BACKGROUND: Chronic irritant contact dermatitis (CICD) is characterized by erythema, scaling, hyperkeratosis, chapping and fissures. It may be the result of skin damage evoked by the cumulative effect of a variety of irritant stimuli. The diagnosis of CICD is made on basis of the patient's history and clinical features. No specific diagnostic tests are available. OBJECTIVE: The histopathologic and cell biological features of CICD have not been extensively studied. Here, we describe the histological and immunohistological changes in CICD. METHODS: Punch biopsies were taken from 11 patients with CICD for hematoxylin eosin and immunohistochemical stainings. Four skin biopsies of the palms of the hands of healthy volunteers served as controls. RESULTS: The histopathologic pattern was characterized by different grades of hyperkeratosis, parakeratosis, spongiosis, exocytosis, acanthosis, and mononuclear perivascular infiltrates. Mitotic activity, as measured by Ki-67-staining in the epidermis, was increased fourfold in involved skin as compared with normal skin. Involucrin, a structural protein of the cornified envelope, was expressed from the stratum granulosum throughout the stratum spinosum in all patients with CICD and was upregulated in comparison with normal skin. Epidermal fatty-acid binding protein (E-FABP), a terminal differentiation marker, was proportionally unaltered in the CICD as compared with the normal skin and was localized from the stratum granulosum to the upper layers of the stratum spinosum. Cytokeratin 16, a differentiation marker expressed in hyperproliferative epidermis, was markedly increased from the stratum granulosum throughout the stratum spinosum in 5 out of 11 patients with CICD. Skin-derived antiproteinase (SKALP)/elafin, a proteinase inhibitor expressed in inflamed epidermis, was only detected within the stratum granulosum in 3 out of 11 patients. CONCLUSION: We conclude that CICD is clinically characterized by features of a chronic dermatitis and, at the histological level, by inflammatory changes, epidermal hyperproliferation and altered differentiation.
BACKGROUND: Chronic irritant contact dermatitis (CICD) is characterized by erythema, scaling, hyperkeratosis, chapping and fissures. It may be the result of skin damage evoked by the cumulative effect of a variety of irritant stimuli. The diagnosis of CICD is made on basis of the patient's history and clinical features. No specific diagnostic tests are available. OBJECTIVE: The histopathologic and cell biological features of CICD have not been extensively studied. Here, we describe the histological and immunohistological changes in CICD. METHODS: Punch biopsies were taken from 11 patients with CICD for hematoxylin eosin and immunohistochemical stainings. Four skin biopsies of the palms of the hands of healthy volunteers served as controls. RESULTS: The histopathologic pattern was characterized by different grades of hyperkeratosis, parakeratosis, spongiosis, exocytosis, acanthosis, and mononuclear perivascular infiltrates. Mitotic activity, as measured by Ki-67-staining in the epidermis, was increased fourfold in involved skin as compared with normal skin. Involucrin, a structural protein of the cornified envelope, was expressed from the stratum granulosum throughout the stratum spinosum in all patients with CICD and was upregulated in comparison with normal skin. Epidermal fatty-acid binding protein (E-FABP), a terminal differentiation marker, was proportionally unaltered in the CICD as compared with the normal skin and was localized from the stratum granulosum to the upper layers of the stratum spinosum. Cytokeratin 16, a differentiation marker expressed in hyperproliferative epidermis, was markedly increased from the stratum granulosum throughout the stratum spinosum in 5 out of 11 patients with CICD. Skin-derived antiproteinase (SKALP)/elafin, a proteinase inhibitor expressed in inflamed epidermis, was only detected within the stratum granulosum in 3 out of 11 patients. CONCLUSION: We conclude that CICD is clinically characterized by features of a chronic dermatitis and, at the histological level, by inflammatory changes, epidermal hyperproliferation and altered differentiation.
Authors: Marion Cornelissen; Antoinette C van der Kuyl; Remco van den Burg; Fokla Zorgdrager; Carel J M van Noesel; Jaap Goudsmit Journal: BMC Cancer Date: 2003-03-18 Impact factor: 4.430
Authors: Klaziena Politiek; Laura Loman; Hendri H Pas; Gilles F H Diercks; Henny H Lemmink; Sabrina Z Jan; Peter C van den Akker; Maria C Bolling; Marie L A Schuttelaar Journal: Contact Dermatitis Date: 2020-06-01 Impact factor: 6.600