Seborrheic Dermatitis (SD) and dandruff are of a continuous spectrum of the same disease that affects the seborrheic areas of the body. Dandruff is restricted to the scalp, and involves itchy, flaking skin without visible inflammation. SD can affect the scalp as well as other seborrheic areas, and involves itchy and flaking or scaling skin, inflammation and pruritus. Various intrinsic and environmental factors, such as sebaceous secretions, skin surface fungal colonization, individual susceptibility, and interactions between these factors, all contribute to the pathogenesis of SD and dandruff. In this review, we summarize the current knowledge on SD and dandruff, including epidemiology, burden of disease, clinical presentations and diagnosis, treatment, genetic studies in humans and animal models, and predisposing factors. Genetic and biochemical studies and investigations in animal models provide further insight on the pathophysiology and strategies for better treatment.

Seborrhoeic Dermatitis (SD) is a very common chronic and/or relapsing inflammatory skin disorder whose pathophysiology remains poorly understood. Yeast of the genus Malassezia has long been regarded as a main predisposing factor, even though causal relationship has not been firmly established. Additional predisposing factors have been described, including sebaceous activity, host immunity (especially HIV infection), epidermal barrier integrity, skin microbiota, endocrine and neurologic factors, and environmental influences. Genetic studies in humans and mouse models—with particularly interesting insights from examining the Mpzl3 knockout mice and their SD‐like skin phenotype, and patients carrying a ZNF750 mutation—highlight defects in host immunity, epidermal barrier and sebaceous activity. After synthesizing key evidence from the literature, we propose that intrinsic host factors, such as changes in the amount or composition of sebum and/or defective epidermal barrier, rather than Malassezia, may form the basis of SD pathobiology. We argue that these intrinsic changes provide favourable conditions for the commensal Malassezia to over‐colonize and elicit host inflammatory response. Aberrant host immune activity or failure to clear skin microbes may bypass the initial epidermal or sebaceous abnormalities. We delineate specific future clinical investigations, complemented by studies in suitable SD animal models, that dissect the roles of different epidermal compartments and immune components as well as their crosstalk and interactions with the skin microbiota during the process of SD. This research perspective beyond the conventional Malassezia‐centric view of SD pathogenesis is expected to enable the development of better therapeutic interventions for the management of recurrent SD.

Seborrheic dermatitis (SD) is a chronic, recurring inflammatory skin disorder that manifests as erythematous macules or plaques with varying levels of scaling associated with pruritus. The condition typically occurs as an inflammatory response to Malassezia species and tends to occur on seborrheic areas, such as the scalp, face, chest, back, axilla, and groin areas. SD treatment focuses on clearing signs of the disease; ameliorating associated symptoms, such as pruritus; and maintaining remission with long-term therapy. Since the primary underlying pathogenic mechanisms comprise Malassezia proliferation and inflammation, the most commonly used treatment is topical antifungal and anti-inflammatory agents. Other broadly used therapies include lithium gluconate/succinate, coal tar, salicylic acid, selenium sulfide, sodium sulfacetamide, glycerin, benzoyl peroxide, aloe vera, mud treatment, phototherapy, among others. Alternative therapies have also been reported, such as tea tree oil, Quassia amara, and Solanum chrysotrichum. Systemic therapy is reserved only for widespread lesions or in cases that are refractory to topical treatment. Thus, in this comprehensive review, we summarize the current knowledge on SD treatment and attempt to provide appropriate directions for future cases that dermatologists may face.

Wound management involves repeated clinical trips and procedures of lab tests over days. To eliminate this time lag and provide real-time monitoring of a wound's progress, we have designed an enzymatic biosensor for determining uric acid (UA) in wound fluid. Uric Acid is a biomarker, having an established correlation with wounds and their healing. This electrochemical biosensor comprises enzyme urate oxidase (uricase, UOx) entrapped in a polyvinyl alcohol based cationic polymer for enhanced stability. Results show that the use of a redox electron shuttle, ferrocene carboxylic acid (FCA), enabled electron transfer between the enzyme and the transducer. The immobilized uricase in the polymer matrix provided stable continuous measurements at body temperature for a week with minimal deviation. Detection of uric acid in wound fluid has been determined from volumes as low as 0.5-50μL. Studies from different wound samples have shown an average recovery of 107%. The sensor has been interfaced with LMP91000 potentiostat and controlled by CC2650 microcontroller on a Kapton tape-based miniaturized flexible platform.

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Pyoderma Gangrenosum (PG) is an inflammatory neutrophilic dermatosis (ND) associated with underlying chronic inflammation and/or malignancy. Diagnosis remains to be challenging as a gold standard diagnostic test is lacking. Initial manifestations may include papules, vesicles, or pustules that subsequently develop into ulceration with features of undermining and violaceous borders. Timely recognition of pyoderma gangrenosum is impeded by clinical findings shared with other etiologies, such as granulomatosis with polyangiitis, polyarteritis nodosa, and antiphospholipid syndrome. As with any other ND, extracutaneous involvement may also occur preceding, during, or following the appearance of skin lesions. Sterile neutrophilic infiltrates have been found to affect internal organs supporting the concept of PG being a systemic disease, with lung being the most common extracutaneous manifestation followed by ocular and visceral compromise. Therefore, in this review, we describe the current knowledge of extracutaneous involvement of PG and its respective clinical manifestations to aid dermatologists in diagnosis, management, and determining prognosis.

Background: Various facial and extrafacial lesions have been reported in frontal fibrosing alopecia (FFA). Facial papules have been associated with worse prognosis. Objectives: We sought to detect the prevalence of facial and extrafacial lesions and to analyze their relation to demographic and clinical variables in a large and ethnically diverse series of patients with FFA. Methods: Charts of patients diagnosed with FFA between January 1, 2015, and December 31, 2017, at the Department of Dermatology, University of Miami, were reviewed retrospectively. Results: 91 patients (87 women and 4 men) met inclusion criteria: 45% (n = 41) were of Hispanic/Latino ethnicity, and 34% (n = 30) were premenopausal. Facial papules were most commonly detected (41% among Hispanic/Latino patients). Significant associations were found between: (1) Hispanic/Latino ethnicity and any FFA-associated facial lesions, facial papules alone, or lichen planus pigmentosus alone, as well as premenopausal status; (2) any FFA-associated facial lesions or facial papules alone and premenopausal status; and (3) Hispanic/Latino ethnicity and simultaneous presence of facial and extrafacial lesions. Conclusions: There is a significant association among Hispanic/Latino ethnicity, facial papules, and premenopausal status, which may portend a susceptibility to severer disease and prompt early and aggressive treatment in this group.