Prolactin-Secreting Pituitary Adenomas (Prolactinomas) The Diagnostic Pathway (11-2K-234)

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1 Prolactin-Secreting Pituitary Adenomas (Prolactinomas) The Diagnostic Pathway (11-2K-234) Common presenting symptoms/clinical assessment: Pituitary adenomas are benign neoplasms of the pituitary gland. About 40% of all pituitary adenomas are prolactinomas. Prolactinomas are more common in women, with a peak incidence during the childbearing years. Occasionally, prolactinomas may be a component of multiple endocrine neoplasia syndrome type I (MEN I). Routine screening for MEN I is not recommended but a family history and basal measurement of calcium are advisable. The clinical features of a prolactinoma predominantly result from hyperprolactinaemia. Prolactin stimulates milk production but also interrupts the pulsatile secretion of GNRH, inhibits the release of LH and FSH, and directly impairs secretion of sex steroid hormones. In very large tumours, hypopituitarism and neurological manifestations are common. Presenting symptoms in men: -impotence, infertility and decreased libido -with larger tumours neurological symptoms may be present such as headaches and visual field defects -this may be due to delayed recognition of symptoms or biological differences in tumour growth Presenting symptoms in women: -most prolactinomas are microadenomas -premenopausal women present with oligo/amenorrhoea, galactorrhoea and anovulatory infertility -these classical symptoms are usually absent in postmenopausal women in whom often these tumours are only recognized when they produce mass effects (headache or visual disturbances) Chronic hyperprolactinaemia-induced hypogonadism is associated with reduced spinal bone mineral density in both sexes. Page 1 of 8

2 Biochemical assessment: -measurement of serum prolactin (ensure sample is obtained without excessive venepuncture stress) -exclude other causes of hyperprolactinaemia (renal failure, hypothyroidism and drug-induced hyperprolactinaemia: neuroleptics, atypical antipsychotics, antidepressants, opiates, verapamil, methyldopa, metoclopramide, domperidone, H2 blockers and oestrogens) - prolactinomas can present with variable elevations in prolactin and there may be dissociation between tumour mass and hormonal secretion -moderate hyperprolactinaemia (prolactin miu/l) may be due to compression of the pituitary stalk by a tumour other than a prolactinoma Radiological assessment: All patients with a suspected prolactinoma should have a MRI scan as per current WCFT imaging protocol for pituitary tumours which includes the following sequences: -T2 axial brain images -T1 sagittal and coronal images of pituitary -Post gadolinium T1 sagittal and coronal images of pituitary Ophthalmological assessment: In patients with macroprolactinomas where optic apparatus involvement is seen on imaging, formal visual field testing should be performed. All cases of resistant macroprolactinomas and new cases of macroprolactinomas with threat to the optic apparatus or VFD to be put through the Regional Pituitary MDT Page 2 of 8

3 The Treatment Pathway (11-2K-235) Primary goal of treatment: -in patients with microprolactinomas is to restore gonadal and sexual function by normalizing prolactin levels -in patients with macroadenomas, control and reduction of tumour size are also important Indications for treatment: -infertility -bothersome galactorrhoea -long-standing hypogonadism -alterations in pubertal development -prevention of bone loss in women because of hypogonadism -Visual field defects (VFD) Premenopausal women with normal menstrual cycles and tolerable galactorrhoea and postmenopausal women with tolerable galactorrhoea who have a microprolactinoma, can be reassured and not actively treated. However, such patients must be carefully followed with periodic prolactin measurements to detect potential enlarging tumours. Medical Therapy: Dopamine agonists: -bromocriptine -cabergoline -quinagolide Bromocriptine and cabergoline are the primary therapy for patients with prolactinomas. These drugs normalize prolactin levels and significantly reduce the volume of the tumour in most patients, and extensive experience has demonstrated their utility in treating prolactinomas of all sizes. Studies with cabergoline have shown superiority in terms of patient tolerability and convenience, reduction in prolactin secretion, restoration of gonadal function, and decrease in tumour volume. Nevertheless, bromocriptine has been used satisfactorily for years and is less expensive. Page 3 of 8

4 Treatment of microprolactinomas The primary clinical objective in treating microprolactinomas is to restore gonadal function and fertility, and medical therapy is remarkably effective in achieving these goals. In 90 95% of cases, microadenomas do not progressively increase in size, so suppression of tumour growth is not a treatment goal. Microadenomas often shrink and sometimes disappear during long-term effective dopamine agonist treatment. Once normal PRL levels are achieved, annual serial assessments of PRL should be performed. Since only 5 10% of microprolactinomas progress to larger tumours, women with microprolactinoma who do not wish to become pregnant may not require therapy with a dopamine agonist. Those who are amenorrhoeic may be treated with oestrogen and should have annual evaluations of serum PRL. An MRI should be repeated if either clinical signs of tumour expansion appear or if the prolactin levels rise significantly. Treatment of macroprolactinomas Dopamine agonist treatment normalizes serum PRL levels and reduces tumour size in most patients with macroprolactinoma. Eighty per cent of prolactinomas treated with dopamine agonists shrink by more than 25% of the original volume, and in almost all patients therapy is associated with a 50% reduction in serum PRL. Tumour shrinkage can often be observed within a week or two after starting therapy, but in some cases may not start for several months. Continued tumour shrinkage may occur for many months or even years. It is useful to repeat the MRI 2 3 months after starting therapy and at longer intervals thereafter. Several studies have demonstrated recovery of impaired anterior pituitary function in association with tumour shrinkage and ovulatory menses return in over 90% of premenopausal women. Dopamine agonists usually restore visual function to an extent similar to that produced by surgical decompression of the chiasm in macroprolactinoma patients. Therefore, patients with macroprolactinomas who have visual field defects are no longer considered to be neurosurgical emergencies Resistant prolactinomas When a patient does not respond adequately to a dopamine agonist, the prolactinoma is considered resistant. Subsequent treatment options include: - achieving the maximally tolerated dose -changing to a different dopamine agonist - considering either pituitary surgery or radiotherapy Page 4 of 8

5 Trans-sphenoidal surgery Trans-sphenoidal surgery does not reliably lead to a long-term cure, and recurrence of hyperprolactinaemia is frequent. Indications: -lack of response to DAs -lack of improvement in VFD as a result of failure of tumour to shrink in response to DAs -cystic macroprolacctinomas causing neurological symptoms that fail to respond to DAs Intolerance of DAs. Radiotherapy External radiation is rarely required to treat prolactinomas and is associated with a significant incidence of major side-effects, including hypopituitarism, damage to the optic nerve, neurological dysfunction and increased risks of stroke and secondary brain tumours. Therefore, radiotherapy is not an acceptable primary therapy for prolactinomas, and is reserved for patients who do not respond to dopamine agonists, those who are not cured by surgery, or for those very rare cases of malignant prolactinoma The Follow Up Pathway (11-2K-236) DA withdrawal When the PRL level has been normal for at least 2-3 years and the size of the tumour decreased by more than 50%, the dose of the dopamine agonist can be gradually decreased, because at this stage low doses are likely to maintain stable PRL levels and tumour size. However, in patients with macroadenomas complete suspension of therapy may lead to tumour expansion and recurrence of hyperprolactinaemia. For this reason, close follow-up is necessary when the drug is withdrawn. Therapy may be tapered and perhaps discontinued altogether in patients who have been treated with dopamine agonists for at least 2 yr, who no longer have elevated serum prolactin, and who have no visible tumour remnant on MRI Page 5 of 8

6 To minimise duplication of clinic appointments and MRI scans the following is proposed: For resistant macroprolactinomas with threat to vision, a joint neurosurgery / neuroendocrinology clinic appointment is desirable this minimises clinic appointments and avoids duplication of follow-up imaging and follow up pituitary function testing and visual perimetry MRI is the modality of choice for follow up and should be performed as per current WCFT imaging protocol for pituitary tumours Once tumour growth control and reduction/normalization of prolactin have been established following the appropriate treatment modalities, follow-up could be transferred and / or shared with the patient s local hospital-based Endocrinology team Referral back to the joint neurosurgery / neuro-endocrinology clinic and the regional Pituitary MDT can take place at any time during the follow-up pathway when evidence of tumour growth/re-growth or rising prolactin levels become evident Radiological follow up: - It is useful to repeat the MRI 2 3 months after starting medical therapy and at longer intervals thereafter depending on clinical and biochemical response to DAs and clinical judgement -repeat MRI will be required before attempting to reduce/suspend DA treatment after at least 2-3 years of successful response to medical therapy Echocardiography: - Echocardiography should be performed at baseline and repeated thereafter depending on baseline findings and change in clinical symptomatology Page 6 of 8

7 REFERENCES 1. Colao A. Pituitary tumours: the prolactinoma. Best Pract Res Clin Endocrinol Metab 2009; 23(5): Casanueva FF, Molitch ME, Schlechte JA et al. Guidelines of the Pituitary Society for the diagnosis and management of prolactinomas. Clin Endocrinol (Oxf) 2006; 65(2): Dekkers OM, Lagro J, Burman P, Jorgensen JO, Romijn JA, Pereira AM. Recurrence of hyperprolactinemia after withdrawal of dopamine agonists: systematic review and metaanalysis. J Clin Endocrinol Metab 2010; 95(1): Melmed S, Casanueva FF, Hoffman AR et al. Diagnosis and treatment of hyperprolactinemia: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2011; 96(2): Page 7 of 8

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