Pulmonary Hypertension Secondary to Fungal Infections: Underexplored Pathological Links

TL;DR

This paper discusses how fungal infections can lead to pulmonary hypertension through various mechanisms, highlighting the need for more research and clinical attention.

Contribution

The paper identifies and explains three key mechanisms linking fungal infections to pulmonary hypertension.

Findings

Fungal infections can cause endothelial injury through emboli or autoimmune reactions.

Chronic fungal infections drive vascular remodeling via inflammation and fibrosis.

Granulomatous diseases like paracoccidioidomycosis can cause distant vascular remodeling post-infection.

Abstract

Background/Objective: Pulmonary fungal infections are a significant diagnostic challenge, primarily affecting immunocompromised individuals, such as those with HIV, cancer, or organ transplants, and they often lead to substantial morbidity and mortality if untreated. These infections trigger acute inflammatory and immune responses, which may progress to chronic inflammation. This process involves myofibroblast recruitment, the deposition of extracellular matrix, and vascular remodeling, ultimately contributing to pulmonary hypertension. Despite its clinical relevance, pulmonary hypertension secondary to fungal infections remains under-recognized in practice and poorly studied in research. Results/Conclusion: This narrative mini-review explores three key mechanisms underlying vascular remodeling in this context: (1) endothelial injury caused by fungal emboli or autoimmune reactions, (2) direct vascular remodeling during chronic infection driven by inflammation and fibrosis, and (3) distant vascular remodeling post-infection, as seen in granulomatous diseases like paracoccidioidomycosis. Further research and clinical screening for pulmonary hypertension in fungal infections are crucial to improving patient outcomes.

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