Inoperable Giant Growth Hormone-secreting Pituitary Adenoma: Radiological Aspects, Clinical Management and Pregnancy Outcome

Dicuonzo, Franca; Purciariello, Stefano; Marco, Aurora De; Guastamacchia, Edoardo; Triggiani, Vincenzo

doi:10.2174/1871530318666180807160712

Cited by 6 publications

(7 citation statements)

References 18 publications

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“…Recent evidence concerning patients who were under medical therapy for a longer period of time during gestation months showed a good safety profile [ 95 ]. Particular aspects concerning surveillance of glucose profile are added by the use of SSAs to cardio-metabolic features in acromegalic pregnancies [ 95 , 96 , 97 , 98 , 99 ].…”

Section: Specific Medical Therapy For Acromegaly During Pregnancymentioning

confidence: 99%

“…Based on the data we currently have, SSAs should be stopped at the moment of pregnancy confirmation, but according to a case-by-case decision, the treatment may be prolonged probably throughout the entire first trimester or even longer in exceptional cases. The main indication of SSA gestational exposure is probably the amelioration of headache to improve the quality of life and to reduce the use of analgesics which is in any case restricted during pregnancy [ 95 , 96 , 97 ]. Headache is related to potential tumor growth which turned out not to be dramatic in most of the published cases.…”

Section: Specific Medical Therapy For Acromegaly During Pregnancymentioning

confidence: 99%

“…The newborn was healthy and remained so for the next 2 years of follow-up [ 96 ]. During the gestation period, tumor expansion may be managed only with medical therapy, especially octreotide, as indicated by most data, unless hypophysectomy is provided in severe cases [ 77 , 95 , 96 , 97 ].…”

Section: Specific Medical Therapy For Acromegaly During Pregnancymentioning

confidence: 99%

“…Another scenario involves inoperable giant somatotropinomas (with a diameter larger than 4 cm) in patients who, through achieving biochemical control under medical treatment, might conceive [ 97 ]. For instance, we mention a young female with macroadenoma severely invasive with respect to the cavernous sinus, the right orbital cavity, the sphenoid sinus, etc., which was rapidly responsive to ocreotide LAR in terms of controlling the headache and bilateral hemianopsia and allowing a good fertility profile in order to get pregnant.…”

Section: Specific Medical Therapy For Acromegaly During Pregnancymentioning

confidence: 99%

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Approach of Acromegaly during Pregnancy

et al. 2022

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Acromegaly-related sub/infertility, tidily related to suboptimal disease control (1/2 of cases), correlates with hyperprolactinemia (1/3 of patients), hypogonadotropic hypogonadism—mostly affecting the pituitary axis in hypopituitarism (10–80%), and negative effects of glucose profile (GP) anomalies (10–70%); thus, pregnancy is an exceptional event. Placental GH (Growth Hormone) increases from weeks 5–15 with a peak at week 37, stimulating liver IGF1 and inhibiting pituitary GH secreted by normal hypophysis, not by somatotropinoma. However, estrogens induce a GH resistance status, protecting the fetus form GH excess; thus a full-term, healthy pregnancy may be possible. This is a narrative review of acromegaly that approaches cardio-metabolic features (CMFs), somatotropinoma expansion (STE), management adjustment (MNA) and maternal-fetal outcomes (MFOs) during pregnancy. Based on our method (original, in extenso, English—published articles on PubMed, between January 2012 and September 2022), we identified 24 original papers—13 studies (3 to 141 acromegalic pregnancies per study), and 11 single cases reports (a total of 344 pregnancies and an additional prior unpublished report). With respect to maternal acromegaly, pregnancies are spontaneous or due to therapy for infertility (clomiphene, gonadotropins or GnRH) and, lately, assisted reproduction techniques (ARTs); there are no consistent data on pregnancies with paternal acromegaly. CMFs are the most important complications (7.7–50%), especially concerning worsening of HBP (including pre/eclampsia) and GP anomalies, including gestational diabetes mellitus (DM); the best predictor is the level of disease control at conception (IGF1), and, probably, family history of 2DM, and body mass index. STE occurs rarely (a rate of 0 to 9%); some of it symptoms are headache and visual field anomalies; it is treated with somatostatin analogues (SSAs) or alternatively dopamine agonists (DAs); lately, second trimester selective hypophysectomy has been used less, since pharmaco-therapy (PT) has proven safe. MNA: PT that, theoretically, needs to be stopped before conception—continued if there was STE or an inoperable tumor (no clear period of exposure, preferably, only first trimester). Most data are on octreotide > lanreotide, followed by DAs and pegvisomant, and there are none on pasireotide. Further follow-up is required: a prompt postpartum re-assessment of the mother’s disease; we only have a few data confirming the safety of SSAs during lactation and long-term normal growth and developmental of the newborn (a maximum of 15 years). MFO seem similar between PT+ve and PT-ve, regardless of PT duration; the additional risk is actually due to CMF. One study showed a 2-year median between hypophysectomy and pregnancy. Conclusion: Close surveillance of disease burden is required, particularly, concerning CMF; a personalized approach is useful; the level of statistical evidence is expected to expand due to recent progress in MNA and ART.

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Section: Specific Medical Therapy For Acromegaly During Pregnancymentioning

confidence: 99%

Section: Specific Medical Therapy For Acromegaly During Pregnancymentioning

confidence: 99%

Section: Specific Medical Therapy For Acromegaly During Pregnancymentioning

confidence: 99%

Section: Specific Medical Therapy For Acromegaly During Pregnancymentioning

confidence: 99%

See 2 more Smart Citations

Approach of Acromegaly during Pregnancy

et al. 2022

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“…Somatotroph adenomas were the second most common functional pituitary adenomas and usually occur with cardiovascular, respiratory, and cerebrovascular disease [1], accompanied by a higher risk of mortality compared to people without the disease [2]. High secretion of growth hormone is often the reason of acromegaly in adults.…”

Section: Introductionmentioning

confidence: 99%

Identification of Serum miRNA-423-5p Expression Signature in Somatotroph Adenomas

Zhao

Feng

et al. 2019

International Journal of Endocrinology

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Circulating miRNAs are novel disease biomarkers that are valuable for diagnosis and prognosis. But the circulating miRNAs profile in somatotroph adenomas is still unknown. Therefore, serum exosomal miRNAs expression profiling in somatotroph adenomas was performed on 6 somatotroph adenomas and 6 normal controls. From the exosomal miRNAs expression profiling, we found 169 miRNAs differently expressed between somatotroph adenomas and healthy pituitary samples (p< 0.05, FC > 2). Among the 169 miRNAs, miR-423-5p was expressed lower in somatotroph adenomas than in healthy pituitary samples, which was proved by miRSCan Panel Chip™ qPCR. PTTG1 and SYT1 were the target mRNAs of miR-423-5p, and transcriptomics and proteomics profile both indicated the high expression of PTTG1 and SYT1 in somatotroph adenomas. H-scores were 223.1 ± 34.7 for PTTG1 and 163.4 ± 42.3 for SYT1 in 62 somatotroph adenomas specimens and 84.2 ± 21.3 for PTTG1 and 47.4 ± 17.2 for SYT1 in 6 healthy pituitary specimens by IHC. miR-423-5p inhibited the expression of SYT1 and PTTG1 at the mRNA and protein levels. Dual luciferase reporter gene assay shown was significantly reduced in the presence of miR-423-5p in GH3 cells transfected with wild-type PTTG1 3'UTR luciferase reporter plasmid but not reduced when transfected with the mutation PTTG1 3'UTR luciferase reporter plasmid (p<0.01). In vitro experiments showed that miR-423-5p induced cell apoptosis, inhibited cell proliferation, and reduced growth hormone release and migration of GH3 cells. The activity of miR-423-5p in GH3 cell was nearly blocked by its inhibitor. These results verified the central role of low miR-423-5p in promoting tumorigenesis in somatotroph adenomas. PTTG1 may act as biomarkers for clinical treatment of somatotroph adenomas.

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