Hyperprolactinemia and Galactorrhea Associated With Marijuana Use : The Endocrinologist

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00019616-200611000-00003ReportThe EndocrinologistThe Endocrinologist© 2006 Lippincott Williams & Wilkins, Inc.16November 2006 p 308-310Hyperprolactinemia and Galactorrhea Associated With Marijuana UseCase ReportRizvi, Ali A. MD, FACP, FACEFrom the Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of South Carolina School of Medicine, Columbia, South Carolina.Reprints: Ali A. Rizvi, MD, FACP, FACE, Two Medical Park, Suite 502, Columbia, SC 29203. E-mail: [email protected] 23-year-old woman presented with breast tenderness and bilateral nipple discharge. She was found to have a prolactin level of 136.9 ng/mL, negative serum pregnancy test, normal pituitary anatomy on imaging, and no other discernible cause for the hyperprolactinemia. Bromocriptine treatment normalized the prolactin and considerably reduced the galactorrhea. After 3 months of therapy, the patient revealed that she had been a heavy weekend marijuana user for more than 1 year but had stopped completely recently. Bromocriptine was discontinued while the patient abstained from further marijuana smoking. One month later, the prolactin level was normal and no breast abnormalities or nipple discharge was evident. In conclusion, periodic, heavy, and regular marijuana use can cause clinically significant hyperprolactinemia over the long term that can present a diagnostic dilemma and lead to unnecessary medical therapy. It should be considered as a reversible cause of elevated prolactin and should be kept in mind in the differential diagnosis of galactorrhea in women.Significant hyperprolactinemia is usually caused by lesions of the hypothalamus and pituitary gland in the form of tumors, cysts, trauma, and infiltrative disease or is a side effect of dopamine–agonist medications like antipsychotic agents. Prolactin elevations are rarely high enough in other situations to be clinically significant. The active compound of marijuana (cannabis), delta9-tetrahydrocannabinol, binds to endogenous receptors on or near the hypothalamus.1 This specific site of action may be the basis for alterations in hormone systems observed with marijuana use.2 Prolactin levels have been reported to be variably affected by cannabis with the limited number of studies reported thus far showing discrepant conclusions. A case is described here in which frequent and chronic marijuana use in a young woman led to elevated serum prolactin and resultant galactorrhea. Dopamine–agonist therapy was instituted with the assumption of either idiopathic or pituitary-based hyperprolactinemia until a link with marijuana smoking was suspected. Stopping the marijuana use led to complete resolution of both the hyperprolactinemia and its clinical manifestations, obviating the need for prolactin-lowering medication. A review of the pertinent medical literature and discussion of the possible underlying mechanisms of cannabis-associated hyperprolactinemia is presented.CASE REPORTA 23-year-old archeology student sought medical attention because of bilateral breast enlargement, tenderness, and galactorrhea for 9 months. The nipple discharge had initially been scant, clear, and on expression only, but subsequently became spontaneous and milky white in color. She had been using oral contraceptives for the past 5 years and had regular menstrual flow without any amenorrhea or menstrual irregularities. There was no history of menstrual difficulties before starting the oral contraceptives. Her medical problems included episodes of occipital neuralgia and bipolar disorder. Except for a laparoscopic knee procedure, she reported no major surgeries in the past. Medications at the time of the initial visit were as follows: 25 mg fluvoxamine twice daily, 150 mg bupropion twice daily, 300 mg zonisamide in the morning and 200 mg in the evening, 500 mg naproxen daily as necessary, and ethinyl estradiol/norgestimate (Ortho Tri-Cyclen) for birth control. She was single, sexually active, and had never been pregnant. She denied current or previous alcohol, tobacco, or substance use. On physical examination, she weighed 83 kg (182 lbs) and was 170 cm (67 inches) tall. There was mild facial acne but no hirsutism, thyromegaly, or visual field abnormality. Cardiac and lung examination was unremarkable. Breast examination revealed general tenderness to palpation and bilateral milky discharge on manual nipple expression. A prolactin level 1 year before this presentation was 26 ng/mL (reference range, 3–30 ng/mL). It had been requested by the patient's personal physician for evaluation of acne prior and unrelated to the onset of breast tenderness and discharge. A breast ultrasound done 6 months before the visit had been read as normal.Laboratory evaluation showed normal glucose, hemoglobin, serum creatinine, and liver and thyroid function. The prolactin level, carefully drawn without any antecedent nipple stimulation, was 136.9 ng/mL. Serum pregnancy test was negative. Magnetic resonance imaging (MRI) of the pituitary gland did not show any evidence of enlargement or adenoma. The patient was started on dopamine–agonist therapy with 1.25 mg bromocriptine daily on the assumption that the hyperprolactinemia was pituitary-based possibly resulting from a microadenoma that was not visible on the MRI scan. The prolactin level decreased to 31.3 ng/mL 10 weeks after initiating bromocriptine therapy and the breast symptoms lessened considerably. At a follow-up visit 3 months later, the patient was free of galactorrhea. However, she revealed that she had been using marijuana heavily and intermittently for the past 1 year, mainly on weekends. She wondered if that could have caused her breast tenderness and discharge. She had resolved to quit all marijuana use approximately 2 weeks before the appointment. In light of this information, it was decided to stop the bromocriptine, and the patient was told to abstain from further marijuana use. A prolactin level 1 month later was normal at 20.7 ng/mL. There has been no subsequent recurrence of galactorrhea or breast discomfort.DISCUSSIONThe endocrine effects of marijuana have received attention since the increased use of the drug as a recreational agent.2,3 Because of the known effects of cannabis on sexual functioning, changes in pituitary and reproductive hormones have been investigated.4,5 Endocrine abnormalities and their clinical effects are summarized in Table 1. By binding to brain receptors, cannabinoids can act on the central neurotransmitter systems involved in the regulation of neuropeptides and thus modulate anterior pituitary hormone secretion.1 A review of studies in the literature on this subject gives no consistent conclusions. The documented hormonal changes seem to depend on such factors as gender, acute versus chronic cannabis use, and the presence of concomitant alcohol and polysubstance dependence. Several small-scale studies showed that short-term (up to a few days) marijuana smoking in a controlled setting caused either a nonsignificant depression or no discernible change of the anterior pituitary hormones (luteinizing hormone, follicle-stimulating hormone, and prolactin) and testosterone in males6–8 and prolactin in females.9 However, the issue of chronic use is more complex with conflicting findings. In one analysis, the frequency of marijuana use seemed to have little effect on the levels of multiple hormones, including prolactin, in both sexes.5 Other reports seem to have very different implications. In chronic male cannabis smokers, depression of plasma testosterone10 and the occurrence of gynecomastia11 has been described. Of interest, Olusi12 reported significantly higher prolactin levels and gynecomastia in 3 young male cannabis users in whom no other cause (eg, liver disease, medications, and tumors) for these abnormalities could be found. Teoh et al13 studied the endocrine profiles of 18 women who were admitted to the hospital for treatment of alcohol/polysubstance dependence. Over 60% had elevated prolactin levels, and the authors suggested that measurement of this hormone might serve as a biologic marker for alcoholism and polysubstance abuse in women.JOURNAL/endst/04.03/00019616-200611000-00003/table1-3/v/2021-02-17T201820Z/r/image-tiff Effects of Marijuana Use on the Endocrine SystemMarkianos and Stefanis14 performed an interesting study in long-term cannabis users, and the ensuing pattern of variations in serum prolactin seen may explain the scenario encountered in the current patient. The subjects were deprived of cannabis for 3 days and allowed to smoke on the fourth day, ie, short periods of deprivation in a background of chronic use. On the third deprivation day, the serum prolactin and dopamine beta-hydroxylase as well as the mean arterial blood pressure were significantly elevated compared with the presmoking values and returned to this latter “baseline” after resumption of cannabis use. Their results suggested that chronic cannabis use reduced noradrenergic and enhanced central dopaminergic activity. They surmised that deprivation might have the opposite effect, possibly by alteration of presynaptic receptor mechanisms. It is worth noting that dopamine suppresses the pituitary release of prolactin and is the “prolactin-inhibitory factor.” With this explanation, it is conceivable that heavy but off-and-on (for example, weekend) use of marijuana in a chronic fashion over months or years can lead to significant hyperprolactinemia through this rebound or cyclic mechanism. In certain individuals, it can ostensibly lead to the distressing clinical manifestations of breast enlargement, tenderness, and nipple discharge. The findings in our patient of unexplained increased prolactin in the setting of chronic, intermittent cannabis use and complete biochemical and clinical resolution after cessation of marijuana smoking attests to this being a likely explanation. It is possible that a similar mechanism causes menstrual abnormalities or anovulation in female marijuana users through prolactin-induced gonadotropin and estrogen changes15; however, this aspect could not be evaluated in the current patient because of her oral contraceptive use.The patient described in this report had no radiologic evidence of a prolactin-producing pituitary tumor, although this was assumed to be the case initially before starting dopamine–agonist therapy. None of the medications she was taking are known to cause clinically significant hyperprolactinemia. Fluvoxamine and bupropion work by inhibition of serotonin reuptake in the brain but have not been known to potentiate the ability of 5-hydroxytryptamine to stimulate prolactin secretion.16 A literature search revealed no clinical reports of these agents inducing hyperprolactinemia. In fact, bupropion may even lower prolactin levels, presumably by blocking the reuptake of dopamine by tuberoinfundibular neurons.16 Oral contraceptives can rarely cause minor prolactin elevations and breast symptoms. However, the patient's complaints started after she had been on the oral contraceptives and the other medications for several years. Of note, her prolactin level was within normal range while she was on these medications, well before the start of cannabis use and the onset of galactorrhea. Her presenting features were temporally associated with cannabis smoking. They remitted when she stopped marijuana use without a change in any of the medications, arguing against the latter having played a role in causing the hyperprolactinemia. Whether concomitantly using these medications can aggravate hyperprolactinemia stemming from marijuana use because of their common property of affecting central neurotransmitter systems, however, is a possibility that cannot be conclusively ruled out in this case.CONCLUSIONCannabis is known to disrupt pituitary and gonadal hormone levels in humans, although the exact effects and mechanisms remain to be elucidated. It is probable that the observed endocrine changes can be quite diverse and depend on several factors. With respect to prolactin, it seems that marijuana acutely suppresses its release as it does of other anterior pituitary hormones. However, the situation may be different with long-term use. Cannabis-induced hyperprolactinemia severe enough to cause hypogonadism and clinical breast changes in males has been reported. Chronic cannabis consumption with short periods of deprivation may cause multiple episodes of “rebound hyperprolactinemia,” which, over time, can be severe, frequent, and sustained enough to result in significant galactorrhea in females. The case described here is the first report that lends credence to this possible underlying etiology. It is evident that more research is required to understand predictable patterns of prolactin changes that are caused by the duration and frequency of marijuana use. The clinical importance of this association lies in the fact that it can contribute to diagnostic confusion in the evaluation of hyperprolactinemia, breast tenderness, galactorrhea, and gynecomastia. Clinicians should keep this possibility in mind and maintain a high index of suspicion regarding cannabis-related biochemical and physical changes in the appropriate circumstances.REFERENCES1. Murphy LL, Munoz RM, Adrian BA, et al. 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MD FACP FACECase ReportCase Report616p 308-310