Dermatitis artefacta masquerading as pyoderma gangrenosum

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the disease, although the doses needed to control pemphigus foliaceus may be similar to those used for pemphigus vulgaris. In conclusion, pemphigus is a relatively common disease in our context, and occurs predominantly in middle-aged persons with a female predominance. Pemphigus vulgaris, the most frequent deep form, is as common as superficial forms in Morocco, as in other Mediterranean series except Tunisia. Hakima Benchikhi Siham Ghafour Asma Disky Leila Bichra Fatna Nejjam Hakima Lakhdar University of Medicine, Ibn Rushd University Hospital, Casablanca, Morocco References 1 Haouet H, Ben Hamida A, Haouet S, et al. Tunisian pemphigus. Apropos of 70 cases. (Experience of the dermatology department of La Rabta Hospital 1974–92). Ann Dermatol Venereol 1996; 123: 9–11. 2 Morini JP, Jomaa B, Gorgi Y, et al. Pemphigus foliaceus in young women. An endemic focus in the Sousse area of Tunisia. Arch Dermatol 1993; 129: 69–73. 3 Bastuji-Garin S, Souissi R, Blum L, et al. Comparative epidemiology of pemphigus in Tunisia and France: unusual incidence of pemphigus foliaceus in young Tunisian women. J Invest Dermatol 1995; 104: 302–305. 4 Belgnaoui F, Bella A, Senouci K, et al. Le pemphigus: à propos de 184 cas colligés à Rabat au Maroc durant les 27 dernières années. Nouv Dermatol 2001; 20: 249–252. 5 Chams-Davatchi C, Valikhani M, Daneshpazhooh M, et al. Pemphigus: analysis of 1209 cases. Int J Dermatol 2005; 44: 470 –476.

Dermatitis artefacta masquerading as pyoderma gangrenosum

Dermatitis artefacta (DA) is a disease that occurs as a result of a self-inflicted injury to the skin.1–5 The representative lesions may vary depending on the creativity of the patient and the methods applied.1–4 DA masquerading as many skin disorders has been reported previously. The case reported here once again shows the ability of these patients to create skin disorders resembling real dermatologic diseases, and their need to be the subject of attention. A 55-year-old female patient, with complaints of pruritic lesions on the right knee after arthroscopy, was referred to our dermatology inpatient clinic in May 1995. Dermatologic examination revealed generalized, violet–pink-colored papules, 3–4 mm in diameter, located on both arms, and ulcerations on the lower legs. The differential diagnosis included pyoderma gangrenosum (PG) and vasculitis. The histopathologic findings were consistent with PG; however, the diagnosis was recorded © 2008 The International Society of Dermatology

6 Uzun S, Durdu M, Akman A, et al. Pemphigus in the Mediterranean region of Turkey: a study of 148 cases. Int J Dermatol 2006; 45: 523–528. 7 Bastuji-Garin S, Turki H, Mokhtar I, et al. Possible relation of Tunisian pemphigus with traditional cosmetics: a multicenter case–control study. Am J Epidemiol 2002; 155: 249–256. 8 Brenner S, Tur E, Shapiro J, et al. Pemphigus vulgaris: environmental factors. Occupational, behavioral, medical, and qualitative food frequency questionnaire. Int J Dermatol 2001; 9: 562–569. 9 Tallab T, Joharji H, Bahamdan K, et al. The incidence of pemphigus in the southern region of Saudi Arabia. Int J Dermatol 2001; 40: 570–572. 10 Micali G, Musumeci ML, Nasca MR. Epidemiologic analysis and clinical course of 84 consecutive cases of pemphigus in eastern Sicily. Int J Dermatol 1998; 37: 197–200. 11 Wohl Y, Brenner S. Pemphigus in Israel; an epidemiologic analysis of cases in search of risk factors. Isr Med Assoc J 2003; 5: 410–412. 12 Diaz LA, Sampaio SAP, Rivitti EA, et al. Endemic pemphigus foliaceus (fogo salvagem). II. Current and historic epidemiologic studies. J Invest Dermatol 1989; 92: 4–12. 13 Bystryn JC, Rudolph JL. Pemphigus. Lancet 2005; 366: 61– 73. 14 Mimouni D, Nousari CH, Cummins DL, et al. Differences and similarities among experts opinions on the diagnosis and treatment of pemphigus vulgaris. J Am Acad Dermatol 2003; 49: 1059–1062. 15 Gharzouri R, Thion P, Revuz J, et al. Risque accru de diabète corticoinduit dans le pemphigus? Ann Dermatol Venereol 2003; 130: 4S2. 16 Zouhair K, El Ouazzani T, Azzouzi S, et al. Surinfection herpétique du pemphigus. Ann Dermatol Venereol 1999; 123: 699–702.

as “atypical” PG. Despite a course of cyclosporine (5 mg/kg/day for 3 months), the patient developed lesions under the breasts; therapy with dapsone (150–200 mg/day) was discontinued because of methemoglobinemia. The patient was lost to follow-up for the next 9 months. On further hospitalizations in 1997, 1999, and 2004, she was given various courses of antimicrobials, including rifampicin, numerous doses of analgesics, dapsone, chlorambucil, clofazimine, and sodium cromoglycate without any benefit. She was lost to follow-up until October 2006, when she finally presented with ulcerations and centrally crusted erythematous papules on the lower legs, accumulating around the ankles, with a duration of 15 days. Multiple biopsies were taken, most of which revealed nonspecific inflammatory changes. With a diagnosis of PG, she was given mycophenolate mofetil (up to 4 g) plus systemic corticosteroids (fluocortolone, intravenous dexamethasone). No response was obtained. The lesions remained active even after two infusions of infliximab (5 mg/kg). Moreover, the patient International Journal of Dermatology 2008, 47, 975–977 970–971

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Figure 1 The lesions started as erythematous patches which

rapidly turned to green, ischemic, anemic areas. These ischemic areas later became heavily crusted, with peripheral erythema, healing to leave cribriform scars. The whole process occurred within a few days

continued to develop new ulcerations in bizarre shapes on the legs, with a strange evolving process (Fig. 1). Only one or two lesions developed every 2 or 3 days, and others improved independent of therapy. The histopathology again ruled out any vascular damage. Constitutional symptoms were lacking and routine laboratory tests remained within normal limits. With a suspicion of DA, all medications were stopped. Surprisingly, rapid improvement was observed under occlusive bandages. Psychiatric consultation was recommended and a mental status examination was found to be positive for inappropriate affect. Psychometric evaluation, including the Minnesota Multiphasic Personality Inventory (MMPI), showed histrionic personality features, a tendency for defense mechanisms of somatization, denial and repression, and a relative weakness of coping strategies, supporting a diagnosis of factitious disorder. Psychoanalytically oriented psychotherapy was planned for further psychiatric evaluation. All photographs of our patient were evaluated retrospectively, and it was concluded that she had been misdiagnosed with PG from the beginning. She still denies playing any role in the occurrence of her lesions. A mixture of wheat oil, pepper, and a herb (Urtica dioica) was found amongst her personal belongings, but it is not known how she created the lesions, as premature confrontation was discouraged by the psychiatrists. We will continue to see her on an ongoing basis for supportive care. International Journal of Dermatology 2008, 47, 975–977 970–971

Our case represents a unique example of DA, in which diagnosis was established after a 12-year delay. The clinical appearance of PG is not always characteristic and the histopathologic features are not diagnostic. Recently, Harries et al.6 reported a case of PG misdiagnosed as DA for years, emphasizing the difficulty of distinguishing between PG and DA. The critical step causing a suspicion of DA in our patient was the strange evolving process of the lesions that did not match that of any natural dermatologic disease. In addition, by contrast with the complexity of the clinical appearance, the histopathologic picture was silent. As emphasized by Sir Norman Walker, “Neither rank, education, intelligence, devotion to duty, nor the most exemplary character exclude the possibility of self infliction.”7 In most cases, however, DA is associated with underlying psychiatric disorders.5,8 One of the most compelling factors of our patient’s disease was its progression under close psychiatric evaluation. She had been diagnosed with depression possibly related to skin disease; however, psychiatrists were not aware of her possible disease until her last hospitalization. Therefore, this experience reflects the need for close dermatologist–psychiatrist collaboration in the diagnosis and treatment of DA. DA is difficult to treat. Direct confrontation is not advised by psychiatrists. Instead, an accepting, empathetic, and nonjudgmental environment should be created between the patient and doctor.1–4 Except in cases triggered by acute stress, the prognosis is not hopeful. The course of the condition tends to recur and is closely related to the underlying psychiatric state.1–4 At least 30% of patients continue to produce skin lesions even after 12 years.4 The desire of these patients to seek attention may result in unnecessary treatments, including surgery or amputation,9 demonstrating their obsessive nature. The latter is particularly true in our patient, who was hospitalized five times during a 12-year period. She had undergone numerous laboratory tests and radiologic procedures, and had received many drugs, including infliximab. In conclusion, a correlation between clinical and pathologic findings is crucial in the diagnosis of dermatologic diseases, and cases that fail to meet these criteria should alert the physician to the possibility of DA. It seems that, in parallel with the development of our understanding of the physiopathology of diseases, our patients will continue to surprise us with their ability to mimic natural skin conditions. Nilsel ilter, MD Esra Adısen, MD Mehmet Ali Gürer, MD Canan Kevlekçi, MD Özlem Tekin, MD Aslıhan Sayın, MD Ankara, Turkey © 2008 The International Society of Dermatology

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References 1 Joe EK, Li VW, Magro CM, et al. Diagnostic clues to dermatitis artefacta. Cutis 1999; 63: 209–214. 2 Koblenzer CS. Dermatitis artefacta. Clinical features and approaches to treatment. Am J Clin Dermatol 2000; 1: 47–55. 3 Lyell A. Cutaneous artefactual disease: a review, amplified by personal experience. J Am Acad Dermatol 1979; 1: 391–407. 4 Sneddon I, Sneddon JL. Self-inflicted injury: a follow-up study of 43 patients. Br Med J 1975; 3: 527–530.

5 Gupta MA, Gupta AK, Ellis CN, et al. Psychiatric evaluation of the dermatology patient. Dermatol Clin 2005; 23: 591–599. 6 Harries MJ, McMullen E, Griffiths CE. Pyoderma gangrenosum masquerading as dermatitis artefacta. Arch Dermatol 2006; 142: 1509–1510. 7 Sneddon IB. Dermatitis artefacta. Proc R Soc Med 1977; 70: 754–755. 8 Gupta MA, Gupta AK. Psychodermatology: an update. J Am Acad Dermatol 1996; 34: 1030–1046. 9 Hollender MH, Abram HS. Dermatitis factitia. South Med J 1973; 66: 1279–1285.

A black plaque on the toe of a white male

A 57-year-old healthy white male physician presented to the dermatology clinic with a black spot on the tip of the left second toe. The skin lesion was asymptomatic and had been noted incidentally in the shower 3 days previously. The patient could not recall any trauma to the toe and was concerned about melanoma. He had traveled to Brazil 1 month prior to presentation, but denied walking barefoot. Physical examination revealed a 1-cm, slightly tender, hyperpigmented, edematous plaque with a central black eschar and mild surrounding erythema (Fig. 1). The remainder of

Figure 2 Histopathology of the flea (see text, hematoxylin and

eosin)

Figure 1 Clinical presentation © 2008 The International Society of Dermatology

the skin examination revealed no additional lesions. After the crust was removed, brown fluid and thick white material were drained and submitted for histopathology. The cavity was curetted and irrigated with sterile saline. The material collected can be seen in Fig. 2, stained with hematoxylin and eosin. Hematoxylin and eosin staining of the specimen revealed ring-shaped structures consistent with respiratory tract and a thick cuticle with a band of striated muscle consistent with intestinal structures of Tunga penetrans. Developing eggs could also be visualized (Fig. 2). The resulting 3-mm wide and 5-mm deep defect was left open, and the patient was treated with mupirocin ointment, cefadroxil 500 mg twice daily for 10 days, and a tetanus booster. A high-resolution sonogram with power Doppler, performed 2 days later, showed intense inflammatory vascularity with no residual collection or foreign body. The defect healed without further problems. Tunga penetrans is a sandflea endemic to Africa, India, the Caribbean, and South America. It is the smallest flea species at only 1 mm in size.1 The female flea penetrates the skin and International Journal of Dermatology 2008, 47, 977–978 970–971

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