Lymphangioleiomyomatosis (LAM) is a rare and progressive multisystem neoplastic disorder that results from the pathological infiltration of abnormal smooth muscle–like LAM cells into the pulmonary interstitium, lymphatic vessels, and abdominopelvic organs. These LAM cells demonstrate inappropriate proliferation and migration as well as heightened proteolytic activity due to dysregulation of the mammalian target of rapamycin (mTOR) signalling pathway [1]. Clinically, patients often present with exertional dyspnoea, recurrent pneumothorax, progressive airflow limitation, or extrapulmonary features such as chylous effusions, lymphadenopathy, or renal angiomyolipomas [2]. In this case report, we describe a 30-year-old woman who developed progressive dyspnoea during pregnancy, with persistence of symptoms into the postpartum period, and subsequently developed painless cervical lymphadenopathy. High-resolution computed tomography (HRCT) of the chest revealed widespread thin-walled pulmonary cysts consistent with LAM, while pulmonary function testing showed preserved spirometry with pronounced gas trapping and a moderately reduced diffusing capacity. Laboratory investigations demonstrated no evidence of autoimmune disease, infection, or malignancy. There were no clinical or radiological features suggestive of tuberous sclerosis complex (TSC). A diagnosis of sporadic pulmonary LAM was therefore established. The patient was managed conservatively with smoking cessation, avoidance of exogenous oestrogen, pneumothorax counselling, and structured long-term radiological and physiological surveillance. This case highlights the importance of recognizing LAM in young women and illustrates how pregnancy may unmask or accelerate disease through hormonal mechanisms [3].