Letters to the Editor

rez-Amor O, Pe rez-Bustillo A, Ruiz-Gonza lez I, Rodrıguez-Prieto 4 Sua MA. Necrobiosis lipoidica therapy with biologicals: an ulcerated case responding to etanercept and a review of the literature. Dermatology 2010; 221: 117–121.

5 Wakusawa C, Fujimura T, Kambayashi Y, Furudate S, Hashimoto A, Aiba S. Pigmented necrobiosis lipoidica accompanied by insulin-dependent diabetes mellitus induces CD163 proinflammatory macrophages and interleukin-17-producing cells. Acta Derm Venereol 2013; 93: 475–476.

Palmoplantar pustulosis associated with necrobiosis lipoidica: A possible role of tumor necrosis factor-a and interleukin-17 Dear Editor, A 62-year-old woman visited our department, complaining of palmar pustules and joint pain. Physical examination revealed multiple pustules, scales and vesicles on her bilateral palms (Fig. 1a). Laboratory investigations showed an increased white blood cell count (10 300/mL) and slightly elevated C-reactive protein (0.69 mg/mL). Blood glucose levels and hemoglobin A1c were within normal ranges. The pustules were sterile. Technetium-99m bone scintigraphy confirmed inflammation in the sternoclavicular joints. Histopathological findings of the pustule revealed neutrophilic infiltration in the epidermis (Fig. 1b). Dental examination revealed several teeth caries and abscess formation in the periodontal pocket. Further clinical examination

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Figure 1. (a) Scattered pustules with scales and vesicles on the palms. (b) Biopsy specimen revealed an intraepidermal pustule (hematoxylin–eosin [HE], original magnification 9200). (c) Border, clear, dark-red plaques on the anterior lower legs. (d) Histopathological findings of the plaque taken from the lower leg showed necrobiosis of collagen fibers and inflammatory granulomatous reaction (HE, 9200). (e) Expression of CD163 in necrobiosis lipoidica (NL) lesion (9100). (f) Expression of interleukin (IL)-17 in NL lesion (9100). (g) IL-17-positive cells infiltrated around the sweat glands (9200).

revealed a few well-circumscribed dark-red plaques on the bilateral shins (Fig. 1c), which had appeared several years before. Histological examination showed necrobiotic changes of collagen in the lower dermis, surrounded with inflammatory granulomatous reaction composed of lymphocytes, histiocytes and giant cells (Fig. 1d). Results of immunohistochemistry showed that the histiocytes were immunoreactive for CD68 and also CD163 (Fig. 1e). Interleukin (IL)-17-positive cells were also detected in the necrobiotic lesions densely, as well as infiltrating cells around the sweat glands in the upper dermis of palmar pustular lesions (Fig. 1f, g). We herein describe a case of necrobiosis lipoidica (NL), palmoplantar pustulosis (PPP) and pustulotic arthro-osteitis in a patient without diabetes mellitus (DM). NL is an uncommon granulomatous skin disease predominantly involving the lower legs of women, often associated with DM or equivocal glucose intolerance. The incidence of NL was estimated to be 0.3% in diabetic patients,1 while the incidence of DM in patients with NL was 11%.2 Microangiopathy has been suggested to be an important initial trigger, and macrophages play an important role in the granuloma formation, via several cytokines such as tumor necrosis factor-a (TNF-a) and IL-1b. Our studies showed a number of CD163-positive macrophages surrounding the degenerated collagen in the dermis of NL lesion. In addition, expression of IL-17 has been localized in PPP lesions.3 Furthermore, recent studies have shown that IL-17 was abundantly detected in NL lesions, suggesting that T-helper (Th)17 cells induce granuloma formation by suppressing regulatory T cells.4 Several recent studies have reported the effectiveness of TNF-a inhibition for recalcitrant NL cases, suggesting an important role of TNF-a in the induction of NL. TNF-a is responsible for the regulation of leukocyte recruitment to the site of evolving or ongoing inflammation, and is also suggested to play a pathogenic role in PPP. Serum levels of TNF-a as well as IL-17, IL-22 and interferon-c have been reported to be increased in patients with PPP,3 and TNF-a targeting therapy has been known to be efficacious in PPP. TNF-a activates Th17 cells leading IL-17 production, and a shared TNF-a-mediated pathogenesis between PPP and NL may exist. To date, coexistence of NL and psoriasis has only been reported in one case with DM.5

Correspondence: Taeko Nakamura-Wakatsuki, M.D., Ph.D., Hikarigaoka 1, Fukushima 960-1295, Japan. Email: [email protected]

© 2014 Japanese Dermatological Association

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Letters to the Editor

This is the first case with an NL and PPP association, however, the rare co-occurrence of NL and psoriasis/PPP suggest that mechanisms other than Th17 may play an important role in the pathogenesis of NL, and further studies are necessary.

CONFLICT OF INTEREST:

None.

Taeko NAKAMURA-WAKATSUKI, Toshiyuki YAMAMOTO Department of Dermatology, Fukushima Medical University, Fukushima, Japan doi: 10.1111/1346-8138.12452

REFERENCES 1 Muller SA, Winkelmann RK. Necrobiosis lipoidica diabeticorum: a clinical and pathological investigation of 171 cases. Arch Dermatol 1966; 93: 272–281. 2 O’Toole EA, Kennedy U, Nolan JJ et al. Necrobiosis lipoidica: only a minority of patients have diabetes mellitus. Br J Dermatol 1999; 140: 283–286. 3 Murakami M, Hagforsen E, Morhenn V et al. Patients with palmoplantar pustulosis have increased IL-17 and IL-22 both in the lesion and serum. Exp Dermatol 2011; 20: 845–847. 4 Wakusawa C, Fujimura T, Kambayashi Y, Furudate S, Hashimoto A, Aiba S. Pigmented necrobiotic lipoidica accompanied by insulindependent diabetes mellitus induces CD163+ proinflammatory macrophages and interleukin-17-producing cells. Acta Derm Venereol 2013; 93: 475–476. 5 Abraham Z, Lahat N, Kinarty A, Feuerman EJ. Psoriasis, necrobiosis lipoidica, granuloma annulare, vitiligo and skin infections in the same diabetic patient. J Dermatol 1990; 17: 440–447.

Three cases of psoriasis vulgaris associated with myasthenia gravis Dear Editor, A 37-year-old Japanese woman suffering from myasthenia gravis (MG) was treated with systemic 4.5 mg prednisolone and 3 mg tacrolimus after thymectomy. Psoriatic lesions initially occurred on her scalp and gradually extended to trunk and four extremities (Fig. 1a). The Psoriasis Area and Severity Index (PASI) score was 16.1. The laboratory examination was normal except for slight elevation of C-reactive protein and detection of anti-acetylcholine receptor antibody. Human leukocyte anti-

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gen (HLA) typing showed that she was positive for HLA-A2/ , B46/ , C1/ and DR4/8. The skin lesions were improved by psoralen plus ultraviolet A therapy treatment combined with topical corticosteroids and active vitamin D3 ointment and PASI scores were decreased to 1.6. The patient’s condition is currently well-controlled by topical therapy alone. A 56-year-old Japanese woman with plaque type psoriasis treated with topical corticosteroids and active vitamin D3 ointment for 8 years in our clinic complained of general fatigue

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Figure 1. Psoriatic lesion of three patients. (a) Case 1, (b) case 2, (c) case 3.

Correspondence: Hidetoshi Takahashi, M.D., Department of Dermatology, Asahikawa Medical University, 2-1-1-1 Midorigaokahigashi, Asahikawa 078-8510, Japan. Email: [email protected]

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© 2014 Japanese Dermatological Association

Palmoplantar pustulosis associated with necrobiosis lipoidica: a possible role of tumor necrosis factor-α and interleukin-17.

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