skin infections

Efficacy of a Topical Lotion Containing Lactoferricin, Glycerophosphoinositol Lysine and Verbascoside for External Otitis Due to Atopic Dermatitis

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The prevalence of atopic dermatitis (AD) in the general dog population is 3-15% it represents the diagnosis for up to 58% of dogs affected with skin disease. Canine AD has been defined by Halliwell in 2006, as a “genetically predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features, associated with IgE antibodies most commonly directed against environmental allergens”. Indeed, genetic factors and familiar predisposition to the disease have been found to play a major role in its pathogenesis, although the full pathogenesis is still unknown. It is certain that the immunological aberration is usually associated with skin barrier dysfunctions; pro-inflammatory cytokines, neuronal itch stimuli and the animal’s pruritic behaviours establish a vicious cycle of itch that perpetuates and potentially exacerbates the skin lesions and defects in the skin barrier function. The initial clinical feature of canine AD is pruritus, which at the beginning may be associated with no lesion or with primary skin lesions such as erythema and occasionally papules. The mediators that elicit the sensation of pruritus have not been elucidated, but histamine does not appear to be a mediator in dogs in contrast to humans and mice. It is usually a life-long pathology which can be controlled, but it can be seldom cured. The diagnosis of canine AD does not require any analytical test, such as IgE determination and/or intradermal skin test, and it can be done on the basis of pruritus associated with skin lesions. The skin lesions are usually associated with the detachment of corneocytes from live skin. Furthermore, the skin lesions are usually associated with the cytological presence and overgrowth of bacteria (mainly Staphylococcus) and fungal or yeast (mainly Malassezia Pachydermatis) in the damaged region, and it has been purpose that this overgrowth could be also responsible for most of the symptoms. Due to the skin infection, canine AD often develops otitis externa and usually, the signs of atopic otitis were noticed by the owners before the other signs of AD.

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2-Octyl Cyanoacrylate Skin Adhesive

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Surgical adhesives have become more prevalent in the Emergency Department (ED) to close #skin lacerations due to their ease of use, more complete surface contact and microbial barrier properties. They also have unique advantages over traditional suturing in the ED. This includes the ease of closure, the speed of closure, decreased or elimination of the need for topical or injectable anaesthetics, and reducing the need for specific aftercare including suture removal. Prior research has found that liquid skin adhesives for laceration closure are less painful and produce similar cosmetic effects when compared to sutures. While skin adhesives offer advantages opportunities for improvement exist. Ease of application is an important characteristic. The viscosity of the adhesive may cause problems if too low, flowing into sensitive areas including eyes and mucous membranes. If too high it may not adequately cover the wound or create a raised area that patients may find irritating, particularly children who may scratch at these raised areas which can increase the risk of infection.

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L 17 Cytokine in Psoriasis

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Psoriasis which was considered a disease of abnormal epidermal keratinocyte proliferation later was identified as T helper-1 (Th1) disease because an increase in Th1 pathway cytokines was observed in the lesions and in serum. Currently, a new paradigm has emerged where Th17 cells which produce IL-17 and IL-22, play a central role in the pathogenesis of psoriasis. The differentiation factors (TGF-beta, IL-6, IL-21), the growth and stabilization factor (IL-23), and the intracellular transcription factors (STAT3, RORγt, and RORalpha) are involved in the development of Th17 cells. IL-17A, part of a group of cytokines, called the IL-17 family plays a critical role in the pathogenesis of psoriasis. IL-17A enhances the expression of S100 proteins, chemokines CCL20, CXCL1, CXCL3, CXCL5, CXCL6, and CXCL8, and VEGF in keratinocytes leading to aberrant cell differentiation, proliferation, and immune activation. IL-17A has pleiotropic effects, but its main effect is recruitment and activation of neutrophils, angiogenesis and tissue remodelling by stimulating the production of angiogenic factors and matrix metalloproteases.

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Radiation dermatitis

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Irritant contact dermatitis accounts for 80% of all contact dermatitis reactions. It occurs when the skin comes in contact with a substance that acts as an irritant. Even though over 2800 substances have been identified as irritants, almost any substance under the right circumstances can act as an irritant.

Skin Barrier in Irritant Contact Dermatitis
The epidermis acts as a barrier with an outer layer composed of dead cells in a water-protein-lipid matrix.

Acute Irritant Contact Dermatitis
Acute irritant contact dermatitis occurs when the skin comes in contact with a strong toxic chemical such as an acid or alkali. The rash occurs within minutes to hours after exposure and in most cases, healing occurs soon after exposure. This rash usually has sharp borders and consists of redness, vesicles, bullae, or skin sloughing.

  • Picture of irritant contact dermatitis on the foot

Chronic Cumulative Irritant Contact Dermatitis
Chronic cumulative irritant contact dermatitis is the more common of the two. This dermatitis occurs after repeated exposure to low-level irritants, such as soaps or shampoos. The rash may take weeks, months, or even years to develop.

The rash usually has poorly-defined borders, is very itchy, and consists of redness, scaling, fissuring, and lichenification.

  • Picture of irritant contact dermatitis on the hand

Treatment of Irritant Contact Dermatitis
The mainstay of treatment for irritant contact dermatitis is avoiding as many of the irritants as possible.

Other helpful measures include:

  • Reduce water exposure – because frequent water exposure actually dries out the skin and disrupts the barrier function of the epidermis, keep water contact to a minimum.
  • Moisturize – Frequent moisturization improves the barrier function of the skin. Avoid the use of moisturizers with perfumes since these may also act as an irritant.
  • Protection – Because the hands are often affected by irritant contact dermatitis, the use of gloves may help reduce exposure to the irritant.
  • Topical steroids – Medium- to high-strength topical steroids may be needed to reduce inflammation and itching.

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