Exponentially elevated testosterone in a middle-aged woman with polycystic ovarian syndrome: A therapeutic response to luteinising hormone-releasing hormone agonist

• Published in: Clinical medicine (London, England) England), 2024-04, Vol.24, p.100097, Article 100097
• Main Authors: Salman, Fareeha, Khattak, Ahmad Ammar, Azam, Kamal Uddin, Muhammad, Fabiha, Saeed, Tamar
• Format: Article
• Language: English
• ISSN: 1470-2118
• DOI: 10.1016/j.clinme.2024.100097

We report a case of a 43-year-old lady referred to the Endocrinology department by her general practitioner (GP) for exponentially elevated testosterone and amenorrhoea persisting for 5 months, excessive weight gain of 153 kg and an elevated testosterone level of 14.8 nmol/L(0.7–2.8 nmol/L). Her body mass index (BMI) was 58.3 kg/m2. Thyroid profile, Prolactin, Cortisol, and 17 hydroxyprogesterone were all within the normal range. Luteinising hormone (LH) and follicle stimulating hormone (FSH) were normal initially. Dehydroepiandrosterone (DHEA) was slightly low. Surprisingly, a contrast-enhanced computer tomography (CT) scan revealed portal vein thrombosis, presenting an unexpected finding in the context of the patient's clinical presentation. Ultrasound pelvis and magnetic resonant imaging (MRI) adrenals did not reveal any abnormalities. The diagnostic process meticulously ruled out potential causes of elevated testosterone, including congenital adrenal hyperplasia, thyroid dysfunction, hyperprolactinemia, adrenal and ovarian tumours, or an exogenous source of testosterone. In view of her amenorrhoea, clinical and biochemical hyperandrogenism, the diagnosis of polycystic ovarian syndrome (PCOS) was reached as per the Rotterdam criteria.1 Although PCOS can be associated with elevated testosterone levels but exponentially high levels of testosterone for example more than 6 nmol/L, as in our patient's case, is not frequently seen in PCOS and such elevated levels warrant further investigations to rule out adrenal or ovarian tumours.2 Given the patient's elevated BMI and the presence of a portal vein thrombus, combined oral contraceptive pills (COCPs) were deemed unsuitable for treatment. Pregnancy was ruled out and given the clinical presentation and laboratory findings, therapeutic intervention was initiated with Leuprorelin, a luteinising hormone-releasing hormone (LHRH) agonist, which is usually used in patients with prostate cancer to lower the testosterone.3,4 She was commenced on Leuprorelin subcutaneous injection once a month for almost 6 months. The response to treatment was notable, resulting in a significant decrease in serum testosterone levels from 14.8 nmol/L to 7.4 nmol/L. Although restoration of regular menstruation wasn't achieved, she started having intermittent spotting and a marked reduction in testosterone levels was noted. However, upon discontinuation of Leuprorelin, testosterone levels began to rise again, reaching 11 nmol/L. In light o