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 Table of Contents  
Year : 2020  |  Volume : 12  |  Issue : 2  |  Page : 90-97

A rational approach to the evaluation and management of patients with hyperprolactinemia

1 Department of Endocrinology, Tawam Hospital; Department of Medicine, College of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates
2 Obesity, Endocrine and Metabolism Center, King Fahad Medical City; Department of Medicine, Faculty of Medicine, King Saud Bin Abdul Aziz University of Health Sciences, Riyadh, Saudi Arabia
3 Department of Medicine, Dubai Medical College; Department of Endocrinology, Mediclinic Airport, Abu Dhabi, United Arab Emirates

Date of Submission03-Apr-2020
Date of Decision04-Apr-2020
Date of Acceptance10-Apr-2020
Date of Web Publication27-Jun-2020

Correspondence Address:
Dr. Khaled M Aldahmani
Department of Endocrinology, Tawam Hospital, Al Ain
United Arab Emirates
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijmbs.ijmbs_38_20

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Prolactin has multiple biological functions. Hyperprolactinemia is a common condition in clinical practice both in women and men. It has multiple etiologies and may present with variable symptoms to different health-care providers. Therefore, a rational and systematic approach is paramount when evaluating patients with hyperprolactinemia to arrive at the correct diagnosis and institute the appropriate therapy. We here review the etiology, clinical presentation, and differential diagnosis of hyperprolactinemia and present a practical plan for further evaluation and management. It is most essential to establish the diagnosis and need for the treatment of patients with micro- and macro-prolactinomas and identify when only observation may be warranted. The biological, medical, and social contexts have to be considered to make the appropriate management decisions on an individual basis.

Keywords: Cabergoline, hyperprolactinemia, pituitary tumors, prolactin

How to cite this article:
Aldahmani KM, AlMalki MH, Beshyah SA. A rational approach to the evaluation and management of patients with hyperprolactinemia. Ibnosina J Med Biomed Sci 2020;12:90-7

How to cite this URL:
Aldahmani KM, AlMalki MH, Beshyah SA. A rational approach to the evaluation and management of patients with hyperprolactinemia. Ibnosina J Med Biomed Sci [serial online] 2020 [cited 2022 Jul 2];12:90-7. Available from: http://www.ijmbs.org/text.asp?2020/12/2/90/288199

  Introduction Top

Prolactin is an important hormone primarily produced by lactotroph cells in the anterior pituitary with multiple biological functions.[1] Prolactin secretion is regulated by several factors in health and disease [Figure 1]. However, dopamine is the main regulatory factor with its prolactin-release inhibiting activity. Hyperprolactinemia denotes serum prolactin level above the laboratory gender-specific normal range, is a relatively common endocrine disorder worldwide.[2],[3],[4] It is more common in females, and its prevalence has increased over the past two decades.[5]
Figure 1: Regulation of prolactin secretion and mechanisms of hyperprolactinemia in different clinical conditions

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The prevalence of hyperprolactinemia is 20 and 90 cases per 100,000 for males and females respectively. The annual incidence in women aged 25–34 years is about 23.9/100,000 person-years.[6] Hyperprolactinemia can cause menstrual disorders, gynecomastia, decreased libido, impotence, and infertility.[7] Hyperprolactinemia may result from physiological changes, pathological conditions, medications, macroprolactin excess, or it can be idiopathic. The leading physiological causes are pregnancy, lactation, and stress, whereas common pathological causes include prolactinomas, other sellar masses, polycystic ovarian syndrome (PCOS), chronic kidney disease, and hypothyroidism [Table 1].[8] Antipsychotics, antidepressants, and anti-emetics are among the most common medications causing hyperprolactinemia.[4],[7],[8] Macroprolactin is a large molecule of prolactin mostly attached to immunoglobulins and can result in hyperprolactinemia due to reduced renal clearance.[9] As patients with hyperprolactinemia may present to different medical specialties, a practical review on the clinical presentations, etiologies, workup, and management will be discussed in this article.
Table 1: Physiological and pathological causes of hyperprolactinemia

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  Clinical Presentations Top

Patients with hyperprolactinemia generally present with symptoms related to hypogonadism (irregular periods, amenorrhea in premenopausal women or decreased libido, erectile dysfunction in men). Galactorrhea and infertility are other common symptoms in hyperprolactinemia.[10] Galactorrhea either spontaneously or after nipple stimulation, may be observed in up to 80% of female patients while it is uncommon in males (8%).[11]

Long-standing hyperprolactinemia may result in osteoporosis in both sexes and is linked to weight gain.[12],[13],[14] In postmenopausal women, hyperprolactinemia may present with the disappearance of hot flushes, as a result of the suppression of luteinizing hormone and follicle-stimulating hormone secretion. Furthermore, hyperprolactinemia is often detected during sellar masses evaluation, screening individuals on high-risk medications or rarely when assessing seizure in the emergency department.[4]

  Etiology Top

Causes of hyperprolactinemia usually fall into three categories physiologic, pharmacologic, and pathologic. The physiologic and pathologic causes are listed in [Table 1]. Recognized physiological states, including exercise, diet, stress, neurogenic stimulation such as chest wall stimulation and nipple stimulation, sexual intercourse, or pregnancy, can cause various degrees of serum prolactin elevation.[15],[16] Another important cause is the intake of some medications.[6] Hyperprolactinemia has been recognized in association with several classes and individual pharmacological agents [Table 2]. Medications that block the central dopaminergic system can potentially increase prolactin levels. These include a group of drugs that antagonize the dopamine receptor on lactotrophs (risperidone, metoclopramide, haloperidol), inhibit dopamine reuptake (serotonin reuptake inhibitors, monoamine oxidase inhibitors, tricyclic antidepressants), deplete dopamine (reserpine, methyldopa), or increase transcription of the prolactin gene (estrogens).[16],[17],[18] Other drugs, such as opiates, can cause hyperprolactinemia through the opioid receptor in the hypothalamus. The mechanism by which verapamil and protease inhibitors elevate prolactin is unclear. Detailed drug history is essential in the diagnostic evaluation of hyperprolactinemia.
Table 2: Classes and examples of pharmacological agents recognized to cause hyperprolactinemia*

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Pathological causes of hyperprolactinemia include a wide range of disorders [Table 1]. Naturally, the most important cause is a prolactin-secreting pituitary adenoma (prolactinoma), which accounts for 30%–40% of all pituitary tumors.[19] Furthermore, any pathology in the hypothalamic-pituitary region such as craniopharyngiomas, granulomatous infiltration of the hypothalamus, and other hypothalamic tumors can cause hyperprolactinemia through interference with the normal dopaminergic inhibitory effect on prolactin secretion stalk effect.[11]

Chronic illness such as chronic renal failure and liver cirrhosis can increase circulating prolactin levels due to decreased clearance.[17] Hypothyroidism can cause moderate hyperprolactinemia by the enhanced release of thyrotropin-releasing hormone (TSH) and reduced prolactin clearance.[18],[20] It is more frequent in overt than subclinical hypothyroidism.[21] One study suggested that a TSH of >7.5 IU/ml may predict the presence of hyperprolactinemia.[22] Cases of adrenal insufficiency-associated hyperprolactinemia have been described.[23] Mild hyperprolactinemia is reported in about 30% of patients with polycystic (PCOS) ovary syndrome.[24],[25] It remains controversial whether any prolactin elevation should trigger a pituitary imaging in PCOS patients. However, serum prolactin of >85.2 ng/ml predicted pituitary abnormality on magnetic resonance imaging (MRI) in one small retrospective study.[26] Chest wall or spinal cord lesions or trauma may increase circulating prolactin levels through stimulation of afferent neural pathways.[11] Finally, idiopathic hyperprolactinemia should be considered when imaging shows normal hypothalamic-pituitary anatomy, and there is no plausible cause of hyperprolactinemia.[27]

  Further Evaluation Top

Clinical history is paramount in evaluating a patient with hyperprolactinemia. History of acute illness, stress, or pain at the time of blood extraction is important to obtain as prolactin might be transiently elevated in such conditions. Similarly, it is essential to document symptoms related to the effect of prolactin on the reproductive system, namely, menstrual irregularities, infertility, galactorrhea in women, and decreased libido and infertility in men.

Symptoms of potential causes of hyperprolactinemia should be elicited, such as headache, vision loss (sellar mass), cold intolerance, constipation, muscle weakness, and weight gain (hypothyroidism). One should focus on medication history, especially those known to elevate prolactin not only at the time of clinic visit but also at the time of prolactin measurement as time may lapse between the first detection of hyperprolactinemia and the visit to health-care physician [Table 2] and [Figure 2].[28] Patients should be asked about any history of renal and liver diseases or their related risk factors.
Figure 2: The relative frequency of psychotropic drug-induced hyperprolactinemia. Frequency of drug-induced hyperprolactinemia is represented as percentages and categorized high, medium and low probabilities (modified from ref 28)

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A single measurement of serum prolactin is usually adequate to document an abnormally high serum prolactin level and establish the diagnosis of hyperprolactinemia.[11] Typical normal range is slightly higher in women than in men. Repeat prolactin to confirm the presence of persistent hyperprolactinemia is recommended in patients with mild hyperprolactinemia, especially if asymptomatic. In general, serum prolactin levels below 200 μg/L may be seen in cases with all causes of hyperprolactinemia [Figure 3]. In contrast, serum prolactin levels >250 μg/L indicate the presence of a prolactinoma.[29],[30],[31],[32],[33]
Figure 3: The degree of hyperprolactinemia and history can help focus the differential diagnosis in the real world. (Data are based on ref 4) Multiply by 21.7 to convert from mcg/l to mIU/L

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Once persistent hyperprolactinemia is confirmed, additional laboratory investigations aim to rule out the common causes of hyperprolactinemia. The decision to consider routine evaluation for the presence of macroprolactin largely depends on the prolactin assay and may need to be discussed with local laboratory specialists. If no obvious cause of hyperprolactinemia is evident, MRI of the pituitary region is recommended to rule out other sellar masses or pathologies. Examples of a microprolactinoma, a macroprolactinoma and an invastive giant prolactinolma are shown in [Figure 4]. In certain patients, no obvious cause of hyperprolactinemia is detected and those are labeled as idiopathic hyperprolactinemia. Small microprolactinomas (below the level of MRI detection) might be present in such patients. [Figure 5] provides an algorithm for practical workup hyperprolactinemia.
Figure 4: MRI coronal sections of the pituitary without contrast demonstrating the three different categories of prolactinomas. (a) Microprolactinoma: A small (6 × 6 mm) hypointense lesion within the left pituitary gland associated with mild depression of the sellar floor in keeping with pituitary microadenoma. The pituitary stalk is located in the midline and the suprasellar optic pathway is unremarkable. (b) Macroprolactinoma: A small (1.1 × 0.9 cm) hypointense lesion within the right pituitary gland in keeping with pituitary macroadenoma. The pituitary stalk is deviated to the left side. (c) Giant invasive prolactinoma with suprasellar extension and compression and upward displacement defect over the optic chiasm. The stalk could not be identified

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Figure 5: Algorithm for a rational evaluation of hyperprolactinemia

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  Rational Management Top

The main aim of hyperprolactinemia management is to treat the underlying cause when possible. If hyperprolactinemia is drug induced, the medication should be stopped when possible. Otherwise, one should consider switching to other drugs with a lesser prolactin-enhancing effect [Figure 2]. It is noteworthy that such modification, especially the psychotropic medications, need to be discussed with the treating specialist to avoid worsening of the underlying clinical condition.

The management of prolactinomas is in the remit of clinical endocrine practice and should be undertaken by the appropriately qualified endocrinologist. For patients with prolactinoma, the primary goals of treatment are the reduction of tumor mass and normalization of prolactin levels, the restoration of gonadal function and fertility and the reduction pressure symptoms such as headaches and visual field defects.[29],[30],[31],[32],[33]

In the decision to treat or not, tumor size and symptoms are important factors to consider. In patients with asymptomatic micorprolactinoma (<10 mm), treatment is not indicated as 90% of the cases do not enlarge during follow-up. Instead, a regular follow-up should be maintained.[31],[32] Therefore, treatment is always indicated for symptomatic patients with microprolactinoma and all macroprolactinoma (≥10 mm) due to a high propensity to grow.[33]

A recent survey of physicians managing prolactinoma in the Middle East and North Africa region revealed that 40% of them would treat microprolactinoms regardless of symptoms.[34] Therefore, it is important to highlight that not all patients with micrporlactinoma need treatment, as the risk of the progression of untreated microprolactinoma is small, and oral contraceptive pill might be an alternative in women with symptoms of estrogen deficiency.[35]

Dopamine agonists (DAs) are the treatment of choice for prolactinoma. An illustrative case of the hormonal and mass responses of a macroprolactinoma to DA therapy is shown in [Figure 6]. Compared to bromocriptine (BRC), cabergoline (CAB) is better tolerated, more convenient, and is more efficacious.[6] The dose of CAB varies with most patients achieving normal prolactin with a dose of 0.25–2 mg weekly. Nausea and dizziness are among the most commonly reported side effects. Hence, patients are advised to take the medication at night after a light snack. Thickening of cardiac valves has been reported mostly in those requiring higher doses of DAs like in Parkinson's disease but not in those treated for prolactinoma. Nonetheless, we suggest that cardiac auscultation is routinely performed on patients receiving DA therapy while considering periodic Echocardiogram in patients on higher doses (CAB ≥ 2 mg/week, BRC ≥ 15 mg/wk). Impulse control disorders such as hypersexuality, impulsive shopping, pathologic gambling, and punding are now increasingly recognized adverse effects of DAs in prolactinoma patients.[35] These behaviors should be explored with all patients and their close family members during the follow-up visits as prompt recognition, and early management may help to avoid serious consequences.
Figure 6: An illustration of the hormonal and mass effect responses of a macroprolactinoma to medical therapy

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Dopamine agonist withdrawal might be considered in patients treated for idiopathic hyperprolactinemia or microprolactinoma with a success rate of about 22%–31%.[37] Factors predicting favorable results include 2–3 years of DA therapy, normal prolactin level before withdrawal, low dose of DA and no or minimal residual tumor on imaging.[6]

Surgical resection of the pituitary adenoma, usually by the transsphenoidal route, is a treatment option in patients with resistance or intolerance to DA, macroprolactinoma with chiasmal compression and visual defect without marked improvement by DA, symptomatic apoplexy or cerebrospinal fluid leak.[38] According to recent data from 50 published series, the remission post surgery occurred on average in 74.7% of microadenomas and 34% of macroprolactinomas, with a recurrence rate of 18% and 23%, respectively.[39] In addition, tumor debulking in patients with partial resistance to DA may help in prolactin normalization with lower doses of DA.[40],[41] Complications from transsphenoidal surgery are limited in the experienced hand, with mortality of <1%.[42] Radiotherapy is rarely needed in the management of prolactinoma and generally reserved for tumors that progress despite combined medical and surgical treatment. Radiation is usually applied as conventional fractionated therapy or stereotactic radiosurgery. The response to treatment is slow with complete normalization of prolactin in 30%–70%.[42],[43] However, local tumor control can be achieved in the majority of patients regardless of the radiotherapy modality.[45],[46] Complications of radiotherapy include the development of hypopituitarism (up to 100% after 10 years), optic nerve injury, cerebrovascular disease, and rarely development of secondary tumors.[47],[48]

  Conclusions Top

Hyperprolactinemia is a frequent encounter in clinical practice with symptoms of abnormal sexual and reproductive function, galactorrhea, and mass effect. The diagnosis can be confirmed with single serum measurement of prolactin level. If the serum prolactin is >250 μg/L, macroprolactinoma should be seriously considered. The majority of patients with hyperproteinemia, including prolactinomas, can be successfully treated with dopaminergic medications as first-line resulting in, restoration of gonadal function, and marked tumor shrinkage in a large proportion of prolactinoma cases. Several studies suggest that DA therapy may be safely withdrawn in many prolactinoma patients after an adequate period of treatment, provided that recommended criteria are applied. In patients with resistant prolactinoma, additional treatment modalities will be needed.

Authors contributions

The authors were assigned specific sections to draft, these were developed into a single manuscript which was reviewed and approved by all authors.

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Conflicts of interest

There are no conflicts of interest.

Compliance with ethical principles

Not applicable. None of the authors reported human or animal studies.

  References Top

Bernard V, Young J, Binart N. Prolactin–A pleiotropic factor in health and disease. Nat Rev Endocrinol 2019;15:356-65.  Back to cited text no. 1
Freda PU, Wardlaw SL, Post KD. Unusual causes of sellar/parasellar masses in a large transsphenoidal surgical series. J Clin Endocrinol Metab 1996;81:3455-9.  Back to cited text no. 2
Vilar L, Freitas MC, Naves LA, Casulari LA, Azevedo M, Montenegro R Jr, et al. Diagnosis and management of hyperprolactinemia: Results of a brazilian multicenter study with 1234 patients. J Endocrinol Invest 2008;31:436-44.  Back to cited text no. 3
Malik AA, Aziz F, Beshyah SA, Aldahmani KM. Aetiologies of Hyperprolactinaemia: A retrospective analysis from a tertiary healthcare centre. Sultan Qaboos Univ Med J 2019;19:e129-e134.  Back to cited text no. 4
Soto-Pedre E, Newey PJ, Bevan JS, Greig N, Leese GP. The epidemiology of hyperprolactinaemia over 20 years in the tayside region of scotland: The prolactin epidemiology, audit and research study (PROLEARS). Clin Endocrinol (Oxf) 2017;86:60-7.  Back to cited text no. 5
Melmed S, Casanueva FF, Hoffman AR, Kleinberg DL, Montori VM, Schlechte JA, et al. Diagnosis and treatment of hyperprolactinemia: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2011;96:273-88.  Back to cited text no. 6
Serri O, Chik CL, Ur E, Ezzat S. Diagnosis and management of hyperprolactinemia. CMAJ 2003;169:575-81.  Back to cited text no. 7
Samperi I, Lithgow K, Karavitaki N. Hyperprolactinaemia. J Clin Med. 2019;13;8:2203.  Back to cited text no. 8
Fahie-Wilson M, Smith TP. Determination of prolactin: The macroprolactin problem. Best Pract Res Clin Endocrinol Metab 2013;27:725-42.  Back to cited text no. 9
Luciano AA. Clinical presentation of hyperprolactinemia. J Reprod Med 1999;44:1085-90.  Back to cited text no. 10
Verhelst J, Abs R. Hyperprolactinemia: Pathophysiology and management. Treat Endocrinol 2003;2:23-32.  Back to cited text no. 11
Di Somma C, Colao A, Di Sarno A, Klain M, Landi ML, Facciolli G, et al. Bone marker and bone density responses to dopamine agonist therapy in hyperprolactinemic males. J Clin Endocrinol Metab 1998;83:807-13.  Back to cited text no. 12
Schlechte J, el-Khoury G, Kathol M, Walkner L. Forearm and vertebral bone mineral in treated and untreated hyperprolactinemic amenorrhea. J Clin Endocrinol Metab 1987;64:1021-6.  Back to cited text no. 13
Greenman Y, Tordjman K, Stern N. Increased body weight associated with prolactin secreting pituitary adenomas: Weight loss with normalization of prolactin levels. Clin Endocrinol (Oxf) 1998;48:547-53.  Back to cited text no. 14
Mann WA. Treatment for prolactinomas and hyperprolactinaemia: A lifetime approach. Eur J Clin Invest 2011;41:334-42.  Back to cited text no. 15
Vilar L, Fleseriu M, Bronstein MD. Challenges and pitfalls in the diagnosis of hyperprolactinemia. Arq Bras Endocrinol Metabol 2014;58:9-22.  Back to cited text no. 16
Kars M, Dekkers OM, Pereira AM, Romijn JA. Update in prolactinomas. Neth J Med 2010;68:104-12.  Back to cited text no. 17
Liu JK, Couldwell WT. Contemporary management of prolactinomas. Neurosurg Focus 2004;16:E2.  Back to cited text no. 18
Molitch ME. Disorders of prolactin secretion. Endocrinol Metab Clin North Am 2001;30:585-610.  Back to cited text no. 19
Prabhakar VK, Davis JR. Hyperprolactinaemia. Best Pract Res Clin Obstet Gynaecol 2008;22:341-53.  Back to cited text no. 20
Hekimsoy Z, Kafesçiler S, Güçlü F, Ozmen B. The prevalence of hyperprolactinaemia in overt and subclinical hypothyroidism. Endocr J 2010;57:1011-5.  Back to cited text no. 21
Sharma LK, Sharma N, Gadpayle AK, Dutta D. Prevalence and predictors of hyperprolactinemia in subclinical hypothyroidism. Eur J Intern Med 2016;35:106-10.  Back to cited text no. 22
Kelver ME, Nagamani M. Hyperprolactinemia in primary adrenocortical insufficiency. Fertil Steril 1985;44:423-5.  Back to cited text no. 23
Milewicz A. Prolactin levels in the polycystic ovary syndrome. J Reprod Med 1984;29:193-6.  Back to cited text no. 24
Delcour C, Robin G, Young J, Dewailly D. PCOS and Hyperprolactinemia: What do we know in 2019? Clin Med Insights Reprod Health 2019;13:1179558119871921.  Back to cited text no. 25
Kyritsi EM, Dimitriadis GK, Angelousi A, Mehta H, Shad A, Mytilinaiou M, et al. The value of prolactin in predicting prolactinoma in hyperprolactinemic polycyctic ovarian syndrome. Eur J Clin Invest 2018;48:e12961.  Back to cited text no. 26
Sluijmer AV, Lappöhn RE. Clinical history and outcome of 59 patients with idiopathic hyperprolactinemia. Fertil Steril 1992;58:72-7.  Back to cited text no. 27
Alosaimi FD, Fallata EO, Abalhassan M, Alhabbad A, Alzain N, Alhaddad B, et al. Prevalence and risk factors of hyperprolactinemia among patients with various psychiatric diagnoses and medications. Int J Psychiatry Clin Pract 2018;22:274-81.  Back to cited text no. 28
Schlechte JA. Long-term management of prolactinomas. J Clin Endocrinol Metab 2007;92:2861-5.  Back to cited text no. 29
Liu JK, Couldwell WT. Contemporary management of prolactinomas. Neurosurg Focus 2004;16:E2.  Back to cited text no. 30
Halperin Rabinovich I, Cámara Gómez R, García Mouriz M, Ollero García-Agulló D, Grupo de Trabajo de Neuroendocrinología de la SEEN. Clinical guidelines for diagnosis and treatment of prolactinoma and hyperprolactinemia. Endocrinol Nutr 2013;60:308-19.  Back to cited text no. 31
Colao A. Pituitary tumours: The prolactinoma. Best Pract Res Clin Endocrinol Metab 2009;23:575-96.  Back to cited text no. 32
Gillam MP, Molitch ME, Lombardi G, Colao A. Advances in the treatment of prolactinomas. Endocr Rev 2006;27:485-534.  Back to cited text no. 33
Beshyah SA, Sherif IH, Chentli F, Hamrahian A, Khalil AB, Raef H, et al. Management of prolactinomas: A survey of physicians from the Middle East and North Africa. Pituitary 2017;20:231-40.  Back to cited text no. 34
Sisam DA, Sheehan JP, Schumacher OP. Lack of demonstrable tumor growth in progressive hyperprolactinemia. Am J Med 1986;80:279-80.  Back to cited text no. 35
Celik E, Ozkaya HM, Poyraz BC, Saglam T, Kadioglu P. Impulse control disorders in patients with prolactinoma receiving dopamine agonist therapy: A prospective study with 1 year follow-up. Endocrine 2018;62:692-700.  Back to cited text no. 36
Dekkers OM, Lagro J, Burman P, Jørgensen JO, Romijn JA, Pereira AM. Recurrence of hyperprolactinemia after withdrawal of dopamine agonists: Systematic review and meta-analysis. J Clin Endocrinol Metab 2010;95:43-51.  Back to cited text no. 37
Glezer A, Bronstein MD. Prolactinomas. Endocrinol Metab Clin N Am 2015;44:71–8.  Back to cited text no. 38
Gillam MP, Molitch ME, Lombardi G, Colao A. Advances in the treatment of prolactinomas. Endocr Rev 2006;27:485-534.  Back to cited text no. 39
Vroonen L, Jaffrain-Rea ML, Petrossians P, Tamagno G, Chanson P, Vilar L, et al. Prolactinomas resistant to standard doses of cabergoline: A multicenter study of 92 patients. Eur J Endocrinol 2012;167:651-62.  Back to cited text no. 40
Primeau V, Raftopoulos C, Maiter D. Outcomes of transsphenoidal surgery in prolactinomas: Improvement of hormonal control in dopamine agonist-resistant patients. Eur J Endocrinol 2012;166:779-86.  Back to cited text no. 41
Sudhakar N, Ray A, Vafidis JA. Complications after trans-sphenoidal surgery: Our experience and a review of the literature. Br J Neurosurg 2004;18:507-12.  Back to cited text no. 42
Rush SC, Newall J. Pituitary adenoma: The efficacy of radiotherapy as the sole treatment. Int J Radiat Oncol Biol Phys 1989;17:165-9.  Back to cited text no. 43
Grossman A, Besser M, Wass J, Rees L. Treatment of prolactinomas with megavoltage radiotherapy. Br Med J (Clin Res Ed) 1984;288:2002.  Back to cited text no. 44
Pouratian N, Sheehan J, Jagannathan J, Laws Jr., ER, Steiner L, Vance ML. Gamma knife radiosurgery for medically and surgically refractory prolactinomas. Neurosurgery 2006;59:255-66.  Back to cited text no. 45
Wilson PJ, Williams JR, Smee RI. Single-centre experience of stereotactic radiosurgery and fractionated stereotactic radiotherapy for prolactinomas with the linear accelerator. J Med Imaging Radiat Oncol 2015;59:371-8.  Back to cited text no. 46
Sheehan JP, Niranjan A, Sheehan JM, Jane JA Jr., Laws ER, Kondziolka D, et al. Stereotactic radiosurgery for pituitary adenomas: An intermediate reviewof its safety, efficacy, and role in the neurosurgical treatment armamentarium. J Neurosurgery 2005;102:678-91.  Back to cited text no. 47
Snyder PJ, Fowble BF, Schatz NJ, Savino PJ, Gennarelli TA. Hypopituitarism following radiation therapy of pituitary adenomas. Am J Med 1986;81:457-62.  Back to cited text no. 48


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]

  [Table 1], [Table 2]


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