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DPN is not a premalignant condition nor is it associated with any underlying systemic disease. DPN lesions show no tendency to regress spontaneously, and often increase in size and number as an individual ages.
DPN lesions are benign and no treatment generally is indicated unless lesions are cosmetically undesirable. Surgical options including curettage, cryotherapy and laser therapy are options Scarring, postoperative skin discoloration or keloid formation are potential complication. Therefore, conservative dpn treatment is advisable.
Visual diagnosis is made by the "stuck on" appearance, horny pearls or cysts embedded in the structure. Darkly pigmented lesions can be challenging to distinguish from nodular melanomas. Furthermore, thin seborrheic keratoses on facial skin can be very difficult to differentiate from lentigo maligna even with dermatoscopy. Clinically, epidermal nevi are similar to seborrheic keratoses in appearance. Epidermal nevi are usually present at or near birth. Condylomas and warts can clinically resemble seborrheic keratoses, and dermatoscopy can be helpful. On the penis and genital skin, condylomas and seborrheic keratoses can be difficult to differentiate, even on biopsy.
To date, the gold standard in the diagnosis of seborrheic keratosis is represented by the histolopathologic analysis of a skin biopsy.
Grover's may be suspected by its appearance, but since it has such a characteristic appearance under the microscope a shave skin or punch biopsy is often performed.
Usually, a common form of treatment for the condition is a type of hand cream which moisturises the hard skin. However, currently the condition is incurable.
No treatment of seborrheic keratoses is necessary, except for aesthetic reasons. Since a slightly increased risk of localized infection caused by picking at the lesion has been described, if a lesion becomes itchy or irritated by clothing or jewelry, a surgical excision is generally recommended.
Small lesions can be treated with light electrocautery. Larger lesions can be treated with electrodesiccation and curettage, shave excision, or cryosurgery. When correctly performed, removal of seborrheic keratoses will not cause much visible scarring except in persons with dark skin tones.
Morbidity and mortality range from both extremes as the significance correlate with the underlying systemic disease.
There seems to be beneficial responses to clindamycin therapy as the lesions regress. This leads to the hypothesis that microorganisms may be playing a role in the initial stages of Kyrle disease.
A family with Kyrle disease were examined which their skin lesions were benign. However, when three of the young adult members were closely examined, they had posterior subcapsular cataracts and two of those three developed multiple tiny yellow-brown anterior stromal corneal opacities. In order to determine if there is any correlation between Kyrle disease and the ocular observations, more cases of Kyrle disease are to be analyzed.
All in all, since Kyrle disease is relatively rare, more cases need to be studied and analyzed in order to understand the underlying pathogenesis and to improve the management of the disease.
Pemphigus is a group of autoimmune blistering diseases that may be classified into the following types:
Sweating causes lesions to form, but lesions aggravated by sweat usually return to "normal" fairly quicklyavoiding sweat is not a reason to avoid exercise. Minor outbreaks can be controlled with prescription strength topical cortisone creams. More severe eruptions usually clear up after treatment for one to three months with Accutane or tetracycline. If these fail or the outbreak is severe, PUVA phototherapy treatments, antifungal pills and cortisone injections are alternatives.
Some research has suggested a correlation of Grover's disease with mercury toxicity in which case Dimercaptosuccinic acid might help.
Treatment is predominantly preventive. Avoidance of topical phenols and diets low in tyrosine may help. Replacement and repair of damaged tissue is also possible.
Hydroquinone-induced exogenous ochronosis is an avoidable dermatosis that is exceedingly difficult to treat.
However, some studies show that treatment may be possible with a Q-switched alexandrite (755 nm) laser.
It is recommended that individuals with this disorder stop using hydroquinone-containing compounds. It is important to be aware of this as dermatologists may think the symptoms a patient is exhibiting are a melasma, and prescribe a hydroquinone-containing cream.
It is self limiting condition
1.reassurence
2.steriod cream for local application
3.moisterizer lotion
This forms a major and critical part in the disease treatment and the shampoo treatment can need to be applied as often as 3 to 4 times per week. An antiseborrheic shampoo removes the scale blocking theolr follicles. The mineral oil soak, whereby the oil remains on the affected animal for at least 2 hours, is needed to replace epidemal lipids as well as to restore normal epidermal barrier function. The oil is then removed through the process of many baths. This oil treatment needs to be repeated at least once a week for 4 to 7 weeks until new hair growth is observed. Once new hair growth is observed, topical treatment can be decreased to every 2 to 4 weeks.
Immunosuppressant and anti-inflammatory therapy serves to stop on-going destruction of the sebaceous glands. Like other inflammatory diseases, most animals receive an initial course to stop the inflammation and treatment is tapered off to the lowest dose that keeps the disease in remission. Oral cyclosporine may be used. Corticosteroids (e.g. prednisone) are used only if pruritus is a major clinical feature.
Erythema dyschromicum perstans (EDP) (also known as ashy dermatosis, and dermatosis cinecienta) is an uncommon skin condition with peak age of onset being young adults, but it may also be seen in children or adults of any age. EDP is characterized by hyperpigmented macules that are ash-grey in color and may vary in size and shape. While agents such as certain medications, radiographic contrast, pesticides, infection with parasites, and HIV have been implicated in the occurrence of this disease, the cause of this skin disease remains unknown.
EDP initially presents as grey or blue-brown circumferential or irregularly shaped macules or patches that appear. While the lesions of EDP are generally non-elevated, they may initially have a slight raised red margin as they first begin to appear. These lesions usually arise in a symmetric distribution and involve the trunk, but also commonly spread to the face and extremities. EDP does not usually have symptoms beside the macules and patches of discolored skin; however, some itching in these areas may occur.
Because EDP is an uncommon disease of the skin, it is important to consider other skin diseases that may resemble erythema dyschromicum perstans, such as infectious diseases (i.e. leprosy or pinta), reaction to drugs, post inflammatory hyperpigmentation, or lichen planus pigmentosus.
There is no cure for EDP. While multiple various topical and systemic therapies have been tried, none have been consistently successful. In children, spontaneous resolution of EDP over the course of months to years is possible; however, this outcome is less likely if EDP presents in adulthood.
Pemphigus defines a group of autoimmune interepithelial blistering diseases that are characterized by loss of normal cell-cell adhesion (acantholysis), and by the presence of pathogenic (predominantly IgG) autoantibodies reacting against epithelial adhesion molecules. Pemphigus is further divided in two major subtypes: pemphigus vulgaris (PV) and pemphigus foliaceus (PF). However, several other disorders such as IgA pemphigus, IgE pemphigus, pemphigus herpetiformis, drug induced pemphigus, Senear Usher syndrome and endemic pemphigus foliaceus exist;recognized by a dermatologist from the appearance and distribution of the skin lesions. It is also commonly diagnosed by specialists practicing otolaryngology- head and neck surgery, periodontists, oral and maxillofacial surgeons and eye doctors, as lesions can affect the eyes and mucous membrane of the oral cavity. Intraorally it resembles the more common diseases lichen planus and mucous membrane pemphigoid. Definitive diagnosis requires examination of a skin or mucous membrane biopsy by a dermatopathologist or oral pathologist. The skin biopsy is taken from the edge of a blister, prepared for histopathology and examined with a microscope. The pathologist looks for an intraepidermal vesicle caused by the breaking apart of epidermal cells (acantholysis). Thus, the superficial (upper) portion of the epidermis sloughs off, leaving the bottom layer of cells on the "floor" of the blister. This bottom layer of cells is said to have a "tombstone appearance".
Definitive diagnosis also requires the demonstration of anti-desmoglein autoantibodies by direct immunofluorescence on the skin biopsy. These antibodies appear as IgG deposits along the desmosomes between epidermal cells, a pattern reminiscent of chicken wire. Anti-desmoglein antibodies can also be detected in a blood sample using the ELISA technique.
There is no standard treatment for PLC. Treatments may include ultraviolet phototherapy, topical steroids, sun exposure, oral antibiotics, corticosteroid creams and ointments to treat rash and itching.
One study identified the enzyme bromelain as an effective therapeutic option for PLC.
Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.
The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.
The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.
The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.
Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.
Diagnosis of tinea nigra causing fungus is made on microscopic examination of skin scrapings, mixed with potassium hydroxide (KOH). The KOH the nonfungal debris.
There are a wide range of depigmenting treatments used for hyperpigmentation conditions, and responses to most are variable.
Most often treatment of hyperpigmentation caused by melanin overproduction (such as melasma, acne scarring, liver spots) includes the use of topical depigmenting agents, which vary in their efficacy and safety, as well as in prescription rules. Several are prescription only in the US, especially in high doses, such as hydroquinone, azelaic acid, and koijic acid. Some are available without prescription, such as niacinamide, or cysteamine hydrochloride. Hydroquinone was the most commonly prescribed hyperpigmentation treatment before the long-term safety concerns were raised, and the use of it became more regulated in several countries and discouraged in general by WHO. For the US only 2% is at present sold over-the-counter, and 4% needs prescription. In the EU hydroquinone was banned from cosmetic applications. Treatments that do not involve topical agents are also available, including fraction lasers and dermabrasion.
Epidermolytic palmoplantar keratoderma has been associated with keratin 9 and keratin 16.
Nonepidermolytic palmoplantar keratoderma has been associated with keratin 1 and keratin 16.
Warty dyskeratoma, also known as an Isolated dyskeratosis follicularis, is a benign epidermal proliferation with distinctive histologic findings that may mimic invasive squamous cell carcinoma and commonly manifests as an umbilicated (Having a central mark or depression resembling a navel) lesion with a keratotic plug, WD have some histopathologic similarities to viral warts but it's not caused by HPV and the majority of these lesions display overall histopathologic features consistent with a follicular adnexal neoplasm. usually limited to the head, neck, scalp or face and vulva. Lesions are generally and sporadic and may be associated with a follicular unit. Oral involvement, particularly the hard palate, and genital involvement have been reported. it can also be thought of as one of the manifestations of focal acantholytic dyskeratosis, an epidermal reaction pattern that can be seen in several disorders, including Darier's disease and Grover's disease. But the main Difference between Darier disease and Warty dyskeratoma, is that Darier disease inherited dermatosis (autosomal dominant) consisting of multiple keratotic papules on the face, trunk, and extremities, while WD occurs as an isolated, noninherited, single keratotic nodule mainly confined to the head and neck as mentioned earlier.
Vaccinating girls with HPV vaccine before their initial sexual contact has been claimed to reduce incidence of VIN.
Warty dyskeratoma must be differentiated from vulvar dysplasia, Bowenoid papulosis, squamous carcinoma, condyloma, and other viral-induced squamous lesions.