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Premature luteinization of one or more developing follicles complicates 1–2 % of controlled ovarian stimulation cycles for assisted reproduction. The management of this complication is controversial, with cycle cancellation likely representing the most commonly used strategy. The aim of this study was to evaluate the efficacy of the “freeze-all” policy—where the entire cohort of blastocysts is cryopreserved for subsequent frozen-thawed embryo transfer—in treating cases of premature luteinization. Patients experiencing premature luteinization during controlled ovarian stimulation—identified by extremely high progesterone levels at induction (P levels ≥3.0 ng/ml and/or P/estradiol ratio ≥1, n= 42)—were included in a “freeze-all” program and compared to controls undergoing a “freeze-all” program with normal progesterone levels at induction (P < 1.5 ng/ml, n= 67). Blastulation rate was comparable between patients with premature luteinization and controls (48.1 ± 20.5 % in Cases vs. 52.3 ± 24.9 % in Controls, p= 0.36). Ongoing pregnancy rates after the first frozen-thawed embryo transfer (38.1 % in Cases and 41.0 % in Controls, p= 0.83) and cumulative ongoing pregnancy rates after three frozen-thawed embryo transfer cycles (40.5 % in Cases vs. 47.8 % in Controls, p= 0.55) were also similar. These results show that extremely marked progesterone elevation throughout controlled ovarian stimulation does not impair blastocyst development and implantation potential in the context of a “freeze-all” strategy. Based on this, adoption of the “freeze-all” strategy represents a valuable tool in treating premature luteinization. In contrast, cycle cancellation—likely the most frequently used method for management of this complication—currently represents a misconduct.

Proopiomelanocortin (POMC) is crucial for several life-essential functions and its regulation has been studied extensively in the past decades. The first studies provided the framework for POMCpromoter activity, namely the identification for the major response elements contained in the promoter, e.g., the glucocorticoid response element, the Nur response element, while subsequent studies showed the importance of cooperation and interplay between transcription factors to achieve optimal promoter activity. The involvement of constitutive repressors of POMCtranscription, such as Bmp4, provided the latest clues to our understanding of POMCpromoter activity. This increased knowledge benefits the clinician as it allows genetic testing and early recognition of patients with congenital ACTH deficiency due to mutations in TPIT and paves the way to new medical treatments in Cushing’s disease. The present review will illustrate the current standing on regulation of the human POMCpromoter, focusing on its activity in corticotropes.