Although soft-tissue fillers are a popular choice for minimally invasive rejuvenation of the face, physicians should be aware of the serious potential adverse effects, recognize their presentations, and have appropriate treatments readily available.

TNF-α, a proinflammatory cytokine central to many autoimmune diseases, has been implicated in the depigmentation process in vitiligo. We reviewed its role in vitiligo by exploring its pro- and anti-inflammatory properties and examined the effects of blocking its actions with TNF-α antagonist therapeutics in reports available in the literature. We found that TNF-α inhibition halts disease progression in patients with progressive vitiligo but that, paradoxically, treatment can be associated with de novo vitiligo development in some patients when used to treat other autoimmune conditions, particularly when using adalimumab and infliximab. These studies reinforce the importance of stating appropriate outcomes measures as most pilot trials proposed to measure repigmentation, whereas halting depigmentation was commonly overlooked as a measure of success. We conclude that TNF inhibition was useful for patients with progressive vitiligo, where TNF-α inhibition is able to quash cytotoxic T cell-mediated melanocyte destruction. However, a lingering concern for initiating de novo disease will likely prevent a more widespread application of TNF inhibitors to treat vitiligo.

SUMMARY Inducible HSP70 (HSP70i) chaperones peptides from stressed cells, protecting them from apoptosis. Upon extracellular release, HSP70i serves an adjuvant function, enhancing immune responses to bound peptides. We questioned whether HSP70i differentially protects control and vitiligo melanocytes from stress and subsequent immune responses. We compared expression of HSP70i in skin samples, evaluated the viability of primary vitiligo and control melanocytes exposed to bleaching phenols, and measured secreted HSP70i. We determined whether HSP70i traffics to melanosomes to contact immunogenic proteins by cell fractionation, western blotting, electron microscopy and confocal microscopy. Viability of vitiligo and control melanocytes was equally affected under stress. However, vitiligo melanocytes secreted increased amounts of HSP70i in response to MBEH, corroborating with aberrant HSP70i expression in patient skin. Intracellular HSP70i colocalized with melanosomes, and more so in response to MBEH in vitiligo melanocytes. Thus whereas either agent is cytotoxic to melanocytes, MBEH preferentially induces immune responses to melanocytes.

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Cutaneous mastocytosis appears to occur sporadically; however, familial inheritance has been reported in 50 families since the mid-1880s. We report four cases of telangiectasia macularis eruptiva perstans (TMEP) occurring in three generations of a family. Whereas most patients with TMEP manifest in adulthood, all of the members of this family developed initial lesions during childhood. This is the third documented instance of familial mastocytosis affecting members of three generations, and the first report of familial TMEP. Although the inheritance pattern is unknown, the presentation of disease in this family further supports the hypothesis of an autosomal dominant mode of transmission with incomplete penetrance.

Glabella and forehead lines can be effectively and safely reduced with neurotoxin alone as well as neurotoxin in combination with fillers. Combination treatment may provide a slightly better cumulative benefit and also increase the persistence of effect.

complete remission and no adverse events were observed. However, 5 patients experienced grade 3 or 4 adverse events (1 patient had sepsis; 2, diabetes; 1, hypertension; and 2, endocrine disorders) between the initial cycle and the first rituximab maintenance infusion. At their last follow-up visit (median [range], 78 [42-147] months after the first cycle of rituximab), all 11 patients remained in complete remission, with 10 patients having discontinued rituximab maintenance therapy. Serum anti-desmoglein 1 and 3 antibody levels, which had been high before rituximab treatment, decreased markedly and remained below 14 U/mL during rituximab maintenance therapy (Table 2). Discussion | The results of this case series indicated that rituximab can be used as single maintenance therapy, without a systemic corticosteroid, with good efficacy and tolerance in patients having severe pemphigus requiring long-term therapy for prevention of relapse. This study supplements a previous one showing the efficacy of rituximab alone in the treatment of relapse to pemphigus initially controlled with a combination of rituximab and corticosteroid. 6 We found that treatment with rituximab alone, even at a low dose, not only prevented relapse but also maintained complete remission with a better benefit to risk ratio than treatment with corticosteroids. The maintenance therapy was shown to be effective for preventing relapse despite shortcomings inherent in retrospective studies (eg, heterogeneity of patient pemphigus history and variable length of rituximab maintenance therapy), highlighting the feasibility of such an approach. A progressive decrease in serum anti-desmoglein autoantibody levels to less than 14 U/mL occurred in all cases along with clinical complete remission even after maintenance therapy cessation. Practical questions remain about the rituximab treatment regimen, including the optimal dose (500 mg or 1 g), frequency of administration (every 6 months or 1 year), and immunologic criteria enabling treatment withdrawal (negative direct immunofluorescence results or low serum autoantibody levels), and the cost-effectiveness of this maintenance therapy in patients with pemphigus. The criteria we used to discontinue rituximab maintenance therapy were persistent complete clinical remission and serum anti-desmoglein 1 and 3 autoantibody levels less than 14 U/mL for at least 1 year. Further prospective studies are warranted to identify patients for treatment with maintenance rituximab therapy and to optimize long-term management of difficult-to-treat pemphigus.