New options in the treatment of Cushing’s disease: a focus on pasireotide
Anne-Gaëlle Poullot,1 Nicolas Chevalier1,2
1Centre Hospitalier Universitaire de Nice, Hôpital de l’Archet, Service d’Endocrinologie, Diabétologie et Médecine de la Reproduction, Nice, France; 2Institut National de la Santé et de la Recherche Médicale (INSERM) UMR U1065/UNS, Centre Méditerranéen de Médecine Moléculaire (C3M), Equipe 5, Environnement, Reproduction et Cancers Hormono-Dépendants, Nice, France
Abstract: Cushing’s disease is caused by a corticotroph pituitary adenoma secreting adrenocorticotropin and can be fatal in the absence of adequate treatment. Transsphenoidal surgery remains the treatment of choice in almost all cases. However, remission rates are relatively low, and recurrence is usual and can be diagnosed up to decades after the initial diagnosis. Repeat surgery or radiation can be useful in these cases, although both have clear limitations with respect to efficacy and/or side effects. Hence, there is a clear unmet need for an effective medical treatment in patients with recurrent or persistent Cushing’s disease. Pasireotide is a novel multireceptor-targeted somatostatin analog with a high affinity for somatostatin receptor (sstr)-1, sstr-2, sstr-3, and sstr-5. Compared with octreotide, pasireotide has an in vitro binding affinity 40-fold higher for sstr-5, which is the major receptor subtype expressed by corticotroph pituitary adenoma. Recent studies have suggested a role for this new multireceptor somatostatin analog in Cushing’s disease. We review in this article the current data available regarding pharmacokinetics, clinical efficiency, and tolerance of pasireotide in patients with de novo, persistent, or recurrent Cushing’s disease, with a special focus on the disturbances of glucose metabolism induced by such a treatment.
Keywords: pasireotide, SOM230, somatostatin analog, Cushing’s disease, Cushing’s syndrome, pituitary adenoma, hypercortisolism
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