Salvatore Domenico Infusino

Cutaneous manifestations in inflammatory bowel diseases: eight cases of psoriasis induced by anti-tumor-necrosis-factor antibody therapy.

Background: Ulcerous rectocolitis and Crohn’s disease are the best known forms of inflammatory bowel disease (IBD). Skin manifestations are not uncommon in IBD and may be divided into specific cutaneous signs, aspecific cutaneous signs, and cutaneous signs caused by drugs used for IBD therapy. The specific signs (fistulas, rhagades and ulcers) are the result of the diffusion of the intestinal inflammatory process into the skin. Aspecific cutaneous signs (stomatic aphthosis, erythema nodosum, pyoderma gangrenosum, Sweet’s syndrome, vasculitis, bullous diseases) are quite frequently found in those suffering from IBD, but also in apparently healthy subjects, and may sometimes be the first sign of the intestinal disease. Cutaneous manifestations due to drugs vary in clinical aspect and are the direct consequence of the therapies adopted, which in IBD patients can be quite numerous: steroids, immunosuppressants, 5-aminosalicylic acid, biological agents, antibiotics. Objective and Methods:Due to the frequent finding of cutaneous manifestations in patients affected by IBD, a collaboration was set up between the Dermatological Clinic of the University of Bologna and the Center for the Study of IBD of the same university hospital. The aim was to diagnose the cutaneous signs appearing during IBD and to establish their etiopathogenesis in order to assess whether they were the result of epiphenomena of the IBD or side effects of the therapies adopted. Results: The cutaneous manifestations we observed can be divided into three distinct groups: signs that were specific to the basic disease, aspecific signs and finally signs attributable to the drugs used for therapy. Particular attention was given to the aspecific signs and those consequential to therapy. The aspecific cutaneous signs seen in our clinic generally reflect those reported in the literature. The cutaneous manifestations due to drugs were further divided into three groups: rosacea, acneiform dermatitis and psoriasis-like dermatitis. The most notable aspect of our series is the high number of patients presenting psoriasiform-type dermatitides with a generally widespread diffusion. Conclusion: We would like to draw attention to the fact that all patients with psoriasis had been undergoing treatment with drugs inhibiting tumor necrosis factor α (TNF-α) as part of IBD therapy. In all cases, the cutaneous reaction started after the third or fourth infusion of the biological drug. Anti-TNF-α agents have also been successfully used to treat psoriasis in the last few years. The reason for this apparently paradoxical effect of the therapy is still unclear.

Chloracne: still cause for concern.

Chloracne, first described by Herxheimer in 1899, is a dermatosis consisting of more or less diffuse acneiform lesions distributed prevalently on the face and on body areas not usually affected by acne and caused by chronic or acute exposure to halogenated chemical compounds. Dioxin is the common name for dibenzo-p-dioxins and dibenzofurans, contaminants nearly ubiquitous in the environment and highly resistant to chemical and biological degradation. These compounds can survive for decades in the environment and accumulate in the human and animal food chains. Chloracne is characterized by the onset of numerous comedo-like lesions and yellowish cysts on the face, particularly on the cheeks, that can spread to the trunk and other body regions not usually affected by acne vulgaris, with diffuse grayish skin pigmentation and sometimes associated with hypertrichosis and areas of folliculitis. The lesions may occasionally be accompanied by skin or systemic manifestations. We report 9 cases of chloracne, 8 of them with rapid onset in patients residing in the same building, and 1 in a patient occupationally exposed to halogenated compounds. In our series, the doses of dioxin and polychlorinated biphenyls in the soil, water and plant material, and the serum titer of dioxin were within the normal range. This consideration raises the issue of the need to revise the serum threshold for dioxin poisoning and the environmental threshold. We wish also to underline the value of dermatopathology in the differential diagnosis of chloracne.

Cutaneous collagenous vasculopathy: report of a case

an itchy facial rash. His medical history was unremarkable apart from acne vulgaris as a teenager. On physical examination, striking tumid erythematous papules, plaques and nodules were seen predominantly on the lower cheeks, and scaly erythematous plaques over the central forehead, upper cheeks, chin and neck (Fig 1a). The eyebrows, beard and scalp appeared normal with no obvious hair loss, and the cutaneous findings were limited to the head and neck. The differential diagnoses considered included granulomatous rosacea, sarcoidosis and lupus erythematosus. Pending histological confirmation, twicedaily topical 0.1% tacrolimus ointment was commenced. On histological examination of an incisional biopsy taken from the left pre-auricular area, a prominent perifollicular inflammatory cell infiltrate was seen, comprised mainly of lymphocytes, with mucinous degeneration of the follicular epithelium (Fig. 2a,b). There was no significant lymphocyte atypia, and the lymphoid immunoprofile was normal. Follicular destruction and granulomatous inflammation were absent. Fungal, bacterial and mycobacterial cultures were negative, as was direct immunofluorescence. Alcian blue staining confirmed the presence of intrafollicular mucin deposits (Fig 2c). Findings were consistent with a diagnosis of benign FM. On review 10 days later, the patient’s facial eruption had dramatically improved (Fig 1b). Full blood count, erythrocyte sedimentation rate, lactate dehydrogenase, human T cell lymphotropic virus (HTLV)1 and HTLV2 serology, and lymphocyte immunophenotyping were all normal or negative. T-cell gene rearrangement studies confirmed a polyclonal population, and a final diagnosis of primary idiopathic FM was made. Treatment with topical 0.1% tacrolimus ointment was tapered over the following 4 weeks, and remission has been maintained for > 1 year. A single case of recalcitrant FM successfully treated with 1% pimecrolimus cream has previously been reported. The response to tacrolimus ointment in our case was unusually rapid, and spontaneous resolution of lesions cannot be excluded. The risk of activating what may be considered a premalignant condition remains a concern, and further studies evaluating the efficacy, safety and tolerability of topical tacrolimus ointment in FM are required before it can be recommended.

Pruritic papular eruption in HIV: a case successfully treated with NB-UVB.

Pruritic papular eruption (PPE) is a skin disease characterized by the eruption of itching papules on the extremities, face, and trunk; it is quite frequent in HIV‐positive patients especially during the advanced immunosuppressive stage. PPE usually improves or heals when antiretroviral therapy restores the immune system function, but in some cases, it can take several months, and a symptomatic treatment for PPE is required. Systemic antihistamines, topical steroids, topical tacrolimus, itraconazole, pentoxyphilline, and ultraviolet B phototherapy have been proposed in cases of persisting PPE, but an elective treatment has not yet been found. We describe the case of a black patient affected by PPE, nonimproving with antiretroviral treatment, and resistant to topical steroids and oral antihistamines; a satisfactory and speedy result was achieved with narrow‐band ultraviolet B phototherapy.

Photodynamic therapy: An option in mycosis fungoides

BACKGROUND Photodynamic therapy (PDT) is a well-known and effective treatment for non-melanoma skin-cancer. Numerous studies have also shown its effectiveness in mycosis fungoides. The aim of the study was to analyse MF patients treated with PDT at the Dermatology Unit of Bologna University. METHODS We retrospectively analysed MF patients treated with PDT over the last ten years. Each PDT protocol consisted of the appliance for 3h under an occlusive film dressing on each lesion of a one-mm-thick layer of 16% methyl aminolaevulinate (MAL) 160mg/g cream (Metvix®, Galderma, Paris, France). The cream was then removed and the skin was exposed to 630nm red light from a diode lamp (Aktilite®, Galderma Benelux, Rotterdam, the Netherlands), with a total radiation dose of 37J/cm2 for 9 mins. A protocol of one session every month was scheduled. The treated lesions were clinically examined, before each treatment. RESULTS Four cases, three male and one female, had been treated with PDT. Two patch lesions on the plantar area, one leg and the pubic area were treated. The number of PDT sessions ranged from 4 to 9. Two complete remissions and two partial remissions were observed. A low-to-mild burning sensation was reported during the treatment, and persisted over the next day; no further side effects were observed. CONCLUSIONS Our series shows that PDT can be considered an effective second-line treatment in patients characterised by a disease located in difficult-to-treat anatomical areas such as the feet and the pubic area.

Minocycline-Induced Blue-Gray Discoloration

At the time of our consultation, we observed a prominent bluegray discoloration characterized by symmetric patches localized on the temporal, preauricular and periorbital skin ( Fig. 1 ), while the trunk, limbs, and the mucosae were spared. Routine blood tests and other recent investigations excluded the most common causes of hyperpigmentation, including Addison disease, hyperthyroidism or malignancy. A skin biopsy from the pigmented skin showing prominent solar elastosis, epidermal thinning, and focal hyperpigmentation of the basal layer was not helpful for a diagnosis. A more detailed medical history revealed that the patient had been taking minocycline 100 mg every other day for nearly 10 years. In fact, he had observed an improvement of a folliculitis of his trunk after minocycline prescription from his physician; he had therefore continued to take the drug autonomously. Minocycline intake was immediately stopped and a diagnosis of minocycline-induced pigmentation was made. At 2 years of follow-up, the face discoloration was still present, although less prominent ( Fig. 2 ). The patient refused any surgical procedure, such as laser treatment or skin bleaching agents. Disorders of pigmentation are usually due to the deposition of melanin and an increase in active melanocytes. The clinical features are characterized by blue-black or blue-gray diffuse or pitted pigmentation primarily of the face, extremities and other photoexposed areas. Various exogenous factors can be involved, including inflammation and injury (postinflammatory hyperpigmentation). Differential diagnosis includes various dermatoses of unknown etiology, such as erythema dyschromicum perstans or ashy dermatosis, lichen planus pigmentosus and melasma or argyria,

Keratosis lichenoides chronica with an atypical clinical presentation and variable histopathological features.

A 44-year-old, otherwise healthy, Moroccan man was referred to us because of rapid onset of erythematous, scaly, raised, slightly pruritic plaques on the trunk, extremities (Figure 1a–c), face, and scalp (Figure 1d). He showed neither nail changes nor mucosal (oral or genital) involvement. His medical history was unremarkable, and he denied any drug intake. A complete blood cell count, liver and kidney function tests, thyroid parameters, and urinalysis were within normal limits. Syphilis screening, hepatitis B, C, and HIV serology, as well as a QuantiFERON-TB test were negative. A chest X-ray and abdominal ultrasound were normal. Multiple skin biopsies were performed. Those taken from the trunk and extremities showed extensive epidermal hyperparakeratosis, psoriasis-like acanthosis, hypogranulosis (Figure 2a–c) as well as neutrophilic microabscesses (Figure 2c). Other findings included necrotic keratinocytes surrounded by lymphocytes (satellite cell necrosis) and a band-like inflammatory infiltrate associated with melanophages (Figure 2d). Periodic acid-Schiff (PAS) staining was negative. Immunocytochemistry showed a reactive inflammatory infiltrate (the makeup of the lymphoid population was as follows: CD3+/–, CD4–/+, CD8+/–, CD20 rare; “+/–” signified 50–75 % of the population; “–/+”, 25–50 %; and “rare”, 10–25 %). Based on these findings, lymphoma was ruled out. Direct immunofluorescence was negative. By contrast, the biopsies taken from the face showed focal hyperparakeratosis, irregular acanthosis, vasodilation, edema (Figure 3a, b), as well as a dermal – predominantly lymphocytic – inflammatory infiltrate (Figure 3b, c) with admixed melanophages (Figure 3b) and “satellite cell necrosis” (Figure 3d). Except for hyperparakeratosis, these findings (in particular the inflammatory infiltrate with melanophages, and the necrotic keratinocytes) were more suggestive of lupus erythematosus. Antinuclear antibodies, anti-extractable nuclear antigen antibodies, anti-DNA antibodies, antiphospholipid antibodies, antineutrophil cytoplasmic antibodies, rheumatoid factor, as well as complement component 3 and 4 were all negative. Therapy with systemic corticosteroids resulted in a good response, however, there was a rebound following treatment discontinuation. Subsequently, many different therapeutic approaches were attempted, including cyclosporine, methotrexate, acitretin, PUVA therapy, topical calcipotriol, and topical corticosteroids. However, they all proved to be ineffective. Despite their variability, the histopathological features showed a certain degree of repetitiveness, which is characteristic of our eventual diagnosis: keratosis lichenoides chronica (KLC). Systemic corticosteroids were the only effective treatment.

Keratosis lichenoides chronica mit untypischer klinischer Präsentation und variblen histopathologischen Merkmalen

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