A 9-month-old girl is brought in by her parents for evaluation of symmetrical brown bands on her ankles that have been present for several weeks. The child is otherwise healthy and appears unbothered by the skin findings. On exam, there are bilateral, linear, well-demarcated hyperpigmented bands encircling the lower legs just above the ankles. There is no erythema, induration, tenderness, or preceding rash.
Which of the following best explains the pathogenesis of this condition?
A. Dermal sclerosis due to immune-mediated fibroblast activation
B. Fixed melanocyte activation following drug hapten exposure
C. Repeated pressure or friction leading to basal layer hyperpigmentation
D. Trauma-induced hemosiderin deposition with vascular leakage
E. Interface dermatitis resulting in pigment incontinence
Rationale:
This patient has a classic presentation of sock-line hyperpigmentation, a benign and self-limited condition typically seen in infants and young children. It presents as symmetrical, band-like hyperpigmented macules that correspond to areas of pressure or compression from socks or snug clothing. Importantly, there is no preceding inflammation, erosion, or systemic illness. Recognizing this condition is important to avoid misdiagnosis as trauma, morphea, or other dermatoses. It is self-resolving and does not require treatment.
Correct answer choice: C. Repeated pressure or friction leading to basal layer hyperpigmentation
The most likely pathogenesis of sock-line hyperpigmentation is repetitive pressure or friction from elastic garments, which triggers dermal and subcutaneous inflammation leading to melanocyte activation and increased melanin deposition in the basal layer. This results in non-indurated hyperpigmentation most noticeable in areas like the ankles where socks apply localized pressure.
Incorrect answer choices:
A. Dermal sclerosis due to immune-mediated fibroblast activation describes the pathogenesis of morphea or localized scleroderma. This involves inflammatory activation of fibroblasts, resulting in indurated, atrophic plaques which is not consistent with this clinical vignette.
B. Fixed melanocyte activation following drug hapten exposure is seen in fixed drug eruption, where drug-specific T cells induce site-specific melanocyte activation and damage. Fixed drug eruptions are typically recurrent, violaceous, and often involve mucosa, not symmetrically distributed pressure areas in infants.
D. Trauma-induced hemosiderin deposition with vascular leakage is seen in traumatic purpura or stasis-related hyperpigmentation, often seen in venous insufficiency, and is associated with erythema, edema, or bruising.
E. Interface dermatitis resulting in pigment incontinence is seen in lichen planus pigmentosus, post-inflammatory hyperpigmentation, or cutaneous lupus, where inflammatory destruction of basal keratinocytes leads to pigment drop-out.
References:
1. Berk DR, Tapia B, Lind A, Bayliss SJ. Sock-line hyperpigmentation: case series and literature review. Arch Dermatol. 2007 Mar;143(3):428-30. doi: 10.1001/archderm.143.3.428.
2. Alkhowailed MS, Otayf M, Albasseet A, Almousa A, Alajlan Z, Altalhab S. Clinical Approach to Linear Hyperpigmentation: A Review Article. Clin Cosmet Investig Dermatol. 2021 Jan 8;14:23-35. doi: 10.2147/CCID.S280819.