Reversible Shrinkage of a Growth Hormone-Secreting Pituitary Adenoma by a Long-Acting Somatostatin Analogue, Octreotide

Barakat, Sawsan; Мелмед, Шломо

doi:10.1001/archinte.1989.00390060149035

Cited by 25 publications

(4 citation statements)

References 15 publications

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“…In the case of Sadoul et al, a significant reduction of a giant mixed GH-prolactin secreting adenoma from 11cm 3 to 0.5cm 3 , after 12 months of combined therapy with octreotide acetate and bromocriptine, was observed. 33 The case that most resembles our own is that reported by Bakarat and Melmed, 34 who observed complete disappearance of a GH secreting adenoma (from 4.6cm 3 to 0) after 4 months of octreotide acetate administration while, the discontinuation of treatment for one month led to an immediate recurrence of the pituitary mass.…”

Section: Discussionsupporting

confidence: 75%

Disappearance of a growth hormone secreting macro adenoma during long-term somatostatin analogue administration and recurrence following somatostatin withdrawal

Livadas¹,

Hadjidakis²,

Argyropoulou³

et al. 2006

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Acromegaly is caused by excessive growth hormone secretion, usually from a pituitary adenoma. The use of somatostatin analogues as primary or adjunctive therapy has been widely applied in the management of acromegaly. We are aware of only three reported cases of complete shrinkage of a pituitary adenoma after long-term analogue administration. However in these cases, the reduction in the dimension of the adenoma was obtained with the everyday use of somatostatin analogues and not with the newer longer acting formulations. We report a patient in whom long term (62 months) lanreotide-L.A.R administration resulted in complete disappearance of a growth hormone secreting pituitary macroadenoma, followed by recurrence of the adenoma six months post therapy discontinuation.

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Section: Discussionsupporting

confidence: 75%

Disappearance of a growth hormone secreting macro adenoma during long-term somatostatin analogue administration and recurrence following somatostatin withdrawal

Livadas¹,

Hadjidakis²,

Argyropoulou³

et al. 2006

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“…Therefore, several long lasting SRIF analogs, such as SMS 201-995 (octreotide), MK 678 (seglitide), and BIM23014 (somatuline), have been developed as anticancer agents (1). Because SRIF was discovered as the key physiological inhibitor of GH secretion in pituitary somatotroph cells, octreotide was first approved for use in treating GH-secreting pituitary somatotroph tumors resulting in acromegaly (2,3). Octreotide and other stable SRIF analogs cause a significant reduction of both GH secretion and pituitary tumor size in acromegaly.…”

Section: Introductionmentioning

confidence: 99%

Somatostatin Acts by Inhibiting the Cyclic 3′,5′-Adenosine Monophosphate (cAMP)/Protein Kinase A Pathway, cAMP Response Element-Binding Protein (CREB) Phosphorylation, and CREB Transcription Potency

Tentler

Hadcock

Gutierrez‐Hartmann

1997

Molecular Endocrinology

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Somatostatin (SRIF) was discovered as an inhibitor of GH secretion from pituitary somatotroph cells. SRIF analogs are very effective agents used to treat neuroendocrine tumors and are now being used with increasing frequency in clinical trials to treat more aggressive malignancies. However, the cellular components mediating SRIF signal transduction remain largely unknown. We have stably overexpressed the SRIF type 2 receptor (SST2) in GH4 rat somatomammotroph cells, establishing a physiologically relevant model system. In this model, the SRIF analog, BIM23014, inhibited forskolin-induced cAMP accumulation, protein kinase A activation, cAMP response element-binding protein phosphorylation, and Pit-1/GHF-1 promoter activation in an okadaic acid-insensitive manner. Pertussis toxin inhibited the effects of BIM23014, documenting that SST2 signaling was coupled to Gi. Moreover, the inhibitory effects of BIM23014 were reversed by overexpression of protein kinase A catalytic subunit, indicating that SRIF does not act via serine/threonine phosphatases, but, rather, by lowering protein kinase A activity. These data define the components of the SRIF/SST2 receptor signaling pathway and provide important mechanistic insights into how SRIF controls neuroendocrine tumors. As SRIF analogs are effective antitumor agents, and many other related compounds are in development, the knowledge gained here will further our understanding of their mechanism of action in other malignancies as well.

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“…Failure to control pituitary adenoma growth in clinical settings has been reported in approximately 10% of cases [73][74][75]. In addition, some Authors reported that the effects of SRIF analogs on tumor size do not appear to be permanent, since GH-secreting pituitary adenomas may reexpand on withdrawal of octreotide [76][77][78][79], suggesting that these drugs induce tumor shrinkage by decreasing adenoma cell size/activity rather than inducing apoptosis [66,80]. On the other hand, octreotide treatment failed to produce significant morphological alterations in GH-secreting pituitary adenoma cells [80].…”

Section: In Vivo Evidence For Antiproliferative Effects On Pituitary mentioning

confidence: 99%

Antiproliferative effects of somatostatin analogs in pituitary adenomas

et al. 2006

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The antisecretory effects of somatostatin (SRIF) and its analogs are widely recognised and provide the basis for treatment of hormonal hypersecretion in pituitary adenomas, especially in the settings of acromegaly. Evidence for an antiproliferative effect of these compounds has also been provided. This review focuses on the mechanisms transducing the antiproliferative effects of SRIF and its analogs on pituitary adenomas, and on the clinical consequences on tumor volume of pharmacological treatment of pituitary adenomas with these drugs.

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Reversible Shrinkage of a Growth Hormone-Secreting Pituitary Adenoma by a Long-Acting Somatostatin Analogue, Octreotide

Cited by 25 publications

References 15 publications

Disappearance of a growth hormone secreting macro adenoma during long-term somatostatin analogue administration and recurrence following somatostatin withdrawal

Disappearance of a growth hormone secreting macro adenoma during long-term somatostatin analogue administration and recurrence following somatostatin withdrawal

Somatostatin Acts by Inhibiting the Cyclic 3′,5′-Adenosine Monophosphate (cAMP)/Protein Kinase A Pathway, cAMP Response Element-Binding Protein (CREB) Phosphorylation, and CREB Transcription Potency

Antiproliferative effects of somatostatin analogs in pituitary adenomas

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