Endocrine studies in heroin addicts

Afrasiabi, M.; Flomm, Michael; Friedlander, Herbert D.; Valenta, Lubomir J.

doi:10.1016/0306-4530(79)90028-3

Cited by 27 publications

(11 citation statements)

References 18 publications

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“…Consistent with this mechanism, several crosssectional studies in heroin-and methadone-dependent subjects have demonstrated decreased gonadotropin and testosterone levels [6][7][8] that may be dose dependent [8] and partially reversed by the administration of opiate antagonists [9]. The effect of opiates on GnRH and gonadotropin secretion, however, may wane over time because of the development of tolerance [9,10]. Although the results of these studies should be interpreted with caution because of observational design, small sample size, and the presence of potentially confounding variables such as malnutrition and comorbid conditions, the finding of central hypogonadism with opiate administration in animal experiments further supports the conclusions drawn in the clinical studies [11,12].…”

Section: Hypothalamic-pituitary-gonadal Axismentioning

confidence: 86%

Opiate Drug Use: A Potential Contributor to the Endocrine and Metabolic Complications in Human Immunodeficiency Virus Disease

2003

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Endocrine and metabolic abnormalities are common in human immunodeficiency virus (HIV) disease and have been attributed to both the disease and its treatment. Other risk factors and behaviors may also be important. Approximately 28% of new HIV infections occur in users of injection drugs, such as opiates. We focus on the effects of opiates on multiple endocrine systems and their potential to contribute to the metabolic and endocrine problems in HIV. Opiate use has been associated with hypogonadism, adrenal dysfunction, reduced bone mineral density, and growth-hormone abnormalities. In addition, some studies have suggested abnormalities in glucose and lipid metabolism among opiate users. Although much of the evidence should be viewed as preliminary, these potential abnormalities should be kept in mind when treating opiate-dependent patients infected with HIV.

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Section: Hypothalamic-pituitary-gonadal Axismentioning

confidence: 86%

Opiate Drug Use: A Potential Contributor to the Endocrine and Metabolic Complications in Human Immunodeficiency Virus Disease

2003

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“…Morphine and morphine analogs increase PRL release acutely [68,69] and chronically in humans [70,71]. Chronic methadone users have normal basal PRL levels but each daily dose causes a transient increase [72].…”

Section: Opiates and Cocainementioning

confidence: 99%

Drugs and prolactin

Molitch

2008

Pituitary

143

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Medications commonly cause hyperprolactinemia and their use must be differentiated from pathologic causes. The most common medications to cause hyperprolactinemia are the antipsychotic agents, although some of the newer atypical antipsychotics do not do so. Other medications causing hyperprolactinemia include antidepressants, antihypertensive agents, and drugs which increase bowel motility. Often, the medication-induced hyperprolactinemia is symptomatic, causing galactorrhea, menstrual disturbance, and erectile dysfunction. In the individual patient, it is important differentiate hyperprolactinemia due to a medication from a structural lesion in the hypothalamic-pituitary area. This can be done by stopping the medication temporarily to determine if the prolactin (PRL) levels return to normal, switching to another medication in the same class which does not cause hyperprolactinemia (in consultation with the patient's physician and/or psychiatrist), or by performing an MRI or CT scan. If the hyperprolactinemia is symptomatic, management strategies include switching to an alternative medication which does not cause hyperprolactinemia, using estrogen/testosterone replacement, or cautiously adding a dopamine agonist.

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“…1,18,34 After being given 5 mg of morphine intravenously, women have rapid development of lower leuteinizing hormone (LH) levels. 22,36 These findings have led to diagnoses of hypogonadotrophic hypogonadism in these populations 1,2,16,18 and demonstration of decreased estriol and DHEAS levels in pregnant heroin addicts receiving lowdose daily methadone maintenance. 2,16 Testosterone levels reported in female opioid consumers are apparently, however, limited to the data of Cofrancesco et al, 8 who reported 16% lower total testosterone values (P Ͻ .03) among the 31 women on methadone maintenance within in a group of 196 subjects at high risk for HIV disease.…”

mentioning

confidence: 97%

“…12 Evidence of opioid-induced inhibition of adrenal function includes inhibited cortisol production immediately after acute intravenous opioid administration 17,54 and soon after oral opioid ingestion, 53 impaired cortisol metabolism during intrathecal 1 or oral 16 therapy, and subnormal levels of dehydroepiandrosterone sulfate (DHEAS), the major adrenal androgen, in a majority of both men and women during chronic use of sustained-action oral or transdermal opioids. 12,16 Evidence of OE in female opioid consumers has been reported infrequently, even though amenorrhea, hypomenorrhea, sexual dysfunction, fatigue, and depression are prominent in many female heroin addicts, including those receiving once daily methadone therapy 2,16,42 and in most women receiving continuous intrathecal opioids for treatment of nonmalignant pain. 1,18,34 After being given 5 mg of morphine intravenously, women have rapid development of lower leuteinizing hormone (LH) levels.…”

mentioning

confidence: 98%