Spontaneous Pregnancies in Hyperprolactinemic Women

Crosignani, Pier Giorgio; Scarduelli, Claudia; Brambilla, Gelma; Cavioni, V.; Ferrari, Carlo

doi:10.1159/000299003

Cited by 17 publications

(11 citation statements)

References 6 publications

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“…However, the present study, as well as other studies (Mornex et al 1978;Zarate et al 1979;Campagnoli et al 1981;Crosignani et al 1981), show that regression of the hyperprolac¬ tinaemic state is a rather frequent finding, especi¬ ally in patients with normal sellar tomography (Bergh et al 1981). Complete clinical and hor¬ monal resolution has also been reported (Isaac 1979;Cowden & Thomson 1979;Crosignani et al 1981), even in patients with pituitary microadenomas (Mornex et al 1978). White et al (1981) showed that only some nonpregnant hyperprolactinaemic women had a Prl surge after administration of exogenous oestradiol.…”

Section: Discussionsupporting

confidence: 75%

“…Therefore, the biochemical regres¬ sion may not only be the result of a large postpartum Prl decrement, but it may also reflect an alteration occurring during pregnancy. The cause of the decreasing Prl levels during gestation is unknown, but resolution of hyperprolactinaemia has been suggested to be caused by adenoma apoplexy (Corkill et al 1981) or infarction (Isaac 1979) probably occurring because of an inadequate vascular supply due to pregnancy-related pituitary enlargement with subsequent infarction of the hypersecreting tissue (Crosignani et al 1981). Alternatively Cowden & Thomson (1979) sugges¬ ted that resolution might occur as the result of a rectification of a minor 'functional' defect during treatment with bromocriptine.…”

Section: Discussionmentioning

confidence: 99%

“…After pregnancy the pathological state is sometimes deteriorated (Rjosk et al 1980), but more fre¬ quently improved (Mornex et al 1978;Zarate et al 1979;Crosignani et al 1981) (White et al 1981). The progressive rise in serum Prl during pregnancy is believed to be caused by the increased oestrogen secretion (Rigg et al 1977), so pregnant hyperprolactinaemic patients could be expected to have a heterogeneous Prl increase during gestation.…”

mentioning

confidence: 99%

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The possible prognostic value of serum prolactin increment during pregnancy in hyperprolactinaemic patients

Starup

Tabor

et al. 1983

Acta Endocrinologica

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In 15 hyperprolactinaemic, infertile patients achieving 17 bromocriptine-induced pregnancies, the presence or absence of prolactin (Prl) increment in the 3rd trimester of pregnancy was correlated to the basal Prl levels before treatment and after pregnancy. The hyperprolactinaemic patients revealed a marked heterogeneity in the Prl increment compared to normal women. Five patients showed a pronounced increase in serum Prl during gestation, whereas Prl levels were unaltered or decreased slightly in 10 patients. In the latter group of patients serum Prl was significantly (P<0.01) lower after pregnancy than before treatment.Our study indicates that some hyperprolactinaemic patients may benefit from a pregnancy, and that these patients probably can be identified, as they do not show any significant changes in Prl levels during pregnancy.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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The possible prognostic value of serum prolactin increment during pregnancy in hyperprolactinaemic patients

Starup

Tabor

et al. 1983

Acta Endocrinologica

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“…Radiotherapy may be effective in controlling tumor growth, although its efficacy in restoring PRL levels to normal is limited. If fertility is a major concern, induction of ovulation is possible in hyperprolactinemic patients even without lowering PRL levels, using clomiphene citrate, gonadotropins, and pulsatile GnRH (332)(333)(334). A number of experimental therapies in various phases of development are available, as discussed in Section XII (Experimental Therapy), although these methods should be reserved for situations in which all other standard therapies have failed.…”

Section: F Treatment Approachesmentioning

confidence: 99%

Advances in the Treatment of Prolactinomas

et al. 2006

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Prolactinomas account for approximately 40% of all pituitary adenomas and are an important cause of hypogonadism and infertility. The ultimate goal of therapy for prolactinomas is restoration or achievement of eugonadism through the normalization of hyperprolactinemia and control of tumor mass. Medical therapy with dopamine agonists is highly effective in the majority of cases and represents the mainstay of therapy. Recent data indicating successful withdrawal of these agents in a subset of patients challenge the previously held concept that medical therapy is a lifelong requirement. Complicated situations, such as those encountered in resistance to dopamine agonists, pregnancy, and giant or malignant prolactinomas, may require multimodal therapy involving surgery, radiotherapy, or both. Progress in elucidating the mechanisms underlying the pathogenesis of prolactinomas may enable future development of novel molecular therapies for treatment-resistant cases. This review provides a critical analysis of the efficacy and safety of the various modes of therapy available for the treatment of patients with prolactinomas with an emphasis on challenging situations, a discussion of the data regarding withdrawal of medical therapy, and a foreshadowing of novel approaches to therapy that may become available in the future.

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“…Radiotherapy can also be effective in controlling tumor growth, although its efficacy in restoring PRL levels to normal is limited (1). If fertility is a major concern, other types of ovulation induction have been found to be successful in hyperprolactinemic patients without lowering the PRL levels, including clomiphene citrate, gonadotropins, and pulsatile GnRH [95][96][97].…”

Section: Treatment Approaches For Patients Resistant To Dopamine Agonmentioning

confidence: 99%

Pharmacologic Resistance in Prolactinoma Patients

2005

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Pharmacologic resistance to dopamine agonists is defined here as failure to normalize PRL levels and failure to decrease macroprolactinoma size by >or=50%. Failure to normalize PRL levels is found in about one-quarter of patients treated with bromocriptine and 10-15% of those treated with pergolide or cabergoline. Failure to achieve at least a 50% reduction in tumor size occurs in about one-third of those treated with bromocriptine and 10-15% of those treated with pergolide or cabergoline. The cause of dopamine resistance is primarily a decrease in D(2) receptors but the receptors have normal affinity for dopamine. Treatment approaches for patients resistant to dopamine agonists include changing to another dopamine agonist and increasing the dose of the drug as long as there is continued response to the dose increases and no adverse effects with higher doses. Transsphenoidal surgery is also an option. Clomiphene, gonadotropins, and GnRH can be used if fertility is desired. For those not desiring fertility, estrogen replacement may be used unless there is a macroadenoma, in which case control of tumor growth is also an issue and dopamine agonists are generally necessary. In many patients modest or even no reduction in tumor size may be acceptable as long as there is not tumor growth. Hormone replacement (estrogen or testosterone) may cause a decrease in efficacy of the dopamine agonist so that it must be carried out cautiously. Reduction of endogenous estrogen, use of selective estrogen receptor modulators, and aromatase inhibitors are potential experimental approaches.

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Spontaneous Pregnancies in Hyperprolactinemic Women

Cited by 17 publications

References 6 publications

The possible prognostic value of serum prolactin increment during pregnancy in hyperprolactinaemic patients

The possible prognostic value of serum prolactin increment during pregnancy in hyperprolactinaemic patients

Advances in the Treatment of Prolactinomas

Pharmacologic Resistance in Prolactinoma Patients

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