Cushing's disease

In addition to the severe hormonal effects related to increased blood cortisol levels, the large tumor can compress adjacent structures.[8] Diagnosing Cushing's disease is a multidisciplinary process involving doctors, endocrinologists, radiologists, surgeons, and chemical pathologists.[12] Once Cushing's syndrome has been diagnosed, the first step towards finding the cause is measuring plasma adrenocorticotropic hormone (ACTH) concentration.Any intermediate values need to be cautiously interpreted and a corticotropin-releasing hormone (CRH) test is advised in order to confirm corticotropin dependency.This is done via a combination of techniques including CRH, high-dose DST, pituitary MRI and bilateral inferior petrosal sinus sampling (IPSS).The sensitivity of the CRH test for detecting Cushing's disease is 93% when plasma levels are measured after fifteen and thirty minutes.[15] A corticotropin gradient sample via BIPSS is required to confirm diagnosis when pituitary MRI imaging and biochemical diagnostic tests have been inconclusive.[11] The UFC test has a specificity of 81% and thus has a high rate of false-positives that are due to pseudo-Cushing states, sleep apnea, polycystic ovary syndrome, familial glucocorticoid resistance, and hyperthyroidism.[11] The late-night or midnight salivary cortisol test has been gaining support due to its ease of collection and stability at room temperature, therefore it can be assigned to outpatients.One of the major complications of this treatment is progression of Nelson's syndrome which is caused by enhance level of tumor growth and ACTH secretion post adrenalectomy in 8–29% of patients with CD.After the completion of collecting urine and blood samples, patients are asked to switch to glucocorticoid such as prednisone to decrease symptoms associated with adrenal withdrawal.The prevalence of hypertension, and abnormalities in glucose metabolism are major predictors of mortality and morbidity in untreated cases of the disease.[24] The disease associated with this increased secretion of cortisol was described by the American neurosurgeon Harvey Cushing in 1912 after he was presented with a unique case of the disease in 1910[28][29] a 23-year-old woman called Minnie G. whose symptoms included painful obesity, amenorrhea, hypertrichosis (abnormal hair growth), underdevelopment of secondary sexual characteristics, hydrocephalus and cerebral tension.[3] However, the most likely explanation, proposed by J. Aidan Carney and based on statistical evidence, was that the basophil adenoma Minnie might have harbored underwent partial infarction, leading to symptom regression.[3] The other hypothesis was that Minnie might have had Primary Pigmented Nodular Adrenocortical Disease (PPNAD), which when associated with Cushing's syndrome (Carney complex) can infrequently cause spontaneous symptom regression of the latter.

Pituitary pars intermedia dysfunctionSpecialtyEndocrinologyCushing's syndromeadrenocorticotropic hormoneanterior pituitaryhypercortisolismadenomacorticotropin releasing hormonecorticosteroidscortisolpurple striaemuscle atrophyosteoporosiskidney stonesmoon faceirregular menstruationinsomniadiabetes mellitussalivarydexamethasone suppression testACTH stimulation testcorticotropin-releasing hormoneinvasive testgold standardpseudo-Cushing statessleep apneapolycystic ovary syndromehyperthyroidismpituitary adenomatranssphenoidal surgerysphenoidal sinusradiation therapyHypopituitarismgrowth hormone deficiencyBilateral adrenalectomyglucocorticoidmineralocorticoidNelson's syndromesteroidprednisoneDiabetes insipiduselectrolytecomorbiditiesprevalenceincidencehypertensionglucose metabolismmortalitymorbidityHarvey Cushingobesityamenorrheahypertrichosishydrocephalusadrenal tumorhyperpituitarismacromegalybasophil cellserectile dysfunctionautopsybasophilinfarctionPrimary Pigmented Nodular Adrenocortical DiseaseCarney complexadrenal glandsBulletin of the Johns Hopkins HospitalThe New York TimesSNOMED CT