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      Chronic Heroin Dependence Leading to Adrenal Insufficiency

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      Case Reports in Endocrinology

      Hindawi Publishing Corporation

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          Abstract

          Opioids have been the mainstay for pain relief and palliation over a long period of time. They are commonly abused by drug addicts and such dependence usually imparts severe physiologic effects on multiple organ systems. The negative impact of opioids on the endocrine system is poorly understood and often underestimated. We describe a patient who developed severe suppression of the hypothalamic-pituitary adrenal (HPA) axis leading to secondary adrenal insufficiency due to long standing abuse of opioids.

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          Most cited references 13

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          DHEAS deficiency during consumption of sustained-action prescribed opioids: evidence for opioid-induced inhibition of adrenal androgen production.

          Dehydroepandrosterone (DHEA)-dehydroepiandrosterone sulfate (DHEAS) deficiency often produces fatigue, depression, weakness, and sexual dysfunction, which improve during replacement therapy. DHEAS deficiency is a sensitive marker for generalized adrenal insufficiency, but it has not been related to opioid ingestion. DHEAS values were determined in 34 male and 32 female opioid-consuming outpatients aged 35-78 years, in stable health, and in 33 male and 53 female nonopioid-consuming control subjects. No subjects used anticonvulsants or corticosteriod medications, and none had malignant, collagen-vascular, or endocrine disease other than menopause or opioid-induced androgen deficiency. Adrenocorticotropic hormone (ACTH) values were measured in 94 of 152 subjects. DHEAS levels were lower in opioid consumers than in control subjects in a dose-related pattern (P < .01), were below age-specific norms in 67% of opioid consumers and 8% of controls (P < .001), and were below our laboratory's lowest detection limit (15 mug/dL) in 29% of opioid users and 1% of controls (P < .001). DHEAS values were also lower in opioid-consuming nonsmokers than in smokers (P < .05) and were unrelated to body mass index or concurrent hormonal replacement therapy. ACTH levels were normal and unrelated to opioid use. The combination of subnormal DHEAS levels in the presence of normal ACTH values in most opioid-consuming patients suggests that these low levels result from factors other than diminished adrenal ACTH stimulation. The study documents a dose-related DHEAS deficiency in a majority of nonhospitalized adults who are chronically consuming sustained-action oral or transdermal opioids for control of nonmalignant pain. This deficiency in these patients has not previously been recognized and is probably symptomatic. Evaluation of replacement therapy should receive high priority.
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            Morphine directly modulates the release of stimulated corticotrophin-releasing factor-41 from rat hypothalamus in vitro.

            The actions of opioids and opiates on the hypothalamo-pituitary-adrenal axis are currently controversial. In the rat, morphine is reported to both stimulate and inhibit ACTH and corticosterone secretion, but the precise sites and mechanisms of these effects have remained unclear. To analyze further the hypothalamic actions of morphine, we have investigated its effect on hypothalamic fragments in vitro and measured the major CRF, CRF-41, by a specific RIA. The acute effects of morphine on both basal and stimulated ACTH release from dispersed pituitary cells were also investigated. Morphine (10(-8)-10(-6) M) did not significantly alter the basal secretion of CRF-41. However, similar concentrations of morphine inhibited CRF-41 release stimulated by norepinephrine in a dose-dependent manner. Similarly, morphine (10(-6) M) inhibited acetylcholine (10(-9) M)- and serotonin (10(-7) M)-stimulated CRF-41 release. The stimulatory effect on CRF-41 release induced by veratridine (10(-6) M) was inhibited by approximately 50% in the presence of morphine. KCl (28 nM)-mediated CRF-41 release was also significantly inhibited by morphine. Naloxone (10(-7)-10(-5) M) had no significant effect on either basal or norepinephrine-induced CRF-41 release, but reversed the inhibitory effect of morphine on norepinephrine-induced CRF-41 secretion in a dose-dependent manner. Morphine (10(-6)-10(-5) M) had no effect on either basal or CRF-41-stimulated ACTH release from dispersed pituitary cells. These data suggest that the predominant effect of morphine on hypothalamic CRF-41 release in vitro is suppression of the release induced by a variety of putative neurotransmitters and depolarizing agents. This inhibitory effect is reversed by naloxone, suggesting that it is mediated by opiate receptors, presumably situated directly on CRF-41 neurons.
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              Acute effects of intravenous heroin on the hypothalamic-pituitary-adrenal axis response: a controlled trial.

              Heroin dependence is associated with a stressful environment and with dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis. The present study examined the acute effects of intravenous heroin versus placebo on the HPA axis response in heroin-dependent patients. Twenty-eight heroin-dependent patients in heroin-assisted treatment and 20 age- and sex-matched healthy participants were included in a controlled trial in which patients were twice administered heroin or saline in a crossover design, and healthy controls were only administered saline. The HPA axis response was measured by adrenocorticotropic hormone (ACTH) levels and by cortisol levels in serum and saliva before and 20 and 60 minutes after substance administration. Craving, withdrawal, and anxiety levels were measured before and 60 minutes after substance application. Plasma concentrations of heroin and its main metabolites were assessed using high-performance liquid chromatography. Heroin administration reduces craving, withdrawal, and anxiety levels and leads to significant decreases in ACTH and cortisol concentrations (P < 0.01). After heroin administration, cortisol concentrations did not differ from healthy controls, and ACTH levels were significantly lower (P < 0.01). In contrast, when patients receive saline, all hormone levels were significantly higher in patients than in healthy controls (P < 0.01). Heroin-dependent patients showed a normalized HPA axis response compared to healthy controls when they receive their regular heroin dose. These findings indicate that regular opioid administration protects addicts from stress and underscore the clinical significance of heroin-assisted treatment for heroin-dependent patients.
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                Author and article information

                Journal
                Case Rep Endocrinol
                Case Rep Endocrinol
                CRIE
                Case Reports in Endocrinology
                Hindawi Publishing Corporation
                2090-6501
                2090-651X
                2014
                20 August 2014
                : 2014
                Affiliations
                Department of Diabetes and Endocrinology, Prince Charles Hospital, Cwm Taf NHS Trust, Gurnos, Merthyr Tydfil, CF47 9DT, UK
                Author notes

                Academic Editor: Anthony J. O'Sullivan

                Article
                10.1155/2014/461816
                4158160
                Copyright © 2014 Gautam Das.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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