Hyperprolactinemia
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Synonyms and keywords: Hyperprolactinaemia; Ahumada-DelCastillo syndrome; Chiari-Frommel syndrome; Forbes-Albright syndrome
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Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Hyperprolactinaemia (BrE) or hyperprolactinemia (AmE) is the presence of abnormally high levels of prolactin in the blood. Normal levels are less than 580 mIU/L for women, and less than 450 mIU/L for men.
The hormone prolactin is downregulated by dopamine and is upregulated by estrogen. A falsely high measurement may occur due to the presence of the biologically inactive macroprolactin in the serum. This can show up as high prolactin in some types of tests, but is asymptomatic.
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Hyperprolactinermia from Other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications, and Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Prevention
References
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Historical Perspective
References
Classification
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Classification
References
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Pathophysiology
References
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Causes
Hyperprolactinaemia may be caused by either disinhibition (e.g. compression of the pituitary stalk or reduced dopamine levels) or excess production from a prolactinoma (a pituitary gland adenoma tumour). A prolactin level of 1000–5000mIU/L could be from either mechanism, but >5000mIU/L is likely due to an adenoma with macroadenomas (large tumours over 10 mm diameter) having levels of up to 100,000mIU/L. Hyperprolactinemia inhibits gonadotropin-releasing hormone (GnRH) by increasing the release of dopamine from the arcuate nucleus of the hypothalamus (dopamine inhibits GnRH secretion), thus inhibiting gonadal steroidogenesis, which is the cause of many of the symptoms described below:
Physiological causes
Physiological causes (i.e. as result of normal body functioning): pregnancy, breastfeeding, stress, sleep.
Prescription drugs
Use of prescription drugs are the most common cause of hyperprolactinaemia. Prolactin secretion in the pituitary is normally suppressed by the brain chemical, dopamine. Drugs that block the effects of dopamine at the pituitary or deplete dopamine stores in the brain may cause the pituitary to secrete prolactin. These drugs include the major tranquilizers (phenothiazines), trifluoperazine (Stelazine), ,and haloperidol (Haldol); some antipsychotic medications like risperidone; metoclopramide (Reglan), used to treat gastroesophageal reflux and the nausea caused by certain cancer drugs; and less often, alpha-methyldopa and reserpine, used to control hypertension. Finally oestrogens and TRH.
Diseases
Prolactinoma or other tumors arising in or near the pituitary—such as those that cause acromegaly or Cushing’s syndrome—may block the flow of dopamine from the brain to the prolactin-secreting cells, likewise division of the pituitary stalk or hypothalamic disease. Other causes include chronic renal failure, hypothyroidism and sarcoidosis. Some women with polycystic ovary syndrome may have mildly elevated prolactin levels.
Apart from diagnosing hyperprolactinaemia and hypopituitarism, prolactin levels are often determined by physicians in patients who have suffered a seizure, when there is doubt whether this was an epileptic seizure or a non-epileptic seizure. Shortly after epileptic seizures, prolactin levels often rise, while they are normal in non-epileptic seizures.
Idiopathic
In many patients elevated levels remain unexplained and may represent a form of hypothalamic-pituitary dysregulation.
References
Differentiating Hyperprolactinemia from other Diseases
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Hyperprolactinemia must be differentiated from other diseases that cause virilization and hirsutism in female. The differentials include 21-hydroxylase deficiency, 17-alpha hydroxylase deficiency, 11-β hydroxylase deficiency, 3 beta-hydroxysteroid dehydrogenase deficiency, polycystic ovarian syndrome, adrenal tumors, ovarian virilizing tumors and cushing’s syndrome.
Differential Diagnosis
Differentials based on virilization and hirsutism
Hyperprolactinemia must be differentiated from diseases that cause virilization and hirsutism in female:[1][2][3]
| Disease name | Steroid status | Other laboratory | Important clinical findings |
|---|---|---|---|
| Non-classic type of 21-hydroxylase deficiency | Increased:
|
|
|
| 11-β hydroxylase deficiency | Increased:
Decreased: |
|
|
| 3 beta-hydroxysteroid dehydrogenase deficiency | Increased:
Decreased: |
|
|
| Polycystic ovary syndrome |
|
|
|
| Adrenal tumors |
|
|
|
| Ovarian virilizing tumor |
|
|
|
| Cushing’s syndrome |
|
||
| Hyperprolactinemia |
|
|
Differentials based on irregular menstruation and hirsutism
Hyperprolactinemia must be differentiated from other causes of irregular menses and hirsutism, The differentials include the following:
| Disease | Differentiating Features |
|---|---|
| Pregnancy |
|
| Hypothalamic amenorrhea |
|
| Primary amenorrhea |
|
| Cushing syndrome |
|
| Hyperprolactinemia |
|
| Ovarian or adrenal tumor |
|
| Congenital adrenal hyperplasia |
|
| Anabolic steroid abuse |
|
| Hirsutism |
|
References
- ↑ Hohl A, Ronsoni MF, Oliveira M (2014). “Hirsutism: diagnosis and treatment”. Arq Bras Endocrinol Metabol. 58 (2): 97–107. PMID 24830586. Vancouver style error: initials (help)
- ↑ White PC, Speiser PW (2000). “Congenital adrenal hyperplasia due to 21-hydroxylase deficiency”. Endocr. Rev. 21 (3): 245–91. doi:10.1210/edrv.21.3.0398. PMID 10857554.
- ↑ Melmed, Shlomo (2016). Williams textbook of endocrinology. Philadelphia, PA: Elsevier. ISBN 978-0323297387.=
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Epidemiology and Demographics
References
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Risk Factors
References
Screening
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Screening
References
Natural History, Complications and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Natural History, Complications, and Prognosis
References
Diagnosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies
Treatment
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Acknowledgements
Acknowledgements
The content on this page was first contributed by: C. Michael Gibson, M.S., M.D.
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