5. Crippa M, Rais O, Gern L. Investigations on the mode and dynamics of transmission and infectivity of Borrelia burgdorferi sensu stricto and Borrelia afzelii in Ixodes ricinus ticks. Vector Borne Zoonotic Dis 2002; 2: 3-9. 6. Kahl O, Janetzki-Mittmann C, Gray JS, Jonas R, Stein J, de Boer R. Risk of infection with Borrelia burgdorferi sensu lato for a host in relation to the duration of nymphal Ixodes ricinus feeding and the method of tick removal. Zentralbl Bakteriol 1998; 287: 41-52. 7. Radolf JD, Caimano MJ, Stevenson B, Hu LT. Of ticks, mice and men: understanding the dual-host lifestyle of Lyme disease spirochaetes. Nat Rev Microbiol 2012; 10: 87-99. 8. Moehrle M. [Removal of ticks with scalpel or disposable razor]. Hautarzt 2002; 53: 579-80. 9. Gammons M, Salam G. Tick removal. Am Fam Physician 2002; 66: 643-5. doi:10.1684/ejd.2014.2489

Leukocytoclastic vasculitis due to duloxetine A 55-year-old woman presented with a 2-week history of ankle pain, fatigue and multiple, symmetrically distributed, palpable purpura on her ankles and lower extremities. She had a history of using pregabalin (150 mg/day, po) and duloxetine (60 mg/day, po) for two weeks for a neuropathic pain diagnosis. The skin symptoms started two weeks after her first dose of these drugs. In her medical history, there was no previous infection or usage of any other drugs apart from 5 years of insulin treatment for diabetes, diagnosed 7 years ago. Physical examination revealed palpable purpura of various sizes, with haemorrhagic crusts in certain lesions, on the patient’s abdomen, ankles and lower legs (figure 1A).

A

B

C

D

Figure 1. A) Palpable purpura, hemorrhagic crusts on lower legs and ankles. B) After 1-year follow-up. C) Endothelial swelling in dermal vessels, deposition of fibrinoid material within the vascular lumen. D) The presence of neutrophilic dust (H&E ×200).

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Laboratory findings, including blood cell count, tests for renal and liver function, C-reactive protein, sedimentation and anti-streptolysin O, C3 and C4, were normal. The presence of ANA cytoplasmic ANCA and perinuclear ANCA were negative. According to viral serology and bacterial cultures, there was no active or chronic infection and, based on physical and laboratory examination, there were no findings of systemic involvement of leukocytoclastic vasculitis (LCV). A biopsy specimen from a palpable purpura demonstrated typical features of LCV: endothelial swelling in the dermal vessels, infiltration of predominantly neutrophilic inflammatory cells, deposition of fibrinoid material within the vascular lumen and the presence of neutrophilic dust (figures 1C, D). Indirect immunofluorescence examination of a frozen biopsy specimen showed no positivity for IgA, C3 or fibrinogen. The patient was diagnosed with LCV due to drugs, based on the clinical, laboratory and histological manifestations. All drugs were stopped, and she received treatment with systemic corticosteroids (prednisolone 40 mg/day) for 2 weeks. The lesions improved in the first week of corticosteroid therapy. Three weeks after this improvement, the patient started to use duloxetine for neuropathic pain, without any physician’s advice. Two weeks after the re-administration of duloxetine, she experienced exacerbation of her skin lesions. At a neurological consultation, duloxetine was immediately replaced with pregabalin and the patient underwent the same steroid treatment for another 2 weeks. She had no new skin symptoms and pregabalin has been the only drug used for neuropathic pain during a 1-year follow-up (figure 1B). Duloxetine, which is one of the two main agents used as serotonin-norepinephrine reuptake inhibitors, has been used in Europe for indications such as major depressive disorder and diabetic peripheral neuropathic pain [1]. The most common side effects are nausea, dry mouth, diarrhoea, fatigue and dizziness [1-4]. Cutaneous side effects, such as an anaphylactic reaction with rash, angioneurotic oedema, erythema multiforme, porphyria, hyperhidrosis, gingival bleeding and flushing, are rarely reported for this drug [1-4]. Additionally, in a case report, atypical StevensJohnson syndrome, which is one of the most important drug-induced skin diseases, was reported during high-dose treatment with duloxetine [5]. In a search of the literature, we found no previous reports of LCV due to duloxetine [5]. There are no specific tests that can identify a drug as the culprit. Therefore, most reported drug-induced eruptions are based on clinical findings. Although patch tests and in vitro tests may support an association between drugs and certain diseases, such as contact dermatitis, a positive re-challenge test with the suspected drug provides more definitive evidence than other tests do. The potential detrimental outcome for the patient limits the use of the re-challenge test in cases such as the present case. Begaud et al. proposed the use of a score for adverse drug reactions, which is widely used in France and Europe [6]. In the present case report, according to the recently revised version of this score, or the so-called “French ‘imputability’ method,” the drug had a probability (I5, B1) of inducing an adverse skin reaction [7]. The patient has not taken other drugs known to induce LCV except pregabalin, which is still part of the treatment protocol for our patient. Withdrawal of duloxetine was followed by improvement of the skin lesions and with re-administration, the same lesions were exacerbated. During the one-year follow-up, the patient has had no skin EJD, vol. 25, n◦ 2, March-April 2015

lesions. To our knowledge, there has been no previous report of LCV due to duloxetine in the literature. In conclusion, considering this case, neurologists should be aware of duloxetine’s rare but possible and potentially serious cutaneous adverse effect, which is not dose dependent.  Disclosure. Financial support: none. Conflict of interest: none. 1

Department of Dermatology, Department of Neurology, 3 Department of Pathology, Namık Kemal University Research Hospital, Poliklinigi Tunca Cad. 100, Yıl mah, Tekirdag, Turkey 2

Gamze ERFAN1 Recep ALP2 Sule ALBAYRAK1 Keriman OGUZ2 Serkan KALAYCI1 Meltem OZNUR3 Mustafa KULAC1

1. Preskorn SH. Duloxetine. J Psychiatr Pract 2004; 10: 375-85. 2. Gross CM, Klöcker M, Jakob T, Klecha D. Dermatological side effects during therapy with serotonin noradrenaline reuptake inhibitors. Nervenarzt 2008; 79: 1307-9. 3. Vey EL, Kovelman I. Adverse events, toxicity and post-mortem data on duloxetine: case reports and literature survey. J Forensic Leg Med 2010; 17: 175-85. 4. Mallinckrodt CH, Prakash A, Andorn AC. Duloxetine for the treatment of major depressive disorder: a closer look at efficacy and safety data across the approved dose range. J Psychiatr Res 2006; 40: 33748. 5. Strawn JR, Whitsel R, Nandagopal JJ, Delbello MP. Atypical Stevens-Johnson syndrome in an adolescent treated with duloxetine. J Child Adolesc Physchopharmacol 2011; 21: 91-2. 6. Begaud B, Evreux JC, Jouglard J, Lagier G. Imputation of the unexpected or toxic effects of drugs. Actualization of the method used in France. Therapie 1985; 40: 111-8. 7. Arimone Y, Bidault I, Dutertre J-P. Update of the French drug reaction assessment method. Therapie 2011; 66: 517-25. doi:10.1684/ejd.2014.2491

Changes of serum lipocalin-2 and retinol binding protein-4 levels in patients with psoriasis and Behc¸et’s disease The correlation between psoriasis, Behc¸et’s Disease (BD) and metabolic syndrome (MetS) is related to chronic inflammation [1, 2]. It is suggested that the inflammation that is caused by increased cytokines leads to an increase in insulin resistance and MetS. It has been shown that Lipocalin-2 (LCN-2), and Retinol-binding protein-4 (RBP-4) are related to obesity and insulin-resistance in humans [3, 4]. The current study aimed to investigate LCN-2 and RBP-4 levels in psoriasis and BD, which are known to have activity in insulin resistance and MetS formation. A total of 60 patients, 30 with psoriasis vulgaris and 30 with BD, admitted to the dermatology policlinics, and 30 healthy volunteers, 15 males and 15 females, who were matched according to body mass index (BMI) and age, were included in the study. The controls were individuals admitted to the EJD, vol. 25, n◦ 2, March-April 2015

hospital for an annual check-up who had no systemic and neurological diseases in their past medical and family history, systemic drug use, alcohol or narcotic drug use, and who were similar with the study group according to age, gender, and BMI. Serum LCN-2/NGAL and RBP-4 levels were determined using commercial kits with the sandwich ELISA method (for LCN-2/NGAL, BOSTER trademark, catalogue number: EK0853; for RBP-4, Assaypro trademark, catalogue number: ER3005-1). Demographic, clinical and laboratory characteristics of the psoriasis and BD patients and the control group are demonstrated in table 1. Serum LCN-2 levels in patients with psoriasis and BD were found to be statistically higher when compared to the controls (p = 0.01 and p

Leukocytoclastic vasculitis due to duloxetine.

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