Psoriasis is an enduring autoimmune disease characterized by abnormal skin patches. These skin patches are usually red, itchy, and scaly. Psoriasis varies in severity from small, local patches to complete body coverage. An injury to the skin can trigger the skin changes of psoriasis in that place, known as Koebner phenomenon.
There are five main types of psoriasis: plaque, guttate, inverse, pustular, and erythrodermic. Psoriasis plaque, also known as psoriasis vulgaris, forms about 90 percent of cases. It usually comes as a red patch with white scales on top. The most commonly affected areas of the body are the back of the forearms, shin, navel area, and scalp. Guttate psoriasis has a drop-shaped lesion. Pustular psoriasis appears as small blisters containing infectious pus. Inverse psoriasis forms red patches in the skin folds. Erythrodermic psoriasis occurs when the rash becomes very large, and can develop from other species. Nails and toenails are affected in most people with psoriasis at some point in time. This may include a hole in the nail or a nail color change.
Psoriasis is generally regarded as a genetic disease triggered by environmental factors. In twin studies, identical twins are three times more likely to be affected than non-identical twins. This suggests that genetic factors affect psoriasis. Symptoms often worsen during the winter and with certain drugs, such as beta blockers or NSAIDs. Psychological infections and pressure can also play a role. Psoriasis is not contagious. The underlying mechanism involves the immune system reacting to the skin cells. Diagnosis is usually based on signs and symptoms.
There is no cure for psoriasis; However, various treatments can help control symptoms. These treatments include steroid creams, vitamin D3 creams, ultraviolet light and immune system suppressants, such as methotrexate. About 75 percent of cases can be treated with cream alone. It affects two to four percent of the population. Men and women are affected with the same frequency. The disease can begin at any age, but usually begins in adulthood. Psoriasis is associated with an increased risk of psoriasis arthritis, lymphoma, cardiovascular disease, Crohn's disease and depression. Psoriatic arthritis affects up to 30 percent of individuals with psoriasis.
Video Psoriasis
Signs and symptoms
Plaque psoriasis
Psoriasis vulgaris (also known as chronic stationary psoriasis or psoriasis such as plaque) is the most common form and affects 85% -90% of people with psoriasis. Psoriasis plaque usually appears as an inflamed skin area that is wrapped in silvery-white scaly skin. These areas are called plaques and are most commonly found in elbows, knees, scalps, and back. Psoriatic erythroderma (erythrodermic psoriasis) involves extensive inflammation and exfoliation on most of the body surface. It may be accompanied by severe itching, swelling, and pain. Often results from exacerbations of plaque psoriasis are unstable, especially after the sudden withdrawal of systemic glucocorticoids. This form of psoriasis can be fatal because extreme inflammation and exfoliation interfere with the body's ability to regulate temperature and perform barrier functions.
Other forms
This type of psoriasis additionally consists of about 10% of cases. They include pustular, inverse, napkin, guttate, oral, and seborrheic-like forms.
Pustular psoriasis
Pustular psoriasis appears as a raised lump filled with uninfectious pus (pustules). The skin underneath and surrounding the red and soft pustules.
Inverse psoriasis
Inverse psoriasis (also known as bending psoriasis) appears as fine and inflamed patches on the skin. Patches often affect the skin folds, especially around the genitals (between the thighs and groin), the armpits, in the overweight abdominal skin creases (known as panniculus), between the buttocks in the intergluteal gap, and under the breasts in the infrared creases. Heat, trauma, and infection are thought to play a role in the development of this atypical form of psoriasis.
Napkin psoriasis
Psoriasis psoriasis is a common subtype of psoriasis in infants characterized by red papules with a silver scale in the diaper area that may extend to the body or limbs. Psoriasis Napkin is often misdiagnosed as napkin dermatitis (diaper rash).
Gutted psoriasis
Guttate psoriasis is characterized by many small lesions such as lute, red, pink, or like droplets (papules). These many psoriasis spots appear over large areas of the body, especially the torso, but also the limbs and scalp. Guttate psoriasis is often triggered by a streptococcal infection, usually streptococcal pharyngitis. The reverse is not true.
Mouth
Psoriasis in the mouth is very rare, in contrast to lichen planus, another common papulosquamous disorder that generally involves the skin and mouth. When psoriasis involves the oral mucosa (the lining of the mouth), it may be asymptomatic, but may appear as white or gray-yellow plaque. Fissured tongue is the most common finding in those with oral psoriasis and has been reported to occur in 6.5 to 20% of people with psoriasis affecting the skin. The emergence of microscopic oral mucosa influenced by a geographical tongue (migratory stomatitis) is very similar to the appearance of psoriasis. However, modern research has failed to show the relationship between the two conditions.
Seborrhoeic psoriasis such as
Seborrhoeic psoriasis is a common form of psoriasis with clinical aspects of psoriasis and seborrheic dermatitis, and may be difficult to distinguish from the latter. This form of psoriasis usually manifests as a red plaque on an oily scale in higher sebum production areas such as scalp, forehead, skin folds in the side of the nose, skin around the mouth, skin over the breastbone, and in the skin folds.
Psoriatic arthritis
Psoriatic arthritis is a form of chronic inflammatory inflammation that has a very varied clinical presentation and often occurs in association with skin and nail psoriasis. It usually involves painful inflammation of the joints and connective tissue around it and can occur in any joint, but most commonly in the joints of the fingers and toes. This can lead to swelling of the finger and toe sausage known as dactylitis. Psoriasis arthritis may also affect the hip, knee, spine (spondylitis), and sacroiliac joints (sacroiliitis). About 30% of individuals with psoriasis will develop psoriasis arthritis. Skin manifestations of psoriasis tend to occur before rheumatic manifestations in about 75% of cases.
Nail changes
Psoriasis can affect the nail and produce various changes in the appearance of fingernails and toes. Nail psoriasis occurs in 40-45% of people with psoriasis that affects the skin and has a lifetime incidence of 80-90% in those with psoriasis arthritis. These changes include nail pitting (pinhead deposition of the nail seen in 70% with nail psoriasis), nail bleaching, small bleeding area of ​​the capillaries under the nail, yellow redness of the nail known as oil drops or salmon, under the nail (subungual hyperkeratosis), loosening and separating the nails (onycholysis), and crushing the nails.
Medical signs
In addition to rash appearance and distribution, certain medical signs may be used by medical practitioners to assist with the diagnosis. This may include the Auspitz sign (indicating bleeding when the scale is removed), Koebner phenomenon (skin lesions of psoriasis caused by trauma to the skin), and the itching and pain are localized to papules and plaques.
Maps Psoriasis
Cause
The cause of psoriasis is not fully understood, but a number of theories exist.
Genetics
About one-third of people with psoriasis report a family history of the disease, and researchers have identified the genetic locus associated with the condition. Identical twin studies show the possibility of 70% of psoriasis developing twins if other twins have a disorder. The risk is about 20% for nonidentical twins. These findings suggest both genetic susceptibility and environmental responses in developing psoriasis.
Psoriasis has a strong genetic component, and many genes are associated with it, but it is not clear how the genes work together. Most of the genes identified are related to the immune system, especially the major histocompatibility complex (MHC) and T cells. Genetic studies are valuable because of their ability to identify molecular mechanisms and pathways for further study and potential drug targets.
Classical genome-wide relationship analysis identified nine loci on different chromosomes associated with psoriasis. They are called psoriasis susceptibility 1 through 9 ( PSORS1 via PSORS9 ). Inside the locus there is a gene in the path that leads to inflammation. Certain variations (mutations) of the gene are commonly found in psoriasis. The genome-wide association scan has identified other genes that are altered for variant characteristics in psoriasis. Some of these genes express inflammatory signal proteins, which affect cells in the immune system that are also involved in psoriasis. Some of these genes are also involved in other autoimmune diseases.
The main determinant is PSORS1 , which may account for 35% -50% heritability of psoriasis. It controls genes that affect the immune system or encode excessive skin protein with psoriasis. PSORS1 is located on chromosome 6 in the major histocompatibility complex (MHC), which controls important immune functions. Three genes in the locus PSORS1 have a strong association with psoriasis vulgaris: HLA-C variant HLA-Cw6 , which encodes a class I MHC protein; CCHCR1 , a WWC variant, which encodes a circular protein that is overexpressed in the epidermis of psoriasis; and CDSN , the variant allele 5, which encodes corneodesmosin, a protein expressed in the granular layer and cornified epidermis and regulated in psoriasis.
The two major immune system genes under investigation are the interleukin-12 beta subunit ( IL12B ) on the 5q chromosome, which expresses interleukin-12B; and IL23R on chromosome 1p, which expresses interleukin-23 receptors, and is involved in T cell differentiation. The Interleukin-23 and IL12B receptors are both closely related to psoriasis. T cells are involved in the inflammatory process leading to psoriasis. These genes are on a pathway that increases tumor necrosis factor-? and nuclear factor? B, two genes involved in inflammation. More recently, the first gene directly associated with psoriasis has been identified. A rare mutation in a gene encoding CARD14 protein plus an environmental trigger is enough to cause plaque psoriasis (the most common form of psoriasis).
Lifestyle
Conditions reported as a worsening disease include chronic infections, stress, and seasonal and climatic changes. Other people who may aggravate the condition include hot water, psoriasis skin lesions scratching, skin dryness, excessive alcohol consumption, smoking, and obesity.
HIV
Levels of psoriasis in HIV-positive people are comparable to HIV-negative individuals; however, psoriasis tends to be more severe in people infected with HIV. Higher levels of psoriasis arthritis occur in HIV-positive people with psoriasis than in those who are not infected. Immune responses in those infected with HIV are usually characterized by cellular signals from the Th2 subset of CD4 helper T cells, whereas the immune response in psoriasis vulgaris is characterized by a typical cellular signal pattern of the Th1 subset of CD4 helper T cells and Th17 helper. T cells. It has been hypothesized that the reduced presence of CD4 T cells leads to the overactivation of T-8 cells, which are responsible for the exacerbation of psoriasis in HIV-positive people. Psoriasis in those with HIV/AIDS is often severe and may not be treated with conventional therapy.
Microbe
Psoriasis has been described as occurring after strep throat, and may be aggravated by colonization of the skin or intestine with Staphylococcus aureus , Malassezia , and Candida albicans .
Drugs
Drug-induced psoriasis may occur with beta blockers, lithium, antimalarial drugs, non-steroidal anti-inflammatory drugs, terbinafine, calcium channel blockers, captopril, glyburide, granulocyte colony-stimulating factor, interleukin, interferon, lipid-lowering drugs, and paradoxically TNF inhibitors such as infliximab or adalimumab. Withdrawal of corticosteroids (topical steroid creams) may aggravate psoriasis because of the rebound effect.
Mechanism
Psoriasis is characterized by an abnormal and rapid growth of the epidermal layer of the skin. Abnormal production of skin cells (especially during wound repair) and overturning of skin cells results from a sequence of pathological events in psoriasis. Skin cells are replaced every 3-5 days in psoriasis rather than usually 28-30 days. This change is believed to be derived from early maturation of keratinocytes caused by a dermisic inflammatory cascade involving dendritic cells, macrophages, and T cells (three subtypes of white blood cells). These immune cells move from the dermis to the epidermis and secrete the chemical signals of inflammation (cytokines) such as interleukin-36, tumor necrosis factor-, interleukin-1, interleukin-6, and interleukin-22. This secreted inflammatory signal is believed to stimulate keratinocytes to multiply. One hypothesis is that psoriasis involves defects in regulator T cells, and in the interleukin-10 regulatory cytokine.
Mutation of protein genes involved in the ability of the skin to function as a barrier has been identified as a marker of susceptibility to the development of psoriasis.
DNA released from dead cells acts as an inflammatory stimulus in psoriasis and stimulates receptors in certain dendritic cells, which in turn produce interferon cytokines. In response to this chemical message from dendritic cells and T cells, keratinocytes also secrete cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor-, which indicate the downstream inflammatory cells come and stimulate additional inflammation.
Dendritic cells mediate the innate immune system and adaptive immune system. They are elevated in psoriatic lesions and induce T cell proliferation and type 1 helper T cells (Th1). Target immunotherapy therapy as well as psoralen and ultraviolet A (PUVA) can reduce the number of dendritic cells and support the secretion of Th2 cell cytokine through the Th1/Th17 cell cytokine profile. Psoriatic T cells move from the dermis to the epidermis and secrete interferon-? and interleukin-17. Interleukin-23 is known to induce the production of interleukin-17 and interleukin-22. Interleukin-22 works in combination with interleukin-17 to induce keratinocytes to secrete neutrophil-attracting cytokines.
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Diagnosis
The diagnosis of psoriasis is usually based on the appearance of the skin. Typical skin characteristics for psoriasis are scaly, erythematous plaques, papules, or patches of skin that may be painful and itchy. There are no specific blood tests or diagnostic procedures that are usually required to make a diagnosis.
The differential diagnosis of psoriasis includes similar dermatological conditions in appearance such as discoid eczema, seborrhoeic eczema, pityriasis rosea (possibly confused with guttate psoriasis), nail fungus (possibly confused with nail psoriasis) or cutaneous T cell lymphoma (50% of individuals with cancer are initially mistaken diagnosed with psoriasis). Dermatological manifestations of systemic diseases such as secondary syphilis rashes may also be confusing with psoriasis.
If the clinical diagnosis is uncertain, biopsy or skin erosion may be performed to rule out other disorders and to confirm the diagnosis. The skin of the biopsy will show the projected epidermal projections that are interdigitate with the dermis on the microscopy. Epidermal thickening is a histological finding of other characteristics of psoriasis lesions. The epidermis granulosum stratum layer is often lost or decreased significantly in psoriatic lesions; skin cells from the most superficial layers of skin are also abnormal because they never fully mature. Unlike their adult counterparts, these superficial cells retain their nuclei. Inflammatory infiltrates can usually be visualized in microscopy when examining skin tissue or joint tissue affected by psoriasis. Epidermal skin tissue that is affected by psoriasis inflammation often has many CD8 T cells while the dominance of CD4 T cells forms an inflammatory infiltrate of the skin and joints of the skin.
Classification
Morphology
Psoriasis is classified as a papulosquamous disorder and is most commonly divided into different categories based on histologic characteristics. Variants include plaque, pustular, guttate, and bending psoriasis. Each form has a special ICD-10 code. Psoriasis can also be classified into nonpustular and pustular types.
Pathogenetik
Other classification schemes consider genetic and demographic factors. Type 1 has a positive family history, beginning before age 40, and is associated with human leukocyte antigen, HLA-Cw6 . Conversely, type 2 does not show a family history, a gift after the age of 40, and is not associated with HLA-Cw6 . Type 1 accounts for about 75% of people with psoriasis.
The classification of psoriasis as an autoimmune disease has triggered a great debate. Researchers have proposed different descriptions of psoriasis and psoriatic arthritis; some authors have classified it as an autoimmune disease while others classify it as distinct from autoimmune disease and refer to them as immune-mediated inflammatory diseases.
Severity
There is no consensus on how to classify the severity of psoriasis. Mild psoriasis has been defined as the percentage of body surface area (BSA) <= 10, Psoriasis Area Severity Index (PASI) score <= 10, and dermatology quality of life index score <= 10. Moderate to severe psoriasis defined by the same group with BSA & gt; 10 or PASI & gt; 10 and DLQI score & gt; 10. The DLQI is a 10 question tool used to measure the impact of some dermatological diseases on daily functioning. The DLQI score ranges from 0 (minimal damage) to 30 (maximum annoyance) and is calculated with each answer given 0-3 points with a higher score indicating greater social or occupational impairment.
The psoriasis area severity index (PASI) is the most widely used measurement tool for psoriasis. PASI assessed the severity of lesions and affected areas and combined these two factors into a single score of 0 (no illness) to 72 (maximal disease). However, PASIs can be too heavy to use outside of the research setting, which has led to efforts to simplify the index for clinical use.
Management
Although there is no cure available for psoriasis, many treatment options are available. Topical agents are commonly used for mild disease, moderate-to-moderate phototherapy, and systemic agents for severe illness.
Topical agents
Topical corticosteroid preparations are the most effective drugs when used continuously for 8 weeks; retinoids and coal tar were found to have limited benefits and may not be better than placebo. Larger benefits have been observed with very potent corticosteroids when compared with potent corticosteroids.
Vitamin D analogues such as paricalcitol were found to be superior to placebo. Combination therapy with vitamin D and corticosteroids is superior to treatment alone and vitamin D is found to be superior to coal tar for chronic plaque psoriasis.
Moisturizers and emollients such as mineral oil, petroleum jelly, calcipotriol, and decubal (oil in emollient water) were found to improve the clearance of psoriasis plaque. Emollients have been shown to be more effective in clearing psoriasis plaque when combined with phototherapy. However, certain emollients have no impact on the clearance of psoriasis plaque or may even decrease the permits achieved with phototherapy. Emolliic salicylate acids are structurally similar to para-aminobenzoic acid (PABA), commonly found in sunscreens, and are known to interfere with phototherapy in psoriasis. Coconut oil, when used as an emollient in psoriasis, has been found to reduce clearance of plaque with phototherapy. Creams and ointments applied directly to the psoriatic plaque can help reduce inflammation, lift scales, reduce skin turnover, and cleanse affected skin of plaque. Ointments and creams containing coal tar, dithranol, corticosteroids (ie desoximetasone), fluocinonide, vitamin D 3 analog (eg, calcipotriol), and retinoids are routinely used. The use of fingertip units can help in guiding how many topical treatments are used.
Vitamin D analogues may be useful with steroids; However, alone has a higher rate of side effects. They may allow less steroids to be used.
Another topical therapy used to treat psoriasis is a form of balneotherapy, which involves bathing daily in the Dead Sea. This is usually done for four weeks with benefits associated with exposure to sunlight and especially UVB rays. It is cost-effective and has been deployed as an effective way to treat psoriasis without drugs. Decrease in PASI score by more than 75% and remission over several months has been frequently observed. Side effects may be mild such as itching, folliculitis, burning skin, poikiloderma, and theoretical risks of nonmelanoma or melanoma skin cancer have been suggested. However, more recent studies have determined that there appears to be no increased risk of melanoma in the long run. The data can not be inferred with respect to the risk of nonmelanoma skin cancer, but it supports the idea that therapy is associated with an increased risk of benign form of sun-damaged skin such as, but not limited to, actinic elastosis or liver spots. Balneotherapy Dead Sea is also effective for psoriatic arthritis.
UV Phototherapy
Phototherapy in the form of sunlight has long been used for psoriasis. The UVB wavelength of 311-313 nanometers is most effective, and special lights have been developed for this application. The exposure time should be controlled to avoid excessive exposure and skin burning. UVB lights should have a timer that turns off the lights when the time is up. The amount of light used is determined by one's skin type. Increased rates of cancer from treatment seem small. Narrow bands of UVB light (NBUVB) phototherapy have been demonstrated to have similar efficacy to Psoralen and ultraviolet A phototherapy (PUVA).
One of the problems with clinical phototherapy is the difficulty many patients get access to the facility. Indoor tanning resources are almost ubiquitous today and can be considered as a means for patients to get UV exposure when dermatologists do not provide phototherapy. Indoor tanning has been used by many as a treatment for psoriasis; one indoor facility reported that 50% of its clients use centers for the treatment of psoriasis; another reported 36% did the same. However, the concern with the use of commercial tanning is that tanning beds that primarily emit UVA may not be effective in treating psoriasis. One study found that plaque psoriasis was responsive to either eryemogenic doses of UVA or UVB, because good exposure can lead to plaque dissociation of psoriasis. It does require more energy to achieve erythemogenic doses with UVA.
UV rays all have risks; Tanning beds are no exception, especially in terms of UV rays and the likelihood of increased skin cancer. There is an increased risk of melanoma, squamous cell and basal cell carcinoma; Younger psoriasis patients, especially those under 35, are at increased risk of melanoma from UV light treatments. The World Health Organization (WHO) registers tanning beds as carcinogens. The study review recommends that people who are prone to skin cancer are cautious when using UV light therapy as a treatment.
The main mechanism of NBUVB is the induction of DNA damage in the form of pyrimidine dimer. This type of phototherapy is useful in the treatment of psoriasis because the formation of this dimer disrupts the cell cycle and stops it. NBUVB induced cell cycle disorders defy the rapid division of skin cell characteristics seen in psoriasis. The activity of various types of immune cells found in the skin is also effectively suppressed by NBUVB phototherapy treatments. The most common short-term side effects of this form of phototherapy are redness of the skin; Less common side effects of NBUVB phototherapy are itching and blistering on treated skin, eye irritation in the form of conjunctival inflammation or corneal inflammation, or cold sores due to reactivation of the herpes simplex virus in the skin around the lips. Eye protection is usually given during phototherapy treatment.
Psoralen and ultraviolet Phototherapy (PUVA) combines oral or topical psoralen administration with exposure to ultraviolet A (UVA) rays. The mechanism of action of PUVA is unknown, but may involve psoralen activation by UVA rays, which inhibit the production of abnormal cells in psoriatic skin. There are several mechanisms of action associated with PUVA, including effects on the skin's immune system. PUVA is associated with nausea, headache, fatigue, burning, and itching. Long-term treatment is associated with squamous cell carcinoma (but not with melanoma). Combination therapy for moderate to severe psoriasis using PUVA plus acitretin results in benefits, but the use of acitretin has been associated with birth defects and liver damage.
Systemic agents
Resistant psoriasis to topical treatment and phototherapy can be treated with systemic therapy including oral medication or injectable treatment. Persons undergoing systemic treatment should have regular blood and liver function tests to check for drug toxicity. Pregnancy should be avoided for most of these treatments. The majority of people experience recurrence of psoriasis after systemic treatment is stopped.
Non-biological systemic treatments often used for psoriasis include methotrexate, ciclosporin, hydroxycarbamide, fumarates such as dimethyl fumarate, and retinoids. Methotrexate and ciclosporin are drugs that suppress the immune system; retinoids are synthetic forms of vitamin A. These agents are also considered to be first-line treatment for erythroderma psoriasis. Oral corticosteroids should not be used, as they may cause severe psoriasis at the time of termination.
Biologically is a protein produced that interferes with the immune processes involved in psoriasis. Unlike common immunosuppressive drug therapies such as methotrexate, the biological special aspects of the immune system contribute to psoriasis. These drugs are generally well tolerated and limited long-term outcome data have shown that biologics are safe for long-term use in moderate to severe plaque psoriasis. However, due to their immunosuppressive action, biology has been associated with a small increase in the risk of infection.
Guidelines consider biology as a third-line treatment for plaque psoriasis after inadequate response to topical medication, phototherapy, and non-biological systemic treatments. Biological safety during pregnancy has not been assessed. European guidelines recommend avoiding biological if pregnancy is planned; anti-TNF therapies such as infliximab are not recommended for use in chronic carriers of hepatitis B virus or HIV-infected individuals.
Some monoclonal antibodies target cytokines, molecules that cells use to send inflammatory signals to each other. TNF-? is one of the main executing inflammatory cytokines. Four monoclonal antibodies (MAbs) (infliximab, adalimumab, golimumab, and certolizumab pegol) and one recombinant TNF? feed receptors, etanercept, have been developed to inhibit TNF-? signaling. Additional monoclonal antibodies, such as ixekizumab, have been developed against pro-inflammatory cytokines and inhibit the inflammatory pathways at different points of anti-TNF-? antibody. IL-12 and IL-23 share a common domain, p40, which is a recently approved FDA-approved ustekinumab target. By 2017, the US FDA approves guselkumab for plaque psoriasis.
Two drugs targeting T cells are efalizumab and alefacept. Efalizumab is a monoclonal antibody that specifically targets the CD11a subunit of LFA-1. It also blocked adhesion molecules on endothelial cells lining blood vessels, which attracted T cells. Efalizumab was voluntarily withdrawn from the European market in February 2009 and from the US market in June 2009 by producers due to drug associations with progressive multifocal leukoencephalopathy cases. Alefacept also blocks the molecules that dendritic cells use to communicate with T cells and even cause natural killer cells to kill T cells as a way to control inflammation. Apremilast can also be used.
Individuals with psoriasis may develop antibody antibodies against monoclonal antibodies. Neutralization occurs when antidrug antibodies prevent monoclonal antibodies such as infliximab from binding antigens in laboratory tests. In particular, neutralization occurs when antidrug antibodies bind antigen sites to binding to infliximab instead of TNF-. When infliximab no longer binds tumor necrosis factor alpha, it no longer reduces inflammation, and psoriasis may worsen. Neutral antibodies have not been reported against etanercept, a biological drug that is a fusion protein consisting of two TNF-? receptors. The lack of neutralizing antibodies against etanercept may be secondary to TNF's presence? receptors, and the development of immune tolerance.
Surgery
Limited evidence suggests elevation of the tonsils may be beneficial for people with chronic plaque psoriasis, guttate psoriasis, and palmoplantar pustulosis.
Diet
Uncontrolled studies have suggested that individuals with psoriasis or psoriasis arthritis may benefit from a diet supplemented with fish oils rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Dietary recommendations include cold-water fish consumption (preferably wild fish, not farmed) such as salmon, herring, and mackerel; extra virgin olive oil; nuts; Vegetables; fruits; and whole grains; and avoid consumption of alcohol, red meat, and dairy products. The effects of caffeine consumption (including coffee, black tea, mate, and dark chocolate) should still be determined.
There is a higher rate of celiac disease among people with psoriasis. When adopting a gluten-free diet, the severity of the disease generally decreases in people with celiac disease and those with anti-gliadin antibodies.
Prognosis
Most people with psoriasis experience are no more than mild skin lesions that can be effectively treated with topical therapy.
Psoriasis is known to have a negative impact on the quality of life of affected people and individual family members. Depending on the severity and location of the outbreak, the individual may experience significant physical discomfort and some disability. Itching and pain can disrupt basic functions, such as self-care and sleep. Participation in sporting activities, specific work, and caring for family members can be a difficult activity for those with plaques that lie on their hands and feet. Plaque on the scalp can be very embarrassing, because the plaque that fluctuates in the hair can be mistaken for dandruff.
Individuals with psoriasis may feel conscious about their appearance and have a poor self-image stemming from fears of public rejection and psychosexual concerns. Psoriasis has been associated with low self-esteem and depression is more common among those with the condition. People with psoriasis often feel prejudiced against because of false beliefs in general that psoriasis is contagious. Psychological pressure can cause significant depression and social isolation; a high level of thinking about suicide is associated with psoriasis. Many tools exist to measure the quality of life of patients with psoriasis and other dermatological disorders. Clinical studies show individuals often experience a decline in quality of life. Children with psoriasis may experience bullying.
Some conditions associated with psoriasis. This happens more often in the elderly. Almost half of individuals with psoriasis over age 65 have at least three comorbidities (concurrent condition), and two thirds have at least two comorbidities.
Cardiovascular Disease
Psoriasis has been linked to obesity and some other cardiovascular and metabolic disorders. The incidence of diabetes was 27% higher in people affected by psoriasis than in those without conditions. Severe psoriasis may be more associated with the development of diabetes than mild psoriasis. Younger people with psoriasis may also be at higher risk for developing diabetes. Individuals with psoriasis or psoriatic arthritis have a slightly higher risk of heart disease and heart attacks when compared with the general population. The risk of cardiovascular disease appears to correlate with the severity of psoriasis and its duration. There is no strong evidence to suggest that psoriasis is associated with an increased risk of death from cardiovascular events. Methotrexate can provide a level of protection for the heart.
The chances of having hypertension 1.58 times higher in people with psoriasis than those without conditions; this possibility is even higher with severe cases of psoriasis. Similar associations were noted in people who had psoriatic arthritis - the possibility of having hypertension was found to be 2.07 times greater than that of the general population. The relationship between psoriasis and hypertension is not currently understood. The mechanisms hypothesized to engage in this relationship include the following: dysregulation of the renin-angiotensin system, elevated levels of endothelin 1 in the blood, and increased oxidative stress. The incidence of heart rhythm of atrial fibrillation abnormalities was 1.31 times higher in people with mild psoriasis and 1.63 times higher in people with severe psoriasis. There may be a slight increase in the risk of stroke associated with psoriasis, especially in severe cases. Treating high cholesterol levels with statins has been associated with reduced severity of psoriasis, as measured by PASI scores, and is also associated with increased risk factors for other cardiovascular diseases such as inflammatory markers. This cardioprotective effect is associated with the ability of statins to improve blood lipid profile and because of its anti-inflammatory effects. The use of statins in those with psoriasis and hyperlipidemia is associated with a decreased level of high sensitivity of C-reactive protein and TNF? as well as decreased activity of LFA-1 immune proteins. Compared with individuals without psoriasis, those affected by psoriasis are more likely to meet the criteria for metabolic syndrome.
Other diseases
The rate of Crohn's disease and ulcerative colitis is increased when compared with the general population, with a factor of 3.8 and 7.5 respectively. People with psoriasis also have a higher risk of celiac disease. Several studies have evaluated the association of multiple sclerosis with psoriasis, and the relationship has been questioned. Psoriasis has been associated with a 16% increase in overall relative risk for non-skin cancer. People with psoriasis had a 52% increased risk of lung and bronchial cancer, an increase of 205% in risk of developing upper gastrointestinal cancer, a 31% increase in the risk of developing urinary tract cancer, a 90% increased risk of developing liver cancer, and a 46% in the risk of developing pancreatic cancer. The risks for the development of non-melanoma skin cancers are also increasing. Psoriasis increases the risk of developing squamous cell carcinoma of the skin by 431% and increases the risk of basal cell carcinoma by 100%. There is no increased risk of melanoma associated with psoriasis.
Epidemiology
Psoriasis is thought to affect 2-4% of the western population. Psoriasis rates vary according to age, region and ethnicity; a combination of environmental and genetic factors is assumed to be responsible for this difference. This can happen at any age, though it most often appears for the first time between the ages of 15 and 25 years. About one-third of people with psoriasis reports are diagnosed before the age of 20. Psoriasis affects both sexes equally.
Psoriasis affects about 6.7 million Americans and occurs more frequently in adults.
People with inflammatory bowel diseases such as Crohn's disease or ulcerative colitis are at an increased risk of developing psoriasis. Psoriasis is more common in countries farther away from the equator. People of white European descent are more likely to have psoriasis and this condition is relatively rare in African Americans and is very rare in Native Americans.
History
Scholars believe psoriasis has been included among various skin conditions called tzaraath (translated as leprosy) in the Hebrew Bible, a condition that is imposed as a punishment for slander. Patients are considered "impure" (see tumah and taharah) during the phase of their suffering and ultimately treated by kohen. However, it is more likely that this confusion arose from the use of the same Greek term for both conditions. The Greeks used the term leprosy (?????) for scaly skin conditions. They use the term psora to describe the condition of itchy skin. He became known as Willan leprosy in the late 18th century when English dermatologists Robert Willan and Thomas Bateman differentiated him from other skin diseases. Leprosy, they say, is distinguished by regular, circular, circular forms, while psoriasis is always irregular. Willan identifies two categories: leprossa graecorum and psora leprossa .
Psoriasis is considered first described in Ancient Rome by Cornelius Celsus. The disease was first classified by British physician Thomas Willan. British physician Thomas Bateman explains the possible link between psoriasis and arthritis symptoms in 1813.
The history of psoriasis is littered with dubious treatments of high effectiveness and toxicity. In the 18th and 19th centuries, Fowler's solution, which contains toxic and carcinogenic arsenic compounds, is used by dermatologists as a treatment for psoriasis. Mercury is also used for the treatment of psoriasis during this time period. Sulfur, iodine, and phenols are also commonly used for the treatment of psoriasis during this era when it is incorrectly believed that psoriasis is a contagious disease. Coal tars were widely used with ultraviolet light irradiation as a topical treatment approach in the early 1900s. During the same period of time, cases of arthritis psoriasis were treated with intravenous gold giving in the same way as rheumatoid arthritis. All of these treatments have been replaced with modern topical and systemic therapies.
Etymology
The word psoriasis comes from the Greek word ????????, meaning "itchy condition" or "itching" of psora , "itch" and - iasis , "action, condition".
Society and culture
The International Psoriasis Association Federation (IFPA) is a global umbrella organization for national and regional psoriasis patient associations and also gathers leading experts in psoriasis and arthritis psoriasis research for scientific conferences every three years. The Psoriasis International Network, a program of the Fondation Renà © à © Touraine, gathers dermatologists, rheumatologists and other caregivers involved in psoriasis management. Nonprofit organizations The National Psoriasis Foundation in the United States, the Psoriasis Association in the UK and the Psoriasis of Australia offer advocacy and education about psoriasis in their respective countries.
Cost
The annual cost of treating psoriasis in the US is estimated at $ 32.5 billion, including $ 12.2 billion in direct costs. Pharmaceutical costs are a major source of direct costs, with the most common biological therapies. These costs increase significantly when co-morbid conditions such as heart disease, hypertension, diabetes, lung disease and psychiatric disorders are taken into account. Expenditures associated with comorbidities are estimated at $ 23,000 per patient per year.
Research
The role of insulin resistance in the pathogenesis of psoriasis is currently under investigation. Early research has shown that antioxidants such as polyphenols can have a beneficial effect on the characteristic of psoriasis inflammation.
Many of the new drugs studied target the Th17/IL-23 axis, especially the IL-23p19 inhibitor, since IL-23p19 is present in increased concentrations in psoriasis skin lesions while contributing less to protection against opportunistic infections. Other cytokines such as IL-17 and IL-22 have also been the target of inhibition because they play an important role in the pathogenesis of psoriasis. Another path of research has focused on the use of vascular endothelial growth factor inhibitors to treat psoriasis. Oral medications investigated as an alternative to drugs given by injection include Janus kinase inhibitors, protein kinase C inhibitors, mitogen-activated protein inhibitors, and phosphodiesterase 4 inhibitors, all of which have been shown to be effective in various phase 2 and 3 clinical trials. However, these agents have severe side effects due to their immunosuppressive mechanism.
References
Further reading
- Baker, Barbara S. (2008). From Arsenic to Biology: History of 200 Year Psoriasis . Beckenham UK: Garner. ISBN: 0-9551603-2-4.
External links
- Psoriasis in Curlie (based on DMOZ)
- "Guidelines for psoriasis assessment and management". US National Guideline Clearinghouse.
Source of the article : Wikipedia
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