Investigation of hypothalamo-pituitary-gonadal axis and glucose intolerance among the firstdegree female relatives of women with polycystic ovary syndrome

7th European Congress of Endocrinology -- SEP 03-07, 2005 -- Gothenburg, SWEDENWOS: 000247150100021PubMed: 17336975Objective: To assess the glucose intolerance and the hypothalamo-pituitary-gonadal (HPG) axis in the first-degree relatives (FDRs) of patients with polycystic ovary syndrome (PCOS). Design: Clinical study of the female FDRs of patients with PCOS. Setting: Outpatients at endocrinology department of a university hospital. Patient(s): Seventy FDRs of PCOS patients and 20 healthy women were evaluated. Intervention(S): Basal hormonal investigations, buserelin test, and 75-g oral glucose tolerance test (OGTT) were performed. Main Outcome Measure(s): Basal hormone levels were measured. Additionally, insulinogenic index, glucose and insulin responses to OGTT, and FSH, LH, E-2, and 17-OHP responses to buserelin test were obtained. Result(S): Four (5.7%) of the FDRs showed impaired glucose tolerance, and the FDRs had significantly higher fasting plasma glucose (P <.05) and basal insulin (P <.01) than control subjects. Peak and area-under-the-curve (AUC) insulin (P <.001) and AUC glucose (P <.05) responses to OGTT were also significantly higher in the FDRs than in control subjects. The FDRs showed higher insulinogenic index than the control subjects (P < 001). The FDRs had significantly (P < 05) higher LH and DHEAS levels and lower (P <.005) 17-OHP levels than the control subjects. Peak (P < 05) and AUC (P <.01) LH responses to buserelin testing were lower in the FDRs than in the control subjects while peak (P <.05) and AUC (P <.01) E, responses to buserelin were higher in the FDRs than in the control subjects. Conclusion(s): These data support the hypothesis that FDRs of PCOS patients may have insulin resistance and the HPG axis is more susceptible than in control subjects. The FDRs also have an increased prevalence of hyperandrogenism and high DHEAS levels compared with the background population

Primary hyperaldosteronism presenting with rhabdomyolysis in emergency room – Case report

Primary hyperaldosteronism, is a well-known cause of secondary hypertension, mostly idiopathic hypertension or arising from aldosterone-producing adenomas. It is characterized with resistant hypertension, hypokalemia and metabolic alkalosis related with aldosterone production excess and plasma renin activity suppression. Hypokalemic rhabdomyolysis usually presents with muscle pain, cramps, fatigability and generalized weakness. Rhabdomyolysis due to hypokalemia is a rare complication of primary hyperaldosteronism reported within a limited number of cases in medical literature. Diagnosis and treatment of primary hyperaldosteronism is fundamentally important because of the probability of certain cure with accurate surgery. Here, we report a 38-year-old female with hypertension related with primary hyperaldosteronism who presented with rhabdomyolysis most likely due to profound hypokalemia

Complete aromatase deficiency in four adult men: detection of a novel mutation and two known mutations in the CYP19A1 gene

The abstract deals with the clinical and genetic description of 4 new cases of aromatase deficiency

The role of apoptosis and autophagy in the hypothalamic-pituitary-adrenal (HPA) axis after traumatic brain injury (TBI)

Traumatic brain injury (TBI) is a major health problem affecting millions of people worldwide and leading to death or permanent damage. TBI affects the hypothalamic–pituitary–adrenal (HPA) axis either by primary injury to the hypothalamic–hypophyseal region or by secondary vascular damage, brain, and/or pituitary edema, vasospasm, and inflammation. Neuroendocrine dysfunctions after TBI have been clinically described in all hypothalamic–pituitary axes. We established a mild TBI (mTBI) in rats by using the controlled cortical impact (CCI) model. The hypothalamus, pituitary, and adrenals were collected in the acute (24 h) and chronic (30 days) groups after TBI, and we investigated transcripts and protein-related autophagy (Lc3, Bcln1, P150, Ulk, and Atg5) and apoptosis (pro-caspase-3, cleaved caspase-3). Transcripts related to autophagy were reduced in the hypothalamus, pituitary, and adrenals after TBI, however, this was not reflected in autophagy-related protein levels. In contrast, protein markers related to apoptosis increased in the adrenals during the acute phase and in the pituitary during the chronic phase. TBI stresses induce a variation of autophagy-related transcripts without modifying the levels of their proteins in the HPA axis. In contrast, protein markers related to apoptosis are increased in the acute phase in the adrenals, which could lead to impaired communication via the hypothalamus, pituitary, and adrenals. This may then explain the permanent pituitary damage with increased apoptosis and inflammation in the chronic phase. These results contribute to the elucidation of the mechanisms underlying endocrine dysfunctions such as pituitary and adrenal insufficiency that occur after TBI. Although the adrenals are not directly affected by TBI, we suggest that the role of the adrenals along with the hypothalamus and pituitary should not be ignored in the acute phase after TBI

Alterations in Serum miR-126-3p levels over time: a marker of pituitary insufficiency following head trauma

Introduction: Traumatic brain injuries (TBIs) pose a high risk of pituitary insufficiency development in patients. We have previously reported alterations in miR-126-3p levels in sera from patients with TBI-induced pituitary deficiency. Methods: To investigate why TBI-induced pituitary deficiency develops only in some patients and to reveal the relationship between miR-126-3p with hormone axes, we used mice that were epigenetically modified with miR-126-3p at the embryonic stage. These modified mice were subjected to mild TBI (mTBI) according to the Marmarou’s weight-drop model at 2 months of age. The levels of miR-126-3p were assessed at 1 and 30 days in serum after mTBI. Changes in miR-126-3p levels after mTBI of wild-type and miR-126-3p* modified mouse lines validated our human results. Additionally, hypothalamus, pituitary, and adrenal tissues were analyzed for transcripts and associated serum hormone levels. Results: We report that miR-126-3p directly affects hypothalamus-pituitary-adrenal (HPA) axis upregulation and ACTH secretion in the acute phase after mTBI. We also demonstrated that miR-126-3p suppresses Gnrh transcripts in the hypothalamus and pituitary, but this is not reflected in serum FSH/LH levels. The increase in ACTH levels in the acute phase may indicate that upregulation of miR-126-3p at the embryonic stage has a protective effect on the HPA axis after TBI. Notably, the most prominent transcriptional response is found in the adrenals, highlighting their role in the pathophysiology of TBI. Conclusion: Our study revealed the role of miR-126-3p in TBI and pituitary deficiency developing after TBI, and the obtained data will significantly contribute to elucidating the mechanism of pituitary deficiency development after TBI and development of new diagnostic and treatment strategies