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UNLABELLED Pregnancy luteomas are rare, benign, neoplasms of the ovary thought to be caused by the hormonal effects of pregnancy. They are usually asymptomatic and found incidentally during imaging or surgery. However, they may present with virilization of the mother or infant or cause complications due to a mass effect or hemorrhage secondary to torsion. Luteomas spontaneously regress postpartum. We present a case of a woman with the classic presentation of a pregnancy luteoma and the common challenges of subsequent management. Pregnancy luteomas present a diagnostic and management challenge in that they can mimic the presentation of malignant ovarian tumors. There have been fewer than 200 case reports of pregnancy luteomas and a relative paucity of data to provide guidance for clinical management. However, certain general principles emerged from a review of modern cases. Management of pregnancy luteomas depends on the clinical situation. Luteomas present most commonly in the second half of pregnancy, with a solid ovarian mass that is frequently bilateral, elevated testosterone levels and some aspects of virilization. With high clinical suspicion for pregnancy luteoma, clinical monitoring and postpartum radiologic follow-up may be an appropriate management strategy to avoid unnecessary surgery. However, in some cases with atypical presentation or with complications from the mass, surgical intervention may be necessary for diagnostic or management purposes. Patients who present in the first half of pregnancy generally have more severe symptoms and are more likely to require surgical intervention for management of mass effect. When there is a high clinical suspicion for pregnancy luteoma, conservative management is appropriate since these tumors will usually regress spontaneously. After completing this CME activity, obstetrician/gynecologists should be better able to evaluate clinical presentations of pregnancy luteomas, examine the complexities involved in diagnosing neoplasms suspicious for pregnancy luteoma, and counsel patients about appropriate management and treatment options. TARGET AUDIENCE Obstetricians & Gynecologists, Family Physicians, Pediatricians Learning Objectives: After completion of this article, the reader should be better able to evaluate the clinical presentations of pregnancy luteomas; examine the complexities involved in the diagnosis of neoplasms suspicious for pregnancy luteoma; and counsel patients on appropriate management and treatment for suspected luteomas.

The incidence of gestational hyperandrogenism secondary to ovarian pathology is low. However, when the condition does exist, diagnosis should be made with minimally invasive modalities. It is important to provide appropriate medical/surgical intervention without disturbing the pregnancy iatrogenically or causing unnecessary maternal morbidity. This case report adds to the existing radiographic data concerning this rare obstetrical condition. Presented is a review of the English literature on virilizing ovarian tumors during pregnancy, and a discussion of an approach to managing these tumors when they occur during pregnancy.

Lacl of masculinization in female infants whose virilized mothers have h. luteinalis is in contrast to the common finding of fetal masculinization when maternal virilization occurs with luteoma of pregnancy. From the data at hand, this variation in fetal response cannot be explained by differences in the quantity of androgen production nor by the stage of pregnancy when maternal virilization becomes evident. Steroid analysis from cases of h. luteinalis suggests that the placenta may serve as an androgen barrier by aromatizing steroids before they reach the fetus. Testosterone conversion by the placenta of an anencephalic fetus confirms that conversion to estrogens occurs even without significant fetal adrenal activity. Understanding of the breakdown of this mechanism, with resultant fetal masculinization, will require careful evaluation of the steroid milieu in conditions like luteoma in which fetal masculinization often occurs. Both cystic and solid ovarian hyperplasia are recognized as are complications of pregnancy which require proper identification and conservative management. The significant difference in patients at risk for luteoma and h. luteinalis and the pathological and hormonal differences clearly indicate that these are distinct and separate entities.

Since its original description in 1963, the pregnancy luteoma has been a controversial entity both clinically and pathologically. The most important questions which have been asked are: Is the luteoma a true neoplasm or does it represent simply an abnormal response to the hormones of pregnancy? What is the relation between the tumor and certain endocrinopathies that are associated with these lesions? This study of 20 cases collected from the files of the Emil Novak Ovarian Tumor Registry and the Pathology Section of the Baltimore City Hospitals directs its attention to these critical clinicopathologic features.

Virilizing luteoma of pregnancy with maternal and fetal virilization is reported in a 19 year old woman. Antepartum steroid determinations in the mother revealed an elevated urinary 17-ketosteroid excretion and markedly increased plasma testosterone levels. The percentage binding of testosterone in plasma was lower than expected for normal pregnancy. Surgical removal of the tumor resulted in complete regression of the signs of virilization in the mother and partial regression of the clitoral hypertrophy in the infant. These changes were associated with a return of the biochemical findings to normal.