Steven Glassman

Vitiligo, reactive oxygen species and T-cells

The acquired depigmenting disorder of vitiligo affects an estimated 1% of the world population and constitutes one of the commonest dermatoses. Although essentially asymptomatic, the psychosocial impact of vitiligo can be severe. The cause of vitiligo remains enigmatic, hampering efforts at successful therapy. The underlying pathogenesis of the pigment loss has, however, been clarified to some extent in recent years, offering the prospect of effective treatment, accurate prognosis and rational preventative strategies. Vitiligo occurs when functioning melanocytes disappear from the epidermis. A single dominant pathway is unlikely to account for all cases of melanocyte loss in vitiligo; rather, it is the result of complex interactions of biochemical, environmental and immunological events, in a permissive genetic milieu. ROS (reactive oxygen species) and H2O2 in excess can damage biological processes, and this situation has been documented in active vitiligo skin. Tyrosinase activity is impaired by excess H2O2 through oxidation of methionine residues in this key melanogenic enzyme. Mechanisms for repairing this oxidant damage are also damaged by H2O2, compounding the effect. Numerous proteins and peptides, in addition to tyrosinase, are similarly affected. It is possible that oxidant stress is the principal cause of vitiligo. However, there is also ample evidence of immunological phenomena in vitiligo, particularly in established chronic and progressive disease. Both innate and adaptive arms of the immune system are involved, with a dominant role for T-cells. Sensitized CD8+ T-cells are targeted to melanocyte differentiation antigens and destroy melanocytes either as the primary event in vitiligo or as a secondary promotive consequence. There is speculation on the interplay, if any, between ROS and the immune system in the pathogenesis of vitiligo. The present review focuses on the scientific evidence linking alterations in ROS and/or T-cells to vitiligo.

Comprehensive analysis of cutaneous T-cell lymphoma (CTCL) incidence and mortality in Canada reveals changing trends and geographic clustering for this malignancy.

Previous reports of geographic clustering of cutaneous T‐cell lymphoma (CTCL) in Texas, Pittsburgh, and Sweden as well as the occurrence of CTCL in married couples and family members raise a possibility of the existence of an external and potentially preventable trigger(s) for this rare skin cancer.

Palmoplantar subcorneal pustular dermatosis following adalimumab therapy for rheumatoid arthritis

Tumour necrosis factor (TNF)‐α inhibitors represent potent new therapies for severe forms of psoriasis, psoriatic arthritis, and several other immune‐mediated disorders. Paradoxical worsening or de novo development of psoriasis has been documented with their use. Palmoplantar pustulosis has been one of the commoner presentations of this unusual side effect. Subcorneal pustular dermatosis (SPD) has some similarity to pustular psoriasis, particularly the acral form of SPD. Thus far there have been no biopsy‐proven cases of SPD associated with TNF‐α inhibitor use.

Distribution and Clustering of Cutaneous T-Cell Lymphoma (CTCL) Cases in Canada During 1992 to 2010

Background: Clustering of patients with cutaneous T-cell lymphoma (CTCL) was reported in several jurisdictions around the world. This rare cancer is known to affect spouses and in some cases multiple members of the same family. These combined results suggest the existence of external disease triggers/promoters. We recently conducted the first comprehensive analysis of CTCL incidence and mortality in Canada, which revealed case clustering in several regions. Objectives: To extend our previous analysis on CTCL incidence across Canada and to provide all the collected data on CTCL patient incidence in Canada during the period of 1992 to 2010. Methods: Clinical parameters for patients with CTCL in Canada were analyzed using 2 independent population-based cancer registries: Canadian Cancer Registry and Le Registre Québécois du Cancer. The CTCL incidence rates were examined on different geographical levels, including provinces/territories, cities, and forward sortation areas. Results: Our findings further corroborate our earlier observations of higher CTCL incidence in Newfoundland and Labrador, maritime provinces (Nova Scotia and New Brunswick), and prairie provinces (Manitoba and Saskatchewan). Also, most cities with high CTCL incidence were located in these provinces. Extensive mapping of high-incidence postal codes supports case clustering in a number of communities that are located in the proximity of industrial centres and seaports. Conclusions: Detailed analysis of CTCL incidence in Canada is critical to fully understand the burden of this disease in our country, to begin the search for a possible external trigger for this lymphoma, and to reform how health care resources are distributed throughout the country to better serve Canadian patients with CTCL.

Actinic superficial folliculitis in a 29-year-old man.

Background: Since actinic superficial follicultis was first described in 1985, only three further cases have been published. The characteristics of this disease are monomorphous, superficial, follicular pustules that appear on the back, upper chest, and shoulders annually after the first sun exposure of the year. The lesions resolve on their own within 10 days. Recurrence occurs under similar conditions after a latency period of at least 4 weeks. Methods: A 29-year-old man presented to our clinic with a 5-year history of an intermittent follicular rash. These eruptions occurred on his back and chest only when he was exposed to the sun, with his shirt off. They developed 24 to 36 hours after the first sun exposure of the year and resolved spontaneously after 5 to 7 days. Photographs of the affected area were impressive, with follicular pustules grouped along his left flank. Conclusion: According to our literature search, this is the sixth reported case of actinic superficial folliculitis. This is the first case in which provocative phototesting was done. We review the clinical and pathologic attributes of actinic superficial folliculitis.

p16+ Squamous cell carcinoma in situ masquerading as genital psoriasis

HPV: human papilloma virus MGUS: monoclonal gammopathy of undetermined significance PIN: penile intraepithelial neoplasia SCCIS: squamous cell carcinoma in situ INTRODUCTION Cutaneous neoplasms of the male genitalia are an important consideration in older men and immunocompromised patients. They are derived from the squamous epithelium and have an association with human papilloma virus (HPV). HPV types 16, 18, and 57b have been isolated, and their DNA is present in approximately 40% to 45% of all penile carcinomas. Squamous cell neoplasia includes both squamous cell carcinoma in situ (SCCIS) and invasive carcinoma. Risk factors include increasing age, immunosuppression, smoking, exposure to ultraviolet light, benzene, and arsenic. Invasive squamous cell carcinoma is uncommon in the genital region. It may advance from SCCIS or present as a more aggressive tumor. In general, both invasive squamous cell carcinoma and SCCIS canpresent as erythematouspatches or plaques with or without significant scale on the penis and inguinal skin. Many conditions mimic SCCIS in the inguinogenital region. Intertrigo, psoriasis, dermatophytosis, candidiasis, Darier disease, Hailey-Hailey, plaque stage cutaneous T-cell lymphoma, and extramammary Paget disease can all resemble SCCIS. Genital psoriasis, in particular, is underrecognized. Involvement of the genital area occurs in 29% to 46% of all psoriasis patients. The symptoms of genital psoriasis are mild to moderate, with itch, pain, and burning most commonly reported. These symptoms closely mimic those of SCCIS. Scale is often absent in genital psoriasis. Here we report a case of SCCIS that closely resembled genital and inverse psoriasis. The tumor

The association between question type and the outcomes of a Dermatology eConsult service

eConsult is a web based service that facilitates communication between primary care providers (PCPs) and specialists, which can reduce the need for face‐to‐face consultations with specialists. One example is the Champlain BASE (Building Access to Specialist through eConsultation) service with dermatology being the largest specialty consulted.

Deep morphea induced by interferon-β1b injection

Morphea, also known as localized scleroderma, is an uncommon fibrosing condition of the skin and underlying tissue. Although the etiology is unknown, morphea is considered an autoimmune condition in which genetic and environmental factors contribute to disease onset.1 Although most cases are spontaneous, several inciting factors are associated with morphea, including trauma, surgery, radiotherapy, and infections.2, 3 Morphea has also apparently been triggered by injections such as vaccination, vitamin B12, and vitamin K.3 However, morphea after interferon-β1b (IFN-β1b) injection is rarely reported. Injection site reactions (ISR) to IFN-β1b range from mild erythema to ulceration,4 and a case of deep morphea after IFN-β1b injection is described here.