We report a 22-year-old Japanese woman with multiple basaloid cell hamartoma with alopecia and autoimmune disease (systemic lupus erythematosus). She presented with infiltrated large annular, brown-violet, erythematous plaques with atrophic areas in the center on her right cheek, left abdomen and left knee. She also had progressive multiple follicular keratotic papules on her scalp, face, neck, and both axilla and hair loss from her scalp, eyebrow, and axilla. Serologically, rheumatoid factor (+ + +), rheumatoid arthritis hemagglutination test (x1280), and anti-nuclear antigen (x160) were positive. Histological findings of the annular lesion showed liquefaction degeneration of basal cells, lymphocytic infiltration around hair follicles and capillaries, and panniculitis with lymphoid cell infiltration, which was diagnosed as lupus erythematosus profundus. The histological findings of multiple follicular papular lesions of the scalp and neck showed aggregations of basaloid cells, partially with hair-bulb-like structures, which was diagnosed as trichoepithelioma. Taken together, the histogenesis of multiple basaloid cell hamartoma is thought to share the same basis with autoimmune disease.

Plasminogen activator inhibitor (PAI) purified from human epidermis ) FEBS Lett. 408, 273-2771 was immunologically identified as placental-type PAI-2. In both fibrinolytic and synthetic substrate assays inhibitory activity of epiderma1 PA1 was neutralized by anti-PAI-2, but not by anti-endothelial type PAI-1. Immunoblotting technique confirmed that the purified epidermal PA1 is reactive with anti-PAI-2, but not with anti-PAI-1. Consequently PA1 in human epidermis was demonstrable by immunohistochemical technique.Placental-type plasminogen activator inhibitor-2; Endothelial-type plasminogen activator inhibitor-l; Urokinase; Tissue-type plasminogen activator; (Human epidermis)

The following is a case study of a 36-year-old Japanese man with a trichoblastoma which exhibited a rippled-pattern on the left temporal region of the scalp. The histological findings of the tumor revealed lobular aggregations composed of immature follicular basaloid cells, lobules of squamous eddy-like foci of incomplete keratinization or small keratinous cysts, and multiple papillary mesenchymal bodies similar to hair germ. Interestingly, a rippled-pattern of basaloid cells and hyalinized matrixes resembling the Verocay bodies of neurilemmoma was also observed. We propose that the rippled-pattern of the basaloid cells and hyalinized matrices is caused by the characteristic stromal induction of trichoblastoma.

The present study reports two cases of basal cell carcinoma arising in seborrheic keratosis. The first case is a seventy-three-year-old female who presented with a blackish nodule arising from a pigmented lesion on her chest. Histopathological analysis of the nodule and the pigmented lesion revealed a basal cell carcinoma with hair follicular differentiation and an acanthotic seborrheic keratosis, respectively. The second case is a seventy-year-old female with a blackish nodule arising from a pigmented lesion on her back. Histological analysis of the nodule revealed an atypical basaloid cell mass surrounded by a seborrheic keratosis lesion. In addition to the coexisting seborrheic keratosis with the basal cell carcinoma, a basaloid follicular hamartoma that showed multiple hamartomatous hair follicles or small cysts replaced by a branching cord or lace-like network of basaloid cells surrounded by fibrovascular stroma was identified. We concluded that both cases presented a rare combination of a seborrheic keratosis which underwent a malignant change to basal cell carcinoma. It appears that both basal cell carcinomas and seborrheic keratosis may derive from a similar source: pluripotential cells of either the epidermis or hair follicle epithelium.

To analyze the degradation system in epidermal cells during their generation, differentiation, and cell death, immunocytochemical localization of lysosomal cysteine and aspartic proteinases, an endo-f3 in islet endocrine cells of the rat pancreas. J. Histochem. Cytochem. 36: 783-791 (1988).