Postmenopausal Uterine Leiomyomas and Chronic Lymphadenopathy: Exploring Epigenetic Changes and Pathophysiology

Uterine leiomyomas (LM) are tumors arising from the non-neoplastic proliferation of smooth muscle cells within the myometrium. Like benign tumors, LM are not generally spread through the lymphatic system, and therefore should not be associated with lymphadenopathy. Herein, we present a case of a 60-year-old female who presented to the clinic with postmenopausal bleeding in the setting of sonographically evident uterine LM and abdominal lymphadenopathy. A lymph node biopsy revealed plasma cells and an eosinophilic material presumptively diagnosed as amyloid. She then underwent an abdominal hysterectomy for definitive treatment of LM. Surgical pathology confirmed the clinical diagnosis of uterine and cervical leiomyoma. Current literature suggests that genetic and epigenetic abnormalities contribute to the pathogenesis of LM in addition to hormonal signals such as estrogen and progesterone. It is unusual for LM to occur in post-menopausal women due to reduced hormonal influence. Therefore, this case explored an alternative mechanism of tumor proliferation. This case hypothesizes that genetic mutations and epigenetic changes resulting from chronic inflammatory offenses contributed to LM growth and lymphadenopathy.