Chika Kawakami

Aberrant aquaporin 5 expression in the sweat gland in aquagenic wrinkling of the palms

Aquagenic wrinkling of the palms (AWP) is an uncommon disease characterized by the rapid and transient formation of edematous whitish plaques on the palms on exposure to water. Although this disease is occasionally accompanied by hyperhidrosis, the pathophysiology of AWP remains unknown. Herein we describe a patient with AWP. The location of wrinkling was limited to the areas positive for iodine-starch test after water exposure, which suggests that AWP is etiologically related to hyperhidrosis. Histologic examination revealed hyperplastic and papillated eccrine glandular epithelium with the enlarged diameter of eccrine coils. Immunohistochemically, while aquaporin 5 (AQP5), one of the water channel AQP families, was present exclusively in the dark cells of sweat glands of healthy donors, an aberrant AQP5 staining, extending to the clear cells, was found in the patient with AWP. The hyperplastic glandular epithelium and aberrant AQP5 staining in the patients sweat glands suggest that AWP stems from dysregulation of sweating.

Increased frequencies of Th17 cells in drug eruptions

c y d TNF-a and IL-6 [8]. Since LCs are commonly activated under IL-1a and TNF-a condition in case of contact hypersensitivity [9], it is conceivable that activated LCs may be an important factor on the occurrence of vitiligo as the interface of melanocyte-specific adoptive immunity cooperating with cytotoxic T cells and may also induce innate immunity in participation with Th17 cells. Following increased infiltration of CD11c+ myeloid dendritic cells and dermal CD1a+ dendritic cells in vitiligo skin can act as antigen trafficking to draining lymph nodes and can produce proinflammatory cytokines such as IL-6 and TNF-a leading to determine helper T cells polarization [10]. Taken together with the effect of Th17 cellrelated cytokines on surrounding keratinocyte and fibroblast [6], this positive feedback linage of local cytokines is possibly important for transient appearance of indeterminate dendritic cells and subsequent mature melanocyte disappearance. Given this idea on the underlying immunogenic mechanism, early therapeutic intervention of molecular targeting biologics is considerable for the treatment with progressive nonsegmental vitiligo.

Valsartan-induced Drug Eruption Followed by CD30+ Pseudolymphomatous Eruption

© 2010 The Authors. doi: 10.2340/00015555-0695 Journal Compilation

Erosive pustular dermatosis of the scalp and leg associated with myasthenia gravis: A possible pathogenetic role for neutrophil-stimulating cytokines and chemokines.

© 2010 The Authors. doi: 10.2340/00015555-0971 Journal Compilation

Circulating Th17 cell fluctuation in psoriatic patients treated with topical calcipotriol and betamethasone butyrate propionate.

References 1 Cui J, Shen LY, Wang GC. Role of hair follicles in the repigmentation of vitiligo. J Invest Dermatol 1991; 97: 410–416. 2 Kim CY, Yoon TJ, Kim TH. Epidermal grafting after chemical epilation in the treatment of vitiligo. Dermatol Surg 2001; 27: 855–856. 3 Laxmisha C, Kumari R, Thappa DM. Surgical repigmentation of leukotrichia in localized vitiligo. Dermatol Surg 2006; 32: 981–982. 4 Commo S, Gaillard O, Bernard BA. Human hair greying is linked to a specific depletion of hair follicle melanocytes affecting both the bulb and the outer root sheath. Br J Dermatol 2004; 150: 435–443. 5 Anbar TS, Abdel-Raouf H, Awad SS et al. The hair follicle melanocytes in vitiligo in relation to disease duration. J Eur Acad Dermatol Venereol 2009; 23: 934–939. 6 Tobin DJ, Swanson NN, Pittelkow MR et al. Melanocytes are not absent in lesional skin of long duration vitiligo. J Pathol 2000; 191: 407–416. 7 Moretti S, Spallanzani A, Amato L et al. New insights into the pathogenesis of vitiligo: imbalance of epidermal cytokines at sites of lesions. Pigment Cell Res 2002; 15: 87–92.

Development of a prominent granulomatous eruption after interferon-gamma therapy in a patient with mycosis fungoides.

© 2010 The Authors. doi: 10.2340/00015555-0788 Journal Compilation

Human T‐lymphotropic virus 1 (HTLV‐1)‐associated lichenoid dermatitis induced by CD8+ T cells in HTLV‐1 carrier, HTLV‐1‐associated myelopathy/tropical spastic paraparesis and adult T‐cell leukemia/lymphoma

Human T‐lymphotropic virus type 1 (HTLV‐1) induces adult T‐cell leukemia/lymphoma (ATLL), HTLV‐1‐associated myelopathy/tropical spastic paraparesis (HAM/TSP) and carrier. ATLL is a mature CD4+CD25+CCR4+ T‐cell neoplasm, and approximately half of patients have direct skin involvement manifesting patch, plaque, tumor, multiple papules, erythroderma and purpura. However, there exist secondary eruptions without tumor cell infiltration in patients with ATLL or HAM/TSP and carriers of HTLV‐1. To clarify the presence of reactive skin eruptions in HTLV‐1‐infected individuals, we reviewed our patients with HTLV‐1‐associated diseases. In 2002–2012, we saw 50 ATLL or HAM/TSP patients and HTLV‐1 carriers presenting with skin lesions. We retrospectively selected cases that histologically showed lichenoid tissue reactions with predominant infiltration of CD8+ T cells, but not CD4+ tumor cells. The cases included erythroderma (HTLV‐1 carrier), lichen planus (HTLV‐1 carrier), alopecia areata (HAM/TSP), chronic actinic dermatitis (HTLV‐1 carrier to acute ATLL conversion) and discoid lupus erythematosus (smoldering ATLL). They were graft‐versus‐host disease‐like, major secondary lesions and seen in HTLV‐1 carriers and patients with HAM/TSP and smoldering ATLL. We coin the term HTLV‐1‐associated lichenoid dermatitis (HALD) to encompass the conditions. HALD may occur in association with the elevated immunity toward HTLV‐1‐infected CD4+ T cells, thus sharing the pathogenetic role of cytotoxic T cells with HAM/TSP.

Tuberculosis verrucosa cutis with elevation of circulating T-helper 1 and 17 cells and their reductions after successful treatment

1 Kanitakis J, Audeffray D, Claudy A. Squamous cell carcinoma of the skin complicating lupus vulgaris. J Eur Acad Dermatol Venereol 2006; 20: 114–116. 2 Yeager J, Findlay R, McAleer I. Penile verrucous carcinoma. Arch Dermatol 1990; 126: 1208–1210. 3 Noel JC, Heenen M, Peny MO et al. Proliferating cell nuclear antigen distribution in verrucous carcinoma of the skin. Br J Dermatol 1995; 133: 868–873. 4 Noel JC, Peny MO, De Dobbeleer G et al. p53 protein overexpression in verrucous carcinoma of the skin. Dermatology 1996; 192: 12– 15. 5 Noel JC, Fayt I, De Dobbeleer G, Simonart T. Pattern of MIB-1 distribution in cutaneous verrucous carcinoma: analysis of 5 cases (abstract). J Invest Dermatol 2002; 118: 907. 6 Harrison PV, Marks JM. Lupus vulgaris and cutaneous lymphoma. Clin Exp Dermatol 1980; 5: 73–77. 7 Sowden J, Paramsothy Y, Smith AG. Malignant melanoma arising in the scar of lupus vulgaris and response to treatment with topical azelaic acid. Clin Exp Dermatol 1988; 13: 353–356. 8 Assaf C, Steinhoff M, Petrov I et al. Verrucous carcinoma of the axilla: case report and review. J Cutan Pathol 2004; 31: 199–204. 9 Noel JC, Peny MO, Detremmerie O et al. Demonstration of human papillomavirus type 2 in a verrucous carcinoma of the foot. Dermatology 1993; 187: 58–61. 10 Pattee SF, Bordeaux J, Mahalingam M, Nitzan YB, Maloney ME. Verrucous carcinoma of the scalp. J Am Acad Dermatol 2007; 56: 506–507.

Therapeutic efficacy of mizoribine for discoid lupus erythematosus with normalized frequency of circulating T helper 17 cells

papillary dermis and acanthotic epidermis in the rete ridges (Fig. 1c), respectively. The dermatoscopic features of CCA have been suggested to resemble those of psoriasis after the scales are removed. However, Zalaudek et al. reported that the dermatoscopy of CCA differs from psoriasis, as in our case. In patients with psoriasis, multiple, homogeneous, dotted vessels are seen with dermatoscopy, whereas in patients with CCA, similar dotted vessels are seen, but in a linear, pearllike distribution, forming a symmetrical reticular vascular network. Cytology is a simple, rapid and inexpensive method, which investigates the characteristics of individual cells. In addition to its use in the pemphigus group of autoimmune bullous diseases and herpesvirus infections, the Tzanck smear test can be used as a diagnostic tool in many other cutaneous diseases. To our knowledge, the cytological findings of CCA have not been defined previously. In our patient, the cytology findings included multiple, cytoplasmic, PAS-positive vacuoles. Both dermatoscopy and Tzanck smear test can be used as diagnostic tools for CCA in daily dermatology practice.

A case of squamous cell carcinoma arising from perianal chronic pyoderma

55歳男性。臀部慢性膿皮症に対し, 約10年前より数回瘻孔部分切除術を受けていた。2008年3月の瘻孔切除標本において有棘細胞癌を認め, 切除断端に腫瘍細胞が陽性であったため, 紹介受診となった。同年4月, 肛門周囲の有棘細胞癌を認めた部位と, 左臀部の慢性膿皮症部の切除を行い, 同部位に分層植皮術を行った。植皮部が肛門周囲であったため, 一時的な人工肛門増設術を行った。繰り返す慢性膿皮症の治療として, 切開, 部分切除のみではなく, 有棘細胞癌の併発を念頭に置き, 全摘除を考慮することが必要である。