Prolactinomas are usually small and rarely grow, but some can become very large.81 They are an important cause of hypogonadism and infertility.82 Prolactinomas, while benign, secrete prolactin and can result in a condition called hyperprolactinemia, a higher than normal level of prolactin in the blood.81
Hyperprolactinemia may result in hypogonadism, infertility, and galactorrhea, or it may remain asymptomatic.82-84 Bone loss occurs secondary to hyperprolactinemia-mediated sex steroid attenuation. Spinal bone density is decreased by approximately 25% in women with hyperprolactinemia and is not necessarily restored with normalization of prolactin levels.85
The most common type of pituitary adenomas are prolactinomas.86 Prolactinomas account for approximately 40% of all pituitary adenomas.82 Table 16 lists the prevalence of prolactinomas. No incidence data were available.
|POPULATION||DATA SOURCE||PREVALENCE PER 100,000||REFERENCE|
|Belgium (n=71,972)||Specialist/general practitioner patient populations, referral hospitals, research centers||62.4||Daly et al. 200675|
|United Kingdom (n=81,149)
|Sixteen general practitioner surgeries covering the area of Banbury.||44.2
|Fernandez et al. 201074|
Abbreviations: UK, United Kingdom; n, number.
Prolactinomas occur in both sexes, but are more common in women.81 These tumors occur most frequently in females aged 20-50 years old, at which time the female-to-male ratio is approximately 10:1. In the pediatric-adolescent age group, prolactinomas have a prevalence of 100/million population, and account for less than 2% of all intracranial tumors. 81
Prolactinomas occur in approximately 30% of patients with multiple endocrine neoplasia type 1, and in this setting they may be more aggressive than their sporadic counterparts. Few studies report familial cases of prolactinoma unrelated to multiple endocrine neoplasia type 1 (known as Familial Isolate Pituitary Adenoma Syndrome).86
The ultimate goals of therapy for prolactinomas are reversal of hypogonadism through the normalization of hyperprolactinemia and control of the tumor mass. Medical therapy with dopamine agonists is highly effective in the majority of cases and represents the mainstay of therapy. There has been a long-held belief that medical therapy is a lifelong requirement; however, a subset of patients has achieved successful withdrawal from dopamine agonists. Complicated situations, such as resistance to dopamine agonists, pregnancy, and giant or malignant prolactinomas, may require multimodal therapy involving surgery, radiotherapy, or both.82,87
Studies have reported the reversal of hypogonadism in 44-62% of cases, usually within 6 months after starting treatment with dopamine agonists.88,89 Furthermore, a study reported the recovery of other hormonal axes following adenoma shrinkage.90 Hormonal re-evaluation should be performed to avoid unnecessary life-long hormone replacement.
Table 17 summarizes treatment outcomes associated with different therapeutic approaches.
|Italy, (n=41 males with macroprolactinoma, age 17-70 years), (n= 10 males with microprolactinoma, age 18-53 years).||Prospective analysis of clinical data||24 months of cabergoline treatment||75.6% patients with macroprolactinoma and 80% with microprolactinoma achieved normal prolactin levels||Colao et al. 200488|
|International cohort (n=3,000)||Eight randomized and 178 non-randomized studies||Dopamine agonists||A median of 68% achieved normalization of prolactin levels||Wang. 201291|
|International cohort (n=2,137 microadenomas; 2,226 macroadenomas)||Data from 50 published papers on surgical resection||Surgical resection||74.7% of microadenomas and 33.9% of macroadenomas achieved normalized PRL levels||Gillam et al. 200682|
Abbreviations: SMR, standardized mortality rate; CVR, cardiac valve regurgitation; yr, year; n, number.