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Diseases of the adrenal gland
Published in J Kellogg Parsons, E James Wright, The Brady Urology Manual, 2019
Bilateral adrenalectomy: Nelson’s syndrome = Caused by ACTH-secreting pituitary adenomaOccurs in 10–20% of patients postoperatively; may occur years laterCharacterized by vision changes, headache, and hyperpigmentation.
Endocrine system
Published in Aida Lai, Essential Concepts in Anatomy and Pathology for Undergraduate Revision, 2018
Nelson’s syndrome Occurs after bilateral adrenalectomyCharacteristic pituitary adenoma and high ACTH levelsSigns: – pigmentationManagement: – surgical resection of pituitary gland– radiotherapy
The adrenal glands and other abdominal endocrine disorders
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
After unilateral adrenalectomy supplemental cortisol should be given postoperatively because the contralateral gland will be suppressed. In total, 15 mg/h is required parenterally for the first 12 hours followed by a daily dose of 100 mg for 3 days, which is gradually reduced thereafter. After unilateral adrenalectomy, the contralateral suppressed gland needs up to 1 year to recover adequate function. A synacthen test to evaluate adrenal fuction prior to stopping cortisol supplements is advised. In 10% of patients with Cushing’s disease who undergo a bilateral adrenalectomy after failed pituitary surgery, the pituitary adenoma causes Nelson’s syndrome due to continued ACTH secretion at high levels, causing hyperpigmentation as a result of chemical synergies between ACTH and melanocyte-stimulating hormone.
Drug design strategies for Cushing’s syndrome
Published in Expert Opinion on Drug Discovery, 2019
S. A. Usanov, A. V. Kliuchenovich, N. V. Strushkevich
The current generally accepted treatments for CS include transsphenoidal pituitary surgery as initial treatment, but, being not always capable of providing complete and permanent remission, it leads to adjunctive therapies: radiotherapy and pharmacological treatment. In selected cases (intolerance of ketoconazole and severe condition), surgical removal of the adrenal glands can be considered, accompanied with the risk of Nelson syndrome development, resulting in the activation of the underlying pituitary tumor due to a loss of inhibition from adrenal secretions [7]. Moreover, patients with CS in pregnancy have high rates of maternal and fetal morbimortality and overall fetal loss of about 25%, with adrenal origins being the most frequent cause in up to 60% of cases. Evidence suggests that patients receiving treatment during pregnancy achieve better fetal outcomes than those without treatment [8]. Surgery may not be a treatment of choice for that cohort of patients, emphasizing the need for the discovery of effective therapeutics with a high safety profile.
Para-ovarian adrenal rest tumors: gynecologic manifestations of untreated congenital adrenal hyperplasia
Published in Gynecological Endocrinology, 2018
Jessica M. Sisto, Fong W. Liu, Mitchell E. Geffner, Michael L. Berman
Ovarian adrenal rest tumors (OARTs) have also been reported, but are very rare with less than 20 documented cases in the literature. Even less often, adrenal rest tumors have been found in the para-ovarian and adnexal areas. A literature search by Zaarour et al. in 2014 revealed a total of 12 documented cases of ovarian and para-ovarian ART, most commonly associated with elevated plasma ACTH levels in women with CAH [5]. Nine of these patients had OARTs, while three had para-ovarian adrenal rest tumors. Two of the patients with para-ovarian masses had elevated ACTH secondary to Nelson syndrome, but not CAH. Chen, et al in 2016 reported three other cases of OARTs in patients with CAH [6]. Our literature search also included an additional OART case documented in 2011 [3]. To our knowledge, our patient would be the fourth para-ovarian adrenal rest tumor documented by pathology in the literature.
Treatment of gingival pigmentation with a 755-nm alexandrite picosecond laser
Published in Journal of Cosmetic and Laser Therapy, 2020
Cristina Pindado-Ortega, Adrián Alegre-Sánchez, Aitana Robledo-Sánchez, Ignacio Tormo-Alfaro, Pablo Boixeda
Gingival pigmentation can be produced by increased biosynthesis and deposition of melanin, increased number of melanocytes (melanocytosis) or deposition of exogenous materials. Hence, a meticulous personal history of the patient is essential in determining whether the oral pigmentation cause is physiological or pathological. Among the etiological factors reported are endocrine disorders such as Addison’s disease, Albright and Nelson’s syndrome or acromegaly, malignant melanoma, Kaposi’s sarcoma, Peutz Jeghers syndrome, Laugier-Hunziker syndrome, hemochromatosis, chronic pulmonary disease, exposure to UV rays, trauma, drugs, tobacco, heavy metal ingestion, amalgam tattoo and genetics(1).