Sonia Sangiuliano

Beyond zoster: sensory and immune changes in zoster-affected dermatomes: a review*.

Neuroepidermal tropism of varicella-zoster virus accounts for cutaneous and nerve lesions following herpes zoster. Skin lesions heal in a few weeks and may or may not leave visible scars. Nerve lesions involve peripheral sensory fibres, sometimes causing permanent damage that results in partial denervation of the affected dermatome. The effects of the nerve injury involve the sensibility function, thus causing neuralgia, itch, allodynia, hypo- or anaesthesia, as well as the immune function that is related to neuropeptide release, thus altering immune control in the affected dermatome. The neuro-immune destabilization in the zoster-infected site paves the way for the onset of many and various immunity-related disorders along the affected dermatome.

Discoid lupus erythematosus at a site of previous injury.

A 71‐year‐old man with three patches of discoid lupus erythematosus (DLE) confined to the right preauricular region drew our attention because of the unusual linear arrangement of the lesions. Twenty‐five years previously, the patient had suffered a trauma in the same area from falling off his motorcycle. We believe that, despite the great lapse in time, this injury may have facilitated the onset of DLE in the very same area, through long‐term destabilization of the local neuroimmune network. The case fits the recently coined concept of the immunocompromised district, a cutaneous region with altered immune control, more susceptible to harbouring opportunistic infections, tumours, and immune disorders.

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.

Tuberculosis and cancer on a BCG vaccination site: an instance of immunocompromised district

1 Lee HY, Chou D, Pang SM, Thirumoorthy T. Acute generalized exanthematous pustulosis: analysis of cases managed in a tertiary hospital in Singapore. Int J Dermatol 2010; 49: 507–512. 2 Posadas SJ, Pichler WJ. Delayed drug hypersensitivity reactions – new concepts. Clin Exp Allergy 2007; 37: 989–999. 3 Sidoroff A, Halevy S, Bavinck JN, et al. Acute generalized exanthematous pustulosis (AGEP) – a clinical reaction pattern. J Cutan Pathol 2001; 28: 113–119. 4 Yesudian PD, Penny M, Azurdia RM, King CM. Ibuprofen-induced acute generalized exanthematous pustulosis. Int J Dermatol 2004; 43: 208–210. 5 Gonzalo-Garijo MA, Pérez-Calderón R, De Argila D, Rodríguez-Nevado I. Metamizole-induced acute generalized exanthematous pustulosis. Contact Dermatitis 2003; 49: 47–48.

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.

Unilateral bullous pemphigoid in a patient with a previous ipsilateral cerebellar hemorrhage.

type of SK often shows a fingerprinting of either light brown, delicate networks in a fingerprint-type pattern or an indistinct structure with a cobblestone-like pattern (Fig. 3). In both cases, comedo-like openings are often seen. The dermoscopic findings of thick SK, such as small milia-like cysts, irregular crypts, fissures or ridges, blue– gray globules, hairpin vessels, and fat fingers, are less common. Cryotherapy of the lesions leads in all cases to resolution of the itch. Incomprehensibly, the literature does not mention SK as a reason for general pruritus, and a search of PubMed did not reveal any papers on this issue. The standard references in Fitzpatrick’s Dermatology in General Medicine and Bolognia et al. do not mention pruritus as a symptom of SK, and the latter bring up pruritus as a sign of only the irritated type of SK. Seborrheic keratoses should be included in the list of causes of generalized pruritus.

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

Tattoo-like contact dermatitis.

DF is a definition in terms of the clinical picture, whereas lipidized fibrous histiocytoma is defined by histologic features. We searched and reviewed the previous literature about giant DF and found 20 cases and verified the histopathologic findings. Of the 20 cases, histopathologic manifestation with ‘foamy cell’ or ‘xanthoma cell’ was recorded in 10 cases. This indicates that foamy cells are a characteristic finding of giant DF. Therefore, some giant DF may consist predominantly of foamy cells, which can be diagnosed as lipidized fibrous histiocytoma. Although our case had hypercholesterolemia, generally there is no relationship between serum lipid level and lipidized fibrous histiocytoma, because no significant difference was observed in serum lipid level between those who had lipidized fibrous histiocytomas and those who had common DF.