Incidence of and Risk Factors for Cutaneous Scarring after Herpes Zoster.

BACKGROUND: About 20% of children have cutaneous scars following chickenpox. In contrast, skin scars are not often reported after herpes zoster (HZ). Risk factors for post-HZ scarring remain undetermined. OBJECTIVE: Our objective was to prospectively study the incidence of and risk factors for post-HZ scarring. METHODS: This was a 3-year prospective study of patients with HZ attending a tertiary university hospital. Baseline data, including age, sex, immunosuppression, prior history of scarring, severity and extension of HZ, afflicted HZ dermatome, and antiviral treatment received, were recorded. At 1 month after the HZ skin lesions had healed, patients were screened for skin scars at the prior HZ site. These patients were followed every 2 months for 6 months. RESULTS: At 6 months, 11 (9.7%) of 113 HZ patients still had post-HZ scarring (fair-skinned patients: hypopigmented [n = 3], hyperpigmented [n = 2], atrophic cicatricial [n = 3], and hypertrophic cicatricial [n = 1]; dark-skinned patients: severe hyperpigmented hypertrophic scarring [n = 2]). HZ was extensive and severe in all cases. Nine of the 11 patients were immunocompromised. Three cases had a history of hypertrophic/keloid scarring but no post-varicella scars. The most frequent location was the trunk (n = 5), followed by the cervical region (n = 3) and the face (n = 3). Given the study setting, it is possible that immunocompromized patients with severe HZ were overrepresented in this study. CONCLUSIONS: Scarring after HZ is probably overlooked. The principal risk factors seem to be severe HZ and immunosuppression. Hence, prompt instigation of antiviral treatment for HZ and HZ vaccination could help reduce the incidence of post-HZ scarring.

Pachyderma in Primary Cutaneous NK and T-Cell Lymphoma and Leukemia Cutis.

BACKGROUND: Pachyderma is defined as severely thickened skin with deep folds and is occasionally observed with primary cutaneous NK and T-cell lymphoma (pCNKTCL), primary cutaneous B-cell lymphoma (pCBCL), and leukemia cutis (LC). AIM: To describe the clinical, histological, and therapeutic particularities of a series of pCNKTCL, pCBCL, and LC patients with pachyderma. RESULTS: In a series of pCNKTCL (n = 70), pCBCL (n = 12), and LC (n = 2) patients followed up during 9 years, 6 cases of pachyderma were observed. Pachyderma occurred on the arms (n = 2), thighs (n = 1), forehead (n = 1), and face (n = 2). The mean age of the patients was 69 years (51-82). The stages were erythrodermic (T4) mycosis fungoides (MF) (n = 1), folliculotropic MF (FMF) (n = 2), classic (T2) MF (n = 2), and chronic myeloid leukemia (n = 1). The erythrodermic MF patient with acute pachyderma on the right arm responded rapidly to oral steroids. The other cases were indolent, appeared progressively, and were highly treatment resistant. Histology revealed dense dermal neoplastic infiltration. The immunohistological profile of the pachydermic lesions was similar to common MF and LC. CONCLUSION: Pachyderma is an atypical manifestation of MF and LC and may occur on the face (FMF) or the extremities (MF). The rapidly appearing pachyderma may be transitory and responds readily to oral steroids.

Melanoma masquerading as nonmelanocytic lesions.

Increased awareness among dermatologists as well as the development of dermoscopy and sequential dermoscopy have contributed significantly toward an increase in the diagnostic accuracy of pigmented melanoma and even of amelanotic melanoma. However, the dermatologist's nightmare is the small group of melanomas that present as common skin diseases, often associated with a significant delay in diagnosis and hence a poor prognosis. The study was carried out to prospectively assess the number of melanomas lacking any clinical suspicion of melanoma and to describe their clinical and histological features over a 6-year observation period in an University Tertiary Skin Cancer Center. Out of 502 cases of newly diagnosed cases of melanoma, seven (1.4%) nonpigmented and nonamelanotic cases of melanoma were identified. The mean age of the patients was 69 years (two females/five males). All cases were discovered by chance on a punch biopsy. The clinical diagnostic suspicions were basal cell carcinoma, fungal intertrigo, keratoacanthoma, lichenoid keratoma, diabetic foot ulcer, eczema, and necrotic pressure ulcer. Dermoscopy, performed after the punch biopsies, was only partially contributive. The mean histological thickness was 2.7 mm, the mean number of mitoses was 7/mm, local micrometastases were present in 5/7 (71%), the mean Ki67 count was 18.9%, and a positive sentinel lymph node was observed in 4/6 (66%) cases. Nonpigmented and nonamelanotic melanomas are rare, are at high risk, and have a poor prognosis because of a delayed diagnosis. Dermoscopy is only of partial diagnostic aid. Treatment resistance or atypical behavior of the above-mentioned lesions should lead to biopsy.

Recurrent in situ melanoma successfully treated with ingenol mebutate.

BACKGROUND: Treatment options for melanoma in situ (MIS) include imiquimod, radiation therapy, cryotherapy, excisional and Mohs surgery. Ingenol mebutate is a new topical treatment option recognized for actinic keratosis. Although in vitro effectiveness has been demonstrated on melanoma cell lines, its therapeutic potential for in vivo melanomas is unknown. CASE REPORT: In 2011, a 91-year-old woman presented a thick melanoma of her cheek. The lateral sections revealed persisting in situ melanoma, which were again excised. She presented for follow-up and a recurrent MIS was evidenced centered on the previous scar. She refused further surgery and ingenol mebutate (0.015% gel) was administered on three consecutive days. One month later, a complete clinical resolution was observed. Histology and immunohistology revealed no residual MIS. CONCLUSION: In this patient, ingenol mebutate was successful and well-tolerated as a topical, alternative therapy for MIS after failure of other treatment options.

Hair loss after varicella zoster virus infection.

Varicella zoster virus (VZV) cutaneous infection occurs predominantly in epidermal and infundibular keratinocytes and accessorily in dermal dendritic cells. These latter cells play a role in cicatricial processes. Two patients are presented with localized alopecia after VZV infection. A 4-year-old girl presented localized hair loss affecting about 20% of her upper right eyelash immediately following the resolution of the varicella skin lesions. No regrowth was observed after 3 months. An 80-year-old woman with a prior history of localized alopecia areata of the left occipital area presented severe left herpes zoster affecting the V1 and V2 dermatomes. At precisely the same site of the previous episode, a localized plaque of alopecia areata recurred. After topical corticosteroid therapy, a progressive hair regrowth occurred after about 3 months. These case reports are the first relating cutaneous VZV infection as the origin for permanent cicatricial alopecia and transitory alopecia areata. Localized hair loss should be added to the cutaneous complications of VZV skin infection.

Photodynamic therapy for multi-resistant cutaneous Langerhans cell histiocytosis.

Langerhans cell histiocytosis is a rare group of proliferative disorders. Beside cutaneous involvement, other internal organs can be affected. The treatment of cutaneous lesions is difficult and relies on topical corticosteroids, carmustine, nitrogen mustard, and photochemotherapy. Systemic steroids and vinblastine are used for recalcitrant skin lesions. However, some cases fail to respond. An 18-month old boy presented a CD1a(+), S100a(+) Langerhans cell histocytosis with cutaneous and severe scalp involvement. Topical corticosteroids and nitrogen mustard failed to improve the skin lesions. Systemic corticosteroids and vinblastine improved the truncal involvement but had no effect on the scalp lesions. Methylaminolevulinate (MAL) based photodynamic therapy (PDT) resulted in a significant regression of the scalp lesions. Control histology revealed an almost complete clearance of the tumor infiltrate. Clinical follow-up after six months showed no recurrence.Although spontaneous regression of cutaneous Langerhans cell histiocytosis is observed, the rapid effect of photodynamic therapy after several failures of other treatment suggests that photodynamic therapy was successful. As far as we know this is the first report of photodynamic therapy for refractory skin lesions. Larger series are needed to determine whether photodynamic therapy deserves a place in the treatment of multiresistant cutaneous Langerhans cell histiocytosis.

Congenital infantile digital fibromatosis: a case report and review of the literature.

Infantile digital fibromatosis (IDF) is a rare benign fibroproliferative tumor of early childhood. IDF preferentially affects the fingers and the toes. Malignant transformation or metastases have never been reported. Surgical treatment has been advocated previously but local recurrences were observed frequently. Recent literature supports clinical surveillance without any medical or surgical intervention as spontaneous regression usually occurs after two to three years. A six-month-old Caucasian girl with IDF on the left fourth digit is presented here. The tumor progressively increased in size after birth. Topical imiquimod cream and diflucortolone valerate cream, both displaying antifibrotic properties, had no effect on tumor growth. Currently the lesion size remains stable without any treatment. Early recognition of IDF is important in order to avoid unnecessary surgical intervention that may prove to be potentially aggravating, unless serious functional or cosmetic concerns intervene. Parents should be reassured concerning the benign nature of IDF and be informed that spontaneous involution of IDF might be expected.

Corynebacterium-associated skin infections.

BACKGROUND: Corynebacterium spp. are diphtheroid bacteria responsible for pitted keratolysis, a common plantar infection confined to the thick stratum corneum. AIM: To study a series of demographic features of patients suffering from pitted keratolysis, and to present a review of the Corynebacterium-associated infections, including pitted keratolysis, erythrasma, and trichobacteriosis. MATERIALS AND METHODS: A 2-year, two-center, prospective survey assessed the demographics of pitted keratolysis, including age, gender, site of infection, symptoms, patients' complaints, the use of protective and/or occlusive shoes, seasonality of diagnosis, drug intake, associated skin signs (including dyshidrosis, erythrasma, and trichobacteriosis), recurrences, and previous diagnoses and treatments. RESULTS: The mean age of the 53 patients with pitted keratolysis was 24.9 years (range, 10-57 years). The male to female ratio was 7.8:1. The soles of both feet were commonly involved (92.4%). Pressure-bearing areas were the usual sites of infection, ranging from restricted involvement of the toes (12/53, 22.6%) to spreading to the entire plantar surface (15/53, 28.3%). A total of 36 (68%) of the 53 patients complained of hyperhidrosis. An unpleasant smell and pain were noted by 35 (66%) and 25 (47%) of the 53 patients, respectively. Occlusive and protective shoes were worn in 51 (96.2%) and 31 (58.4%) of the 53 cases, respectively. CONCLUSION: Pitted keratolysis commonly affects young male patients wearing protective shoes for professional reasons, inducing a moist and warm environment. Hyperhidrosis, an unpleasant smell, and pain are the main clinical complaints.

Oral antifungal-exacerbated inflammatory flare-up reactions of dermatomycosis : case reports and review of the literature.

Inflammatory flare-up reactions of some dermatomycoses, particularly those caused by zoophilic fungi, are typical and potentially severe adverse effects following the intake of some oral antifungals. However, this condition has not previously been reported with the most frequently used antifungals in dermatology, namely fluconazole, itraconazole, and terbinafine. In this report, we describe five patients, observed over a 10-year period, who presented with inflammatory exacerbations following oral antifungal therapy for dermatomycoses. We also review the literature on inflammatory reactions exacerbated by oral antifungal agents. Details of the patients' age, sex, occupation, and atopic background; the site of the lesion, its clinical and histologic features, and any systemic signs; the identity of the fungal pathogen; the antifungal agent taken by the patient; the time between drug intake and occurrence of the flare-up; the approach to management; and the outcome were documented for each patient. A PubMed literature search was also conducted, focusing on inflammatory exacerbations induced by griseofulvin, ketoconazole, itraconazole, fluconazole, and terbinafine. The patients were four farmers and one veterinarian (all male). All primary lesions were inflammatory dermatophytoses, including one kerion. Inflammatory exacerbation of the skin lesions started 12-24 hours after the intake of oral antifungals. Mild systemic changes, including slight fever and malaise, occurred in two cases. Itraconazole 400 mg/day was implicated as the causative agent in four cases and terbinafine 250 mg/day in one case. Mycologic cultures grew Trichophytonverrucosum in four cases. Antifungal treatment was discontinued in all patients. Oral and topical corticosteroids were administered to the two patients with systemic changes; the other three patients were treated with topical corticosteroids only. Two days after the onset of corticosteroids, lower doses of itraconazole (100 mg/day) and terbinafine (125 mg/day) were reintroduced. All lesions healed after 4-5 weeks. The PubMed search did not identify any articles that described inflammatory exacerbations of dermatomycoses induced by oral antifungals. Inflammatory flare-up of dermatomycoses is a rare but potentially severe cutaneous complication of oral antifungal use. Occupational contact with animals, inflammatory dermatomycoses, and zoophilic fungi represent common features in these patients. Although evidence-based data are not available, clinical experience shows that, in addition to antifungal therapy, topical and/or systemic corticosteroids are helpful to reduce the inflammatory reactions. The cases described in this article represent the first published report of oral antifungal-exacerbated inflammatory flare-up reactions of dermatomycosis in patients taking itraconazole or terbinafine.

Cutaneous adverse reactions following anti-infective vaccinations.

Although widely administered, anti-infective vaccinations are rarely responsible for cutaneous adverse effects. In this context, hepatitis B and bacillus Calmette-Guerin vaccines are the most frequently incriminated products. Cutaneous adverse effects are less frequently encountered following administration of vaccines against varicella, diphtheria/tetanus/pertussis (primary and booster doses), measles, poliomyelitis, rubella, pneumococcus, tick-borne encephalitis, smallpox, Meningococcus and influenza. The adverse effects can occur at the site of or at a distance from the injection. The patho-mechanisms of local adverse cutaneous reactions include predominantly nonspecific lymphoid or granulomatous reactions. Allergic reactions to the vaccine strain, adjuvants, conservatives or other components are less frequently involved in local vaccine adverse effects. Systemic reactions are mainly mediated by immediate type or immune complex-related allergic reactions to toxoid-, ovalbumin-, gelatin- or pneumococcal-containing vaccines. Systemic reactions are sometimes related to a specific vaccine strain. Other cutaneous reactions may also occur through unknown patho-mechanisms. No vaccine type or strain is specifically associated with a particular type of cutaneous adverse effect. This article presents seven case reports of cutaneous adverse effects following anti-infective vaccination then reviews the relevant literature on this subject.

Revisiting childhood herpes zoster.

Herpes zoster is rare in otherwise healthy children, but it is more common in association with immunosuppression. Maternal varicella infection during pregnancy and varicella occurring in the newborn represent risk factors for childhood herpes zoster. However, some controversies persist about risk factors, diagnosis, and the natural history of childhood disease. In a 2-year prospective study, 18 children with herpes zoster were clinically diagnosed in outpatient consultations in a hospital dermatology unit. Data about age, dermatome involvement, underlying disease, and history of previous varicella were recorded. Tzanck smears, biopsy specimens, and sera were obtained from 18, 4, and 10 children, respectively. The varicella zoster virus major envelope glycoprotein gE was detected in 16 of 18 smears and all four biopsies. Herpes simplex virus I was demonstrated in one of the smears. The established risk factors for childhood herpes zoster were only found in one child. Evidence for previous full-blown varicella and varicella with few lesions was recorded in 7 and 4 of the 17 immunocompetent children, respectively. No history of varicella was recalled in 6 of 17 cases, although a serologic clue of past varicella infection (IgM negative, IgG positive) was disclosed. Recurrent herpes zoster was diagnosed in one immunocompromised child. Zoster-associated pain was localized and the disease severity remained mild in all children. Established risk factors for childhood herpes zoster were only rarely found in our series of patients. In contrast, unrecognized varicella and varicella with few lesions were frequently recorded and may represent additional risk factors for shingles in childhood. Zosteriform herpes simplex virus infections should be differentiated from childhood herpes zoster, emphasizing the importance of precise viral identification.