INTRODUCTION

Progesterone (P4) is essential for maintaining canine pregnancy. Unlike other domestic species, the canine placenta does not synthesize P4; therefore, the bitch relies entirely on the ovarian corpus luteum (CL) throughout gestation [1]. Consequently, premature luteolysis or functional disruption of the CL results in pregnancy failure [2, 3].

Hypoluteodism, or luteal insufficiency, is defined as a primary dysfunction in which the CL fails to secrete sufficient P4 to sustain pregnancy. This condition is typically identified by serum P4 concentrations falling below the critical threshold (commonly 2–5 ng/mL) in the absence of other abortifacient factors [4, 5]. However, in high-risk breeds or clinical cases exhibiting a precipitous decline, early intervention before reaching these critical levels may be warranted to prevent irreversible fetal loss. Although its precise incidence is underreported, largely because of challenges in establishing consistent diagnostic criteria, recent retrospective analyses indicate that hypoluteodism is a significant contributor to non-infectious pregnancy loss [6, 7]. As a result, the condition is particularly insidious, often presenting without overt clinical signs until fetal compromise has already occurred [8].

Physiologically, the regulation of the canine CL undergoes a critical transition during mid-gestation, shifting from autonomous function to reliance on hormonal support. During early gestation, the CL operates relatively independently, but beginning around days 25–30 post-ovulation, it becomes dependent on pituitary support, particularly luteinizing hormone (LH) and prolactin [9, 10]. This "critical window" of shifting luteotrophic dependency represents a period of increased vulnerability to luteal failure, as described by Kowalewski et al. [11]. Recent studies suggest that certain breeds may be predisposed to premature luteolysis during this transitional phase, further amplifying the risk [12]. However, distinguishing true primary hypoluteodism from secondary P4 declines associated with infectious agents, such as _Brucella _canis and Escherichia coli, or uterine pathology remains a diagnostic challenge for clinicians, particularly during this vulnerable interval [6].

The clinical management of confirmed hypoluteodism necessitates exogenous P4 supplementation to compensate for inadequate endogenous production. Historically, synthetic progestins, such as medroxypro-gesterone acetate (MPA), have been widely used because of their potent progestational activity and broad availability [6]. Although effective, the use of long-acting progestins remains controversial because of adverse effects, including masculinization of female fetuses, insulin resistance in the dam, and prolonged gestation with potential fetal loss when withdrawal is mistimed [13]. Although recent protocols using micronized natural P4 or altrenogest have gained popularity, MPA remains an important therapeutic option, particularly in resource-limited settings or when alternative formulations are unavailable or unsuitable. Zhelavskyi et al. [14] demonstrated that hormonal supplementation can effectively support pregnancy maintenance in bitches with luteal insufficiency.

Despite the recognized clinical importance of hypoluteodism, several important gaps remain in the current literature. Most available reports are limited to isolated case descriptions or small case series, with relatively few studies providing systematic longitudinal monitoring of P4 dynamics throughout gestation. In addition, previous investigations have largely involved heterogeneous canine populations, making it difficult to identify breed-specific patterns of luteal dysfunction or periods of increased susceptibility to pregnancy loss. Information regarding predisposed breeds, particularly the Shetland Sheepdog, remains scarce. Furthermore, although MPA has historically been used for pregnancy support, concerns regarding fetal virilization, prolonged gestation, and maternal adverse effects have limited its application, and contemporary evidence evaluating the safety and efficacy of low-dose MPA protocols with planned late-gestation withdrawal is limited. Consequently, there is a lack of practical clinical guidelines regarding the optimal timing for P4 surveillance, initiation of therapy, and withdrawal of exogenous progestins to facilitate elective cesarean section while minimizing fetal and maternal complications.

Therefore, this retrospective study aimed to characterize the temporal pattern of P4 decline in bitches diagnosed with hypoluteodism and to evaluate the clinical efficacy and safety of a tailored low-dose MPA protocol combined with standardized prepartum withdrawal. Particular emphasis was placed on identifying a critical period of luteal vulnerability in predisposed breeds, especially the Shetland Sheepdog, and on determining whether systematic P4 monitoring, coupled with timed cessation of treatment, could successfully maintain pregnancy to term without compromising maternal health or neonatal viability. By providing data from one of the largest documented cohorts with serial hormonal monitoring and a standardized withdrawal strategy, this study seeks to establish a practical framework for the clinical management of canine hypoluteodism and to offer veterinarians an evidence-based approach for reducing pregnancy loss while facilitating planned cesarean delivery.