Laugier-Hunziker syndrome: A case report and review of the literature.

Laugier-Hunziker syndrome (LHS) is a rare acquired disorder characterized by diffuse macular hyperpigmentation of the oral mucosa and, at times, longitudinal melanonychia. Although LHS is considered a benign disease with no systemic manifestations or malignant potential, it is important to rule out other mucocutaneous pigmentary disorders that do require medical management. Prompt clinical recognition also averts the need for excessive and invasive procedures and treatments. To date, only four cases have been reported in the United States. We present a 77-year-old man who had clinical features typical of LHS and we then provide a review of the literature on LHS and its mimickers.

A paradigm for facial skin rejuvenation.

There is a significant desire by patients to reverse the signs of aging caused by photodamage. Numerous procedures for facial skin rejuvenation have been developed in an attempt to minimize the erythema, dyspigmentation, and rhytides associated with photoaging. The initial procedures developed for facial rejuvenation involve skin resurfacing via complete ablation of layers of skin. Of these procedures, ablative laser resurfacing is the most precise technique and is considered the gold standard for facial skin rejuvenation. Although ablative procedures are quite efficacious, they carry significant patient downtime and risks of adverse effects such as scarring and dyspigmentation. Concerns regarding patient morbidity have led to the development of nonablative procedures that target dermal collagen without damaging the epidermis. Of these technologies, intense pulsed light is the most commonly used because it effectively targets both the erythema and dyspigmentation seen in photoaging. Nonablative techniques minimize side effects and patient downtime; however, they do not match the results seen in fully ablative procedures. Fractional laser technologies-first nonablative and more recently ablative-represent the most recent attempt to match the results seen in fully ablative procedures with less patient downtime. Their results are promising but require further study.

Irritant contact dermatitis from plants.

Irritant contact dermatitis (ICD) from plants is a very common phenomenon as potentially irritant plants and plant products are commonly found in the everyday environment, including the home, garden, workplace, and recreational setting. It is therefore essential to have a basic understanding of the various plant-derived physical and chemical irritants. ICD from plants is commonly divided into mechanical irritant contact dermatitis (MICD) and chemical irritant contact dermatitis (CICD). The common mechanical plant irritants include thorns, spines, glochids, trichomes, and sharp-edged leaves. Many chemical irritants have yet to be elucidated, but known culprits include calcium oxalate, protoanemonin, isothiocyanates, bromelain, diterpene esters, alkaloids, and other chemical irritants such as naphthoquinone and acids. This review details the major plant contributors to MICD and CICD, along with their respective irritants. The clinical presentations seen in ICD (versus other plant dermatoses) will also be described, along with diagnostic considerations and exposure data. We also review mechanisms for the development of ICD and current treatments for ICD from plants.

Evidence-based therapy for cutaneous sarcoidosis.

Although healthcare providers have arrived at a relatively comfortable zone of accepted clinical practice in the management of cutaneous sarcoidosis, virtually every treatment is based on minimal evidence-based data and relies almost exclusively on anecdotal information. Although it would be convenient to blame this state of affairs on the lack of certainty about disease aetiology, the unavoidable fact is that little has been executed, even in the realm of well designed comparative trials. Nonetheless, worldwide accepted standard therapies for sarcoidosis include the administration of corticosteroids, antimalarials and methotrexate. A stepwise approach to patient care is appropriate, and potent topical corticosteroids (e.g. clobetasol) or repeated intralesional injections of triamcinolone (3-10 mg/mL) may be all that is needed in mild skin-limited disease. In patients requiring systemic therapy for recalcitrant or deforming skin lesions (or for widespread disease), corticosteroids (e.g. prednisone 40-80 mg/day, tapered accordingly) used alone or in combination with antimalarials or methotrexate may be indicated. Antimalarials and methotrexate are considered second-line interventions and may be used as monotherapy for steroid-resistant sarcoidosis or in patients unable to tolerate steroids. Given the concern regarding ocular toxicity, the maximum dosages of chloroquine and hydroxychloroquine should not exceed 3.5 and 6.5 mg/kg/day, respectively. Methotrexate is given in weekly doses of 10-30 mg, with the caveat that haematological, gastrointestinal, pulmonary and hepatic toxicities are possible. Despite universal acceptance as standard care, the aforementioned treatments often result in an incomplete clinical response or unacceptable adverse events. In such situations, more innovative treatment options may be used. Treatments that may well gain widespread future use include the tumour necrosis factor-alpha inhibitors infliximab and adalimumab. Experience is limited, but early reports are promising. Infliximab is administered via intravenous infusion at doses of 3-10 mg/kg at 0, 2 and 6 weeks and as indicated thereafter, whereas adalimumab is injected subcutaneously at doses of 40 mg either weekly or every 2 weeks. Because adalimumab is not approved for the management of sarcoidosis, the optimum dose administration interval is uncertain. However, it has been given in both weekly and every other week regimens. Isotretinoin, 0.5-2 mg/kg/day, has been used successfully in a handful of reported cases. However, the teratogenic potential of isotretinoin is often prohibitive considering that the primary demographic group likely to develop sarcoidosis is women of childbearing potential. Thalidomide at dosages of 50 to >400 mg/day has limited, albeit promising, supporting data. However, access is restricted in many countries because of a deserved pregnancy category X rating. Melatonin (20 mg/day) and allopurinol (100-300 mg/day) are not well studied in cutaneous sarcoidosis, and the clinical experience with tetracycline derivatives has been mixed. That said, there are compelling reports of therapeutic benefit with both doxycycline and minocycline. Because neither of these agents is associated with the severe toxicity of cytotoxic drugs, they may serve as effective therapy in some patients. Pentoxifylline (400 mg three times daily) has been of use in a small number of reported cases of pulmonary sarcoidosis, but there are no reports on its use in patients with primarily cutaneous disease. Both ciclosporin and chlorambucil have been largely abandoned given their associated toxicity and disappointingly unreliable efficacy. Finally, laser therapy is a newer modality that may provide patients with a quick and non-invasive treatment option for cutaneous sarcoidosis.

Abnormal expression of interleukin-23 in mycosis fungoides/Sézary syndrome lesions.

Progression of mycosis fungoides (MF) to Sézary syndrome (SS) is accompanied by a shift from a T(H)1 to a T(H)2 cytokine profile. Interleukin (IL)-23 is a novel cytokine that shares a common p40 subunit with the T(H)1 inducer, IL-12. IL-23 induces a third profile, T(H)IL-17, that is dominant in inflammation and autoimmunity. Although IL-23 induces an eczematous-like skin reaction in mice, and is expressed in T(H)1-mediated skin disorders such as psoriasis, it has not been evaluated in MF/SS. To study the role of IL-23 in MF/SS development, 40 MF/SS lesions of all stages were immunohistochemically analyzed with a novel anti-human IL-23 antibody raised against full-length human IL-23. IL-23 was detected with the catalyzed signal amplification system. The intensity and frequency of IL-23 staining were semi-quantitatively graded in both the dermal infiltrate and the epidermis. Increased expression of IL-23 was observed throughout the epidermal keratinocytes and in dermal lymphocytes compared to normal skin. IL-23 intensity did not differ significantly among the stages of MF/SS; however, in stage IVB patients, we observed lower frequency of IL-23 expression in dermal lymphocytes than in other stage patients [P = 0.13, analysis of variance (ANOVA)]. Interestingly, clusters of atypical lymphocytes, especially the epidermotropic tumor cells, demonstrated weak or absent IL-23 staining in 18 of 40 (45%) lesions. This finding was present in 4 of 5 (80%) of the stage IVB lesions and 7 of 11 (64%) of the lesions from Sézary patients. These findings indicate that abnormal IL-23 expression may play a role in the pathogenesis and progression of MF/SS.