Prolactin secretion before, during, and after chronic gonadotropin-releasing hormone agonist treatments in children

Massart, Francesco; Parrino, Roberta; Placidi, Giulia; Massai, G.; Federico, Giovanni; Saggese, Giuseppe

doi:10.1016/j.fertnstert.2005.03.041

Cited by 5 publications

(6 citation statements)

References 23 publications

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“…Interestingly, reduction of testosterone and estradiol levels with depot gonadotropin-releasing hormone analogues has been reported in some patients when used for treatment of prostate cancer in men [117,118] and precocious puberty in children [119,120].…”

Section: Estrogensmentioning

confidence: 99%

Drugs and prolactin

Molitch

2008

Pituitary

142

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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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Section: Estrogensmentioning

confidence: 99%

Drugs and prolactin

Molitch

2008

Pituitary

142

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“…Thus, the previous GnRH analogue did not seem to be the cause of mild hyperprolactinemia in 1 of our adolescents, because she stopped triptorelin depot administration >2 years before our evaluation and revision of her clinical records did not reveal any hormone increase during treatment. We also excluded a false positive increase due to macroprolactinemia [17, 26], while this possibility was not explored in the other report [25]. …”

Section: Discussionmentioning

confidence: 99%

Body Mass Index and Body Composition in Adolescents Treated with Gonadotropin-Releasing Hormone Analogue Triptorelin Depot for Central Precocious Puberty: Data at Near Final Height

Chiocca

Dati²,

Baroncelli³

et al. 2009

Neuroendocrinology

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Background/Aim: In children with central precocious puberty (CPP), gonadotropin-releasing hormone (GnRH) analogue treatment has been associated with an increase in body mass index (BMI). We evaluated BMI and body composition in adolescents treated with GnRH analogue at their near final height to assess the long-term effects of therapy on these parameters. Patients and Methods: We studied 20 patients (14.8 ± 1.6 years; 17 females) previously treated with triptorelin depot for CPP (3.75 mg/28 days) from 8.1 ± 0.8 to 11.5 ± 0.8 years. 23 healthy adolescents with normal onset of puberty (14.7 ± 2.1 years, 19 females) were the controls. BMI and body composition (dual-energy x-ray absorptiometry) were assessed. Results: Patients reached their near adult height (–0.5 ± 1.1 standard deviation score (SDS)); the girls were menstruating and the majority (15/17) had regular cycles, the boys showed normal testicular function. BMI was unchanged from the start of GnRH analogue therapy (0.4 ± 1.0 SDS) to near adult height (0.2 ± 1.0 SDS, p = NS vs. 0). Total fat mass (TFM) was significantly increased (16,144 ± 8,065 g; controls 10,712.1 ± 4,120.4 g, p < 0.02); glucose homeostasis and lipid profile corresponded to reference ranges. Conclusions: GnRH analogue therapy did not show long-term detrimental effects on BMI, but it may increase TFM, suggesting that body composition should be monitored till adulthood.

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“…Few studies have compared GnRHa-induced hormonal patterns in children to ascertain if there is clinical equivalence between LA- and TR-based depot preparations for treatment of CPP [19,20,21,25]. Regarding gonadotropin secretion, adult studies comparing LA and TR depot preparations observed a difference in their potency and duration of action [17,18].…”

Section: Discussionmentioning

confidence: 99%

“…These analyses were restricted to the first 4–12 weeks after administration of the analog [12,17,18]. Few studies have been performed in children with longer GnRHa treatment (2.5–3.5 years) and investigate different GnRHa-induced clinical aspects [19,20,21]. Furthermore, to the best of our knowledge, the impact of GnRHa treatment on growth of spCPP patients has not been previously evaluated.…”

Section: Introductionmentioning

confidence: 99%

Growth Outcome during GnRH Agonist Treatments for Slowly Progressive Central Precocious Puberty

et al. 2009

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Background: Gonadotropin-releasing hormone agonists (GnRHa) represent the gold-standard treatment for central precocious puberty (CPP). In CPP children, GnRHa treatment slows bone age progression and preserves adult height (Ht) by suppressing sexual steroid secretion. In some patients, however, GnRHa induce an inappropriate growth deceleration impairing Ht outcome. Furthermore, slowly progressive CPP (spCPP) forms were reported which do not need GnRHa treatment. Methods: We evaluated the growth outcome of 26 spCPP girls treated with triptorelin (TR) and 21 with leuprorelin acetate (LA) for 36.5 ± 0.7 months. Results: GnRHa treatment induced a progressive growth deceleration in both spCPP groups. No difference in bone maturation was detected (p > 0.05; TR vs. LA group), however compared to LA, TR treatment resulted in significantly higher Ht after 24 months (p < 0.05; LA vs. TR group). Although target height (TH) standard deviation score (SDS) and predicted adult height (PAH)-SDS at diagnosis were similar in both spCPP groups (p > 0.05; LA vs. TR group), final height (FH-SDS) was lower in LA-treated subjects (p < 0.05; LA vs. TR group). In both spCPP groups, FH-SDS was significantly lower than TH-SDS (p < 0.001) but not lower than PAH-SDS at diagnosis (p > 0.05). Ht-SDS correlated with 17β-estradiol (E₂) blood levels in both spCPP groups (p < 0.0001) throughout GnRHa treatment, and E₂ values were higher in the TR- than in the LA-treated patients during the 12 months after GnRHa administration (p < 0.05; LA vs. TR group). GnRHa-induced E₂ secretion and Ht-SDS at GnRHa withdrawal correlated positively with FH (p < 0.01 and p < 0.001, respectively). Conclusions: The effectiveness of GnRHa treatment in improving FH in spCPP girls was doubtful.

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Prolactin secretion before, during, and after chronic gonadotropin-releasing hormone agonist treatments in children

Cited by 5 publications

References 23 publications

Drugs and prolactin

Drugs and prolactin

Body Mass Index and Body Composition in Adolescents Treated with Gonadotropin-Releasing Hormone Analogue Triptorelin Depot for Central Precocious Puberty: Data at Near Final Height

Growth Outcome during GnRH Agonist Treatments for Slowly Progressive Central Precocious Puberty

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