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Physiologic Changes
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Other hormonal alterations include an increase in aldosterone, cortisol, parathyroid hormone, parathyroid-related hormone, and renin [2]. Deoxycorticosterone increases. Androstenedione increases with an increase in the transformation to estrone and estradiol [1]. Fasting levels of both insulin and glucagon increase [1]. There is an increase in melanocyte-stimulating hormone to which can be attributed the pregnancy-related increases in pigmentation seen in the areola and the linea nigra and in chloasma [1].
Normal physiology of pregnancy
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Rawan El-Amin, Loren Custer, Jennifer Silk
Increases in cortisol levels are caused by increased corticosteroid-releasing hormone (CRH). Outside of pregnancy, CRH is only produced by the hypothalamus. In pregnancy, it is also produced by the placenta and fetal membranes. Increased CRH signals the anterior pituitary to increase adrenocorticotropic hormone (ACTH), which in turn stimulates cortisol production from the adrenal glands. Increases in other adrenal hormones including aldosterone and deoxycorticosterone also occur.1
Resetting of the Arterial Baroreflex: Peripheral and Central Mechanisms
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Mark W. Chapleau, George Hajduczok, Francois M. Abboud
In deoxycorticosterone acetate (DOCA)-salt hypertension, baroreflex responses are also impaired before the development of hypertension. Reflex decreases in splanchnic sympathetic nerve activity, heart rate, and arterial pressure in response to graded electrical stimulation of aortic baroreceptor afferents are all impaired in DOCA-salt rats both prior to and after the development of hypertension (Nakamura et al., 1988).
Moyamoya syndrome in a male pseudohermaphrodite patient with congenital adrenal hyperplasia – a rare association. Case report and review of literature
Published in British Journal of Neurosurgery, 2023
Remesh Chirayil Vasudevan, Reshma Vachali Madayi, Rohit Ravindranath Nambiar
CAH is a rare disorder that results from defective biosynthesis of steroid hormones in the adrenal cortex. CAH with 17 alpha-hydroxylase and 11 beta-hydroxylase deficiencies is associated with hypertension. Pathogenesis of CAH is due to various genetic mutations in the enzymes involved in steroid synthesis. As a result, cortisol production is reduced and the negative feedback control on adrenocorticotropic hormone (ACTH) is lost. Elevated ACTH level results in overproduction and accumulation of steroids precursors prior to the enzyme defect.6 There is hyperplasia of adrenal cortex. The clinical features depend on the level of enzyme defect. Patients with ambiguous genitalia, hypogonadism, hypertension and associated hypokalemia should be evaluated for possible CAH. In CAH due to 17 alpha-hydroxylase deficiency, both adrenal and gonadal steroid hormones production will be impaired. In male patients, lack of testosterone will impair Wolffian duct development. They will have gonads but no internal genitalia.7 High 11 deoxycorticosterone levels will cause sodium retention, potassium loss and hypertension due to potent mineralocorticoid action.
Kidney microbiota dysbiosis contributes to the development of hypertension
Published in Gut Microbes, 2022
Xin-Yu Liu, Jing Li, Yamei Zhang, Luyun Fan, Yanli Xia, Yongyang Wu, Junru Chen, Xinyu Zhao, Qiannan Gao, Bing Xu, Chunlai Nie, Zhengyu Li, Aiping Tong, Wenjie Wang, Jun Cai
Our study has several limitations. First, we only examined samples from SHRs with essential hypertension and found IgA-coated bacteria or L-forms, which were confirmed in biopsy samples from patients with essential hypertension. In a rat model of secondary hypertension, deoxycorticosterone acetate (DOCA)-salt hypertensive rats and Dahl salt-sensitive (SS) rats (SSR) remain to be determined. SSR is a typical model of secondary hypertension caused by the interaction between a high-salt diet (environmental factor) and genetic factors. A high-salt diet inevitably leads to high osmolarity in the gastrointestinal tract, which is conducive to the translocation and colonization of L-forms. Similarly, essential hypertension is also characterized by a genetic component that interacts with environmental risk factors including diet. Possibly, genetic predisposition alone may not play as great a role as is currently believed. The kidney microbiome, could be a factor independent of host heredity, and is transmitted from parents. Second, the data based on live bacteria detected in the kidney from 4-week-old SHRs with normal BP and TBWF intervention reconstructing hypertensive renal flora to lower blood pressure suggest that kidney microbiota dysbiosis is the cause rather than the result of hypertension. However, we could not confirm the bacterial species that promote the occurrence and development of hypertension.
An up-to-date evaluation of abiraterone for the treatment of prostate cancer
Published in Expert Opinion on Pharmacotherapy, 2021
Jason Shpilsky, Julia Stevens, Glenn Bubley
Mineralocorticoid excess syndrome (MES) is a key on–target effect of abiraterone (Figure 1). By inhibiting CYP17A1, abiraterone reduces production of downstream DHEA and testosterone. However, inhibition of CYP17A1 also reduces production of cortisol, which decreases negative feedback to the pituitary, increasing levels of ACTH [16]. This causes an increase in the mineralocorticoid deoxycorticosterone, leading to hypokalemia, hypertension, and fluid retention. Coadministration of glucocorticoids suppresses ACTH and prevents MES. Abiraterone is approved with concomitant prednisone 5 mg twice daily (mCRPC) or prednisone 5 mg daily (mCSPC) [18]. One randomized phase II trial found that prednisone 5 mg twice daily had higher rates of freedom from MES compared to prednisone 5 mg daily (71% vs 37%), without significant impacts on insulin resistance or bone mineral density [32]. A corticosteroid regimen should be selected and adjusted based on a patient’s comorbidities and presence of MES.