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Fetal programming
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Katherine E. Pelch, Jana L. Allison, Susan C. Nagel
To date, 17-hydroxyprogesterone is the formulation of greatest efficacy in preventing preterm deliveries in women with a previous spontaneous preterm birth. In a retrospective cohort study by Waters et al., women receiving weekly injections of 17-hydroxyprogesterone caproate were 3.3 times more likely to develop gestational diabetes, controlling for maternal age, BMI, and maternal race (46). Progesterone may increase insulin resistance by affecting glucose transport at the glucose transporter type 4 (GLUT-4) receptor (46). Gestational diabetes can lead to insulin resistance in utero and permanently modify expression of genes responsible for glucose transport and beta cell development, predisposing fetuses to type II diabetes mellitus in adulthood (47). As use of progesterone to prevent preterm birth continues to gain momentum, the postnatal effects will continue to be elucidated as exposed fetuses reach adolescence and adulthood.
Practice exam 3: Answers
Published in Euan Kevelighan, Jeremy Gasson, Makiya Ashraf, Get Through MRCOG Part 2: Short Answer Questions, 2020
Euan Kevelighan, Jeremy Gasson, Makiya Ashraf
Persistent progestogenic side effects may be alleviated by changing the type of progestogen (e.g. from a 19-nortestosterone to a 17-hydroxyprogesterone compound) or reducing the dose, but it is important to give sufficient progestogen to protect the endometrium. Reducing the duration of progestogen from 14 to 10 days or utilizing long-cycle HRT where the patient ingests progestogen on only 14 days every three months may help. Changing the route of administration (e.g. to intrauterine or transdermal patches) may reduce unwanted symptoms (4).
Endocrinology and gonads
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
Plasma 17-hydroxy progesterone levels are high in congenital adrenal hyperplasia. The plasma Cortisol levels are normal or low. CAH should be considered in the differential diagnosis of ambiguous genitalia in the newborn and may present with low serum sodium (due to salt loss in the urine) and hyperkalemia. Infertility is a complication of poor control during puberty.
Determination of estrone sulfate, testosterone, androstenedione, DHEAS, cortisol, cortisone, and 17α-hydroxyprogesterone by LC-MS/MS in children and adolescents
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2020
Carina Ankarberg-Lindgren, Mats X. Andersson, Jovanna Dahlgren
17α-hydroxyprogesterone (17OHP) is predominantly synthesized in the adrenal glands but also in the gonads, and it is a metabolic precursor of cortisol. Elevated levels of 17OHP co-occurring with elevated concentrations of androstenedione (A4) and testosterone (T) is indicative of congenital adrenal hyperplasia (CAH) in the newborn or non-classical CAH in children and adolescents [10]. In many countries, determination of 17OHP is routinely used as neonatal screening and monitoring of optimal hydrocortisone treatment in CAH [11]. However, with MS/MS technology, quantitation of 17OHP together with A4 and T is also useful in the investigation of suspected hyperandrogenism and its origin [12–14]. Although the underlying mechanism of hyperandrogenism in females with polycystic ovarian syndrome (PCOS) is not fully understood yet, a recent study on obese adolescent girls showed that A4 and T are key steroid hormones to distinguish between PCOS and non- PCOS [15]. Reference intervals during pubertal development are needed for further research studies, assessing differential diagnosis and monitoring of replacement therapy.
Abiraterone acetate in combination with prednisone in the treatment of prostate cancer: safety and efficacy
Published in Expert Review of Anticancer Therapy, 2020
Cécile Manceau, Loic Mourey, Damien Pouessel, Guillaume Ploussard
CYP17A1 is an enzyme expressed in steroidogenic tissue like testes and adrenal cortex. It’s also expressed in prostatic tumor tissue. This enzyme is involved in the conversion of cholesterol to the androgen precursor and steroid hormone synthesis. The generation of glucocorticoid such as cortisol requires 17 α-hydroxylase as it converts pregnenolone and progesterone to 17-hydroxypregnenolone and 17-hydroxyprogesterone. So, 17 α-hydroxylase deficiency impairs glucocorticoids production, pregnenolone, and progesterone increase. The decrease in cortisol levels includes a compensatory increase in adrenocorticotropic hormone (ACTH) and the increase in pregnenolone and progesterone is treated to form mineralocorticoids [6]. Prednisone is associated to compensate cortisol reduction due to 17 α-hydroxylase inhibition, therefore, decreasing the mineralocorticoid excess [6] (Figure 1).
Virilising ovarian tumour in a postmenopausal woman after bilateral oophorectomy
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2020
Ankia Coetzee, Jocelynn Ann Hellig, Candice Sher-Lockitz, Annelize Barnard, Viju Thomas, Magda Conradie
Baseline biochemical results are tabulated in Table 1. Biochemical testing documented elevated serum luteinising hormone (LH) and follicle stimulating hormone (FSH) levels along with low circulating oestradiol in keeping with the patient’s postmenopausal state. The serum total testosterone was markedly high at 10.8 nmol/l (normal female range: 0.5–2.6 nmol/l). The weaker androgens, dehydroepiandrosterone sulphate (DHEAS) and androstenedione, respectively predominantly from adrenal and ovarian origin, were both within the normal laboratory reference ranges. A random, unstimulated 17α- hydroxyprogesterone (17OHP) level was slightly elevated at 4.3 nmol/l (female reference range 0.6–2.2). Pathological cortisol excess was excluded based on an 8:00 am serum cortisol level that suppressed following administration of low dose (1 mg) exogenous dexamethasone to less than 50 nmol/l (32 nmol/l).