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 rare case of pancreatic exocrine carcinoma with an endocrine component secreting adrenocorticotropic hormone (ACTH) is reported and discussed in relation to other cases previously published. The patient initially presented with a severe form of diabetes, which was treated accordingly. Persistence of hyperglycemia, along with other metabolic alterations and marked hypokalemia, led to the suggestion of abnormal ACTH secretion. In this patient, however, a florid Cushing's syndrome was not observed. The patient also developed hematological alterations, mainly leukopenia and thrombocytopenia, whose origins were unclear. At autopsy, a poorly-defined mass was discovered between the body and tail of the pancreas. Standard histology showed a moderately-differentiated adenocarcinoma. Immunohistochemical analysis of the tumor specimen demonstrated the presence of some neoplastic cells immunoreactive for chromogranin A, neuron-specific enolase and ACTH. These findings are consistent with the existence of an endocrine component within the exocrine carcinoma with ACTH differentiation.
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PMID:Pancreatic exocrine carcinoma producing adrenocorticotropic hormone. 131 74

This study evaluated the effects of naloxone hydrochloride in the treatment of Escherichia coli-induced shock in baboons. The baboons were studied for 12 hours and monitored for survival times. All baboons were intravenously infused for two hours with E coli and treated as follows: group 1, E coli (control); group 2, E coli plus naloxone hydrochloride, 0.5 mg/kg bolus plus 0.5 mg/kg/h for 9.5 hours; and group 3, E coli plus naloxone hydrochloride, 2.0 mg/kg bolus plus 2.0 mg/kg/h for 3.8 hours. Naloxone was administered after arterial pressure had reached the nadir (more than two hours following initiation of E coli infusion). Mean arterial pressure was supported by the lower dose of naloxone; however, sustained leukopenia and neutropenia were not reversed by its infusion. Naloxone prevented the increase in plasma beta-endorphin level and blunted the increase in plasma cortisol level. Despite these effects, naloxone did not prevent multiple-organ disease and did not decrease mortality.
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PMID:Evaluation of naloxone therapy for Escherichia coli sepsis in the baboon. 296 70

1. Tumour necrosis factor (TNF-alpha) is involved in the pathogenesis of splanchnic artery occlusion (SAO) shock. On the other hand, inhibition of TNF-alpha is an important component of the mechanism of action of melanocortins in reversing haemorrhagic shock. We therefore investigated the effects of the melanocortin peptide ACTH-(1 - 24) (adrenocorticotropin fragment 1 - 24) on the vascular failure induced by SAO shock. 2. SAO-shocked rats had a decreased survival rate (0% at 4 h of reperfusion, while sham-shocked rats survived for more than 4 h), enhanced serum TNF-alpha concentrations (755+/-81 U ml-1), decreased mean arterial blood pressure, leukopenia, and increased ileal leukocyte accumulation, as revealed by means of myeloperoxidase activity (MPO=9.4+/-1 U g-1 tissue). Moreover, aortic rings from shocked rats showed a marked hyporeactivity to phenylephrine (PE, 1 nM - 10 microM) (Emax and ED50 in shocked rats=7.16 mN mg-1 tissue and 120 nM, respectively; Emax and ED50 in sham-shocked rats=16.31 mN mg-1 tissue and 100 nM, respectively), reduced responsiveness to acetylcholine (ACh, 10 nM-10 microM) (Emax and ED50 in shocked rats=30% relaxation and 520 nM, respectively; Emax and ED50 in sham-shocked rats=82% relaxation and 510 nM, respectively) and increased staining for intercellular adhesion molecule-1 (ICAM-1). 3. ACTH-(1 - 24) [160 microg kg-1 intravenously (i.v.), 5 min after SAO] increased survival rate [SAO+ACTH-(1 - 24)=80% at 4 h of reperfusion], reversed hypotension, reduced serum TNF-alpha (55+/-13 U ml-1), ameliorated leukopenia, reduced ileal MPO (1.2+/-0.2 U g-1 tissue), restored the reactivity to PE, improved the responsiveness to ACh and blunted the enhanced immunostaining for ICAM-1 in the aorta. 4. Adrenalectomy only in part - but not significantly - reduced the ACTH-induced shock reversal, the survival rate of SAO+ACTH-(1 - 24) adrenalectomized rats being 60% at 4 h of reperfusion; and methylprednisolone (80 mg-1 i.v., 5 min after SAO) had a non-significant effect (10% survival) at 4 h of reperfusion. 5. The present data show that melanocortins are effective also in SAO shock, their effect being, at least in part, mediated by reduced production of TNF-alpha. Furthermore, they demonstrate, for the first time, that this inhibition is responsible for the adrenocorticotropin-induced reversal of vascular failure and leukocyte accumulation.
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PMID:Adrenocorticotropin reverses vascular dysfunction and protects against splanchnic artery occlusion shock. 1051 67

In this crossover study, we compared the peak responses of cortisol to low-dose (1 microg/1.73 m(2)) and standard-dose (250 microg/1.73 m(2)) adrenocorticotropic hormone (ACTH) stimulation tests in 90 full-term newborns (37 to 42 weeks gestational age, birthweight > 2,500 g, aged 4 to 7 days): 30 with sepsis syndrome, 30 with respiratory distress (RD) and 30 normal infants. Basal cortisol and ACTH were measured in a fasting venous sample. Serum cortisol concentrations were measured 30 minutes after low-dose ACTH and 60 minutes after standard-dose ACTH by radioimmunoassay (RIA). The mean basal circulating cortisol concentration and peak cortisol responses to low-dose and standard-dose ACTH tests were higher in stressed infants with sepsis and RD compared to normal. Basal but not ACTH-stimulated cortisol concentrations were significantly higher in newborns with sepsis versus those with RD. Circulating cortisol concentrations after the low-dose ACTH test were correlated significantly with those obtained after the standard-dose ACTH test (r = 0.814, P <.001). Clinical subgrouping of septic newborns showed that those with leukopenia (5/10 died) and with meningitis (6/12 died) had significantly lower basal and peak cortisol responses to the low-dose ACTH test (but not the standard-dose ACTH test) versus those with leukocytosis (3/20 died) and without meningitis (2/18 died), respectively. In addition, septic newborns who died had significantly lower circulating cortisol concentrations and lower cortisol responses to the low-dose ACTH test (but not the standard-dose test) versus those who survived the stress. On an individual basis, only 2 septic newborns (both died) had low basal cortisol levels (<5 microg/dL) and cortisol responses less than 15 microg/dL after the low-dose ACTH test. Four more septic newborns had basal cortisol above 5 microg/dl but cortisol responses below 20 microg/dL after the low-dose ACTH test. These 4 newborns (4/30) with inadequate adrenocortical response to low-dose ACTH during sepsis had high mortality (3/4 died) and represented a subgroup of septic newborns that should be diagnosed, using a low-dose ACTH test, and treated early. These data suggest that the low-dose ACTH test may be more disciminatory than the standard-dose test among babies under stress. Increasing the cut-point level of basal cortisol in stressed infants to the lowest level of cortisol response to low-dose ACTH in normal newborns, followed by the use of a low-dose ACTH test, appears to select some newborns who need and may improve on corticosteroid therapy. Further studies are required to investigate whether supplementation with stress doses of hydrocortisone may improve the outcome in these patients.
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PMID:Circulating adrenocorticotropic hormone (ACTH) and cortisol concentrations in normal, appropriate-for-gestational-age newborns versus those with sepsis and respiratory distress: Cortisol response to low-dose and standard-dose ACTH tests. 1476 73