Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pituitary control of pigmentation has known for more than 60 years. Since 1969, beta-melanocyte-stimulating hormone (beta-MSH) has been accepted as the main pituitary pigmentary hormone in man. Its "constant companionship" with adrenocorticotrophic hormone (ACTH) has also been repeatedly demonstrated. Current investigations challenge both of these concepts. Human beta-MSH immunoreactivity has been shown to be actually due to beta-lipotropic hormone (beta-LPH), a larger molecule that within itself contains the entire amino acid sequence of beta-MSH. Human beta-MSH does not exist in vivo; it is merely an extraction artifact formed by enzymatic degradation of beta-LPH. It would appear likely that beta-LPH, not beta-MSH, is the constant companion of ACTH.
JAMA 1978 Sep 15
PMID:Pituitary pigmentary hormones. Relationship of melanocyte-stimulating hormone to lipotropic hormone. 21 Mar 1

Corticotropin is one of the few accepted treatments for acute exacerbations of multiple sclerosis and retrobulbar neuritis. Psychosis is a serious side effect usually necessitating discontinuation of the drug therapy. Because mood disorders preponderated in most patients previously described with this psychosis, 27 patients were empirically treated with lithium carbonate concurrently with corticotropin. In none of the patients treated with lithium did a psychotic reaction occur, although in a comparable group of 44 patients previously treated identically with corticotropin but without lithium, six (14%) became psychotic.
JAMA 1979 Mar 09
PMID:Lithium prophylaxis of corticotropin-induced psychosis. 21 18

Corticotropin deficiency may occur after pituitary surgery, and, if unrecognized and untreated, it can be fatal. In this study the insulin tolerance test was used to assess hypothalamic-pituitary-adrenal reserve five to seven days after pituitary surgery, and postoperative morning serum cortisol concentration was compared with the insulin tolerance test for predicting corticotropin deficiency. In 35 patients with pituitary tumors studied prospectively, 27 had normal insulin tolerance test results five to seven days after pituitary surgery; in these patients, the morning serum cortisol concentration two to three days after surgery was 250 nmol/L (9 micrograms/dL) or greater. Eight patients had subnormal insulin tolerance test results or clinical evidence of adrenal insufficiency; the morning serum cortisol concentration in these patients was 80 nmol/L (3 micrograms/dL) or less. Postoperative adrenal insufficiency was transient (one to three months) in five of these eight patients. We retrospectively identified 45 patients whose postoperative morning serum cortisol values were 200 nmol/L (7 micrograms/dL) or greater; none of these patients had clinical evidence of adrenal insufficiency. We conclude that a morning serum cortisol level obtained two to three days after surgery and 24 hours after the discontinuation of hydrocortisone accurately predicts postoperative corticotropin reserve.
JAMA 1988 Feb 05
PMID:Rapid assessment of corticotropin reserve after pituitary surgery. 282 32

We describe a woman who developed adrenal insufficiency after removal of an apparently nonfunctional adrenal adenoma. She displayed no stigmata of Cushing's syndrome and had normal plasma and urinary cortisol levels. A second patient without clinical findings of Cushing's syndrome also had normal basal steroid levels. This patient displayed partial suppressibility with dexamethasone, had low-normal levels of serum corticotropin, and excreted a low concentration of urinary 17-ketosteroids. She also developed mild adrenal insufficiency after the operation. We believe the adrenal adenomas in these patients secreted enough cortisol to suppress the contralateral adrenal gland but not enough hormone to elevate basal steroid levels. Therefore, we suggest that all patients with adrenal masses be studied with the overnight dexamethasone suppression test rather than basal steroid hormone measurements to detect low levels of autonomous cortisol secretion. In addition, patients with adrenal masses that are not removed surgically should have serial adrenal function tests performed.
JAMA 1989 Feb 10
PMID:Adrenal insufficiency after operative removal of apparently nonfunctioning adrenal adenomas. 291 87

A 37-year-old woman with documented primary aldosteronism died of a cerebral hemorrhage. At postmortem examination she was found to have bilateral, adrenal hyperplasia and nodular basophilic hyperplasia of the anterior and intermediate lobe of the pituitary. Based on these findings and experimental evidence suggesting the existence of a pituitary factor that stimulates aldosterone secretion, we postulate that idiopathic aldosteronism is caused by an abnormality of the intermediate lobe of the pituitary gland leading to overproduction of non-adrenocorticotropic hormone peptides derived from pro-opiomelanocortin that increase aldosterone production and cause hyperplasia of the adrenal glands.
JAMA 1984 May 18
PMID:Idiopathic aldosteronism. A possible disease of the intermediate lobe of the pituitary. 671 84

A 44-year-old woman reported several weeks of fatigue, somnolence, pain in the large joints, nausea, and decreased appetite. She had also noted an unintentional 11-kg weight loss over a period of 6 months. She had a remote history of amenorrhea, but she was presently menstruating regularly. She was taking no medications, with the exception of acetaminophen as needed for knee pain. The diagnosis of adrenal insufficiency (AI) was considered. Serum cortisol level after adrenocorticotropin hormone (ACTH) stimulation was abnormal. Because her plasma ACTH level was not increased, a diagnosis of secondary AI (due to deficiency in ACTH) was made. Magnetic resonance imaging of the brain performed to exclude the presence of a sellar or suprasellar mass showed reduction in size of the pituitary gland and an increased cerebrospinal fluid content within the sella, consistent with a partially empty sella. The patient's symptoms improved rapidly with hydrocortisone therapy but during follow-up, the dose of hydrocortisone was found to be excessive. Important differences exist between primary and secondary AI, and the diagnosis of secondary AI may be challenging. The therapy of AI should be carefully tailored to the requirements of the individual patient.
JAMA 2005 Nov 16
PMID:Adrenal insufficiency. 1652 31