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      Adrenal insufficiency in acute oral opiate therapy

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          Summary

          Opiate drugs such as morphine are in extensive use for pain relief and palliation. It is well established that these drugs can cause changes in endocrine function, but such effects are not always sufficiently appreciated in clinical practice, especially in relation to the hypothalamic–pituitary–adrenal (HPA) axis. Herein, we report on an 18-year-old man who was diagnosed with a slipped left femoral epiphysis following a long history of pain in his leg. On examination, he was thought to look relatively young for his age and therefore the orthopaedic surgeons arranged an endocrine assessment, which showed an undetectable concentration of serum cortisol and a suppressed concentration of testosterone; therefore, he was referred urgently with a diagnosis of hypopituitarism. We elicited a history that he had been treated with opiate analgesics for 3 days at the time of his original blood tests. Full endocrine assessment including a short Synacthen test revealed that he now had normal adrenal and pituitary function. We conclude that his morphine therapy had caused profound suppression of his HPA and pituitary–gonadal axes and suggest that clinicians should be aware of these significant changes in patients on even short-term opiate therapy.

          Learning points

          • Therapy with opiates is the standard therapy for severe acute and chronic pain.

          • Such drugs cause profound changes in endocrine function.

          • Importantly, opiates suppress the HPA axis at a central level.

          • Short-term therapy with morphine could be the cause of biochemical adrenocortical insufficiency.

          • Morphine and related drugs also suppress the pituitary–gonadal axis.

          • After discontinuation of therapy with such drugs, adrenal function improves.

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          Most cited references 8

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          The effect of opioid therapy on endocrine function.

           A. J. Brennan (2013)
          Opioids are an established option in the analgesic armamentarium for managing moderate-to-severe chronic pain. Long-term opioid use, however, is associated with several potential adverse effects and toxicities, such as peripheral edema, immune suppression, hyperalgesia, sleep apnea, and changes in endocrine function, many of which are not fully appreciated. Opioid endocrinopathy can greatly affect patients, causing reduced sexual function, decreased libido, infertility, mood disorders, osteoporosis, and osteopenia. Furthermore, although opioid endocrinopathy appears to be common, many patients do not report their symptoms, thus causing this adverse effect to go unnoticed and without clinical monitoring, particularly in patients chronically taking the equivalent of ≥ 100 mg of morphine daily. Indeed, diagnosing hypogonadism as opioid-related can be challenged by other influences on endocrine function, such as pain pathophysiology, comorbidities, other drug therapies, and patient age. Management options for opioid endocrinopathy include discontinuing opioid therapy, reducing the opioid dose, switching to a different opioid, and hormone supplementation. Copyright © 2013 Elsevier Inc. All rights reserved.
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            Opioid induced hypogonadism

            Hypogonadism in both sexes is a common result of ongoing treatment with opioid analgesics and can be treated with suitable hormone replacement therapy
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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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                Author and article information

                Journal
                Endocrinol Diabetes Metab Case Rep
                Endocrinol Diabetes Metab Case Rep
                edm
                EDM Case Reports
                Endocrinology, Diabetes & Metabolism Case Reports
                Bioscientifica Ltd (Bristol )
                2052-0573
                01 January 2014
                2014
                : 2014
                Affiliations
                Department of Endocrinology and Metabolic Diseases Università Cattolica del Sacro Cuore RomeUK
                [1 ]Oxford Centre for Diabetes, Endocrinology and Metabolism Oxford University Hospitals NHS Trust Old Road, Oxford, OX3 7LEUK
                Author notes
                Correspondence should be addressed to V Stokes Email: vickystokes22@ 123456hotmail.com
                Article
                EDM130071
                10.1530/EDM-13-0071
                3965279
                © 2014 The authors
                Categories
                Unusual Effects of Medical Treatment

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