were no significant associations between hormone variables and Lp(a) values. This study suggests that variation in sex hormone production accounts for some of the variation in serum lipid levels.

Thyrotropin stimulation of the lutropin/choriogonadotropin receptor: different sites mediate agonist activity and high affinity binding.

Surprisingly, thyrotropin (TSH) can increase cAMP and inositol phosphate (IP) levels in Cos-7 cells transfected with the lutropin (LH)/choriogonadotropin (CG) receptor (LH/CGR) as well as LH or CG, as evidenced by similar EC50 and maximal stimulation values. Additionally surprising, TSH activation is evident, despite markedly reduced levels of high affinity TSH binding by comparison to CG (Hidaka A, et al. 1993 Biochem Biophys Res Commun 196:187-195). In this report, we questioned whether the unusual TSH activity, as well as the discrepancy between TSH activity and binding, might reflect the existence of distinct agonist and binding sites on the LH/CGR extracellular domain and the ability of TSH to interact with the former despite a minimal interaction with the latter. We evaluated this possibility by using two chimeras spanning the extracellular domain of the TSHR and the LH/CGR:Mc1 + 2, where residues 8-165 of the TSHR are substituted, and Mc2 + 3 + 4, where residues 90-370 are replaced with the corresponding peptide segment from the LH/CGR. After transfection in Cos-7 cells, Mc2 + 3 + 4 exhibits higher affinity for CG than wild-type LH/CGR, but has no CG agonist response in assays measuring cAMP or inositol phosphate (IP) levels. Conversely, the Mc1 + 2 chimera exhibits significantly decreased affinity for CG, but CG agonist activity is comparable to wild-type LH/CGR in cAMP and IP assays. These data show that the extracellular domain of the LH/CGR does have distinct sites for CG binding and agonist activity: the C-terminus in Mc2 + 3 + 4 is important for high affinity CG binding, whereas the N-terminus in Mc1 + 2 is able to exhibit a CG agonist response, despite low affinity binding. When evaluated using TSH, Mc1 + 2, with the C-terminus of the TSHR present, exhibits high affinity TSH binding comparable to wild-type TSHR. Unexpectedly, Mc1 + 2, with the substitution of the N-terminus of the extracellular domain of the LH/CGR, exhibits even better TSH agonist activity than wild-type TSHR, not a loss of activity. Thus, the N-terminus of the extracellular domain of the LH/CGR can couple TSH binding to signal transduction events even better than the N-terminus of the TSHR. This may, in part, explain why TSH has an unusual agonist activity in cells transfected with LH/CGR, despite relatively low affinity binding. Although distinct agonist and binding sites exist in the linear sequence of the extracellular domain, the activity of the two sites is interdependent.(ABSTRACT TRUNCATED AT 400 WORDS)

Histochemical, clinical, and in vitro beta cell responses in a neonate with persistent hyperinsulinaemic hypoglycaemia of infancy.

When treatment with diazoxide and somatostatin for persistent hyperinsulinaemic hypoglycaemia of infancy failed, subtotal pancreatectomy was performed on a neonate on day 41. The pancreatic tissue was saved and used for immunohistochemical and cell culture studies. The initial immunohistochemistry of beta cells for insulin was negative, using a 1 in 200 dilution of insulin antiserum, but positive results were obtained with an increased concentration of the antiserum. The insulin to somatostatin cell ratio in islets of Langerhans was about 1:1, with no somatostatin cells outside the islets. Glucose stimulated insulin secretion in a concentration dependent manner in vitro. Isobutyl methyl xanthine doubled insulin secretion, but lithium had no effect. The glucose stimulated insulin secretion was inhibited by somatostatin, epinephrine, and in the absence of Ca2+. In view of the normal in vitro responses of beta cells to various secretory analogues, the lack of responsiveness to somatostatin analogue before pancreatectomy may not have been due to deficiency or resistance to somatostatin, but to beta cell hyperplasia overwhelming the paracrine regulatory mechanism(s).

Prednisolone levels in plasma and leukemia cells during therapy of chronic lymphocytic leukemia.

The capacity of chronic lymphocytic leukemia cells to concentrate prednisolone has been evaluated in vivo and in vitro employing a radioimmunoassay for prednisolone. No evidence to suggest that leukemia cells are capable of selectively concentrating glucocorticoid was found. The relative uptake of glucocorticoid by leukemia cells was found to be greater in vitro than in vivo. This may be attributable to differences in steroid bioavailability to cells. Substantially lower levels than previously reported of free prednisolone were found in plasma of patients receiving oral treatment with prednisolone. This may result from the failure in previous studies to remove derivatives of prednisolone and other steroids prior to assay for hormones.

The contribution of steroids to digoxin-like immunoreactivity in cord blood.

Samples of cord serum from 29 healthy neonates were analysed for digoxin-like immunoreactive substance (DLIS), cortisol, 17 beta-oestradiol, progesterone, dehydroepiandrosterone-sulphate (DHEAS), 17 alpha-hydroxyprogesterone (17OHP), androstenedione, oestriol and ouabain-like activity (OLA; by inhibition of Na+, K+ATPase activity). The mean serum concentration of DLIS was 0.91 (SD = 0.19) nmol/L and the mean OLA was 26.1 (SD = 11.5) nmol/L. There was no correlation between DLIS and OLA. DLIS correlated significantly with oestriol (r = 0.521), progesterone (r = 0.534) and 17OHP (r = 0.43). Stepwise multiple regression analysis showed that 17 beta-oestradiol, progesterone and androstenedione contributed to DLIS and the intercept was 0.64 (SD = 0.127). The concentrations of steroids (17 beta-oestradiol, progesterone, androstenedione) required to displace digoxin by 50% in the digoxin immunoassay and inhibit Na+,K+ATPase in the OLA assay were 10(3)-10(4)-fold higher than those found in cord serum. We conclude that the contribution of these steroids to DLIS is small and that DLIS and OLA measure different compounds.

Reference intervals for thyroid hormones in pregnant Chinese women.

OBJECTIVE: To establish gestation-related reference intervals for thyroid hormones in a Chinese population. MATERIALS AND METHODS: A prospective study with 343 healthy pregnant women (5-41 weeks) and 63 non-pregnant controls. Thyroid stimulating hormone (TSH), free thyroxine (T4) and tri-iodothyronine (T3) (and human chorionic gonadotrophin) were measured by immunoassays. The median, 2.5th and 97.5th percentiles at 4-week intervals were calculated. Data were also analysed for significant trends using ANOVA. RESULTS: Free T3 decreased during pregnancy, whereas free T4 initially increased, peaking between 9-13 weeks and then decreased, the decline becoming significant by week 21. TSH mirrored changes in free T4. CONCLUSION: The gestation-related reference intervals for thyroid hormones should alleviate the misinterpretation of thyroid function in pregnancy.

Salivary oestradiol and progesterone after in vitro fertilization and embryo transfer using different luteal support regimens.

Salivary oestradiol (E2) and progesterone (P) levels have been shown to reflect the biologically active fractions in the serum. The luteal-phase status of stimulated cycles was investigated after in vitro fertilization and embryo transfer (IVF-ET). Thirty patients were randomly allocated to one of three luteal therapy groups: group A had no support, group B had intramuscular P and group C had intramuscular P and human chorionic gonadotrophin (hCG). One pregnancy was achieved in group A, two in group B and three in group C. Significant correlations between salivary and serum levels of E2 and of P in matched samples during luteal phase were found. Salivary E2 levels from luteal day 8 through day 14 and P levels from day 3 through day 14 were significantly higher in the pregnant than in the nonpregnant cycles. Among the nonpregnant cycles, salivary E2 and P levels were significantly higher in group C than in group A or B. These findings suggest that, in stimulated cycles for IVF-ET, determination of salivary E2 and P levels may be used as reliable alternatives to serum concentrations for assessing the luteal phase. Also, the additional hCG has an enhanced luteotrophic effect, as reflected by the higher salivary E2 and P levels, which may lead to a better pregnancy rate.

Transient neonatal hyperthyrotropinaemia.

Of 48 consecutive newborns with elevated umbilical venous plasma thyrotropin (TSH) concentration, only two (4%) were subsequently proved to have congenital hypothyroidism, while the other 46 had transient elevation of TSH. Compared with matched controls, these 46 newborns were all delivered vaginally (P less than 0.0003) and had a longer second stage of labour (P less than 0.002), together with higher incidences of nuchal encirclement of the cord (P less than 0.05) as well as female babies (P less than 0.05). There was no difference in the incidence of antenatal complications, mean gestational age, birth weight, or birth asphyxia. There were no small-for-gestational age infants in the study group, while four were found in the controls. The results indicate that elevated umbilical cord plasma TSH concentration may represent a response to the stress of difficult or complicated delivery in the healthy appropriate- or large-for-gestational age newborn who does not have congenital hypothyroidism.

The effect of labour on prolactin and cortisol concentrations in the mother and the fetus.

Concentrations of prolactin and cortisol were determined in maternal and umbilical cord serum of women delivered by elective Caesarean section and by vaginal delivery. There was no difference in the concentration of prolactin in the two groups of women. Similarly, cord blood prolactin concentrations were not significantly different in the two groups. Cortisol concentrations in the women undergoing Caesarean section were similar to the vaginal delivery group before the onset of labour. However, there was a significant increase in cortisol concentration at delivery following labour. The cord blood cortisol concentration was significantly higher in the neonates delivered vaginally, and it correlated with the maternal cortisol concentration at delivery. The relevance of these findings is discussed.

Salivary estradiol and progesterone during the normal ovulatory menstrual cycle in Chinese women.

Salivary and serum levels of estradiol and progesterone were measured by radioimmunoassay in 10 Chinese women during their normal menstrual cycles. Changes in salivary estradiol and progesterone levels followed a similar pattern to that in the serum. Significant correlation was found between salivary and serum levels of estradiol and progesterone (p less than 0.001). Measurements of these salivary steroids may be used to assess follicular dynamics. Moreover, salivary sampling is simple, convenient and stress free.