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)

The hippocampus is a major center for the regulation of the hypothalamic-pituitary-adrenal axis. There is experimental evidence that chronic exposure to high levels of glucocorticoids may be toxic to the hippocampus. We observed elevated mean basal and 60-min cortisol (F) levels in response to adrenocorticotropin stimulation (0.25 mg cortrosyn, i.v. bolus infusion) in 15 children with HIV infection. Furthermore, in eight of the children for whom data was available, in addition to high peripheral cortisol levels, neurologic dysfunction and hippocampal atrophy were noted on CT scan. These preliminary data suggest that in HIV-infected children an altered cortisol secretion may be associated with specific central nervous system damage.
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PMID:Altered cortisol response and hippocampal atrophy in pediatric HIV disease. 826 54

alpha-Melanocyte-stimulating hormone (alpha-MSH), adrenocorticotrophic hormone (ACTH), beta-endorphin, cortisol, and the cytokines interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF alpha) were measured in 80 AIDS patients (group IV CDC) and in healthy hospital personnel. The average plasma alpha-MSH was significantly greater in AIDS patients than in control subjects; no significant differences between groups were observed in the average concentrations of ACTH, cortisol, and beta-endorphin; plasma cytokines were likewise similar in the two groups. Plasma concentrations of alpha-MSH and ACTH were inversely related in AIDS patients and a similar inverse relation between alpha-MSH and IL-6 was also observed in these patients. There were positive relations among elevated circulating ACTH, cortisol, IL-6, and high fever in AIDS patients with severe concomitant disease. Plasma alpha-MSH concentrations within a specific range correlated positively with 6 month survival. Because cytokines can stimulate HIV expression in certain cell types and they are believed to have a role in disease progression in HIV-infected patients, it may be that a potent endogenous modulator of cytokine action such as alpha-MSH is crucial to survival in these patients.
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PMID:Proopiomelanocortin-derived peptides and cytokines: relations in patients with acquired immunodeficiency syndrome. 838 70

From among patients hospitalized at Kenyatta National Hospital, 6 subjects diagnosed as HIV positive by at least one HIV ELISA antibody test and 10 HIV negative control patients were enrolled into a study and matched for age, sex, level of education, and ethnic group. A baseline blood sample was obtained from each patient at 2.00 p.m. for complete blood count biochemical assays for B endorphin and adrenocorticotropic hormone (ACTH) as well as an HIV ELISA test. HIV positive patients were informed of ELISA test results and transferred to isolation rooms. Blood was drawn on the next 3 consecutive days. Concentration of ACTH was measured by radio-immunoassay. B-endorphin assay was almost the same as for ACTH. Assay sensitivity was 5 pg/ml with a range of 5-500 pg/ml. Multivariate and univariate analyses of variance with repeated measures were used to evaluate the differences in biochemical responses between HIV positive (under stress) patients and HIV negative (with no stress) patients. (ACTH and B endorphin concentrations in plasma were obtained on the day of diagnosis and at different times 1 and 72 hours thereafter. Change scores (pre-post 72 hours) in plasma ACTH and B- endorphin concentrations support the hypothesis that patients diagnoses to have AIDS experience stress mediated biochemical changes. The change score distributions predominantly indicated elevated concentrations of each neurohormone. By contrast, HIV, negative patients exhibited more random patterns of change following diagnosis. The results could be used in situations of stress-induced immuno-incompetency. Identification of significant effect of stress on neuroendocrine response and immune competence in patients diagnoses as HIV positive may suggest methods of prolonging the life of patients who otherwise have no definitive treatment. B endorphin antagonists such as Naltrexone may exert beneficial effects in selected HIV positive patients by modifying the endogenous opioid systems.
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PMID:Behavioural mechanisms in AIDS patients under stress. 839 Mar 50

Patients with acquired immune deficiency syndrome (AIDS) are reported to have increased basal cortisol and reduced stimulated cortisol release, but the dysfunction in the hypothalamic-pituitary-adrenal (HPA) axis is not yet understood in patients with human immunodeficiency virus (HIV) infection during the advanced stage of disease that precedes the development of AIDS. To understand the status of the HPA axis during this phase of HIV infection, 25 non-AIDS ambulatory patients with advanced HIV infection and without evidence of adrenal or pituitary insufficiency were studied. Ovine corticotropin-releasing hormone was administered (1 microgram/kg BW) intravenously and plasma cortisol and adrenocorticotropin (ACTH) were measured over the following 120 minutes. Based on a standard response curve, obtained from CRH testing of 10 HIV negative volunteers with no HPA abnormalities, 13 patients were found to have normal response (group 1), 6 patients had reduced ACTH and cortisol response (group 2) and 6 patients had normal ACTH with reduced cortisol response (group 3). Basal cortisol and basal ACTH were comparable for control subjects and groups 1, 2, and 3. This suggests that, in advanced non-AIDS HIV patients with no clinical evidence of pituitary or adrenal disease, about 25% (group 2) have reduced pituitary reserve with high basal ACTH and cortisol, and about 25% (group 3) have reduced adrenal reserve with high basal cortisol and inappropriately normal basal ACTH, whereas about 50% (group 1) maintain normal HPA axis activity with increased basal cortisol secretion. The exact physiopathologic mechanism is not yet known, but an enhanced CRH production by the hypothalamus may explain the alterations in the HPA axis in advanced HIV disease.
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PMID:Hypothalamic-pituitary-adrenal function in non-AIDS patients with advanced HIV infection. 848 93

There is increasing evidence that cytokines contribute to the immunopathogenesis of human immunodeficiency virus (HIV) infection. It may be, therefore, that compensatory rises in circulating cytokine antagonists also occur in HIV infection and that such changes mark disease progression. To test this idea, plasma concentrations of the cytokine antagonists alpha-melanocyte-stimulating hormone (alpha-MSH), interleukin-1 receptor antagonist (IL-1ra), and soluble tumor necrosis factor receptor (sTNFr) were measured in patients of different Centers for Disease Control (CDC) categories of HIV infection and in seronegative controls. Plasma levels of all these cytokine antagonists were higher in HIV-infected patients. IL-1ra and sTNFr concentrations were correlated with indicators of disease activity: positively with plasma neopterin and negatively with CD4+ T lymphocyte counts. alpha-MSH and sTNF r were greater in CDC groups III and IV, whereas IL-1ra was elevated only in the latter group. Because cytokines activate the hypothalamic-pituitary-adrenal axis and adrenal steroids inhibit cytokine production, we measured circulating adrenocorticotropic hormone (ACTH) and cortisol in HIV-infected patients and investigated relations among these hormones, cytokine antagonists, and markers of disease progression. It appears that these physiological modulators of cytokine activity are not closely linked to sTNFr, IL-1ra and alpha-MSH: there were no significant correlations between plasma concentrations of ACTH or cortisol and those of cytokine antagonists, nor were there correlations between hormones and markers of disease progression such as neopterin or CD4+ T cell counts. It is notable that severe adrenal insufficiency was extremely rare (3%) in HIV-infected patients; it was confined to the AIDS group and was consistently secondary to ACTH deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma concentration of cytokine antagonists in patients with HIV infection. 852 84

To examine the potential role of stress hormones in the progression of HIV infections, we developed an in vitro model system that investigates the effects of cortisol, adrenocorticotropin-releasing hormone (ACTH) and beta-endorphin on the natural killer cell activity of lymphocytes from normal subjects and AIDS patients. The system employs a 4 hr 51Cr release assay and K562 target cells. Direct addition of cortisol (0.05, 0.1, and 0.2 microgram/ml) or ACTH (10(-6) to 10(-8) M) to the mixture of effector and prelabeled target cells did not produce any significant immunoregulatory effects on the NK cell activity of normal lymphocytes. Direct addition of beta-endorphin (10(-13) to 10(-17) M) to the mixture of effector and prelabeled target cells did not produce any significant immunoregulatory effects on the NK cell activity of lymphocytes from normal or AIDS subjects. However, cortisol and ACTH significantly inhibited the NK activity of lymphocytes from AIDS patients. The selective inhibitory effects of cortisol and ACTH in patients with HIV infections are consistent with a model which proposes that stress related neurohormones and/or neuropeptides may be involved in the progression of HIV infections.
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PMID:Selective inhibitory effects of stress hormones on natural killer (NK) cell activity of lymphocytes from AIDS patients. 854 34

The objective of the study was to relate plasma dehydroepiandrosterone sulfate (DHEA-S) concentrations to the progression of HIV infection in individual HIV-infected men with hemophilia and to obtain information on the cause of DH EA-S alterations. Blood samples were obtained from 16 men with hemophilia; in 9 men serial samples were available for up to 11 years after HIV-1 infection. Control samples were obtained from men of comparable ages without hemophilia or HIV infection. Measurements were made of CD4+ cell counts, plasma adrenocorticotropic hormone (ACTH), cortisol, DHEA, DHEA-S, and prolactin. Before HIV infection, men with hemophilia had significantly lower plasma levels of DHEA-S than control men. After infection, 3 of 9 subjects studied serially had little or no change in plasma DHEA-S levels or in CD4+ cell counts over 11 years. Four of the 9 i n whom AIDS developed had progressive decreases in plasma DHEA-S concentrations that, in some cases, preceded a precipitous fall in CD4+ cell counts. Major decreases in plasma DHEA-S levels before falls in CD4+ counts were observed in 2 ot her subjects who had other severe illnesses. None of the decreases in DHEA-S levels were associated with decreased concentrations of plasma cortisol, ACTH, or prolactin. We conclude that plasma DHEA-S is an indicator of general health rather than a specific indicator for progression of HIV. The decrease in plasma DHEA-S is not related to ACTH stimulation of the adrenal gland or to cortisol secretion, but it may be related to cytokines that can inhibit 17-hydroxylation of DH EA-S precursors.
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PMID:Longitudinal study of adrenal steroids in a cohort of HIV-infected patients with hemophilia. 864 55

Interactions between HPA (Hypothalamic-pituitary-axis) and immune system seem to involve the EPO (endogenous opioid peptides) system, as shown by some recent findings. Possible relationships between beta-endorphin (beta-End) synthesis and severity rate of immunodeficiency have been studied in 48 HIV Ab positive patients, at different stages of infection. A statistically significant decrease in the beta-End synthesis was observed in these patients, as compared to a control group of 19 healthy subjects, but this decrease was not related to the CD4+T lymphocytes number. Plasmatic levels modifications of HPA-related peptides were not observed in the IVC1 CDC group.
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PMID:Beta-endorphins ACTH and cortisol in CSF and plasma of HIV infected patients. 876 83

Documented evidence supports the "cortisol connection' theory of acquired immune deficiency syndrome, linking glucocorticoid metabolism with immune function, and human immunodeficiency virus with them both. The peptide T subregion of gp 120 of human immunodeficiency virus apparently utilizes cellular melanocyte stimulating hormone receptors to competitively inhibit the blocking of interleukin-1 by melanocyte-stimulating hormone. Interleukin-1 stimulates CD8+ T-lymphocyte proliferation, as well as causing the release of corticotropin-releasing hormone, thereby stimulating the release of adrenocorticotrophic hormone and cortisol. Gp 120 also induces upregulation of adrenocorticotrophic hormone-related messenger ribonucleic acid. This apparently separate glucocorticoid metabolic route utilized by human immunodeficiency virus is the basis of the cortisol excess seen in human immunodeficiency virus infection. In vitro glucocorticoid-resistant lymphoid cells are resistant to human immunodeficiency virus infection as well. Viral resistance is also observed in patients who demonstrate glucocorticoid resistance. Glucocorticoid-responsive elements are contained in the human immunodeficiency virus (proviral and viral) genome that appear to regulate human immunodeficiency virus replication. Similarly, lymphoid-cell development and regulation depend on glucocorticoids. One may take advantage of this view of human immunodeficiency virus pathogenesis to create new methods of treatment.
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PMID:Acquired immune deficiency syndrome: the glucocorticoid solution. 881 17

The circadian rhythms of plasma growth hormone (GH), insulin-like growth factor type I (IGF-I), cortisol, adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), and prolactin (PRL) were evaluated in 13 HIV-seropositive patients (8 males and 5 females; mean age [+/-SD], 30 +/- 5 years), classified as CDC C2. Sixteen clinically healthy subjects (9 males and 7 females; mean age [+/-SD], 32 +/- 8 years) were chosen as control group. Samples were taken every 4 hr from 04:00 to 20:00 and every 2 hr from 20:00 to 04:00. Plasma GH was evaluated by IRMA procedure, plasma IGF-I by RIA (after separation of soluble IGF-I from IGF-I-binding proteins, using acid-ethanol extraction), plasma cortisol by a solid-phase RIA, plasma ACTH by double-antibody RIA, and serum TSH and serum PRL by a solid-phase two-site fluoroimmunometric assay. Rhythmometric data were analyzed by single and population mean cosinor analysis; the comparison of the parameters of the rhythm between patients and controls was carried out by the mesor test and the amplitude-acrophase Hotelling test. Alterations of the circadian pattern of GH, IGF-I, cortisol, ACTH, TSH, and PRL were demonstrated in HIV-seropositive patients. In fact, the circadian profiles of these hormones were clearly flattened and no statistically significant 24-hr rhythm was detectable (with the exception of cortisol). These results are consistent with the hypothesis that alterations of the circadian temporal structure may already be present in HIV-seropositive patients without wasting and infectious complications.
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PMID:Circadian secretory pattern of growth hormone, insulin-like growth factor type I, cortisol, adrenocorticotropic hormone, thyroid-stimulating hormone, and prolactin during HIV infection. 931 Feb 92


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