Development of acromegaly in patients with prolactinomas

Andersen, Marianne; Hagen, Claus; Frystyk, Jan; Schroeder, H D

doi:10.1530/eje.0.1490017

Cited by 36 publications

(25 citation statements)

References 28 publications

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“…In patients with hyperprolactinaemia, we found that three of 78 patients developed acromegaly (58). In line with the paper by Sakharova et al (62), our findings highlight the need for careful endocrine evaluation of patients with a prolactinoma (58).…”

Section: Gh Excess and Hyperprolactinaemiasupporting

confidence: 91%

“…interconversion of somatotrophs and lactotrophs, has been described in pregnancy (56) and in pituitary hyperplasia (57). Pituitary hormone secretion from an adenoma is a dynamic process, and acromegaly may thus be diagnosed in a patient with hyperprolactinaemia (58). Similarly, GH hypersecretion may be detected despite not being accompanied by obvious clinical stigmata of acromegaly.…”

Section: Gh Excess and Hyperprolactinaemiamentioning

confidence: 99%

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MANAGEMENT OF ENDOCRINE DISEASE: GH excess: diagnosis and medical therapy

Andersen

2014

European Journal of Endocrinology

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Acromegaly is predominantly caused by a pituitary adenoma, which secretes an excess of GH resulting in increased IGF1 levels. Most of the GH assays used currently measure only the levels of the 22 kDa form of GH. In theory, the diagnostic sensitivity may be lower compared with the previous assays, which have used polyclonal antibodies. Many GH-secreting adenomas are plurihormonal and may co-secrete prolactin, TSH and a-subunit. Hyperprolactinaemia is found in 30-40% of patients with acromegaly, and hyperprolactinaemia may occasionally be diagnosed before acromegaly is apparent. Although trans-sphenoidal surgery of a GH-secreting adenoma remains the first treatment at most centres, the role of somatostatin analogues, octreotide long-acting repeatable and lanreotide Autogel as primary therapy is still the subject of some debate. Although the normalisation of GH and IGF1 levels is the main objective in all patients with acromegaly, GH and IGF1 levels may be discordant, especially during somatostatin analogue therapy. This discordance usually takes the form of high GH levels and an IGF1 level towards the upper limit of the normal range. Pasireotide, a new somatostatin analogue, may be more efficacious in some patients, but the drug has not yet been registered for acromegaly. Papers published on pasireotide have reported an increased risk of diabetes mellitus due to a reduction in insulin levels. Pegvisomant, the GH receptor antagonist, is indicated -alone or in combination with a somatostatin analogue -in most patients who fail to enter remission on a somatostatin analogue. Dopamine-D2-agonists may be effective as monotherapy in a few patients, but it may prove necessary to apply combination therapy involving a somatostatin analogue and/or pegvisomant.

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Section: Gh Excess and Hyperprolactinaemiasupporting

confidence: 91%

Section: Gh Excess and Hyperprolactinaemiamentioning

confidence: 99%

MANAGEMENT OF ENDOCRINE DISEASE: GH excess: diagnosis and medical therapy

Andersen

2014

European Journal of Endocrinology

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“…Since Andersen and cols. (12) showed that GH hypersecretion not detected at diagnosis of the prolactinoma can arise subsequently, it is possible that the onset of hypersecretion occurred after the diagnosis in some of the patients and the frequency found in this cross-sectional study may still increase over time.…”

Section: Discussionmentioning

confidence: 75%

Biochemical acromegaly in patients with prolactinoma during treatment with dopaminergic agonists

Rosário

Purisch

2010

Arq Bras Endocrinol Metab

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Objective: To evaluate the frequency of subclinical acromegaly (in the absence of clinical phenotype but biochemically uncontrolled) in patients with prolactinoma during treatment with dopaminergic agonists. Subjects and methods: One hundred twenty one patients without a phenotype suggestive of acromegaly were studied. Results: Initially, the laboratory diagnosis of acromegaly was unequivocal (elevated IGF-1 for gender and age with nadir GH > 1 µg/L) in two patients, and likely (elevated IGF-1 with nadir GH > cut-off but < 1 µg/L) in another patient. In two other patients, this diagnosis was possible (normal IGF-1 with nadir GH > 1 µg/L). Repetition of the tests 6 months after withdrawal of the dopaminergic agonist confirmed the diagnosis of subclinical acromegaly (elevated IGF-1 for gender and age with nadir GH > 1 µg/L) in these 5 patients. False-positive results were excluded in all cases. Conclusion: In patients with prolactinomas, acromegaly should be investigated not only in cases with a clinical phenotype. Arq Bras Endocrinol Metab. 2010;54(6):546-9 Keywords Acromegaly; prolactinoma; growth hormone; IGF-1 RESUMO Objetivo: Avaliar a frequência de acromegalia subclínica (na ausência de fenótipo clínico, mas bioquimicamente não controlada) em pacientes com prolactinoma em tratamento com agonistas dopaminérgicos. Sujeitos e métodos: Cento e vinte e um pacientes sem fenótipo de acromegalia foram estudados. Resultados: Inicialmente, o diagnóstico laboratorial de acromegalia foi inequívoco (IGF-1 elevado para sexo e idade com nadir do GH > 1 µg/L) em dois pacientes, e provável (IGF-1 elevado com nadir do GH > valor de corte ensaio-específico mas < 1 µg/L) em outro paciente. Em outros dois, esse diagnóstico foi possível (IGF-1 normal com nadir do GH > 1 µg/L). A repetição dos testes seis meses após a suspensão dos agonistas dopaminérgicos confirmou o diagnóstico de acromegalia subclínica (IGF-1 elevado para sexo e idade com nadir do GH > 1 µg/L) em cinco desses pacientes. Os resultados falso-positivos foram excluídos em todos os casos. Conclusão: Em pacientes com prolactinomas, a acromegalia deveria ser investigada não apenas nos casos com fenótipo clínico. Arq Bras Endocrinol Metab. 2010;54(6):546-9 Descritores Acromegalia; prolactinoma; hormônio de crescimento; IGF-1

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“…Acromegaly was diagnosed clinically and biochemically after 33 months, despite cabergoline and sandostatin treatment. This is probably due to the ability of pituitary mammosomatotroph cells to produce both hormones (44)(45)(46).…”

Section: Discussionmentioning

confidence: 99%

Temozolomide treatment of a pituitary carcinoma and two pituitary macroadenomas resistant to conventional therapy

Schroeder¹,

Hansen

Hagen³

et al. 2009

European Journal of Endocrinology

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112

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Objective: Aggressive pituitary tumours may be difficult to treat. Temozolomide (TMZ) is an alkylating cytostaticum. In a small number of cases, TMZ therapy has been reported to reduce pituitary tumour size and hormone hypersecretion. Design: We present three patients with pituitary tumours treated with TMZ. One tumour was initially a macroprolactinoma that developed into a mixed GH-and prolactin-secreting carcinoma (patient A). To our knowledge, this is the first published in English literature. Two adenomas, a macroprolactinoma (patient B) and a clinically non-functioning pituitary adenoma (patient C), were highly invasive. The three patients suffered from extensive tumour mass effects, and all tumours were resistant to conventional treatment. Method: TMZ, 150-200 mg/m 2 of body surface area was administered orally for 5 days during each 28-day cycle. Result: During TMZ therapy, tumour sizes were significantly reduced, hormone levels normalized and symptoms of mass effects decreased in all three cases. The carcinoma was treated from 2004 to 2006 (23 months). Three years after the terminating treatment, the tumour has not regrown and hormone levels are normalized. Immunohistochemical staining for methylguanine DNA methyltransferase (MGMT) was negative in two patients (A and B), and in one patient (C) a few nuclei stained positive. Conclusion: TMZ therapy significantly decreased tumour volume, hormone hypersecretion and symptoms in all three patients, corresponding to the pathological findings regarding MGMT. TMZ therapy may be a new option for the treatment of resistant pituitary adenomas.

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Development of acromegaly in patients with prolactinomas

Cited by 36 publications

References 28 publications

MANAGEMENT OF ENDOCRINE DISEASE: GH excess: diagnosis and medical therapy

MANAGEMENT OF ENDOCRINE DISEASE: GH excess: diagnosis and medical therapy

Biochemical acromegaly in patients with prolactinoma during treatment with dopaminergic agonists

Temozolomide treatment of a pituitary carcinoma and two pituitary macroadenomas resistant to conventional therapy

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