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Renato Cozzi
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Lindsay Dong
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Cozzi, R.;  Brunetti, A.;  Antonini, S.;  Saladino, A.;  Lavezzi, E.;  Zampetti, B. Somatostatin Receptor Ligands in Clinical Management of Acromegaly. Encyclopedia. Available online: https://encyclopedia.pub/entry/25326 (accessed on 17 July 2025).
Cozzi R,  Brunetti A,  Antonini S,  Saladino A,  Lavezzi E,  Zampetti B. Somatostatin Receptor Ligands in Clinical Management of Acromegaly. Encyclopedia. Available at: https://encyclopedia.pub/entry/25326. Accessed July 17, 2025.
Cozzi, Renato, Alessandro Brunetti, Simone Antonini, Andrea Saladino, Elisabetta Lavezzi, Benedetta Zampetti. "Somatostatin Receptor Ligands in Clinical Management of Acromegaly" Encyclopedia, https://encyclopedia.pub/entry/25326 (accessed July 17, 2025).
Cozzi, R.,  Brunetti, A.,  Antonini, S.,  Saladino, A.,  Lavezzi, E., & Zampetti, B. (2022, July 20). Somatostatin Receptor Ligands in Clinical Management of Acromegaly. In Encyclopedia. https://encyclopedia.pub/entry/25326
Cozzi, Renato, et al. "Somatostatin Receptor Ligands in Clinical Management of Acromegaly." Encyclopedia. Web. 20 July, 2022.
Somatostatin Receptor Ligands in Clinical Management of Acromegaly
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This entry is adapted from the peer-reviewed paper 10.3390/medicina58060794

Somatostatin receptor ligands (SRLs) represent a true milestone in the medical therapy for acromegaly. The first-generation SRLs (FG-SRLs), octreotide and lanreotide, have demonstrated good efficacy in disease control and tumor shrinkage, and are still considered first-line medical therapies. The development of long-acting release (LAR) formulations has certainly improved the therapeutic tolerability of these drugs.  In the case of FG-SRL-resistant disease, pasireotide, the only second generation SRL currently available, demonstrated superiority in disease control and tumor shrinkage compared to FG-SRLs. However, its use in clinical practice is still limited due to concern for impairment in glucose homeostasis.

pituitary acromegaly therapy somatostatin SSA

1. Introduction

Acromegaly is a rare disorder characterized by excessive circulating growth hormone (GH) levels, which in more than 95% of cases is caused by a GH-secreting pituitary adenoma. Due to the wide range of comorbidities associated to GH excess (i.e., hypertension, diabetes type 2, osteoporosis and arthritis, cardiovascular and respiratory disease, increased oncological risk), acromegaly may significantly impair quality of life (QoL) and increase risk of death [1][2].
Universally, the first-line therapy for acromegaly is the surgical removal of the pituitary adenoma via a trans-sphenoidal approach. In specialized centers, surgery results are effective in 80–90% of microadenomas and 50–75% of macroadenomas, with minor efficacy in the case of very large or invasive adenomas [3][4]. When surgery cannot reach resolution or is not feasible, other therapeutic strategies include medical treatment or radiotherapy, although the latter is currently mostly considered a third level therapy to be reserved for selected cases [5].
The goal of medical therapy is to achieve optimal disease control from both a clinical and biochemical perspective, normalizing insulin-like growth factor 1 (IGF-1) levels within an age-specific reference range and limiting the development of disease-related complications. In addition to biochemical control, treatment aims to prevent tumor growth or, ideally, induce tumor shrinkage. Medical therapy includes somatostatin receptor ligands (SRLs), pegvisomant, and dopamine agonists, although the role of the latter is currently considered suitable for patients with minor hormonal hypersecretion.
The release of FG-SRLs, octreotide and lanreotide, dates back to 1980s [6]. Both drugs act as somatostatin analogues with a high affinity for somatostatin-receptor type 2 (SSTR2) and to a lesser extent for SSTR5, inhibiting GH release from pituitary cells and preventing tumor growth. Prospective studies have demonstrated an overall efficacy of 40% in clinical and biochemical disease control, and a significant tumor shrinkage in about 60% of patients, mostly in de novo patients [7][8].
In patients unresponsive to FG-SRLs, the second line of therapy includes pegvisomant (PEGV), a GH receptor antagonist, or pasireotide (PAS), the only second-generation SRLs currently available [5]. PEGV is a genetically engineered GH-receptor antagonist prevalently blocking the GH-induced production of IGF-1 in the liver. In the 2021 update on ACROSTUDY, a 10-year-long global multicenter non-interventional study involving 2221 patients, PEGV showed IGF-1 normalization in 53.7% of the patients after 1 year and in 75.4% after 10 years of treatment. However, due to its mostly peripheral action, PEGV has no impact on pituitary tumor volume, and in ACROSTUDY an increase in tumor size was documented in 7.1% of patients [9].
PAS is a multi-receptor somatostatin ligand approved for acromegaly by both FDA and EMA in 2014, which compared to FG-SRLs expresses a significantly higher affinity for SSTR5 and a lower affinity for SSTR2 [10]. In both phase 3 clinical trials and real-life studies, PAS has proved to be more effective than FG-SRLs in achieving biochemical control and tumor shrinkage [11][12]. It also demonstrated an overall good tolerability profile, with similar side effects to FG-SRL except for an increased risk of developing glucose homeostasis alterations up to overt diabetes. Nevertheless, glucose metabolism alterations occur only in a minority of patients and hyperglycemic events are commonly controlled with standard anti-diabetic therapy [13].

2. Octreotide and Lanreotide

The most widely used formulations of FG-SRLs are octreotide in long-acting-release formulation (octreotide LAR), administered via intramuscular injection at a standard dose of 10–30 mg every 4 weeks, and lanreotide Autogel, administered via deep subcutaneous injection at a standard dose of 60–120 mg every 4 weeks.
Despite an overall improved QoL thanks to disease control, patients treated with FG-SRLs still experience reduced QoL because of therapy-related burden [14].
An oral formulation of octreotide was approved by Food and Drug Administration (FDA) in June 2020 for acromegalic patients already responsive to injective SRLs. This new formulation was tested in two sponsored randomized controlled trials (CH-ACM-01 and CHIASMA OPTIMAL) including one-hundred-and-fifty-five patients and fifty-six patients, respectively, who were already controlled in FG-SRLs therapy [15][16]. Therapy was administered through oral capsules taken two times a day with water, on an empty stomach, at least 1 h before a meal or at least 2 h after a meal. Both studies demonstrated that about 60% of patients maintained an optimal biochemical response during the follow-up period, which was 52 and 36 weeks, respectively.
The main limitation of the study was the inclusion in the treatment phase only of patients already responsive to oral octreotide, despite demonstrating the efficacy and safety of the oral formulation. Moreover, despite the presence of substantially overlapping side effects between the two formulations, the satisfaction in patients undergoing oral treatment proved to be significantly superior to injective formulation, as measured with AcroTSQ [17]. Oral octreotide may, therefore, represent an interesting therapeutic strategy in patients with a well-controlled disease under injective FG-SRLS, who have difficulty or are reluctant to parenteral administration.
An octreotide subcutaneous (SC) depot formulation (name CAM2029), is also under development. This formulation uses FluidCrystal technology, allowing both monthly administration and use of thin needles. In a phase 2 trial performed on patients with either acromegaly or functioning neuroendocrine tumors, the SC depot formulation demonstrated to increase octreotide plasma levels more than the IM formulation, with good biochemical control of disease and safety profile [18].
In addition, a prolonged release formulation (PRF) of lanreotide is under development, with the purpose of increasing the interval of therapy administration from 4 to 12 weeks. In a phase 2 clinical trial, lanreotide PRF was administered at multiple doses of 180 mg, 270 mg, and 360 mg. The primary endpoint of the study was to find the maximum tolerated dose (MTD), demonstrating good tolerability. Moreover, GH and IGF-1 levels remained substantially stable throughout the study [19]. Therefore, a PRF capable of extending the dose interval appears certainly possible, although further studies are required to better define efficacy and tolerability.

3. Pasireotide

PAS is currently considered in acromegaly therapeutic scenario as a second-line therapy. While for Cushing’s disease the drug is only approved in a short acting formulation, acromegalic patients can benefit from a LAR formulation to be administered at the standard dose of 20–60 mg every 4 weeks. PAS-LAR is suggested for treatment of patients poorly responsive to FG-SRL, especially if there is concern for tumor growth [5]. Indeed, in the phase 3 PAOLA study, PAS-LAR obtained biochemical control of disease in up to 20% of patients previously uncontrolled in FG-SRL therapy, with a further increase to 37% at the end of the extension phase [12][19]. A head-to-head superiority trial comparing PAS-LAR to octreotide LAR on naïve patients with acromegaly confirmed that patients receiving PAS-LAR were 63% more likely to achieve disease control [20]. Regarding tumor shrinkage, clinical trials documented a significant reduction (intended as either >20% or >25%) in up to 80% of treatment naïve patients and about 20% of patients unresponsive to FG-SRLs, with a medium tumor volume reduction of 40% [12]. In real-life settings, patients with uncontrolled disease in FG-SRLs achieved IGF-1 normalization after switching to PAS-LAR in up to 60% of cases, and most of them experienced a significant reduction or even disappearance of headaches [21][22].

The positive effect of PAS in acromegaly may go beyond simple control of disease. A longitudinal retrospective study performed by Chiloiro et al. on patients with resistant acromegaly showed that treatment with PAS reduced the incidence of vertebral fractures (VF), also independently from IGF-1 levels [23].

PAS may also represent the best therapeutic option for rare types of acromegaly associated with large pituitary tumors, such as X-linked acrogigantism (X-LAG) or aryl hydrocarbon receptor-interacting protein (AIP) mutation positive acromegaly, which are often resistant to FG-SRLs [24].

The use of PAS is still limited in clinical practice by concerns about the development of alterations in glucose metabolism.

The pathophysiology underpinning PAS-induced hyperglycemia depends on its higher affinity for SSTR5 than SSTR2. In fact, SSTR5 is highly expressed in pancreatic beta cells, responsible for insulin production, and in entero-endocrine cells is responsible for incretin release (i.e., glucagone-like peptide type 1), while SSTR2 expression prevails in alpha pancreatic cells, mainly responsible for glucagon production. As such, PAS affinity for SSTR5 induces a marked inhibition on both insulin and GLP-1 secretion, with a minor effect on glucagon, whose secretion is instead inhibited by FG-SRLs (Figure 1). A study performed by Henry et al. on healthy volunteers confirmed that a twice-daily subcutaneous administration of 600 or 900 µg of PAS significantly decreased plasma levels of insulin, GLP-1, and glucose-dependent insulinotropic polypeptide, and only slightly affected glucagon secretion [25]. As such, monitoring glucose profile is mandatory during PAS treatment, although diabetes mellitus occurs only in a minority of patients. 
/media/item_content/202207/62d8b75d22bc3medicina-58-00794-g001.png
Figure 1. Mechanism of Pasireotide-induced Hyperglycemia.
Aside from alterations in glucose metabolism, PAS has demonstrated both in clinical trials and in real-life settings mostly minor adverse drug reactions (AE). In the PAOLA extension study, cholelithiasis occurred in almost 30% of patients, although not requiring significant intervention except for one case reported of bile duct stone and cholecystitis. In the ACCESS study, evaluating safety of PAS-LAR 40 mg in forty-four acromegalic patients, gastrointestinal symptoms were reported as the most common non-glucose-related AEs: diarrhea in 38.6% of patients, nausea in 27.3%, and abdominal pain in 18.2% [26]. FDA also warned treatment with PAS with possible bradycardia and QT prolongation, recommending caution in subjects with congenital long QT prolongation, uncontrolled or significant cardiac disease, or under treatment with drugs inducing QT prolongation [27]. However, no significant arrhythmias or episodes of severe bradycardia have been reported in larger clinical trials and real-life settings.

4. SRLs in Combination Therapy with Pegvisomant

Combining FG-SRLs with PEGV is a therapeutic strategy increasingly used in real-world setting. At the moment, expert consensus recommends combination therapy in patients with resistance to monotherapy and concern for tumor growth and impaired glucose metabolism [5].
Regarding the addition of PEGV to SRLs, the main reason is the raise of IGF-1 levels in the presence of an aggressive disease or tumor with extrasellar invasion. SRLs and PEGV combination therapy has actually proved to achieve a better biochemical control of disease than SRLs alone [28]. Bonert et al. in their single-center prospective study of fifty-one patients treated with weekly PEGV (40 up to 160 mg/week) plus octreotide LAR or lanreotide Autogel, described 96% of biochemical control rate in patients with both previously well and poorly controlled disease [29]. Moreover, despite that the ACROSTUDY clearly demonstrated that PEGV monotherapy is not significantly associated to tumor growth, the discontinuation of SRLs may reduce control on tumor volume to its pre-treatment size [30].
While adding PEGV to SRLs appears to be a logical therapeutical escalation, it is more difficult to justify the addition of SRLs to PEGV, whose main reasons may be uncontrolled disease in PEGV monotherapy, concerning tumor growth and the reduction of frequency of PEGV injections. In the French ACROSTUDY, authors report that 53.3% of patients with uncontrolled disease achieved IGF-1 normalization after addition of SRLs and that PEGV frequency of administration significantly reduced (16% vs. 44.3% of patients receiving less than seven injections per week) [31].
Regarding glucose metabolism, two recent meta-analyses showed an overall neutral effect of combination therapy on fasting glucose and HbA1c with a significant reduction of fasting plasmatic insulin [32][33]. Associating FG-SRLs with PEGV, therefore, might represent a feasible choice in patients with resistant disease and overt diabetes in whom PAS might be not recommended.
In selected cases, a novel therapeutic perspective is represented by the combination therapy of PEGV with PAS-LAR [34]. Potential benefits of this combination may be treatment with PEGV and PAS-LAR may be treatment of resistant acromegaly, a PEGV dose reduction and a reduction of altered glycemic control experienced with PAS monotherapy.

References

  1. T’Sjoen, G.; Bex, M.; Maiter, D.; Velkeniers, B.; Abs, R. Health-related quality of life in acromegalic subjects: Data from AcroBel, the Belgian Registry on acromegaly. Eur. J. Endocrinol. 2007, 157, 411–417.
  2. Holdaway, I.M.; Bolland, M.; Gamble, G. A meta-analysis of the effect of lowering serum levels of GH and IGF-I on mortality in acromegaly. Eur. J. Endocrinol. 2008, 159, 89–95.
  3. Mortini, P.; Barzaghi, L.R.; Albano, L.; Panni, P.; Losa, M. Microsurgical therapy of pituitary adenomas. Endocrine 2017, 59, 72–81.
  4. Buttan, A.; Mamelak, A.N. Endocrine Outcomes After Pituitary Surgery. Neurosurg. Clin. N. Am. 2019, 30, 491–498.
  5. Giustina, A.; Barkhoudarian, G.; Beckers, A.; Ben-Shlomo, A.; Biermasz, N.; Biller, B.; Boguszewski, C.; Bolanowski, M.; Bollerslev, J.; Bonert, V.; et al. Multidisciplinary management of acromegaly: A consensus. Rev. Endocr. Metab. Disord. 2020, 21, 667–678.
  6. Bauer, W.; Briner, U.; Doepfner, W.; Haller, R.; Huguenin, R.; Marbach, P.; Petcher, T.J.; Pless, J. SMS 201–995: A very potent and selective octapeptide analogue of somatostatin with prolonged action. Life Sci. 1982, 31, 1133–1140.
  7. Colao, A.; Auriemma, R.S.; Pivonello, R.; Kasuki, L.; Gadelha, M.R. Interpreting biochemical control response rates with first-generation somatostatin analogues in acromegaly. Pituitary 2015, 19, 235–247.
  8. Giustina, A.; Mazziotti, G.; Torri, V.; Spinello, M.; Floriani, I.; Melmed, S. Meta-Analysis on the Effects of Octreotide on Tumor Mass in Acromegaly. PLoS ONE 2012, 7, e36411.
  9. Fleseriu, M.; Führer-Sakel, D.; van der Lely, A.J.; De Marinis, L.; Brue, T.; van der Lans-Bussemaker, J.; Hey-Hadavi, J.; Camacho-Hubner, C.; Wajnrajch, M.P.; Valluri, S.R.; et al. More than a decade of real-world experience of pegvisomant for acromegaly: ACROSTUDY. Eur. J. Endocrinol. 2021, 185, 525–538.
  10. Lesche, S.; Lehmann, D.; Nagel, F.; Schmid, H.A.; Schulz, S. Differential Effects of Octreotide and Pasireotide on Somatostatin Receptor Internalization and Trafficking in Vitro. J. Clin. Endocrinol. Metab. 2009, 94, 654–661.
  11. Gadelha, M.R.; Bronstein, M.D.; Brue, T.; Coculescu, M.; Fleseriu, M.; Guitelman, M.; Pronin, V.; Raverot, G.; Shimon, I.; Lievre, K.K.; et al. Pasireotide versus continued treatment with octreotide or lanreotide in patients with inadequately controlled acromegaly (PAOLA): A randomised, phase 3 trial. Lancet Diabetes Endocrinol. 2014, 2, 875–884.
  12. Colao, A.; Bronstein, M.D.; Freda, P.; Gu, F.; Shen, C.-C.; Gadelha, M.; Fleseriu, M.; van der Lely, A.J.; Farrall, A.J.; Reséndiz, K.H.; et al. Pasireotide Versus Octreotide in Acromegaly: A Head-to-Head Superiority Study. J. Clin. Endocrinol. Metab. 2014, 99, 791–799.
  13. Samson, S.L. Management of Hyperglycemia in Patients with Acromegaly Treated with Pasireotide LAR. Drugs 2016, 76, 1235–1243.
  14. Wolters, T.L.C.; Roerink, S.H.P.P.; Sterenborg, R.; Wagenmakers, M.A.E.M.; Husson, O.; A Smit, J.W.; Hermus, A.R.M.M.; Netea-Maier, R.T. The effect of treatment on quality of life in patients with acromegaly: A prospective study. Eur. J. Endocrinol. 2020, 182, 319–331.
  15. Melmed, S.; Popovic, V.; Bidlingmaier, M.; Mercado, M.; Van Der Lely, A.J.; Biermasz, N.; Bolanowski, M.; Coculescu, M.; Schopohl, J.; Racz, K.; et al. Safety and Efficacy of Oral Octreotide in Acromegaly: Results of a Multicenter Phase III Trial. J. Clin. Endocrinol. Metab. 2015, 100, 1699–1708.
  16. Samson, S.L.; Nachtigall, L.B.; Fleseriu, M.; Gordon, M.B.; Bolanowski, M.; Labadzhyan, A.; Ur, E.; Molitch, M.; Ludlam, W.H.; Patou, G.; et al. Maintenance of Acromegaly Control in Patients Switching from Injectable Somatostatin Receptor Ligands to Oral Octreotide. J. Clin. Endocrinol. Metab. 2020, 105, e3785–e3797.
  17. Fleseriu, M.; Dreval, A.; Bondar, I.; Vagapova, G.; Macut, D.; Pokramovich, Y.G.; E Molitch, M.; Leonova, N.; Raverot, G.; Grineva, E.; et al. Maintenance of response to oral octreotide compared with injectable somatostatin receptor ligands in patients with acromegaly: A phase 3, multicentre, randomised controlled trial. Lancet Diabetes Endocrinol. 2021, 10, 102–111.
  18. Pavel, M.; Borson-Chazot, F.; Cailleux, A.; Hörsch, D.; Lahner, H.; Pivonello, R.; Tauchmanova, L.; Darstein, C.; Olsson, H.; Tiberg, F.; et al. Octreotide SC depot in patients with acromegaly and functioning neuroendocrine tumors: A phase 2, multicenter study. Cancer Chemother. Pharmacol. 2018, 83, 375–385.
  19. Neggers, S.; Badiu, C.; Biagetti, B.; Durand-Gasselin, L.; Petit, A.; Petrossians, P.; Regnault, B.; Rich, D.; Shafigullina, Z.; Shustov, S.; et al. Pharmacological and safety profile of a prolonged-release lanreotide formulation in acromegaly. Expert Rev. Clin. Pharmacol. 2021, 14, 1551–1560.
  20. Colao, A.; Bronstein, M.D.; Brue, T.; De Marinis, L.; Fleseriu, M.; Guitelman, M.; Raverot, G.; Shimon, I.; Fleck, J.; Gupta, P.; et al. Pasireotide for acromegaly: Long-term outcomes from an extension to the Phase III PAOLA study. Eur. J. Endocrinol. 2020, 182, 583–594.
  21. Witek, P.; Bolanowski, M.; Szamotulska, K.; Wojciechowska-Luźniak, A.; Jawiarczyk-Przybyłowska, A.; Kałużny, M. The Effect of 6 Months’ Treatment with Pasireotide LAR on Glucose Metabolism in Patients with Resistant Acromegaly in Real-World Clinical Settings. Front. Endocrinol. 2021, 12, 139.
  22. Shimon, I.; Adnan, Z.; Gorshtein, A.; Baraf, L.; Khazen, N.S.; Gershinsky, M.; Pauker, Y.; Abid, A.; Niven, M.J.; Shechner, C.; et al. Efficacy and safety of long-acting pasireotide in patients with somatostatin-resistant acromegaly: A multicenter study. Endocrine 2018, 62, 448–455.
  23. Chiloiro, S.; Giampietro, A.; Frara, S.; Bima, C.; Donfrancesco, F.; Fleseriu, C.M.; Pontecorvi, A.; Giustina, A.; Fleseriu, M.; De Marinis, L.; et al. Effects of Pegvisomant and Pasireotide LAR on Vertebral Fractures in Acromegaly Resistant to First-generation SRLs. J. Clin. Endocrinol. Metab. 2019, 105, e100–e107.
  24. Beckers, A.; Lodish, M.B.; Trivellin, G.; Rostomyan, L.; Lee, M.; Faucz, F.R.; Yuan, B.; Choong, C.S.; Caberg, J.-H.; Verrua, E.; et al. X-linked acrogigantism syndrome: Clinical profile and therapeutic responses. Endocr.-Relat. Cancer 2015, 22, 353–367.
  25. Henry, R.R.; Ciaraldi, T.P.; Armstrong, D.; Burke, P.; Ligueros-Saylan, M.; Mudaliar, S. Hyperglycemia Associated with Pasireotide: Results from a Mechanistic Study in Healthy Volunteers. J. Clin. Endocrinol. Metab. 2013, 98, 3446–3453.
  26. Fleseriu, M., on behalf of the ACCESS Study Investigators; Rusch, E.; Geer, E.B. Safety and tolerability of pasireotide long-acting release in acromegaly—Results from the acromegaly, open-label, multicenter, safety monitoring program for treating patients who have a need to receive medical therapy (ACCESS) study. Endocrine 2016, 55, 247–255.
  27. Breitschaft, A.; Hu, K.; Darstein, C.; Ligueros-Saylan, M.; Jordaan, P.; Song, D.; Hudson, M.; Shah, R. Effects of subcutaneous pasireotide on cardiac repolarization in healthy volunteers: A single-center, phase I, randomized, four-way crossover study. J. Clin. Pharmacol. 2013, 54, 75–86.
  28. Strasburger, C.J.; Mattsson, A.F.; Wilton, P.; Aydin, F.; Hey-Hadavi, J.; Biller, B.M.K. Increasing frequency of combination medical therapy in the treatment of acromegaly with the GH receptor antagonist pegvisomant. Eur. J. Endocrinol. 2018, 178, 321–329.
  29. Bonert, V.; Mirocha, J.; Carmichael, J.; Yuen, K.C.J.; Araki, T.; Melmed, S. Cost-Effectiveness and Efficacy of a Novel Combination Regimen in Acromegaly: A Prospective, Randomized Trial. J. Clin. Endocrinol. Metab. 2020, 105, e3236–e3245.
  30. Neggers, S.J.C.M.M.; Franck, S.E.; De Rooij, F.W.M.; Dallenga, A.H.G.; Poublon, R.M.L.; Feelders, R.A.; Janssen, J.A.; Buchfelder, M.; Hofland, L.J.; Jorgensen, J.O.L.; et al. Long-Term Efficacy and Safety of Pegvisomant in Combination With Long-Acting Somatostatin Analogs in Acromegaly. J. Clin. Endocrinol. Metab. 2014, 99, 3644–3652.
  31. Kuhn, E.; Caron, P.; Delemer, B.; Raingeard, I.; Lefebvre, H.; Raverot, G.; Cortet-Rudelli, C.; Desailloud, R.; Geffroy, C.; Henocque, R.; et al. Pegvisomant in combination or pegvisomant alone after failure of somatostatin analogs in acromegaly patients: An observational French ACROSTUDY cohort study. Endocrine 2020, 71, 158–167.
  32. Feola, T.; Cozzolino, A.; Simonelli, I.; Sbardella, E.; Pozza, C.; Giannetta, E.; Gianfrilli, D.; Pasqualetti, P.; Lenzi, A.; Isidori, A.M. Pegvisomant Improves Glucose Metabolism in Acromegaly: A Meta-Analysis of Prospective Interventional Studies. J. Clin. Endocrinol. Metab. 2019, 104, 2892–2902.
  33. Ma, L.; Luo, D.; Yang, T.; Wu, S.; Li, M.; Chen, C.; Zhou, S.; Wu, Y.; Zhou, Y.; Cui, Y. Combined therapy of somatostatin analogues with pegvisomant for the treatment of acromegaly: A meta-analysis of prospective studies. BMC Endocr. Disord. 2020, 20, 126.
  34. Maia, B.; Kasuki, L.; Gadelha, M.R. Novel therapies for acromegaly. Endocr. Connect. 2020, 9, R274–R285.
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Renato Cozzi
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Alessandro Brunetti
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Simone Antonini
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Andrea Saladino
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Elisabetta Lavezzi
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Benedetta Zampetti
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