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Endocrine Disorders, Contraception, and Hormone Therapy during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Diagnosis of Cushing is confounded because many of the symptoms (hypertension, weight gain, fatigue, striae, and increased pigmentation) are common in normal pregnancies. Symptoms more specific to Cushing syndrome include thinning of skin, spontaneous bruising, and muscle weakness are symptoms. Increased adrenal androgens cause hirsutism and acne in pregnant women with Cushing syndrome (Grimes et al., 1973). Pregnancy outcomes are usually extremely poor. An estimated 50 percent of recognized pregnancies end in spontaneous abortion, premature delivery or stillbirth (Aaron et al., 1990; Gormley et al., 1982; Grimes et al., 1973).
Endocrine diseases and pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Clinical manifestations of Cushing’s syndrome include central obesity, moon-like plethoric face, dorsal cervical and supraclavicular fat pads, thin skin with easy bruising and wide, deeply recessed, reddish or violaceous striae, proximal muscle wasting and weakness, osteoporosis, and hirsutism. Hypokalemia, hypertension, and diabetes mellitus commonly complicate Cushing’s syndrome, but are not invariably present. Anovulatory oligomenorrhea and infertility frequently prevent pregnancy, so Cushing’s syndrome during pregnancy is an unusual occurrence. However, the presence of gonadotropin receptors in pigmented nodular adrenal hyper-plasia and in some adrenal adenomas may account for first expression of Cushing’s syndrome manifestations during pregnancy (69). When pregnancy does accompany Cushing’s syndrome, pre-eclampsia, hypertension, miscarriage, premature labor, intrauterine growth retardation, and stillbirth are distinct risks (58,70). However, neonatal ACTH suppression and adrenal insufficiency are rare, and fetal virilization does not occur. Thus, most therapeutic attention and diagnostic efforts are directed toward maternal health during the pregnancy.
Endocrine Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
As estrogens and androgens play a role in the growth of certain tumor types (e.g., hormone-responsive breast and prostate, respectively), inhibiting their production with an agent such as aminoglutethimide can reduce growth rate. Furthermore, tumors of the adrenal glands are usually associated with excess steroid production which can ultimately cause Cushing’s syndrome. Thus, aminoglutethimide suppresses the production of these steroids, and so is used in this context to decrease symptoms.
Posterior reversible encephalopathy syndrome in carcinoid tumor
Published in Baylor University Medical Center Proceedings, 2022
Thuy-Tien Ho, Venkatesh Aiyagari
The diagnosis of Cushing syndrome includes the finding of elevated 24-hour urine cortisol, midnight plasma and salivary cortisol, and a lack of suppression of serum cortisol after administration of dexamethasone. Cushing syndrome either is caused by hypercortisolism or is ACTH independent. Abdominal CT is usually the first diagnostic test. ACTH-dependent Cushing syndrome can be due to an ACTH-secreting pituitary adenoma and rarely due to a nonpituitary source such as small cell lung carcinoma, carcinoid tumors, medullary thyroid cancer, pheochromocytoma, or poorly differentiated neuroendocrine tumors. Plasma ACTH levels are typically high, more so with ectopic ACTH production.2 Pituitary MRI with gadolinium contrast detects approximately 50% of ACTH-producing pituitary tumors. If the pituitary MRI is normal, inferior petrosal sinus sampling will determine if the pituitary is the source of the ACTH production. An alternate approach is to perform a high-dose dexamethasone suppression or a corticotrophin-releasing hormone test. If the pituitary is not the source of ACTH production, CT and MRI of the neck, chest, and abdomen as well as scintigraphy with [111In]-pentetreotide for detection of neuroendocrine tumors is recommended.3 Surgical excision of tumors producing ACTH or cortisol is the optimal treatment for Cushing syndrome. Radiotherapy is an option for treatment of pituitary tumors. If surgery is not feasible, ketoconazole or metyrapone can be used. If medical treatment fails, bilateral adrenalectomy can be considered.
Adrenocortical carcinoma arising from the colonic mesentery
Published in Baylor University Medical Center Proceedings, 2022
Samuel Z. See, Sinan Ali Bana, Nuvaira Ather, Amy Haberman
Clinical presentation depends on whether the tumors are functioning or nonfunctioning. Patients with functioning tumors typically present with symptoms of the Cushing syndrome and/or virilization.8 Many nonfunctioning tumors are detected incidentally on radiographic studies performed for another reason. Imaging generally shows an inhomogeneous hypervascular tumor with irregular margins with or without necrosis and hemorrhage.9,10 Biopsy and subsequent histopathologic evaluation are required for diagnosis. Immunohistochemistry findings of positive alpha-inhibin, Melanin-A, and SF-1 can confirm the primary adrenal origin.11 The Modified Weiss Criteria use histopathologic characteristics to differentiate an adrenal adenoma from carcinoma. These characteristics include a mitotic rate >5 per 50 high-power fields, clear cytoplasm compromising ≤25% of the tumor, abnormal mitoses, necrosis, and capsular invasion, with each criterion receiving a score of 0 when absent and 1 when present. Using the formula 2× mitotic rate criterion + 2× clear cytoplasm criterion + abnormal mitoses + necrosis + capsular invasion, a score of 3 or more suggests malignancy.12
Peripheral clock system circadian abnormalities in Cushing’s disease
Published in Chronobiology International, 2020
Vinicius Reis Soares, Clarissa Silva Martins, Edson Zangiacomi Martinez, Leonardo Domingues Araujo, Silvia Liliana Ruiz Roa, Lucas Ravagnani Silva, Ayrton Custodio Moreira, Margaret De Castro
We studied 13 healthy women and 12 CD patients. Patients were investigated between 2015 and 2017 in the Division of Endocrinology at HCFMRP-USP, one of the referral services for Cushing’s syndrome in Brazil. The diagnosis of Cushing’s syndrome was based on clinical signs and symptoms and subsequent confirmation of hypercortisolism by biochemical testing, according to international established criteria (Nieman et al. 2008). Briefly, biochemical diagnosis was based on increased levels of urinary-free cortisol and/or late-night salivary cortisol (LNSC), and non-suppression of plasma or salivary cortisol after low-dose (1 mg overnight) dexamethasone suppression test (LDDST). To diagnose endogenous hypercortisolism, we used as a cutoff for LNSC values above 350 ng/dL (or 9.8 nmol/L) and salivary cortisol levels after LDDST above 150 ng/dl (or 4.2 nmol/L) (Elias et al. 2014). The criteria for a normal salivary cortisol circadian rhythm was late-night cortisol (2300 h) lower than 83.5% of morning basal cortisol (0900 h) and lower than 350ng/dl (9.65 nmol/l) (Castro et al. 1999). Values below the limit of detection of the method, for statistical analysis, were substituted by the limit of detection.