Effect of Oral Contraceptives on Serum Prolactin: A Longitudinal Study in 126 Normal Premenopausal Women

Hwang, Peter; Ng, Charmaine; Cheong, S. T.

doi:10.1111/j.1365-2265.1986.tb00754.x

Cited by 28 publications

(11 citation statements)

References 25 publications

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“…We assume that the reduction of ovarian mass, which had caused the decrease in estrogen and progesterone levels, was a trigger for the appearance of galactorrhea as in the case of normal postpartum galactorrhea or after the discontinuation of oral contraceptives (21). Later, gallactorrhea persisted, probably due to the mass effect of the adenoma, although supranormal serum estradiol level may have also been the reason for the elevated PRL (4).…”

Section: Discussionmentioning

confidence: 99%

Evolution of clinical symptoms in a young woman with a recurrent gonadotroph adenoma causing ovarian hyperstimulation

Pentz-Vidovic

Škorić

Grubišić

et al. 2000

European Journal of Endocrinology

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Objective: To demonstrate the clinical course in a young female with gonadotroph adenoma causing ovarian stimulation. Patient and methods: Our patient was a 23-year-old woman with a history of oligomenorrhea who had previously undergone bilateral ovarian wedge resection owing to the clinical appearance of polycystic ovaries. Two years later, she sought treatment for headache, galactorrhea, history of spotting and lower abdominal distension. FSH, LH, b-LH, inhibin A and B, estradiol, prolactin (PRL), and bchorionic gonadotrophin (b-CG) were measured, and the responses of FSH, LH and b-LH to thyrotrophin-releasing hormone (TRH) were documented. Immunohistochemical analysis of the tumor tissue was performed after surgery. Five years after the trans-sphenoidal surgery, the patient again became oligomenorrheic. A large recurrent adenoma was diagnosed on CT one year later. Transvaginal ultrasound showed ovaries of normal size with multiple small cystic formations simulating a polycystic pattern, While the patient was awaiting surgery, a pituitary apoplexy occurred. Emergency decompressive surgery was performed and the patient fully recovered. Results: Enlarged ovaries were found on ultrasound examination simulating a hyperstimulationlike pattern. At that time, elevated levels of FSH (13.4 IU/l) and marginally elevated levels of b-LH (1.43 ng/ml) were found, whereas the level of LH (0.5 IU/l) was subnormal. Plasma estradiol was markedly supranormal (6150 pmol/l). Levels of inhibin A and B were elevated (326 pg/ml and 588 pg/ml respectively). The prolactin level (70 ng/ml) was increased, whereas b-chorionic gonadotrophin (b-CG) was normal. Signi®cantly increased FSH, LH, and b-LH responses to TRH stimulation were documented. Pituitary macroadenoma was found on MRI scan and removed by trans-sphenoidal surgery. Immunohistochemical examination showed high positivity for b-CG and LH, and slight positivity for FSH. Five years after the surgery, estradiol was elevated (1160 pmol/l), whereas basal levels of LH (4.65 IU/l) and FSH (3.98 IU/l) were not suppressed. After the second operation, immunostaining of the adenoma tissue con®rmed the previous ®ndings. Conclusions: Measurement of gonadotrophins in our case did not prove to be a method for identifying a large recurrent gonadotroph pituitary adenoma. The sonographic ovarian imaging varied from a polycystic-to an ovarian hyperstimulation-like pattern during the evolution of the tumour.

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Section: Discussionmentioning

confidence: 99%

Evolution of clinical symptoms in a young woman with a recurrent gonadotroph adenoma causing ovarian hyperstimulation

Pentz-Vidovic

Škorić

Grubišić

et al. 2000

European Journal of Endocrinology

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“…Whether the estrogens in oral contraceptives or hormone replacement therapy are sufficient to cause hyperprolactinemia is controversial. Some studies have shown that estrogen-containing oral contraceptives can indeed cause hyperprolactinemia in percentages ranging from 12 to 30% of treated women, with little influence of the dose of estrogen [105,106] but others have shown either a minimal or no increase in PRL levels [107][108][109][110][111]. On the other hand most studies have shown either no [112][113][114][115] or minimal effect [116] on PRL levels of estrogen replacement therapy following oophorectomy or at menopause with varying doses of estrogens up to 1.25 mg of conjugated estrogens or 50 lg of estradiol daily.…”

Section: Estrogensmentioning

confidence: 99%

Drugs and prolactin

Molitch

2008

Pituitary

143

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Medications commonly cause hyperprolactinemia and their use must be differentiated from pathologic causes. The most common medications to cause hyperprolactinemia are the antipsychotic agents, although some of the newer atypical antipsychotics do not do so. Other medications causing hyperprolactinemia include antidepressants, antihypertensive agents, and drugs which increase bowel motility. Often, the medication-induced hyperprolactinemia is symptomatic, causing galactorrhea, menstrual disturbance, and erectile dysfunction. In the individual patient, it is important differentiate hyperprolactinemia due to a medication from a structural lesion in the hypothalamic-pituitary area. This can be done by stopping the medication temporarily to determine if the prolactin (PRL) levels return to normal, switching to another medication in the same class which does not cause hyperprolactinemia (in consultation with the patient's physician and/or psychiatrist), or by performing an MRI or CT scan. If the hyperprolactinemia is symptomatic, management strategies include switching to an alternative medication which does not cause hyperprolactinemia, using estrogen/testosterone replacement, or cautiously adding a dopamine agonist.

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“…Some studies have shown that estrogen-containing oral contraceptives can cause hyperprolactinemia in percentages ranging from 12 to 30% of treated women, with little influence of the dose of estrogen [35,36] but others have shown either a minimal or no increase in PRL levels [37][38][39][40][41]. On the other hand most studies have shown either no [42][43][44][45] or minimal effect [46] on PRL levels of estrogen replacement therapy following oophorectomy or at menopause with varying doses of estrogens up to 1.25 mg of conjugated estrogens or 50 µg of estradiol daily.…”

Section: Late Development Of Dopamine Agonist Resistancementioning

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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Effect of Oral Contraceptives on Serum Prolactin: A Longitudinal Study in 126 Normal Premenopausal Women

Cited by 28 publications

References 25 publications

Evolution of clinical symptoms in a young woman with a recurrent gonadotroph adenoma causing ovarian hyperstimulation

Evolution of clinical symptoms in a young woman with a recurrent gonadotroph adenoma causing ovarian hyperstimulation

Drugs and prolactin

Pharmacologic Resistance in Prolactinoma Patients

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