Medication use is a common cause of hyperprolactinemia, and it is important to differentiate this cause from pathologic causes, such as prolactinomas.

To ascertain the frequency of this clinical problem and to develop treatment guidelines, the medical literature was searched by using PubMed and the reference lists of other articles dealing with hyperprolactinemia due to specific types of medications.

The medications that most commonly cause hyperprolactinemia are antipsychotic agents; however, some newer atypical antipsychotics do not cause this condition.

Other classes of medications that cause hyperprolactinemia include antidepressants, antihypertensive agents, and drugs that increase bowel motility.

Hyperprolactinemia caused by medications is commonly symptomatic, causing galactorrhea, menstrual disturbance, and impotence.

It is Important to ensure that hyperprolactinemia in an Individual patient is due to medication and not to a structural lesion in the hypothalamic/pituitary area; this can be accomplished by (1) stopping the medication temporarily to determine whether prolactin levels return to normal, (2) switching to a medication that does not cause hyperprolactinemia (in consultation with the patient’s psychiatrist for psychoactive medications), or (3) performing magnetic resonance imaging or computed tomography of the hypothalamic/pituitary area. If the patient’s hyperprolactinemia is symptomatic, treatment strategies include switching to an alternative medication that does not cause hyperprolactinemia, using estrogen or testosterone replacement, or, rarely, cautiously adding a dopamine agonist.

Medications That May Cause Hyperprolactinemia

  • Antidepressants
    • Tricyclic and tetracyclic antidepressants
    • Monoamine oxidase inhibitors
    • Selective serotonin reuptake inhibitors
    • Other
  • Opiates and cocaine
  • Antihypertensive medications
    • Verapamil
    • Methyldopa
    • Reserpine
  • Gastrointestinal medications
    • Metoclopramide
    • Domperidone
    • Histamine2 receptor blockers?
  • Protease inhibitors?
  • Estrogens

Introduction: Fluoxetine is a commonly prescribed drug which is used in the psychiatric practice and adenomyosis is a common medical problem in women of the reproductive age group.

Objective: To explore the role of fluoxetine in the causation of adenomyosis.

Methods: Female Wistar rats (n=18) were divided into three groups (group I (the control), group II and group III) and they were treated with normal saline and oral fluoxetine (4mg/kg and 8 mg/kg) respectively for 100 days. Periodic serum prolactin measurements and histopathological examinations of the uterine horns of all the rats were done at the end. Comparison of the mean serum prolactin levels between the patients (n=15) who were diagnosed with adenomyosis, the healthy age sex matched controls and the female patients (n=20) who received fluoxetine for more than 3 months, before and after the fluoxetine administration, was done separately. Appropriate (paired or unpaired) t tests were used for the data analysis.

Results: Out of the 12 test group rats, 10 rats showed the features of adenomyosis histopathologically, along with significantly (p < 0.05) raised serum prolactin levels. The mean serum prolactin levels of the patients of adenomyosis in comparison to those of the controls and of the patients who were treated with fluoxetine (before and after the fluoxetine administration), were significantly high (p=0.001 in both the cases).

Conclusion: Fluoxetine may have some role in the causation of adenomyosis (via raising serum prolactin levels); although for a stronger evidence, the follow-up of the patients who are treated with fluoxetine on a long term basis should be ideal.

An excess of DRD2 polymorphism 2 was found in exon 7 in women with peritoneal moderate/severe endometriosis. The presence of polymorphism 2 could cause a defect in a post-receptor
signaling mechanism, resulting in a mild increase in serum prolactin levels. Thus, the potential angiogenic role of prolactin may play a role in the implantation of ectopic endometriosis tissue.

Dopamine receptor agonist Quinagolide induced a 69.5% reduction in the size of the lesions, with 35% vanishing completely. Histologic analysis showed tissue degeneration, which was supported by down-regulation of VEGF/VEGFR2, three proangiogenic cytokines (CCL2, RUNX1, and AGGF1) and plasminogen activator inhibitor (PAI) 1, a potent inhibitor of fibrinolysis in the L2 lesions.

By interfering with angiogenesis, enhancing fibrinolysis, and reducing inflammation, quinagolide reduces or eliminates peritoneal endometriotic lesions in women with endometriosis.

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