Jennifer Clay Cather

Update on botulinum toxin for facial aesthetics

The use of botulinum toxin has revolutionized the treatment of facial lines with an incomparable safety record over the past 14 years. The most common used injection sites are shown in Fig. 9. With the recent FDA approval for Botox in the treatment of glabellar lines, its use will likely increase dramatically. It is essential that practitioners have a detailed and specific knowledge of the facial and neck musculature to be injected to minimize untoward side effects, especially in the early days of new users learning curve. The specifics of the dilutions and units per amount used for the various different commercial forms of botulinum toxin types A and B need to be understood fully and standardized together with the potential for antigenicity with the higher protein load of type B. In addition, specific indications for the use of botulinum toxin as adjunctive therapy for specific facial surgical procedures (i.e., blepharoplasty, surgical brow lift, and laser resurfacing) will become better understood. [figure: see text] Finally, even though the anatomy of the facial musculature is well described, individual differences in men and women, in different population groups, and in tissue qualities, such as turgor and elasticity [87], are important factors to be considered before undertaking botulinum toxin injections. It is likely that the use of specific measuring devices, such as digital imaging, will further help define the use of botulinum toxin for different muscle groups and facial aesthetic indications.

Use of biologic agents in combination with other therapies for the treatment of psoriasis.

Psoriasis is a chronic inflammatory skin disorder, which is associated with a significant negative impact on a patient’s quality of life. Traditional therapies for psoriasis are often not able to meet desired treatment goals, and high-dose and/or long-term use is associated with toxicities that can result in end-organ damage. An improved understanding of the involvement of cytokines in the etiology of psoriasis has led to the development of biologic agents targeting tumor necrosis factor (TNF)-α and interleukins (ILs)-12/23. While biologic agents have improved treatment outcomes, they are not effective in all individuals with psoriasis. The combination of biologic agents with traditional therapies may provide improved therapeutic options for patients who inadequately respond to a single drug or when efficacy may be increased with supplementation of another treatment. In addition, combination therapy may reduce safety concerns and cumulative toxicity, as lower doses of individual agents may be efficacious when used together. This article reviews the current evidence available on the efficacy and safety of combining biologic agents with systemic therapies (methotrexate, cyclosporine, or retinoids) or with phototherapy, and the combination of biologic agents themselves. Guidance is provided to help physicians identify situations and the characteristics of patients who would benefit from combination therapy with a biologic agent. Finally, the potential clinical impact of biologic therapies in development (e.g., those targeting IL-17A, IL-17RA, or IL-23 alone) is analyzed.

Efficacy of Secukinumab on Moderate-to-severe Plaque Psoriasis Affecting Different Body Regions: a Pooled Analysis of Four Phase 3 Studies

IntroductionThe impact of psoriasis varies with the body region affected. In addition, patients have different perceptions of disease improvement and treatment satisfaction based on the location of skin clearance with treatment. The monoclonal antibody secukinumab selectively targets interleukin-17A—a central cytokine of psoriasis—and provides rapid and sustained clearance for moderate-to-severe psoriasis affecting all body regions. The objective of this study was to evaluate the efficacy of secukinumab on moderate-to-severe psoriasis affecting the trunk, upper limbs, and lower limbs.MethodsData were pooled from four phase 3 studies. To be included in the analysis for each body region, patients were required to have a Psoriasis Area and Severity Index (PASI) score ≥12 for that body region and psoriasis covering ≥10% of the surface area of that region. Secukinumab was administered at Baseline, Weeks 1, 2 and 3, and then every 4xa0weeks from Week 4 to 48.ResultsAcross the trunk, upper limbs, and lower limbs, initial PASI subscore responses were sustained to Week 52. At Week 52, trunk (T) PASI 90/100 responses were achieved by 78.4%/71.1% of patients receiving secukinumab 300xa0mg, respectively, and by 66.3%/56.9% of patients receiving secukinumab 150xa0mg, respectively. At Week 52, upper limb (UL) PASI 90/100 responses were achieved by 67.3%/59.1% of patients receiving secukinumab 300xa0mg, respectively, and by 50.3%/43.3% of patients receiving secukinumab 150xa0mg, respectively. At Week 52, lower limb (LL) PASI 90/100 responses were achieved by 63.9%/55.3% of patients receiving secukinumab 300xa0mg, respectively, and by 45.1%/36.4% of patients receiving secukinumab 150xa0mg, respectively. A 50% reduction in mean PASI subscore occurred after 2.8, 2.9, and 3.4xa0weeks with secukinumab 300xa0mg on the trunk, upper limbs, and lower limbs, respectively.ConclusionSecukinumab provided robust and sustained efficacy for moderate-to-severe psoriasis affecting the trunk, upper limbs, and lower limbs.FundingNovartis Pharmaceuticals Corporation.Trial registrationClinicalTrials.gov identifiers: NCT01365455, NCT01358578, NCT01555125, and NCT01636687.

Hyperpigmented macules and streaks

Phytophotodermatitis is an ultraviolet-induced contact dermatitis due primarily to plant- (= phyto), fruit-, or vegetable-derived photosensitizing compounds such as furocoumarins (psoralens). Two prerequisites must be filled for phytophotodermatitis to occur: 1) the skin must have had contact with a sensitizing phototoxin (allergen), and 2) there must be subsequent exposure to ultraviolet radiation (1). Psoralens may be transferred directly when leaves, rinds, or juice come into contact with the skin or indirectly through person-to-person contact. The majority of these phototoxins are activated by ultraviolet light in the long-wave or ultraviolet A (UVA) spectrum (320–400 nm) (2). n nFigures u200bFigures11 and u200b22 are examples of “margarita photodermatitis” in 2 different patients (1). While sunbathing at the beach and preparing margaritas, our patients squeezed limes, which left juice on their skin. Juice on the hands is easily spread or even dripped onto distant sites or other people. Lime juice contains furocoumarin, a lipid-soluble 8-methoxypsoralen. After sunbathing (a potent source of UVA), the 8-methoxypsoralen covalently binds to keratinocyte DNA (forming cyclobutane dimers), producing irreversibly damaged DNA (3). n n n nFigure 1 n nBizarre streaks and linear erythematous vesicular plaques with hyper- pigmentation on the abdomen. n n n n n nFigure 2 n nLinear erythematous vesicular plaques with hyperpigmentation on the arm.

Violaceous-rimmed ulcers.

A 40-year-old man presented with a violaceous-rimmed ulceration on his inner thigh. He complained of crusting and drainage, but the lesion was otherwise asymptomatic. It began as a pimple, expanded into a small erosion, and then progressed to an ulceration (Figure). Medications at the time of presentation included prednisone and delayed-release mesalamine. n n n nFigure n nViolaceous-rimmed ulceration on the inner thigh. n n n nWhat is the diagnosis? What are the therapy options? n nDIAGNOSIS: Pyoderma gangrenosum (PG) associated with Crohns disease.

Hair loss and plaquelike skin lesions.

A healthy 35-year-old African American woman presented for evaluation of hair loss (Figure u200b(Figure11). Examination of her scalp revealed areas of alopecia with absent hair follicles, erythematous papules, and a few pustules, consistent with a scarring (cicatricial) form of alopecia. Additionally, there were hypopigmented lesions on her arms (Figure u200b(Figure22) and targetoid plaquelike lesions on her legs (Figure u200b(Figure33). n n n nFigure 1 n nPosterior scalp with areas of scarring alopecia and erythematous papules and plaques n n n n n nFigure 2 n nHypopigmented macules on the arm. n n n n n nFigure 3 n nLower legs with targetoid plaques. n n n nWhat is your diagnosis? n nDIAGNOSIS: Sarcoidosis.

Purplish, pruritic papules on the limbs

A 46-year-old white man presented with an acute 3- to 4-week history of an intensely pruritic eruption that mainly involved the limbs. Individual lesions appeared to predominate around the wrist flexures. Examination revealed multiple, flat, purplish lesions, 5 to 15 mm in diameter, with coalescence in areas of scratching (Figure u200b(Figure11). Whitish plaques were seen on the oral mucous membrane (Figure u200b(Figure22). The patient was otherwise well, although on further questioning he stated that he felt less energetic than usual. He reported no recent illness or medication ingestion. n n n nFigure 1 n nPurplish, flat-topped papules on the wrist; a few are in a linear arrangement. n n n n n nFigure 2 n nA white reticulated pattern can be seen inside the right cheek; lesions cannot be removed with a tongue blade. n n n nWhat is the diagnosis, and what further laboratory tests are indicated? n nDIAGNOSIS: Lichen planus.

Diffuse eruption of pigmented papules

A 33-year-old African American woman presented for evaluation of an itchy eruption of approximately 6 months duration that began on the hand dorsa before spreading to the arms, ears, and knees. Initial examination revealed clusters of pigmented, 1-mm papules on the hand dorsa, especially the knuckles, and on the distal forearms. Multiple lesions were present in areas of scratching (Koebners phenomenon), producing a linear pattern. After the initial evaluation, these lesions continued to spread and involved the forehead (Figure u200b(Figure11), the back of neck (Figure u200b(Figure22), and the distal extremities (Figure u200b(Figure33). On further questioning, the patient stated that she had suffered a flulike illness 2 months previously and that her muscles felt sore, particularly in her arms and legs. n n n nFigure 1 n nClusters of pigmented papules on the forehead. n n n n n nFigure 2 n nMultiple pigmented papules on the back of the neck. n n n n n nFigure 3 n nPigmented papules with a linear distribution. n n n nWhat is your diagnosis? n nDIAGNOSIS: Papular mucinosis (scleromyxedema).

Painful nodule with induration and spreading erythema

A young woman presented with a 2-day history of a 2-to 3cm erythematous painful papule on her right flank, which she thought was a spider bite. Initially, the lesion was a nodule that was warm, tender, and fluctuant on palpation. Clinically the lesion was most consistent with an abscess, spider bite, or inflamed cyst. The lesion was incised, drained, and cultured. Empiric therapy with cephalexin was started. Within 24 hours, the patient presented to the dermatology clinic with a low-grade fever (38.3°C, 101°F), and the lesion had become more tender. The erythema had spread to 20 cm, and the central induration had spread to 9 cm (Figure).

Pruritic eruption on the chest, arms, and buttocks

An otherwise healthy middle-aged white man presented with a long-standing, extremely pruritic eruption on his chest, arms, and buttocks. Previous therapies, including multiple topical steroids, systemic antihistamines, and an occasional course of oral steroids, had provided limited relief. Examination revealed erythematous and urticarial papules and discrete small bullae and vesicles (Figure u200b(Figure11). Closer examination revealed numerous crusted lesions along with the vesicles (Figure u200b(Figure22). A skin biopsy taken from the edge of a small vesicle is shown in Figure u200bFigure33. n n n nFigure 1 n nErythematous papules, vesicles, and tense bullae on the chest of a middle-aged man. n n n n n nFigure 2 n nFew intact vesicles and excoriated lesions with crusting are seen on the elbows. n n n n n nFigure 3 n nSkin biopsy of a vesicle reveals a subepidermal split with a collection of neutrophils in the suprapapillary dermis (hematoxylin-eosin). n n n nWhat is the diagnosis? n nDIAGNOSIS: Dermatitis herpetiformis (Duhrings disease).