Letters to the Editor

Finally, our patient did not have any electronic or metallic device but suture thread. Therefore, it seems that there is a common element in all cases: a foreign body. Taking it into account, we consider that the most plausible origin of reticular telangiectatic erythema is local microcirculatory changes secondary to mechanical obstruction of blood flow caused by the foreign body, as suggested previously.2 The clinical resolution after foreign body removal observed in our patient and in others1 supports this explanation. In all reported cases the histology showed dermal telangiectasia and variable perivascular lymphohistiocytic infiltrate. These histological features are unspecific, but allow its differentiation from cutaneous reactive angiomatosis (reactive angioendotheliomatosis, acroangiodermatitis, diffuse dermal angiomatosis, intralymphatic histocytosis, glomeruloid angioendotheliomatosis and angiopericytomatosis). These reactive angioproliferations may clinically resemble reticular telangiectatic erythema, but they are histologically characterized by intravascular or extravascular hyperplasia of endothelial cells, pericytes or histiocytes.6 Moreover, the absence of mucin exclude a diagnosis of reticular erythematous mucinosis.1 In conclusion, the descriptive term reticular telangiectatic erythema describes the distinctive clinical features of a reactive cutaneous phenomenon to foreign bodies characterized histologically by dermal telangiectasia and variable inflammatory infiltrate. This phenomenon is probably related to an alteration of microvascular blood flow caused by the implicated foreign body.

Acknowledgements We thank Dr. Francisco Javier Miquel and Dr. Mercedes Rodrıguez Serna for their assistance in allergy patch testing. M. Armengot-Carbo,1,* V. Sabater,2 R. Botella-Estrada3 , Department of Dermatology, Hospital General Universitari de Castello , Spain, 2Department of Pathology, Hospital General Universitario Castello de Valencia, Valencia, Spain, 3Department of Dermatology, Hospital Universitario La Fe, Valencia, Spain *Correspondence: Miquel Armengot-Carbo. E-mail: [email protected] 1

References 1 Aneja S, Taylor JS, Billings SD, Honari G, Sood A. Post-implantation erythema in 3 patients and a review of reticular telangiectatic erythema. Contact Dermatitis 2011; 64: 280–288. 2 Mercader-Garcıa P, Torrijos-Aguilar A, de La Cuadra-Oyanguren J, Vilata-Corell JJ, Fortea-Baixauli JM. Telangiectatic reticular erythema unrelated to cardiac devices. Arch Dermatol 2005; 141: 106–107. 3 Inzinger M, Tilz H, Komericki P, Schuster C, Wolf P, Kr€anke B. Heattriggered reticular telangiectatic erythema induced by a spinal cord stimulator. Mayo Clin Proc Mayo Clin 2013; 88: 117–119. 4 Morgan MB, Scalf LA, Hanno R. Sternal erythema: a distinctive postsurgical eruption. J Am Acad Dermatol 2005; 53: 893–896.

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5 Bowers JW, Morgan MB. Is postsurgical sternal erythema synonymous with reticular telangiectatic erythema? J Am Acad Dermatol 2007; 56: 892–893. 6 Rongioletti F, Rebora A. Cutaneous reactive angiomatoses: patterns and classification of reactive vascular proliferation. J Am Acad Dermatol 2003; 49: 887–896. DOI: 10.1111/jdv.12707

Sweet’s syndrome in a patient affected by ankylosing spondylitis and ulcerative colitis under treatment with adalimumab Editor Sweet’s syndrome is an acute febrile neutrophilic dermatosis clinically characterized by the eruption of multiple, usually tender, papules, plaques and nodules with red to violaceous colouration, associated with general symptoms such as fever, malaise, arthralgia and routine laboratory alterations, mainly leucocytosis, C-reactive protein elevation and neutrophilia. The disease can be classified into three subtypes: classical (or idiopathic), associated with malignancy and drug-induced. To the best of our knowledge, this is the second report of Sweet’s syndrome in a patient with a longstanding inflammatory bowel disease and ankylosing spondylitis. A 44-year-old Italian woman was referred to our clinic with an eruption of tender papules, plaques and nodules that began 7 days before presentation. Her medical history revealed a diagnosis of ulcerative colitis and ankylosing spondylitis 12 years before. Past treatments of both conditions included azathioprine, suspended due to unacceptable nausea; infliximab, interrupted for eruptive vaginal condylomatosis; mercaptopurine, interrupted in 2011 when she underwent a complete rectocolectomy; sulphasalazine, and oral methylprednisolone, discontinued due to lack of response. The patient also had an enterovaginal fistula with chronic urinary infection, which was managed by prophylactic antibiotic therapy. Two months before the appearance of cutaneous manifestations the patient switched to adalimumab 40 mg subcutaneously every 2 weeks with an excellent control of the arthritis. Upon presentation, dermatologic examination revealed multiple erythematous papules, plaques and nodules. The lesions were widely distributed, symmetrical, spared the head and neck area, and were more numerous on the arms. The colour of the lesions ranged from a bright to a more dusky red, and the surface was smooth (Fig. 1). The patient referred concomitant malaise, fatigue, diffuse arthralgia and the body temperature was 38.1 °C.

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Complete blood cell count showed no alterations, but erythrocyte sedimentation rate (ESR) was increased (82 mm h1), as white blood cell count showed leucocytosis (12 000 mm3) with neutrophilia (78%). Urine exams were unremarkable and urinary cultures were negative. Incisional biopsy of a papule on the left arm was performed and histological examination revealed a diffuse neutrophilic infiltrate within the superficial and deep dermis (Fig. 2). On this basis, we confirmed the clinical suspicion of Sweet’s syndrome. The patient was treated with oral prednisone 1 mg kg1 day1 for 1 week and tapered to 0.25 mg kg1 day1 in 4 weeks of treatment; she obtained the complete resolution of the disease. Complete blood test examination was unremarkable, including ESR and white blood cell count, and the patient endorsed no fever or other general symptoms. Sweet’s syndrome, or acute febrile neutrophilic dermatosis, was been first described in 1964 by Robert D. Sweet.1 The disease is characterized by abrupt eruption of tender, erythematous papules, plaques and nodules, sometimes vesicles and general symptoms. These general symptoms include fever, malaise, diffuse arthralgia and laboratory alterations. The disease can be classified in classical, malignancy-associated and drug-induced. The currently used diagnostic criteria for classical form are those by von den Driesch,2 whereas adapted criteria for drug-induced form are those by Walker and Cohen3 According to the previous criteria, we could exclude that our case was drug-induced for the long temporal relationship between drug intake and the clinical presentation, that occurred with a latency of 2 months. A review by Ali and Duerksen4 reports only 15 cases in literature of ulcerative colitis associated with Sweet’s syndrome, and most of them in patients with bowel disease activation, whereas our case had proctocolectomy many years before the eruption. While the combination of Sweet’s syndrome and ankylosing spondylitis has been reported in only three previous articles, one of them describing a similar case to ours, characterized by the acute onset

Figure 2 Histopathological examination shows a diffuse neutrophilic infiltrate in the superficial and deep dermis (haematoxylin and eosin original magnification 910).

of this syndrome in a patient with Crohn’s disease and longstanding ankylosing spondylitis.5–7 Both Sweet syndrome and the ankylosing spondylitis share the same association with the inflammatory bowel diseases, and this reason may probably explain the rare but possible conjunction of these particular disorders as in our case. Therefore, we conclude that Sweet’s syndrome should be included into the list of cutaneous associations linked to ankylosing spondylitis. N. Bruscino,1 V. Grandi,1,* S. Gunnella,1 V. Maio2 1

Division of Dermatology, 2Division of Pathological Anatomy, Department of Surgery and Translational Medicine, University of Florence, Florence, Italy *Correspondence: V. Grandi. E-mail: [email protected]

References 1 Sweet RD. An acute febrile neutrophilic dermatosis. Br J Dermatol 1964; 76: 349–356. 2 Von den Driesch P. Sweet’s syndrome (acute febrile neutrophilic dermatosis). J Am Acad Dermatol 1994; 31: 535–556. 3 Walker DC, Cohen PR. Trimethoprim-sulfamethoxazole-associated acute febrile neutrophilic dermatosis: case report and review of druginduced Sweet’s syndrome. J Am Acad Dermatol 1996; 34: 918–923. 4 Ali M, Duerksen DR. Ulcerative colitis and Sweet’s syndrome: a case report and review of the literature. Can J Gastroenterol 2008; 22: 296–298. 5 Petermann A, Tebbe B, Distler A, Sieper J, Braun J. Sweet’s syndrome in a patient with acute Crohn’s colitis and longstanding ankylosing spondylitis. Clin Exp Rheumatol 1999; 17: 607–610. 6 Wendling D, Leaustic M, Toussirot E, Prati C. Ankylosing spondylitis and Sweet’s syndrome. Clin Rheumatol 2008; 27(Suppl. 1): S27–S28. 7 Mansouri S, Abourazzak FE, Aradoini N et al. Ankylosing spondylitis associated with Sweet’s syndrome: a case report. J Med Case Rep 2013; 7: 16.

Figure 1 Right shoulder, few eruptive erythematous tender papules and plaques.

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DOI: 10.1111/jdv.12710

© 2014 European Academy of Dermatology and Venereology

Sweet's syndrome in a patient affected by ankylosing spondylitis and ulcerative colitis under treatment with adalimumab.

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