No abstract available.

No abstract available.

No abstract available.
Diagnosis* ; Female ; Oligomenorrhea ; Polycystic Ovary Syndrome*

BACKGROUND: Diabetic patients develop hypoaldosteronism which frequently caused hyperkalemia and metabolic acidosis and diabetic hypoaldosteronism is associated with selective unresponsiveness of aldosterone to angiotensin A-II, but mechanism of defect in A-II stimulated aldosterone response still remain unclear. METHODS: To elucidate the mechanism of defect in A-II stimulated aldosterone response, author evaluated the responses of aldosterone production to A-II, K+, and ACTH in adrenal glomerulosa cells prepared from streptozotocin induced diabetic rats, Inositol triphosphate (IP3) generated by activation of phospholipase C (PLC) and arachidonic acid and lysophospholipids generated by activation of phospholipase A2 (PLA2) were measured in A-II stimulated glomerulosa cells. Radiocalcium efflux and aldosterone response to second messenger of A-II such as PLC, IP3, PLA, AA and protein kinase C activator, 12-o-tetradecanoylphorbol 13 acetate (TPA). RESULTS: 1. Plasma renin activity and aldosterone levels were not different among control rats, untreated and insulin treated diabetic rats. 2. Basal, ACTH and K+ -stimulated aldosterone production were similar in cells from the three groups (p<0.05), but A-II stimulated aldosterone production was significantly decreased in cells from untreated diabetic rats compared with control and insulin treated diabetic rats (p0.05). 4. Aldosterone responses to PLC, IP3, AA and TPA were significantly decreased in glomerulosa cells from diabetic rats compared with control and insulin treated diabetic rats (p<0.05), but aldosterone response to PLA2 was similar among the three groups (p>0.05). 45Ca efflux to PLC, IP3 PLA2 and AA were similar among the three groups (p>0.05). CONCLUSION: These results suggested that decreased A-II-stimulated aldosterone response was present in glomerulosa cells from streptozotocin induced diabetic rats and reversed by insulin treatments. The main defect of altered A-II response of zona glomerulosa might be located in the step after activation of phospholipase and increase of intracellular calcium, and activation of PKC, or distal to that could be one of the causative mechanism.
Acidosis ; Adrenocorticotropic Hormone ; Aldosterone* ; Angiotensin II ; Angiotensins* ; Animals ; Arachidonic Acid ; Calcium* ; Diabetes Mellitus ; Humans ; Hyperkalemia ; Hypoaldosteronism ; Inositol ; Insulin ; Lysophospholipids ; Phospholipases A2 ; Phospholipases* ; Plasma ; Protein Kinase C ; Rats* ; Renin ; Second Messenger Systems ; Streptozocin ; Type C Phospholipases ; Zona Glomerulosa*

OBJECTIVES: Subacute thyroiditis is a nonsuppurative inflammation of thyroid gland and is probably caused by a cytopathic virus. Typical clinical symptoms and features of subacute thyroiditis vary widely during the course of illness. It has a clinical course, evolving from hyperthyroidism through a temporary hypothyroidism to recovery. However, the final outcome of this disease remains unpredictive in some patients. Permanet hypothyroidism occurs infrequently. METHODS: Thirty-three patients proven to have subacute thyroiditis at the Ewha Womans University Hospital from September 1993 to November 1995 were studied. We analyzed their clinical features, laboratory findings, and duration of recovery to cha- racterize the course of the disease. RESULTS: 1) Total 33 patients were studied: 31 patients were female and 2 patients were male. Their mean age was 42.6+/-8.3 years old. The peak months were August through October in this study. 2) Initial mean ESR was 73.0+/-35.2mm/hr, mean T3 was 217.3+/-73.9ng/dl, mean T4 was 15.2+/-8.5microgram/ dl, and TSH was 0.06+/-0.09microIU/ml. The positive rates of antithyroglobulin and anitmicrosomal antibodies were 31% and 6% respectively, and TSH receptor antibody was elevated in one patient. 3) In the thyroid scan, 91% showed both lobes nonvisualisation, and 9% showed one lobe nonvisualization. Radioactive iodine uptake(RAIU) at 24 hour was 2.4+/-3.3%. 4) With the predisolone therapy, 90% of patients completely recovered, 57% of these patients had no hypothyroid phase and remaining 33% of them had hypothyroid phase during course of the disease. Three of the patients had permanent hypothyroidim. 5) The average duration of recovery was 3.2+/-1.4 months and it has no correlation with initial thyroid hormone levels, antithyroid antibodies and duration of steroid administration. CONCLUSION: There was no historical, physical, laboratory findings that help us predict those patients likely to have an exacerbation of the disease.
Antibodies ; Female ; Humans ; Hyperthyroidism ; Hypothyroidism ; Inflammation ; Iodine ; Male ; Prednisolone ; Receptors, Thyrotropin ; Thyroid Gland ; Thyroiditis, Subacute

Background: Postpartum thyroiditis is a painless, destructive lymphocytic inflammation of the thyroid gland that occurs during the postpartum period and is associated with a high prevalence of serum thyroid autoantibodies. Clinical symptoms and laboratory fi#ndings of postpartum thyroiditis vary widely during the course of illness and the final outcome of this disease remains unpredictive in some patients. The purpose of this study is to investigate the clinical course and the predictors of the outcome of the disease. Methods: Thirty-eight patients proven to have postpartum thyroiditis at the Ewha Womans University Hospital were studied. We analyzed their clinical features, laboratory findings and duration of recovery to characterize the course of the disease. Results: Their mean age was 29.0±3.3 years and the time of diagnosis was 4.9±1.9 months after delivery. The prevailed months of delivery were November through January in this study. Twenty six patients were hypothyroid and 12 were thyrotoxic at initial thyroid function. The positive rates of antithyroglobulin and anitmicrosomal antibodies were 92%, 67% in the hypothyroid group and 75%, 67% in th thyrotoxic group respectively. TSH receptor antibodies were negative in all patients. In the hypothyroid group the titers of antimicrosomal antibodies were significantly higer than the thyrotoxic group. The titers of antimicrosomal antibodies were positively correlated with serum TSH and negatively correlated with serum T4. In all patients, the titers in thyroid function tests returned to the normal range without long-term hypothyroidism. Conclusion: The titers of antimicrosomal antibodies were significantly higher in the hypothyroid group than the thyrotoxic group. Thus the titers of antimicrosomal antibodies can help guide the physician in the care of patients with postpartum thyroiditis who will probably be hypothyroid. In this study, we were surprised that all patients became euthyroid without permanent hypothyroidism.
Antibodies ; Autoantibodies ; Clinical Study ; Diagnosis ; Female ; Humans ; Hypothyroidism ; Inflammation ; Postpartum Period ; Postpartum Thyroiditis ; Prevalence ; Receptors, Thyrotropin ; Reference Values ; Thyroid Function Tests ; Thyroid Gland ; Thyroiditis

Polycystic ovary syndrome (PCOS) is the commonest endocrine disorder in women of reproductive age and now recognized as an important metabolic and reproductive disorder. The majority of women with PCOS have insulin resistance and this is regarded to have a central etiological role in PCOS. Insulin resistance and concomitant hyperinsulinemia modifies reproductive function by driving androgen production, suppression of sex hormone-binding globulin (SHBG) and disruption of insulin signaling pathways in the central nervous system. Insulin resistance, together with defects in insulin secretion, confers markedly increased risk for type 2 diabetes mellitus and metabolic syndrome. There are post-binding defects in insulin receptor signaling, with selective resistance to insulin's metabolic actions and preserved other actions. Genetic and environmental abnormalities interact to produce peripheral insulin resistance in PCOS. The numerous in vivo and in vitro data supporting the central role of insulin resistance in the pathogenesis of PCOS have led a new therapy for PCOS with insulin-sensitizing agents.
Central Nervous System ; Diabetes Mellitus, Type 2 ; Female ; Humans ; Hyperinsulinism ; Insulin ; Insulin Resistance ; Polycystic Ovary Syndrome ; Receptor, Insulin ; Sex Hormone-Binding Globulin

Hyperandrogenism refers to classical androgen-dependent signs such as hirsutism, acne and androgenetic alopecia. Disorders that result in androgen excess include specific identifiable disorders (i.e. disorders of inclusion), but the great majority of women presenting with hirsutism and other symptoms or signs of hyperandrogenism suffer from polycystic ovary syndrome (PCOS). Hirsutism is the main hyperandrogenic symptom, defined as an excess of body hair in androgen-sensitive regions of skin in women. In this review, I attempt to focus on the pathogenesis of hirsutism, as well as clinical and biochemical features that are important in choosing therapeutic options. PCOS is the most common disorder of premenopausal women, affecting 4 to 8% of this population, and therefore, diagnostic issues of PCOS in Korean women will be addressed, specifically the reproductive and metabolic derangements and criteria for hyperandrogenism based on hirsutism and serum androgen concentrations.
Acne Vulgaris ; Alopecia ; Female ; Hair ; Hirsutism ; Humans ; Hyperandrogenism ; Polycystic Ovary Syndrome ; Skin

There is an evidence to suggest that testosterone is an important regulator of insulin sensitivity in men via effects on body fat distribution and insulin action in muscle. Observational studies have shown that metabolic syndrome is strongly associated with low testosterone levels in men and hypogonadism is likely a fundamental component of metabolic syndrome. Low testosterone could be not only an early marker of metabolic syndrome but also involved in the pathogenesis of disease processes from the prospective studies. Although obesity, insulin resistance and hypogonadism are certainly thought to be linked, the exact causal relationships among them remain unclear. Large population based prospective observational and intervention studies are needed to elucidate the exact causal relationship among testosterone and the components of metabolic syndrome.
Body Fat Distribution ; Humans ; Hypogonadism ; Insulin ; Insulin Resistance ; Clinical Trial ; Male ; Obesity ; Testosterone*

No abstract available.
Aging* ; Gonadal Hormones* ; Gonads*