A Review of Post-Inflammatory Pigmentation Changes: Pathophysiology, Diagnosis and Treatment

Post-inflammatory hyperpigmentation (PIH) and hypopigmentation are heterogenous conditions that often occur secondary to dermatoses (eg, psoriasis, acne, or atopic dermatitis), cutaneous injury (eg, burns or radiation therapy), infection (viral, bacterial, or fungal), or allergic/immunologic dysregulation (eg, contact dermatitis or insect bite reactions). The pathophysiology of PIH is complex with multiple pathways implicated in hypermelanosis including ultraviolet radiation exposure, local skin inflammation, and cytokine and growth factor signalling between keratinocytes, melanocytes, and dermal fibroblasts. PIH is a clinical diagnosis based on patient history and clinical examination and may persist for months to years following the resolution of underlying pathophysiological mechanisms, emphasizing the need for prompt diagnosis and management. PIH can be disfiguring and associated with substantial impairments in quality of life and psychosocial well-being. Patients with skin of colour (ie, Fitzpatrick skin types III-VI) have an increased risk of PIH and often present with more pronounced dyspigmentation, highlighting a high unmet need for improved recognition, awareness, and management in this population. Photoprotection is the cornerstone of PIH management given the photosensitive nature of the condition and is recommended in tandem with other treatment options including topical agents (eg, hydroquinone, retinoids, tranexamic acid), light/laser-based therapies, or chemical peels (glycolic acid and salicylic acid). Despite their use, high-level clinical evidence for these treatment options in PIH remains limited. This review provides an up-to-date overview of PIH pathophysiology, diagnosis and differential diagnosis, and management, and offers expert clinical commentary on practical strategies for identifying, preventing, and managing PIH in routine practice.