Pulmonary hypertension (PH) is a significant but underrecognised complication of numerous parenchymal lung diseases beyond the well-characterised conditions of COPD and idiopathic pulmonary fibrosis. This chapter explores the spectrum of pulmonary vascular disease in association with less commonly discussed pulmonary conditions, including post-tuberculosis lung disease (PTLD), cystic fibrosis (CF), non-CF bronchiectasis, lymphangioleiomyomatosis (LAM), neurofibromatosis (NF), pulmonary Langerhans cell histiocytosis (PLCH), and silicosis. Although these diseases differ in aetiology and pathology, they share mechanisms that contribute to the development of PH, including chronic hypoxia, vascular remodelling, inflammation, fibrosis, and in some cases, direct vascular involvement or venous occlusion. For instance, PTLD-associated PH is increasingly recognised in high TB-burden settings, with risk factors such as recurrent TB, fibrocavitary disease, and venous thromboembolism contributing to pathogenesis. In non-CF and CF bronchiectasis, PH prevalence ranges widely and is associated with disease severity, hypoxia, and structural lung damage. LAM, NF1, and PLCH are rare, multisystem or neoplastic disorders with complex pathophysiology leading to PH, currently thought predominantly via parenchymal destruction or pulmonary vascular remodelling. While PH in these conditions may be mild in early stages, it frequently portends worse outcomes and is associated with increased morbidity and mortality, particularly in patients being evaluated for lung transplantation. The diagnosis of PH in the context of parenchymal lung disease remains challenging due to overlapping clinical features and limitations of non-invasive screening tools, especially in resource-constrained settings. Right heart catheterisation remains the gold standard but is often inaccessible. Treatment strategies are similarly limited, with most patients managed conservatively through optimisation of underlying lung disease, oxygen therapy, and supportive care. The recent approval of inhaled treprostinil for interstitial lung disease-associated PH provides hope for expanded therapeutic options in group 3 PH, but is not proven. This chapter emphasises the need for heightened clinical suspicion, targeted screening in high-risk populations, and further research to elucidate disease mechanisms and guide future therapeutic interventions in this neglected subset of pulmonary hypertension.