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)

A 54-year-old man who had an appearance strongly suggestive of Cushing's syndrome, collapsed after the removal of a carcinoid tumour of the thymus. The clinical suspicion of acute adrenal insufficiency was supported by invasive haemodynamic data and the diagnosis was subsequently confirmed biochemically. These post-operative events were subsequently ignored and a further crisis was probably prevented by tumour recurrence (and hence resumption of adrenocorticotropic hormone (ACTH) production). The ectopic production of ACTH from a carcinoid tumour of the thymus is recognised but a report of acute adrenal insufficiency from its removal is probably unique.
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PMID:Post-thymectomy collapse: an unusual case of acute adrenal insufficiency. 778 88

Seventy-two long-surviving liver transplant recipients were evaluated prospectively, including a baseline allograft biopsy for weaning off of immunosuppression. Thirteen were removed from candidacy because of chronic rejection (n = 4), hepatitis (n = 2), patient anxiety (n = 5), or lack of cooperation by the local physician (n = 2). The other 59, aged 12-68 years, had stepwise drug weaning with weekly or biweekly monitoring of liver function tests. Their original diagnoses were PBC (n = 9), HCC (n = 1), Wilson's disease (n = 4), hepatitides (n = 15), Laennec's cirrhosis (n = 1), biliary atresia (n = 16), cystic fibrosis (n = 1), hemochromatosis (n = 1), hepatic trauma (n = 1), alpha-1-antitrypsin deficiency (n = 9), and secondary biliary cirrhosis (n = 1). Most of the patients had complications of long-term immunosuppression, of which the most significant were renal dysfunction (n = 8), squamous cell carcinoma (n = 2) or verruca vulgaris of skin (n = 9), osteoporosis and/or arthritis (n = 12), obesity (n = 3), hypertension (n = 11), and opportunistic infections (n = 2). When azathioprine was a third drug, it was stopped first. Otherwise, weaning began with prednisone, using the results of corticotropin stimulation testing as a guide. If adrenal insufficiency was diagnosed, patients reduced to < 5 mg/day prednisone were considered off of steroids. The baseline agents (azathioprine, cyclosporine, or FK506) were then gradually reduced in monthly decrements. Complete weaning was accomplished in 16 patients (27.1%) with 3-19 months drug-free follow-up, is progressing in 28 (47.4%), and failed in 15 (25.4%) without graft losses or demonstrable loss of graft function from the rejections. This and our previous experience with self-weaned and other patients off of immunosuppression indicate that a significant percentage of appropriately selected long-surviving liver recipients can unknowingly achieve drug-free graft acceptance. Such attempts should not be contemplated until 5-10 years posttransplantation and then only with careful case selection, close monitoring, and prompt reinstitution of immunosuppression when necessary.
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PMID:Weaning of immunosuppression in long-term liver transplant recipients. 783 42

There is increasing evidence that the hypercortisolemia in inflammatory diseases suppresses the elaboration of proinflammatory cytokines, thus protecting the host from its own defence reactions. In severe sepsis and septic shock cortisol levels are usually elevated, but some patients may have relative adrenal insufficiency. This may contribute to the overwhelming systemic inflammatory response syndrome. We evaluated the impact of low-dose hydrocortisone infusion (10 mg/h) on the course of the systemic inflammatory response syndrome. This dose corresponds to a maximum secretory rate of cortisol achieved in corticotropin-stimulated healthy humans. In a prospective observational study 57 surgical patients with severe sepsis or septic shock were studied, of which in addition to the conventional treatment 12 patients were infused with low-dose hydrocortisone, and 45 were treated without any corticosteroid. In the longitudinal analysis the systemic inflammatory response--as judged by body temperature, cardiovascular response, and kinetics of inflammatory mediators such as phospholipase A2, C-reactive protein, and neutrophil elastase--started to differ in favor of the hydrocortisone-treated patients after 2 days of treatment (P < 0.05, Mann-Whitney U test). The difference disappeared after withdrawal of exogenous cortisol. Shock reversal was achieved in all patients treated with low-dose hydrocortisone. The data provide evidence that low-dose hydrocortisone infusion attenuates the systemic inflammatory response in human septic shock. From an immunological point of view a relative cortisol deficiency may contribute to the amplified immune response in systemic inflammatory diseases. A randomized clinical trial must clarify the impact of low-dose hydrocortisone infusion on the clinical course and outcome of septic shock patients.
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PMID:Low-dose hydrocortisone infusion attenuates the systemic inflammatory response syndrome. The Phospholipase A2 Study Group. 786 82

In order to know the prevalence rate of adrenal insufficiency among patients with renal failure due to amyloidosis; we have performed a stimulation test with synthetic corticotropin hormone (Nuvacthen test) in nine patients diagnosed of renal amyloidosis and in five controls. We also measured ACTH and plasma cortisol levels. In two out of nine patients (22%) a low ACTH, low plasmatic cortisol and an abnormal response to Nuvacthen test were detected being diagnosed of primary adrenal insufficiency. We conclude that adrenal insufficiency is not an infrequent finding in systemic amyloidosis and may be due to secondary amyloidotic infiltration of adrenal or pituitary glands. Though Nuvacthen test is a useful test to diagnose subclinical adrenal insufficiency, in our series patients with an abnormal response also had low levels of basal cortisol and ACTH and no one patient with normal basal levels had an abnormal response to the stimulation test.
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PMID:[Adrenal insufficiency in patients with kidney failure secondary to amyloidosis. Its detection by a stimulation test]. 773 87

A dose of 1.5 micrograms/kg of MCI-028, human corticotropin-releasing hormone (hCRH), was administered intravenously to 38 children with non-endocrine short stature with normal function in the hypothalamo-pituitary-adrenocortical axis and to 71 children with a disorder in the same axis. Blood levels of adrenocorticotropic hormone (ACTH) and cortisol were determined to evaluate the axis. The 95% confidence limits of peak responses of ACTH and cortisol in non-endocrine short stature were between 17.2 and 135.3 pg/ml, and between 13.1 and 35.6 micrograms/dl, respectively, and were used as standards for children. When compared with these standards, the hormonal responses in children with various disorders in the hypothalamo-pituitary-adrenocortical axis were as follows: in two children with Cushing's syndrome caused by adrenal tumor, ACTH values were decreased and were not responsive to hCRH, while cortisol values, though within the normal limit, were not responsive; in children with primary adrenal insufficiency or congenital adrenal hyperplasia, cortisol values were decreased and not responsive, whereas ACTH values tended to be increased and ACTH response high except for 21 alpha-hydroxylase deficiency of congenital adrenal hyperplasia. In two cases of pituitary dwarfism complicated with ACTH deficiency, both ACTH and cortisol values were decreased and poorly responsive; and in children who were receiving glucocorticoid, both ACTH and cortisol values tended to be decreased and to respond poorly to hCRH. As for side effects, hot flushing was observed among 8.0% of the subjects after administration of hCRH. But this symptom was not severe and no other side effects of clinical importance were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of hypothalamo-pituitary-adrenocortical function in children by human corticotropin-releasing hormone (MCI-028) test. 795 24

The authors studied 15 patients at risk for central adrenocortical insufficiency to evaluate the role of naloxone in establishing the integrity of the hypothalamic-pituitary-adrenal axis. Each patient was admitted to the General Clinical Research Center for 2 days. Naloxone, 125 micrograms/kg body weight, was administered intravenously, and plasma adrenocorticotropic hormone (ACTH) and cortisol concentrations were measured at -15, 0, 30, 45, 60, 90, and 120 minutes. Metyrapone, 30 mg/kg body weight, was administered orally at 11 PM on the second day of hospitalization. Plasma ACTH, cortisol, and 11-deoxycortisol concentrations were measured at 8 AM pre- and postmetyrapone. The results of the metyrapone test were used to distinguish patients who had central adrenal insufficiency from those who were normal. In 11 patients who had a normal metyrapone test, the plasma ACTH level increased from 6 +/- 1 pmol/L at baseline to 11 +/- 2 pmol/L 30 minutes after naloxone administration. The plasma cortisol increased from 191 +/- 21 nmol/L at baseline to 379 +/- 47 nmol/L 45 minutes after naloxone administration. In four patients with central adrenal insufficiency, the plasma ACTH and cortisol concentrations did not increase after naloxone administration. Reliance solely on the individual ACTH and cortisol responses to naloxone would have permitted a correct decision regarding glucocorticoid replacement therapy in 14 (93%) of 15 patients. Naloxone stimulation testing may have a role in the clinical evaluation of patients with suspected central adrenocortical insufficiency.
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PMID:Naloxone-induced activation of the hypothalamic-pituitary-adrenal axis in suspected central adrenal insufficiency. 807 33

The reactivity of the hypothalamic-pituitary-adrenal (HPA) axis was investigated in 10 female patients fulfilling the Yunus criteria for the primary fibromyalgia syndrome (PFS) and in 10 matched, healthy and sedentary controls. The 2 groups were subjected to a dexamethasone suppression (DXM) test, a corticotropin-releasing hormone (CRH) test and an insulin induced hypoglycemia (IH) test. In the DXM test there was no escape from suppression in patients or controls. The CRH and the IH tests showed a markedly enhanced, and statistically significant, adrenocorticotropic hormone (ACTH) release in patients with PFS versus controls, while the cortisol response in both groups was not different. Our data suggest that fibromyalgia is related to a neuroendocrine disorder characterized by hyperreactive pituitary ACTH release and a relative adrenal hyporesponsiveness. This HPA response pattern is unique and contrasts to the hypercortisolemic responses observed in affective disorders, e.g., depression, which like PFS, are often thought to be precipitated by chronic stress. Our findings seem to indicate a relative adrenal insufficiency in PFS, which might serve clinically as an explanation for the reduced aerobic capacity and impaired muscle performance these patients display.
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PMID:Altered reactivity of the hypothalamic-pituitary-adrenal axis in the primary fibromyalgia syndrome. 847 45

We describe three critically ill patients who displayed indirect evidence of transient corticotropin deficiency. All these patients were elderly, were poorly nourished, and had unexplained hypotension intraoperatively or immediately postoperatively. During the hypotensive episodes, they had inappropriately low plasma cortisol levels (10, 12, and 6 micrograms/dl) and responded dramatically to the administration of glucocorticoids. A normal response to infusion of synthetic corticotropin excluded primary adrenal insufficiency. Two patients tested had low thyroxine levels without increased thyrotropin concentrations and depressed levels of gonadotropins. In all three patients, the dose of glucocorticoids was successfully tapered and then discontinued. After recovery, serum thyroxine levels increased, gonadotropins reverted to normal concentrations, and the administration of metyrapone to two patients demonstrated normal hypothalamic-pituitary-adrenal function. Cortisol levels of less than 15 micrograms/dl in critically ill patients suggest the presence of adrenal insufficiency. The infusion of synthetic corticotropin may not exclude adrenal insufficiency attributable to corticotropin deficiency. If direct tests of corticotropin reserve are impractical, treatment with glucocorticoids is warranted.
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PMID:Transient corticotropin deficiency in critical illness. 838 90

Since the discovery and structural elucidation of corticotropin-releasing factor (CRF) synthetic ovine and human CRF have become useful tools for the diagnosis of pituitary and adrenocortical disorders. The stimulation of release of adrenocorticotropic hormone (ACTH) after a dose of 100 micrograms CRF allows differentiation of the various causes of secondary adrenal insufficiency. In patients with specific autoimmune corticotroph disorders or general inflammatory or tumorous destruction of the anterior pituitary there is no rise of ACTH after intravenous administration of CRF. In contrast, patients with secondary adrenal failure due to suprasellar lesions show a rise of ACTH from a low or unmeasurable basal level without an accompanying cortisol response, demonstrating the integrity of the corticotroph and the atrophy of the cRF neuron and the adrenocortical cell. Similar observations are made in patients with secondary adrenal failure resulting from long-term glucocorticoid treatment. This demonstrates that the main reason for adrenal insufficiency after glucocorticoid treatment is the persisting suppression of the activity of CRF neurons. In patients with adrenocortical hyperfunction (Cushing's syndrome) the CRF stimulation test differentiates unequivocally between autonomous adrenal hypercortisolism and ACTH-dependent bilateral adrenal hyperplasia. However, the differential diagnosis between eutopic pituitary (Cushing's disease) and paraneoplastic ACTH secretion (ectopic ACTH syndrome) is difficult. Recent results show that catheterization of the sinus petrous inferior and measurement of ACTH in central and peripheral blood before and after CRF injection allows this differential diagnosis to be made with confidence. The usefulness of measuring CRF plasma levels is not established. The only exception to this is in cases of ectopic CRF syndrome, which is a rare cause of Cushing's syndrome.
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PMID:The role of corticotropin-releasing factor in the investigation of endocrine diseases. 849 Oct 93

No clear criteria exist to rule out hypoadrenal shock by cosyntropin (alpha 1-24-corticotropin, a synthetic subunit of adrenocorticotropic hormone) testing in persons who have critical nonadrenal illness. Four patients in the surgical intensive care unit with critical multisystem disease and refractory high cardiac output, low vascular resistance shock had significantly diminished or terminated vasopressor requirements after institution of hydrocortisone sodium succinate infusion in doses simulating physiologic stress response (100 to 300 mg of hydrocortisone per day). In each case, cosyntropin testing revealed serum cortisol levels higher than those usually associated with hypoadrenal shock. Positive response was defined as maintenance of blood pressure with a decrease to less than 25% of baseline pressor requirements within 48 hours of treatment. We hypothesize a syndrome of functional hypoadrenalism in patients with multisystem critical illness and refractory shock responsive to glucocorticoid administration in doses simulating physiologic stress response despite cosyntropin stimulation test results that would rule out hypoadrenalism in a normal person.
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PMID:Occult hypoadrenalism in critically ill patients. 815 74


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