Rosa Valentina Puca

Contact pemphigus: a side‐effect of imiquimod therapy

carcinoma. Akiyama et al. have recognized the development of squamous cell carcinomas on chronic ulcers, scars, and burns, but association with this fungal infection is not completely understood. Associations with melanoma are rare; yet, we found this one previous report of chromoblastomycosis in association with melanoma. With both malignant tumors, we only found a description that appeared on a burn scar. Fonsecaea pedrosoi is the most common etiological agent in chromoblastomycosis, but it rarely affects nails. We did not find cases of onychomycosis caused by F. pedrosoi in the literature.

Etanercept in the Treatment of Generalized Annular Pustular Psoriasis

1. Some authors consider a separate variant of generalized psoriasis, well described by Lapiere, as recurrent circinate erythematous psoriasis. It presents with erythematous, annular or polycyclic lesions, and an eruption of small sterile pustules and fine desquamation. The patches extend from the center and resolve within some weeks, leaving scales and changes in pigmentation and pigmentary changes. Frequent relapses are described in the bordering areas 2,3 . In this study, we report the case of a woman affected by generalized annular pustular (Lapiere) psoriasis. This patient had previously been treated with conventional therapeutics, and demonstrated a significant improvement after treatment with etanercept. This 70-year-old Caucasian woman, described in our report, has a 35-year history of psoriasis. Physical examination revealed the presence of small erythematous papules, centered by a pustule, a few millimeters in diameter (Fig. 1). Histological examination showed Kogoj-Lapiere spongiform multilocular typical pustules (an epidermal pustule formed by infiltration of neutrophils into necrotic areas of the epidermis, where the cell walls form a swampy network), features compatible with the clinical diagnosis of Lapiere psoriasis. The patient had previously been treated with other topical and systemic drugs (colchicine, acitretin, ciclosporin, methotrexate) and ultraviolet B narrow band phototherapy, with partial and temporary benefits, side effects, and frequent relapses. Differential diagnosis of our case included other generalized pustular psoriasis: acute generalized exanthematous pustolosis (AGEP) was perhaps the most important differential diagnosis. AGEP, which occurs as an acute, spontaneously healling reaction to drugs (usually antibiotics), was excluded on the basis of the absence of vasculitis associated with spongiform pustules and based on the presence of psoriatic anamnesis. Lapiere psoriasis can be differentiated from pustular lesions caused by prolonged application of topical steroids or tar ointments on the periphery of pre-existent psoriatic plaques. Unlike the Von Zumbusch generalized form, the general state of health is not compromised. The patient was treated with 50 mg of etanercept twice weekly subcutaneously for three months. There was an

A case of figurate urticaria by etanercept

Etanercept is a competitive inhibitor of tumor necrosis factor-alpha (TNF-α) a polypeptide hormone, involved in the development of the immune system, in host defense and immune surveillance. Even if the etanercept mechanism of action is not completely understood, it is supposed that it negatively modulates biological responses mediated by molecules (cytokines, adhesion molecules, or proteinases) induced or regulated by TNF. For this reason, it is widely used in the treatment of immunologicals diseases, such as rheumatoid and psoriatic arthritis, polyarticular juvenile idiopathic active, ankylosing spondylitis, and plaque psoriasis. Etanercept has a good tolerability profile. Adverse events related to skin are rare, arising usually in about 5% of patients treated with anti-TNF α. In this scenario, we describe a case of figurate urticaria arose after the re-administration of etanercept in a patient affected by psoriasis and hepatitis B. A 65-year-old man, affected by psoriasis, was hospitalized in September 2014 to the Regional Center for the treatment of psoriasis and Biological Drugs of Second University of Naples for progressive extension of psoriatic skin lesions. The laboratory analysis detected positivity for hepatitis B virus (HBV) antigens. For this reason, it was administered to him lamivudine 100 mg/die about 30 days before to start etanercept treatment. The etanercept therapy has resulted in a progressive improving of skin manifestations, and the patient decided individually to stop the therapy. Afterwards, for worsening of the psoriatic lesions, he was again hospitalized and treated with the same therapeutic schedule (lamivudine followed by etanercept). Ten days after the start of therapy, the patient showed the onset of urticarial rash. Due to this, the treatment with lamivudine and etanercept was suspended and the patient′s clinical conditions improved. It is probably that immunological disorders due to etanercept therapy and HBV infection could explain the onset of figurate urticaria in our patient. In this contest, the post-marketing surveillance confirms its important role in the monitoring of drugs tolerability and effectiveness.

Cefuroxime-induced pemphigus erythematosus in a young boy.

Pemphigus erythematosus (Senear–Usher syndrome) is a variant of superficial pemphigus with features of both lupus erythematosus and pemphigus. It affects mainly middle‐aged adults, and is rarely observed before the age of 20 years. The case of a 14‐year‐old boy who showed cutaneous lesions suggestive for pemphigus erythematosus is described. Not all laboratory and histopathological investigations confirmed the hypothesis, so a diagnosis of clinical pemphigus erythematosus was made. Systemic steroid therapy was effective in controlling the disease. This case is interesting because of the rare occurrence of pemphigus erythematosus in adolescence and the possibility of another drug being added to the list of pemphigus inducers.

Pemphigus Vulgaris after Coxsackievirus Infection and Cephalosporin Treatment : A Paraviral Eruption?

Pemphigus is an autoimmune disease that results from the interaction between predisposing genetic factors and exogenous agents, mainly drugs and viruses. Herein we report the case of a 66-year-old woman referred to our department for the onset of painful oral erosions and bullous lesions on the torso. Clinical, laboratory and histopathological investigations led to the diagnosis of pemphigus vulgaris. Two weeks before the outbreak of the lesions, the patient had suffered from a viral pharyngitis, subsequently diagnosed as herpangina, and had been taking an oral cephalosporin (cefixime) for 1 week to prevent possible bacterial complications. A relationship between the onset of pemphigus and coxsackievirus infection or cefixime administration or both was supposed. The case may represent a peculiar paraviral eruption, where a predisposing pemphigus-prone genetic background paved the way for the acantholytic autoimmune disorder as a consequence of the combined effect of the coxsackievirus infection and the cephalosporin treatment.

Pemphigus erythematosus relapse associated with atorvastatin intake

Statins, also known as 3-hydroxy-3-methylglutaril-CoA reductase inhibitors, are well-tolerated drugs used for prevention of atherosclerosis and cardiovascular events. Although they are generally considered safe, some serious adverse effects, such as myositis, myopathy, and rhabdomyolysis can rarely occur. Furthermore, recent data from long-term follow-up on patients who have been taking statins for a long period of time suggest that prolonged exposure to statins may trigger autoimmune reactions. The exact mechanism of statin-induced autoimmune reactions is unclear. Statins, as proapoptotic agents, release nuclear antigen into the circulation and may induce the production of pathogenic autoantibodies. Herein we report the case of a 70 year-old man who developed a relapse of pemphigus erythematosus, a syndrome with features of both lupus erythematosus and pemphigus, after atorvastatin intake.

Pemphigus and drug addiction

© 2009 The Authors JEADV 2009, 23, 954–982 Journal compilation

Statinat®-induced pemphigus: over-the-counter drugs too may be harmful!

Editor We describe a patient with pemphigus in remission from 12 years, which suddenly exacerbated after the assumption of Statinat®, a compound aimed to the control of cholesterol plasmatic levels. Statinat® contain polyphenols, which are substances that are able to induce pemphigus. 1 In September 1995, a 44-year-old woman presented for the first time to our Department with a 2-week history of oral erosions accompanied by severe pain and multiple bullae all over the body. The diagnosis of pemphigus vulgaris was established by the skin biopsy, which showed intraepithelial blistering, and Tzanck-test, which revealed the typical acantholytic cells or ‘Tzanck cells’, indirect immunofluorescence positive for intercellular substance (1 : 375). Human leucocyte antigen (HLA) molecular typing showed HLA class II DR 14; DQ 1, 4. Systemic therapy with corticosteroids resulted in a complete remission of the disease within 3 months. The patient remained healthy until February 2007 when she returned to our Department for the development of typical bullous lesions on her trunk. On admission, physical examination revealed several crusting bullae and erosions on the trunk, whereas visible mucous membranes were disease-free. A skin biopsy of a fresh bulla showed suprabasal splitting with formation of intraepithelial cavities. The routine clinical tests were normal, whereas high antibody titres against Desmoglein 1 (1 : 80) and Desmoglein 3 (1 : 100) were measured by enzyme-linked immunosorbent assay. The clinical history disclosed that, because of hypercholesterolemy, the patient had been assuming for 1 month, and on her physician’s advice, a bioactive compound called Statinat® to avoid the assumption of the statins, the commonest types of cholesterol-lowering drugs. She was not taking any medications excepted for Statinat®; therefore, a diagnosis of pemphigus relapse induced by Statinat® was suspected. The withdrawal of Statinat® and the therapy with topical clobetasol propionate (Clobesol® 0.05%) were sufficient to achieve a remission of the disease after 1 month, which confirmed our suspicion. Statinat® is a non-prescription drug aimed to the control of cholesterol plasmatic levels, containing: DIF1STAT® (patent complex of natural substances), polyphenols, folic acid and vitamin E-B 6 -B 12 . Drugs implicated in the induction of pemphigus can be divided into three main groups according to their chemical structure: thiol drugs (containing a sulfhydryl group), phenol drugs (containing a phenol ring) and amidic drugs (containing an amidic group). 2 The causal relationship between drug and bullous disorders has usually been based on a temporal correlation in both outbreak and remission of the disease. Numerous phenol drugs, such as pyritinol, 5-thiopyridoxine (combined phenol and thiol drugs), 3 cephalosporins, 4 rifampicin, 5 levodopa, 6 aspirin, heroin, 7 phenobarbital and pentachlorophenol, 8 are known to induce pemphigus The phenol compounds stimulate interleukin-1 α and tumour necrosis factorα release by keratinocytes. 9 These cytokines are involved in the pathomechanism of acantholysis. Brenner et al . proposed a possible explanation for phenolinduced pemphigus lesions in genetically predisposed individuals that accounts for in vitro observations of biochemical acantholysis as well as clinical cases of pemphigus induced by phenols. 10 The interaction between predisposing and inducing pemphigus factors was present: HLA class II DR14, DQ1, 4 and a phenol compound in an over the counter drug (Statinat®). In accordance with Brenner et al ., we recommend caution in the use of phenols in pemphigus-prone patients. In fact, it has been proposed that drugs, food and water containing phenols and polyphenolic compounds may induce and promote pemphigus.

Pemphigus and chrysotherapy: all that glitters is not gold!

To our knowledge, the occurrence of LS in the neonatal period has not been reported previously. Onset in a boy in the neonatal period, with extragenital involvement, familial occurrence, and lack of an associated autoimmune disorder, were interesting observations in this case. Chandra Naik, MD Gurcharan Singh, MD Department of Dermatology, Sri Devraj Urs Medical College, Tamaka, Kolar Kavnataka, India