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Alcoholism
Published in Mark S. Gold, R. Bruce Lydiard, John S. Carman, Advances in Psychopharmacology: Predicting and Improving Treatment Response, 2018
Charles A. Dackis, Mark S. Gold
Before proceeding to a discussion of treatment for major depression, certain other diagnostic considerations should be mentioned. Alcoholics are susceptible to a number of medical diseases, some of which can mimic depression. Thyroid abnormalities are often seen in alcoholics and can be evaluated with the TRH infusion test. Augmented TSH responses or abnormalities in T3, T4, or baseline TSH could indicate the need of thyroid hormone replacement. Alcohol-induced, pseudo-Cushing’s syndrome is characterized by a transient but marked elevation in plasma cortisol,9 and can be ruled out by measurements of plasma or urinary cortisol, or with the 2-mg dexamethasone suppression tests. Hepatic or pancreatic disease, often seen in alcoholics, can also mimic depression. Medical illnesses associated with depression have been described in this volume, and should be carefully ruled out during the evaluation process.
Cushing’s syndrome, cortical carcinoma, and estrogen- and androgen-secreting tumors
Published in Demetrius Pertsemlidis, William B. Inabnet III, Michel Gagner, Endocrine Surgery, 2017
In general, the first step is to rule out exogenous glucocorticoid ingestion by history. This is followed by confirmation of hypercortisolism. Physiologic hypercortisolism—aka pseudo-Cushing’s syndrome—may be indicated by a history of polycystic ovary syndrome, severe stress or infection, chronic alcoholism, long-standing major depression, and morbid obesity. The diagnosis of Cushing’s syndrome is made once confirmed hypercortisolism is found to be pathologic in nature. Initial tests recommended by the Endocrine Society include the urine free cortisol (UFC), late-night salivary cortisol, 1 mg (low-dose) overnight dexamethasone suppression test (DST), and 2-day low-dose DST. Tests not recommended include the random serum cortisol or ACTH, urinary 17-ketosteroids, an insulin tolerance test, the loperamide test, and any specific test reserved for the diagnosis of a cause of hypercortisolism [15].
Neuroendocrine disease
Published in Philip E. Harris, Pierre-Marc G. Bouloux, Endocrinology in Clinical Practice, 2014
Harvey Cushing first described the chromophobe pituitary adenoma as being the underlying cause of some cases of the condition,191 thereafter referred to as Cushing’s disease. Although florid cases of Cushing’s syndrome are easy to diagnose, subtler cases can be extremely difficult. Alcohol abuse, obesity, and depression can all give rise to “pseudo-Cushing’s syndrome,” not only mimicking Cushing’s syndrome clinically but also, on occasion, biochemically. In addition, some cases of Cushing’s disease “cycle” in and out of active disease. A recent review of 201 patients identified 30 (14%) patients with a median intercyclic period of 4 years, although the period can be highly variable.192 Once the diagnosis of Cushing’s syndrome has been confirmed, it is necessary to make a specific etiological diagnosis. Although the differentiation of Cushing’s syndrome into ACTH-dependent and ACTH-independent disease is usually straightforward, the identification of the source of ACTH in the former can be very difficult. Neurosurgery should only be carried out by a dedicated neuroendocrine surgeon. An experienced endocrine surgeon should be available for bilateral adrenalectomy, and there should be ready access to thoracic surgery.
Sensitivity of Different ACTH and Cortisol Concentration Values in Corticotropin-Releasing Hormone Based Tests in Cushing’s Disease
Published in Endocrine Research, 2023
Shehrban Sobeh Khalil, Mohammad Sheikh Ahmad, Talia Sarah-Hefer, Ekaterina Yovanovich, Maria Reut, Limor Chen-Konak, Nariman Saba-Khazen, Leonard Saiegh
Pseudo-Cushing’s syndrome (PCS) results from over activity of the hypothalamic–pituitary–adrenal axis, leading to hypercortisolism and may complicate the diagnosis of CS. Examples for PCS states are alcoholism, psychiatric disorders, severe obesity and poorly controlled diabetes mellitus.4 In 1993, Yanovski et al5 developed the combined test of Corticotropin-releasing hormone (CRH) stimulation after low-dose dexamethasone suppression (DEX-CRH test) to distinguish between CS and PCS. The test is based on the assumption that ACTH secreting pituitary tumors in Cushing’s disease (CD) patients respond to exogenous CRH stimulation despite pre-treatment with dexamethasone, while normal pituitary cells in PCS subjects do not. The initial report found that cases with serum cortisol concentration >1.4 µg/dl (38 nmol/L) in response to CRH after dexamethasone suppression were considered true CS, with 100% specificity and sensitivity. However, subsequent studies reported a lower diagnostic performance of the test, and different cutoff values for CS diagnosis were proposed.6–9