# Sequential Dermoscopic, Histopathologic, and Immunopathologic Documentation of Regressing Seborrheic Keratosis: A Multimodal, Time‐Resolved Visual Case Study

**Authors:** Tomoaki Takada

PMC · DOI: 10.1002/ccr3.72274 · Clinical Case Reports · 2026-03-09

## TL;DR

This case study documents the rare spontaneous regression of a seborrheic keratosis over 8 weeks using multiple imaging and analysis techniques.

## Contribution

The study provides the first fully time-resolved clinicodermoscopic-immunopathologic sequence of cytotoxic regression in seborrheic keratosis.

## Key findings

- Sequential imaging showed structural changes in seborrheic keratosis during regression.
- Immunohistochemistry revealed CD8+/TIA-1+ cytotoxic T-cell activation and keratinocyte apoptosis.
- Keratinocyte-derived amyloid deposition was observed during the regression process.

## Abstract

Seborrheic keratosis (SK) typically shows stable behavior, and spontaneous regression is rarely documented. We report a unique case of SK that underwent complete involution within 8 weeks. Sequential clinical and dermoscopic imaging demonstrated a transition from classical SK structures to red‐blue homogeneous areas and, ultimately, to whitish regression zones. Histopathology revealed interface inflammation, keratinocyte degeneration, and epidermal remodeling. Immunohistochemistry confirmed a stepwise regression mechanism involving CD8+/TIA‐1+ cytotoxic T‐cell activation, cleaved caspase‐3–mediated apoptosis, and keratinocyte‐derived amyloid deposition. To our knowledge, this is the first case to demonstrate a fully time‐resolved clinicodermoscopic‐immunopathologic sequence of cytotoxic regression in SK.

Seborrheic keratosis may undergo rapid spontaneous regression driven by cytotoxic T‐cell activation. Sequential dermoscopy and immunopathology revealed a stepwise process involving keratinocyte apoptosis and keratinocyte‐derived amyloid deposition.

## Linked entities

- **Proteins:** CD8A (CD8 subunit alpha), TIA1 (TIA1 cytotoxic granule associated RNA binding protein)
- **Diseases:** seborrheic keratosis (MONDO:0008420)

## Full-text entities

- **Genes:** KRT20 (keratin 20) [NCBI Gene 54474] {aka CD20, CK-20, CK20, K20, KRT21}, TIA1 (TIA1 cytotoxic granule associated RNA binding protein) [NCBI Gene 7072] {aka ALS26, TIA-1, WDM}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, CASP3 (caspase 3) [NCBI Gene 836] {aka CPP32, CPP32B, SCA-1}, CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}
- **Diseases:** melanoma (MESH:D008545), fibrosis (MESH:D005355), inflammation (MESH:D007249), cytotoxic injury (MESH:D014947), primary cutaneous amyloidosis (MESH:C562642), benign epidermal tumors (MESH:D009369), cutaneous amyloidosis (MESH:C564461), Keratosis (MESH:D007642), keratoacanthoma (MESH:D007636), hemorrhage (MESH:D006470), SK (MESH:D017492), amyloid (MESH:C000718787), dermatitis (MESH:D003872), erythema (MESH:D004890), cysts (MESH:D003560)
- **Chemicals:** H&amp;E (MESH:D006371), hematoxylin (MESH:D006416)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12968886/full.md

## References

7 references — full list in the complete paper: https://tomesphere.com/paper/PMC12968886/full.md

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Source: https://tomesphere.com/paper/PMC12968886