Subject(s)
Pemphigoid, Bullous , Humans , Biomarkers , Chemokine CCL17 , Chemokines , Pemphigoid, Bullous/diagnosisSubject(s)
Hyperpigmentation , Lentigo , Papillomavirus Infections , Photosensitivity Disorders , Humans , Hyperpigmentation/diagnosis , Leg , Lentigo/diagnosisSubject(s)
Nevus, Blue , Skin Neoplasms , Female , Humans , Nevus, Blue/diagnosis , Nevus, Blue/genetics , Skin Neoplasms/genetics , Vulva , Exome SequencingSubject(s)
Antimetabolites, Antineoplastic/adverse effects , Capecitabine/adverse effects , Drug Eruptions/etiology , Eosinophilia/chemically induced , Folliculitis/chemically induced , Skin Diseases, Vesiculobullous/chemically induced , Aged , Eosinophilia/pathology , Folliculitis/pathology , Humans , Male , Skin Diseases, Vesiculobullous/pathologyABSTRACT
BACKGROUND: In extramammary Paget disease (EMPD), Paget cells are sometimes detected outside the clinical border (subclinical extension). However, the spreading pattern of Paget cells in subclinical extension remains unclear. In addition, the macroscopic appearances of lesions accompanied by subclinical extension are totally unknown. OBJECTIVES: To characterize the spreading pattern of Paget cells as well as the macroscopic appearance of lesions of EMPD with subclinical extension. METHODS: Nineteen patients with primary anogenital EMPD underwent mapping biopsies and excisional surgeries; biopsy samples were then taken at the periphery of well-demarcated lesions. Samples were transparentized and subjected to whole-mount immunostaining with anticytokeratin 7 antibody to label Paget cells. The histological border was evaluated in three dimensions by two-photon microscopy. The shape and location of the histological border were compared with those of the clinical border. RESULTS: In 21 samples taken at the lesion where subclinical extension was not shown by mapping biopsy, the shape and location of the histological border were almost identical to those of the clinical border. However, two samples exhibited small foci of Paget cells outside the clinical border, showing subclinically extended satellite lesions. In the two samples taken at the lesions where subclinical extension was shown by mapping biopsy, a continuous arrangement of Paget cells extending beyond the clinical border was identified. Subclinically extended Paget cells were detected solely outside hypopigmented patches with erythema. CONCLUSIONS: In EMPD, at least two patterns of subclinical extension exist: continuous and satellite lesions. Subclinical extension might exist preferentially outside hypopigmented patches with erythema.
Subject(s)
Anus Neoplasms/pathology , Paget Disease, Extramammary/pathology , Skin Neoplasms/pathology , Urogenital Neoplasms/pathology , Adult , Aged , Aged, 80 and over , Dermoscopy/methods , Female , Humans , Hypopigmentation/pathology , Male , Middle Aged , Neoplasm Recurrence, Local/pathology , Paget Disease, Extramammary/surgery , Photons , Preoperative Care , Skin Neoplasms/surgeryABSTRACT
It has been reported that basic fibroblast growth factor (bFGF) promotes the healing of skin ulceration by inducing fibroblast proliferation, yet the role of bFGF on epidermal barrier function, especially from the perspective of scratch-induced skin abrasion, remains unknown. To this end, we initially developed an epidermal abrasion mouse model induced by scratching with a stainless-steel wire brush, and examined the effects of bFGF on the wound healing induced by skin abrasion. This procedure induced a significant elevation of transepidermal water loss (TEWL) in a scratch-count-dependent manner. This elevated TEWL was significantly decreased following topical application of bFGF to the skin. In addition, bFGF increased the expression of Ki67 in keratinocytes following mechanical scratching. These results suggest that bFGF enhances keratinocyte proliferation, which, in turn, repairs the skin barrier disruption and wounds caused by scratching in mice. Consistently, bFGF stimulated proliferation of normal human epidermal keratinocytes (NHEK). Intriguingly, the effect of bFGF and other growth factors on NHEK proliferation was additive. However, high cell density diminished the effect of bFGF on NHEK proliferation. This particular result can be explained by our observation that FGF receptor mRNA expression in NHEK was low under conditions of high cell density. Our findings suggest that bFGF stimulates keratinocyte proliferation, especially in a lower cell density environment, to repair skin wound in accord with skin barrier recovery.
Subject(s)
Fibroblast Growth Factor 2/administration & dosage , Keratinocytes/drug effects , Skin/drug effects , Wound Healing/drug effects , Administration, Topical , Adult , Animals , Cell Proliferation/drug effects , Cells, Cultured , Coculture Techniques , Epidermal Cells , Fibroblasts/cytology , Fibroblasts/drug effects , Fibroblasts/metabolism , Humans , Keratinocytes/cytology , Keratinocytes/metabolism , Mice , Mice, Inbred C57BL , RNA, Messenger/metabolism , Receptors, Fibroblast Growth Factor/genetics , Skin/injuries , Skin/metabolism , Water/metabolismABSTRACT
BACKGROUND: Cholinergic urticaria (CU) has well-described characteristic clinical presentations, yet the precise pathological mechanism remains incompletely understood. A variety of pathogeneses has been proposed, which suggests that there exists several clinical subtypes. CONCLUSIONS: In this review, we categorize CU into four subtypes: (i) CU with poral occlusion; (ii) CU with acquired generalized hypohidrosis; (iii) CU with sweat allergy; and (iv) idiopathic CU, and discuss diagnostic and treatment options.
