These guidelines offer a rapid method to assess disease severity and to treat primary focal hyperhidrosis according to severity.

Recent advancements, including more versatile facial fillers, refined injection techniques and the adoption of a global facial approach, have contributed to improved patient outcome and increased patient satisfaction. Nine Canadian specialists (eight dermatologists, one plastic surgeon) collaborated to develop an overview on volume restoration and contouring based on published literature and their collective clinical experience. The specialists concurred that optimal results in volume restoration and contouring depend on correcting deficiencies at various layers of the facial envelope. This includes creating a foundation for deep structural support in the supraperiosteal or submuscular plane; volume repletion of subcutaneous fat compartments; and the reestablishment of dermal and subdermal support to minimize cutaneous rhytids, grooves and furrows. It was also agreed that volume restoration and contouring using a global facial approach is essential to create a natural, youthful appearance in facial aesthetics. A comprehensive non-surgical approach should therefore incorporate combining fillers such as high-viscosity, low-molecular-weight hyaluronic acid (LMWHA) for structural support and hyaluronic acid (HA) for lines, grooves and furrows with neuromodulators, lasers and energy devices.

A total of 238 patients with a clinical diagnosis of localized hyperhidrosis (HH) were treated on 332 anatomic sites (axillae, feet, hands, and groin). The purpose of the study was to evaluate the effectiveness of aluminum chloride hexahydrate (AC), in a salicylic acid gel base (SAGB) containing 4% salicylic acid (SA), for the treatment of localized HH. The SAGB was similar to a keratolytic gel, 1Keralyt® (Westwood Squibb). Because SAGB and anhydrous alcohol (AA), the standard vehicle for AC, have different consistencies, double blinding was not possible. Bromhidrosis (BH) was documented when present, whether of apocrine (axillae and groin) or eccrine (feet) origin. For the sake of uniformity, AC in SAGB was compounded by the same pharmacist. The concentration of AC varied from 10 to 40%, depending on the site to be treated. The improvement of HH was subjectively assessed through a questionnaire as follows: nil = no improvement; poor = <25%; fair = 25–50%; good = 50–75%; and excellent = >75%. Armpits: 20% AC was used to control axillary HH. When 20% AC failed to control HH, its concentration was gradually increased to 25% and, rarely, to 30%. When irritation occurred, the concentration of AC was decreased to 15 or 10%, and 1% hydrocortisone (HC) was added to the preparation. Patients were instructed to apply the medication initially 2–3 nights per week, gradually decreasing the frequency as required. When possible, only the active focal area of HH was treated. 2As with AC in AA, the medication was applied at bedtime. Patients were instructed to avoid rubbing and the application of the medication on recently shaved skin. Hands and feet: for these areas, the concentration of AC was 30% initially, but could be increased up to 40% if necessary. 3Application was daily at bedtime, and later at gradually longer intervals. Occlusion was never used.

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A 43-year-old woman with an unremarkable medical history was admitted with severe polyarthralgia, purpuric papules on her lower legs (Fig. 1), and recent pain with blue discoloration of her third left finger. She was faking no medication. At the time of presentation the abdominal examinafion was normal. Laboratory evaluation showed normal or negative values of BUN, creatinine, AST, WBC, Hb, VDRL, rheumatoid facfor, HBSAg, ANA, ASO, cryoglobulins, cryofibrinogen, anticardiolipins, anti-Sm, anti-RNP, anfi-Ro, anti-La, anfi-SCI70, and anfi-cenfromere. Hepatitis C titer was not obtained. Sedimentation rate was 61 mm/h and immune circulating complexes were present (14.2 |ig/ml; normal, <1.5 ng/ml). Urine sediment analysis revealed the presence of cellular, hyalin, granular, and erythrocytic casts. IgA level was 1.98 g/l (normal, 0.5-3.0 g/l). Skin biopsy showed extensive leucocytoclastic vasculitis. Deposits of IgA, IgM, and C3 were observed in the dermal vessels under direct immunofluorescence microscopy.