Sickle cell Disease<\/strong><\/p>\n Gender Diversity<\/strong><\/p>\n Success Rates for Fertility Preservation<\/strong><\/p>\n Patient Preferences and Parental Regret<\/strong><\/p>\n On the Horizon: The Future of Fertility Preservation<\/strong><\/p>\n American College of Obstetrics and Gynecology<\/strong> American Academy of Pediatrics<\/strong> Children\u2019s Oncology Group<\/strong> American Urological Association<\/p>\n Orphanet J Rare Dis.<\/a>\u00a02015 Oct 21;10:136. doi: 10.1186\/s13023-015-0332-8.<\/p>\n Immunosuppressive drugs and\u00a0fertility.<\/strong><\/p>\n Leroy C<\/a>1,2<\/sup>,\u00a0Rigot JM<\/a>3<\/sup>,\u00a0Leroy M<\/a>4<\/sup>,\u00a0Decanter C<\/a>5<\/sup>,\u00a0Le Mapihan K<\/a>6<\/sup>,\u00a0Parent AS<\/a>7<\/sup>,\u00a0Le Guillou AC<\/a>8<\/sup>,\u00a0Yakoub-Agha I<\/a>9<\/sup>,\u00a0Dharancy S<\/a>10<\/sup>,\u00a0Noel C<\/a>11<\/sup>,\u00a0Vantyghem MC<\/a>12,13<\/sup>.<\/p>\n Author information<\/strong><\/a><\/p>\n Abstract<\/strong><\/p>\n Immunosuppressive drugs are used in the treatment of inflammatory and autoimmune diseases, as well as in transplantation. Frequently prescribed in young people, these treatments may have deleterious effects on\u00a0fertility, pregnancy outcomes and the unborn child. This review aims to summarize the main gonadal side effects of immunosuppressants, to detail the effects on\u00a0fertility\u00a0and pregnancy of each class of drug, and to provide recommendations on the management of patients who are seen prior to starting or who are already receiving immunosuppressive treatment, allowing them in due course to bear children. The recommendations for use are established with a rather low level of proof, which needs to be taken into account in the patient management. Methotrexate, mycophenolate, and le- and teri-flunomide, cyclophosphamide, mitoxanthrone are contraindicated if pregnancy is desired due to their teratogenic effects, as well as gonadotoxic effects in the case of cyclophosphamide. Anti-TNF-alpha and mTOR-inhibitors are to be used cautiously if pregnancy is desired, since experience using these drugs is still relatively scarce. Azathioprine, glucocorticoids, mesalazine, anticalcineurins such as cyclosporine and tacrolimus, \u00df-interferon, glatiramer-acetate and chloroquine can be used during pregnancy, bearing in mind however that side effects may still occur. Experience is limited concerning natalizumab, fingolimod, dimethyl-fumarate and induction treatments.<\/p>\n CONCLUSION:\u00a0<\/strong><\/p>\n At the time of prescription, patients must be informed of the possible consequences of immunosuppressants on\u00a0fertilityand of the need for contraception. Pregnancy must be planned and the treatment modified if necessary in a pre-conception time period adapted to the half-life of the drug, imperatively in relation with the prescriber of the immunosuppressive drugs.<\/p>\n PMID:26490561<\/p>\n Blood Purif.<\/a>\u00a02018;45(1-3):194-200. doi: 10.1159\/000485157. Epub 2018 Jan 26.<\/p>\n Pregnancy and End-Stage Renal Disease.<\/strong><\/p>\n Tangren J<\/a>1<\/sup>,\u00a0Nadel M<\/a>1<\/sup>,\u00a0Hladunewich MA<\/a>2<\/sup>.<\/p>\n Author information<\/strong><\/a><\/p>\n Abstract<\/strong><\/p>\n Pregnancy is uncommon in women with end-stage renal disease (ESRD).\u00a0Fertility\u00a0rates are low in women on dialysis, and physicians still frequently counsel women with ESRD against pregnancy. Advancements in the delivery of dialysis and obstetric care have led to improved live birth rates in women on dialysis, so pregnancy for young women with ESRD is now more feasible and safer. However, these pregnancies remain high-risk for both maternal and fetal complications, necessitating experienced multidisciplinary care. In this article, we review\u00a0fertility\u00a0issues in women with ESRD, discuss pregnancy outcomes in women on dialysis, and provide an approach for management of pregnant women with ESRD.<\/p>\n KEYWORDS:\u00a0<\/strong><\/p>\n End-stage renal disease; Intensive hemodialysis; Pregnancy<\/p>\n PMID:29478065<\/p>\n Rev Endocr Metab Disord.<\/a>\u00a02017 Mar;18(1):117-130. doi: 10.1007\/s11154-016-9385-9.<\/p>\n Gonadal dysfunction in chronic kidney disease.<\/strong><\/p>\n Palmer BF<\/a>1<\/sup>,\u00a0Clegg DJ<\/a>2<\/sup>.<\/p>\n Author information<\/strong><\/a><\/p>\n Abstract<\/strong><\/p>\n Sexual dysfunction is a common finding in both men and women with chronic kidney failure. Common disturbances include erectile dysfunction in men, menstrual abnormalities in women, and decreased libido and\u00a0fertility\u00a0in both sexes. These abnormalities are primarily organic in nature and are related to uremia as well as the other comorbid conditions that frequently occur in the chronic kidney failure patient. Fatigue and psycho social factors related to the presence of a chronic disease are also contributory factors. Disturbances in the hypothalamic-pituitary-gonadal axis can be detected prior to the need for dialysis but continue to worsen once dialytic therapy is initiated. Impaired gonadal function is prominent in uremic men while the disturbances in the hypothalamic-pituitary axis are more subtle. By contrast, central disturbances are more prominent in uremic women. Therapy is initially directed towards optimizing the delivery of dialysis, correcting anemia with recombinant erythropoietin, and controlling the degree of secondary hyperparathyroidism with vitamin D. For many practicing nephrologists sildenafil has become the first line therapy in the treatment of impotence. In the hypogonadal man whose only complaint is decreased libido, testosterone may be of benefit. Regular gynecologic follow up is required in uremic women to guard against potential complications of unopposed estrogen effect. Uremic women should be advised against pregnancy while on dialysis. Successful transplantation is the most effective means of restoring normal sexual function in both men and women with chronic kidney failure.<\/p>\n KEYWORDS:\u00a0<\/strong><\/p>\n Amennorhea; Anovulation; Dialysis; Erectile dysfunction; Estrogen; Gonadotropin deficiency; Impotence; Pituitary-gonadal axis; Sildenafil; Testosterone; Transplantation erectile dysfunction; Uremia<\/p>\n PMID:27586847<\/p>\n Pediatr Nephrol.<\/a>\u00a02015 Jul;30(7):1099-106. doi: 10.1007\/s00467-014-2897-1. Epub 2014 Sep 5.<\/p>\n Fertility\u00a0preservation in patients receiving cyclophosphamide therapy for renal disease.<\/strong><\/p>\n Gajjar R<\/a>1<\/sup>,\u00a0Miller SD<\/a>,\u00a0Meyers KE<\/a>,\u00a0Ginsberg JP<\/a>.<\/p>\n Author information<\/strong><\/a><\/p>\n Abstract<\/strong><\/p>\n Cyclophosphamide continues to have an important role in the treatment of renal disease, including nephrotic syndrome and lupus nephritis, despite known complications of gonadotoxicity and potential infertility in both male and female patients. It is important that the physician recommending this therapy mitigates the effect of the drug on\u00a0fertility\u00a0by adhering to recommendations on dosing limits and offering\u00a0fertility-preserving strategies. In addition to well-established methods, such as sperm banking and embryo cryopreservation, advances in reproductive technology have yielded strategies such as oocyte cryopreservation, resulting in more\u00a0fertility-preserving options for the pediatric patient. Despite these advances, there continues to be a significant barrier to referral and access to sperm banks and\u00a0fertility\u00a0specialists. These issues are further complicated by ethical issues associated with the treatment of pediatric patients. In this review we explore the development of recommended dosing limits and include a discussion of the available\u00a0fertility-preserving methods, strategies for increasing access to\u00a0fertility\u00a0specialists, and the ethical considerations facing the pediatric healthcare provider.<\/p>\n PMID:25190492<\/p>\n J Neuroendocrinol.<\/a>\u00a02008 Dec;20(12):1368-75. doi: 10.1111\/j.1365-2826.2008.01791.x.<\/p>\n Evaluation <\/strong>of endocrine profile, hypothalamic-pituitary-testis axis and semen quality in multiple sclerosis.<\/strong><\/p>\n Safarinejad MR<\/a>1<\/sup>.<\/p>\n Author information<\/strong><\/a><\/p>\n Abstract<\/strong><\/p>\n Several endocrine and sexual disturbances have been demonstrated in multiple sclerosis (MS) patients of both sexes. The endocrine profile, hypothalamic-pituitary-testis (HPT) axis and semen quality were evaluated in male patients with MS. A total of 68 male MS patients aged 18 years or older were recruited. Forty-eight age-matched healthy male volunteers served as controls. All subjects underwent complete physical examination and routine semen analysis. Two blood samples were drawn from each participant at 15-min intervals for the determination of the resting levels of: luteinising-hormone (LH), follicle-stimulating hormone (FSH), prolactin, testosterone, oestradiol and sex hormone binding globulin. The HPT axis was assessed using gonadotrophin-releasing hormone (GnRH) and human chorionic gonadotrophin tests. The mean basal serum levels for LH, FSH and testosterone in MS patients were significantly lower than the mean for normal controls (P = 0.01). The injection of GnRH analogue did not yield a significant increase in FSH and LH levels in the MS patients compared to normal controls (P = 0.001). Total sperm count, sperm motility and percent normal sperm morphology were lower in MS patients compared to controls. MS subjects with progressive disease had higher and more severe HPT axis abnormalities than that for patients with relapsing remitting MS. Most subjects with MS have hypogonadotrophic hypogonadism state and\u00a0fertility\u00a0impairment. It appears that the damage to HPT axis is both in pituitary and testicular levels. Further studies are needed to better elucidate the underlying pathophysiology of HPT axis dysregulation.<\/p>\n PMID: 19094084<\/p>\n Transgend Health.<\/a>\u00a02016 Jan 1;1(1):41-44. doi: 10.1089\/trgh.2015.0010. eCollection 2016.<\/p>\n Preservation of\u00a0Fertility\u00a0Potential for\u00a0Gender\u00a0and Sex Diverse Individuals.<\/strong><\/p>\n Johnson EK<\/a>1,2,3<\/sup>,\u00a0Finlayson C<\/a>4,5<\/sup>.<\/p>\n Author information<\/strong><\/a><\/p>\n Abstract<\/strong><\/p>\n Gender\u00a0and sex diverse individuals-transgender individuals and those with disorders of sex development (DSD)-both face medical treatments that may impair biological\u00a0fertility\u00a0potential. Young DSD patients also often have abnormal gonadal development.\u00a0Fertilitypreservation for these populations has historically been poorly understood and rarely addressed. Future\u00a0fertility\u00a0should be discussed with\u00a0gender\u00a0and sex diverse individuals, particularly given recent advances in\u00a0fertility\u00a0preservation technologies and evolving views of\u00a0fertilitypotential. Key ethical issues include parental proxy decision-making and uncertainty regarding prepubertal\u00a0fertility\u00a0preservation technologies. Many opportunities exist for advancing\u00a0fertility-related care and research for transgender and DSD patients.<\/p>\n KEYWORDS:\u00a0<\/strong><\/p>\n disorders of sex development;\u00a0fertility\u00a0preservation;\u00a0gender dysphoria; transgender<\/p>\n PMID:29159296<\/p>\n J Clin Endocrinol Metab.<\/a>\u00a02017 Nov 1;102(11):3869-3903. doi: 10.1210\/jc.2017-01658.<\/p>\n Endocrine\u00a0Treatment of Gender-Dysphoric\/Gender-Incongruent\u00a0Persons: An\u00a0Endocrine\u00a0SocietyClinical Practice\u00a0Guideline.<\/strong><\/p>\n Hembree WC<\/a>1<\/sup>,\u00a0Cohen-Kettenis PT<\/a>2<\/sup>,\u00a0Gooren L<\/a>2<\/sup>,\u00a0Hannema SE<\/a>3<\/sup>,\u00a0Meyer WJ<\/a>4<\/sup>,\u00a0Murad MH<\/a>5<\/sup>,\u00a0Rosenthal SM<\/a>6<\/sup>,\u00a0Safer JD<\/a>7<\/sup>,\u00a0Tangpricha V<\/a>8<\/sup>,\u00a0T’Sjoen GG<\/a>9<\/sup>.<\/p>\n Author information<\/strong><\/a><\/p>\n Abstract<\/strong><\/p>\n OBJECTIVE:\u00a0<\/strong><\/p>\n To update the “Endocrine\u00a0Treatment of Transsexual\u00a0Persons: An\u00a0Endocrine\u00a0Society\u00a0Clinical Practice\u00a0Guideline,” published by the\u00a0Endocrine\u00a0Society\u00a0in 2009.<\/p>\n PARTICIPANTS:\u00a0<\/strong><\/p>\n The participants include an\u00a0Endocrine\u00a0Society-appointed task force of nine experts, a methodologist, and a medical writer.<\/p>\n EVIDENCE:\u00a0<\/strong><\/p>\n This evidence-based\u00a0guideline\u00a0was developed using the Grading of Recommendations, Assessment, Development, and Evaluation approach to describe the strength of recommendations and the quality of evidence. The task force commissioned two systematic reviews and used the best available evidence from other published systematic reviews and individual studies.<\/p>\n CONSENSUS PROCESS:\u00a0<\/strong><\/p>\n Group meetings, conference calls, and e-mail communications enabled consensus.\u00a0Endocrine\u00a0Societycommittees, members and cosponsoring organizations reviewed and commented on preliminary drafts of the\u00a0guidelines.<\/p>\n CONCLUSION:\u00a0<\/strong><\/p>\n Gender affirmation is multidisciplinary treatment in which endocrinologists play an important role. Gender-dysphoric\/gender-incongruent\u00a0persons\u00a0seek and\/or are referred to endocrinologists to develop the physical characteristics of the affirmed gender. They require a safe and effective hormone regimen that will (1) suppress endogenous sex hormone secretion determined by the person’s genetic\/gonadal sex and (2) maintain sex hormone levels within the normal range for the person’s affirmed gender. Hormone treatment is not recommended for prepubertal gender-dysphoric\/gender-incongruent\u00a0persons. Those clinicians who recommend gender-affirming\u00a0endocrine\u00a0treatments-appropriately trained diagnosing clinicians (required), a mental health provider for adolescents (required) and mental health professional for adults (recommended)-should be knowledgeable about the diagnostic criteria and criteria for gender-affirming treatment, have sufficient training and experience in assessing psychopathology, and be willing to participate in the ongoing care throughout the\u00a0endocrine\u00a0transition. We recommend treating gender-dysphoric\/gender-incongruent adolescents who have entered puberty at Tanner Stage G2\/B2 by suppression with gonadotropin-releasing hormone agonists. Clinicians may add gender-affirming hormones after a multidisciplinary team has confirmed the persistence of gender dysphoria\/gender incongruence and sufficient mental capacity to give informed consent to this partially irreversible treatment. Most adolescents have this capacity by age 16 years old. We recognize that there may be compelling reasons to initiate sex hormone treatment prior to age 16 years, although there is minimal published experience treating prior to 13.5 to 14 years of age. For the care of peripubertal youths and older adolescents, we recommend that an expert multidisciplinary team comprised of medical professionals and mental health professionals manage this treatment. The treating physician must confirm the criteria for treatment used by the referring mental health practitioner and collaborate with them in decisions about gender-affirming surgery in older adolescents. For adult gender-dysphoric\/gender-incongruent\u00a0persons, the treating clinicians (collectively) should have expertise in\u00a0transgender-specific diagnostic criteria, mental health, primary care, hormone treatment, and surgery, as needed by the patient. We suggest maintaining physiologic levels of gender-appropriate hormones and monitoring for known risks and complications. When high doses of sex steroids are required to suppress endogenous sex steroids and\/or in advanced age, clinicians may consider surgically removing natal gonads along with reducing sex steroid treatment. Clinicians should monitor both\u00a0transgender\u00a0males (female to male) and\u00a0transgender\u00a0females (male to female) for reproductive organ cancer risk when surgical removal is incomplete. Additionally, clinicians should persistently monitor adverse effects of sex steroids. For gender-affirming surgeries in adults, the treating physician must collaborate with and confirm the criteria for treatment used by the referring physician. Clinicians should avoid harming individuals (via hormone treatment) who have conditions other than gender dysphoria\/gender incongruence and who may not benefit from the physical changes associated with this treatment.<\/p>\n Copyright \u00a9 2017\u00a0Endocrine\u00a0Society<\/p>\n PMID:28945902<\/p>\n Pediatr Endocrinol Rev.<\/a>\u00a02010 Dec;8 Suppl 1:178-81.<\/p>\n Fertility\u00a0preservation in adolescents with Klinefelter’s syndrome.<\/strong><\/p>\n De Sanctis V<\/a>1<\/sup>,\u00a0Ciccone S<\/a>.<\/p>\n Author information<\/strong><\/a><\/p>\n Abstract<\/strong><\/p>\n Klinefelter’s syndrome (KS) is one the most common sex chromosomal abnormalities and is characterized by hypergonadotropic\u00a0hypogonadism\u00a0and infertility. Some men with non-mosaic syndrome have azoospermia and only few have oligospermia. In adult 47,XXY, germ cell aplasia, total tubular atrophy or hyalinising fibrosis and relative hyperplasia of Leydig cells are found. Occasionally, single foci of spermatogenesis do exist in the testes. The mechanisms leading to degeneration of seminiferous tubules are unknown. But this process accelerates dramatically at the time of puberty. Therefore, the preservation of reproductive potential for a chromosopathy that for years has been synonymous of sterility may offer to KS subjects the ability to father genetically own their child and may have significant psychological consequences in adulthood. In non-mosaic KS, pregnancy have been reported using intracytoplasmic sperm injection (ICSI) with ejaculated spermatozoa. In azoospermic KS men, ICSI using testicular spermatozoa retrieved with micro-testicular extracted sperm (TESE) is the sole mode of treatment that can be offered, besides sperm donation. These issues are addressed here with the aim of assisting physicians in the management of adolescents with KS.<\/p>\n PMID:21217610<\/p>\n Acta Endocrinol (Copenh).<\/a>\u00a01989 Feb;120(2):129-33.<\/p>\n Gonadal function and ovarian galactose metabolism in classic galactosemia.<\/strong><\/p>\n Kaufman FR<\/a>1<\/sup>,\u00a0Xu YK<\/a>,\u00a0Ng WG<\/a>,\u00a0Silva PD<\/a>,\u00a0Lobo RA<\/a>,\u00a0Donnell GN<\/a>.<\/p>\n Author information<\/strong><\/a><\/p>\n Abstract<\/strong><\/p>\n Evaluation of ovarian steroid secretion, histologic examination of ovarian tissue, and incubation studies with radiolabelled galactose in ovarian tissue slices were performed in a 21-year-old woman with galactosemia and incipient ovarian failure. After exogenous gonadotropin administration in an attempt to achieve\u00a0fertility, there was no evidence of ovulation by ultrasound; estrogen and androgen production were deficient indicating ovarian unresponsiveness. Histologic examination of the ovary revealed that the ovarian stroma had an increase in fibrous tissue and that a few hyalinized atretic follicles were present with no intermediate or evolving Graafian follicles. After incubation with galactose-1-14C, there was absence of labelled CO2 production and only labelled galactose-1-phosphate was identified as compared to controls in which several labelled intermediates could be seen. The incorporation of galactose into the TCA-insoluble fraction was drastically reduced in the patient compared to controls, suggesting that there may be a deficiency of ovarian galactose-containing glycolipids, glycoproteins and mucopolysaccharides in the galactosemic ovary. Deficiency in the production of galactose containing compounds, or galactose-1-phosphate accumulation or both, may lead to the development of hypergonadotropic\u00a0hypogonadism\u00a0seen in women with galactosemia.<\/p>\n PMID:2492704<\/p>\n Eur J Endocrinol.<\/a>\u00a02018 Mar;178(3):285-294. doi: 10.1530\/EJE-17-0862. Epub 2018 Jan 16.<\/p>\n Gonadal function in adult male patients with congenital adrenal hyperplasia.<\/strong><\/p>\n Engels M<\/a>1,2<\/sup>,\u00a0Gehrmann K<\/a>3<\/sup>,\u00a0Falhammar H<\/a>4,5<\/sup>,\u00a0Webb EA<\/a>6,7<\/sup>,\u00a0Nordenstr\u00f6m A<\/a>8<\/sup>,\u00a0Sweep FC<\/a>2<\/sup>,\u00a0Span PN<\/a>9<\/sup>,\u00a0van Herwaarden AE<\/a>2<\/sup>,\u00a0Rohayem J<\/a>10<\/sup>,\u00a0Richter-Unruh A<\/a>10<\/sup>,\u00a0Bouvattier C<\/a>11<\/sup>,\u00a0K\u00f6hler B<\/a>3<\/sup>,\u00a0Kortmann BB<\/a>12<\/sup>,\u00a0Arlt W<\/a>6,7<\/sup>,\u00a0Roeleveld N<\/a>13<\/sup>,\u00a0Reisch N<\/a>14<\/sup>,\u00a0Stikkelbroeck NMML<\/a>15<\/sup>,\u00a0Claahsen-van der Grinten HL<\/a>16<\/sup>;\u00a0dsd-LIFE group<\/a>.<\/p>\n\n
\n
Guidelines for Fertility Preservation in Children<\/h3>\n
\nRecommendations for Fertility Preservation in Children<\/a><\/p>\n
\nRecommendations for Fertility Preservation in Children<\/a><\/p>\n
\nRecommendations for Fertility Preservation in Children<\/a><\/p>\nOther<\/h3>\n
Nephrology<\/h3>\n
\n
\nNeurology<\/h3>\n
Endocrinology\/Gender\/DSD\/Genetics<\/h3>\n
\n
\n
\n
\n