Psoriasis
Psoriasis is a long-term autoimmune disease characterized by abnormal patches of skin. The affected area has red, itchy, scaly, and scaly skin. The severity of psoriasis varies, from small localized patches to complete coverage of the body. About 30% of patients have psoriatic arthritis. Psoriasis is believed to affect 2-4% of the population of the Western world, with incidence varying by age, region, and ethnicity; The incidence of psoriasis in people of European descent is about five times that of people of Asian descent, and psoriasis is estimated to affect about 6.7 million Americans.
Psoriasis can occur at any age, although it is more common in adults and usually first appears between the ages of 15 and 25. About one-third of people with psoriasis are diagnosed before the age of 20, with the incidence being the same in both sexes.
Signs and symptoms
Psoriasis can be divided into five main types:
- Plaque psoriasis, also known as psoriasis vulgaris, usually presents as inflamed raised areas of the skin covered with silvery-white, scaly skin, accounting for about 90% of cases. Most commonly found on the elbows, knees, scalp, and back.
- Pustular psoriasis, which appears as a raised mass filled with noninfectious pus (pustules). The skin below and around the pustules is red and soft, and can be localized or more widespread throughout the body. There are two types of local pustular psoriasis, both confined to the hands and feet.
- Skinfold psoriasis, also known as curvature psoriasis. Presents as smooth, inflamed patches of skin. These plaques often affect skin folds, especially around the genitals (between the thighs and groin), in the armpits, in the skin folds of the overweight abdomen, between the buttocks in the gluteal space, and in the submammary folds under the breasts.
- Guttate psoriasis is an inflammatory disease characterized by many small, scaly, red, or pink droplet-like papules. These numerous pimples appear over large areas of the body, mainly the trunk, extremities, and scalp, but usually do not include the palms and soles of the feet. Gutate psoriasis is usually caused by an oropharyngeal or perianal streptococcal infection and usually develops 1 to 3 weeks after infection. Guttate psoriasis is most common in children and young adults and is usually diagnosed based on history and clinical findings. Guttate psoriasis has a better prognosis than plaque psoriasis and usually resolves within 1-3 weeks; However, up to 40% of people with guttate psoriasis eventually transition to plaque psoriasis.
- Erythrodermic psoriasis, which involves extensive inflammation and skin flaking of most of the body surface, usually involving more than 90% of the body surface area. It may be accompanied by severe dryness, itching, swelling, and pain. It can develop from any type of psoriasis. Erythrodermic psoriasis is usually the result of exacerbation of unstable plaque psoriasis, especially after abrupt withdrawal of systemic glucocorticoids. This form of psoriasis can be fatal, and extreme inflammation and exfoliation disrupt the body’s ability to regulate temperature and the skin’s barrier function.
Etiology and pathophysiology
The cause is not fully understood. Genetics, seasonal changes, skin damage, climate, immunocompromised states, specific infections, and the use of certain medications are associated with different types of psoriasis.
The pathophysiology of Psoriasis is characterized by abnormal hyperand rapid growth of the epidermis layer of the skin. The sequence of pathological events begins with the initial phase, in which skin trauma, infection or drugs lead to the activation of the immune system, followed by the maintenance phase, which includes the chronic progression of the disease. Skin cells in silver speculation are replaced every 3-5 days instead of the usual 28-30 days. These changes are thought to result from premature keratinocytes maturation induced by an inflammatory cascade involving dendritic cells, macrophages, and T cells in the dermis. These immune cells move from the dermis to the epidermis and secrete inflammatory cytokines such as IL-36, TNFa, IL-10, IL-6, and IL-22. These factors stimulate the proliferation of keratinocytes. One hypothesis is that silver speculation involves defects in regulatory T cells and IL-10. Dendritic cells are linked to increase in psoriasis lesions and induce the proliferation of T cells and type 1 helper T cells (Th1). Targeted immunotherapy as well as psoralen and ultraviolet A (PUVA) therapy can reduce the number of dendritic cells, from which psoriasis T cells enter the epidermis and secrete IF-y and IL-17. IL-23 is known to induce the production of IL-17 and IL-22. IL-22 binds to IL-17 and induces keratinocytes to secrete cytokines that attract neutrophils.
Diagnosis
Usually based on the appearance of the skin. Typical skin features of psoriasis are scaly, erythematous, papules, or patches of skin that may be painful and itchy. In addition to the appearance and distribution of the rash, doctors may use specificsMedical signsto assist in diagnosis. These may include: Ospits’ sign（Auspitz’s sign, that is, precise bleeding when removing scales), Koebner phenomenon (psoriasis skin lesions caused by skin trauma) and confined to papules and plaquesItching and pain.
Treat
Although there is no cure for psoriasis, many treatment options exist. Topical drugs are usually used for mild disease, phototherapy for moderate disease, and systemic drugs for severe disease. There is no evidence to support the effectiveness of conventional topical and systemic agents, biological therapies, or phototherapy for acute guttate psoriasis or acute guttate episodes of chronic psoriasis that is not supported by clinical evidence. In short, treatment is divided into the following areas:
Ointments and creams containing coal tar, anthranol, corticosteroids (i.e., deoxymethasone), fluocinolin, vitamin D3 analogues (e.g., calcipotriene), and retinoids are routinely used.
Another topical remedy is a form of balneotherapy that involves daily bathing in the Dead Sea. This usually lasts for four weeks, and its benefits are attributed to sun exposure, especially UVB light.
Ultraviolet phototherapy, phototherapy in the form of sunlight, has long been used for psoriasis. UVB wavelengths 311313 nanometers are the most common. These lamps were developed for this treatment. A 2013 meta-analysis found no difference in efficacy between NB-UVB and PUVA in the treatment of psoriasis, but NB-UVB was generally more convenient.
Psoriasis resistant to topical treatments and phototherapy can be treated with systemic therapies, including oral medications or injections.
Commonly used nonbiological systemic treatments include methotrexate, cyclosporine, hydroxyurea, fumarate, and retinoids. Methotrexate and cyclosporine are drugs that suppress the immune system; Retinoids are synthetic forms of vitamin A. These drugs are also considered first-line treatments for psoriasis erythroderma. Oral corticosteroids should not be used because they can cause severe psoriasis attacks after discontinuation.
Biologics are manufactured proteins that interrupt the immune process of psoriasis. Unlike generalized immunosuppressive medical therapies such as methotrexate, biologics target specific aspects of the immune system that cause psoriasis. These drugs are generally well tolerated, and biologics are safe for long-term use in moderate to severe plaque psoriasis. Guidelines consider biologics as third-line treatment for plaque psoriasis that does not respond adequately to topical therapy, phototherapy, and non-biological systemic therapy.
a) TNF-a is one of the main actuator inflammatory cytokines. Four monoclonal antibodies (MAb) (infliximab, adalimumab, golimumab, and certolizumab) and a recombinant TNF-a bait receptor, etanercept, have been developed to inhibit TNF-a signaling. Ustekinumab is an FDA-approved drug targeting a common domain shared by IL-12 and IL-23, p40.
The drug Alefacept, which targets T cells, can block 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.
There is strong evidence that infliximab, bizizumab, ixekizumab, and risankizumab are the most effective biologics for treating moderate to severe psoriasis cases. There is also some evidence to support the use of thokinumab, bromidazimab, guselculumab, certolizumab, and ustekinumab. In general, anti-IL17, anti-IL12/23, anti-IL23, and anti-TNFα biologics are more effective than traditional systemic therapies. The immune pathway of psoriasis involves Th9, Th17, Th1 lymphocytes and IL-22. These biologics impede different aspects of these pathways.
Another group of treatments for moderate to severe psoriasis is fumarate (FAE), which may be similar in effectiveness to methotrexate.
Apremilast (Otezla, Celgene®) is an oral small molecule inhibitor of phosphodiesterase 4, which plays an important role in chronic inflammation associated with psoriasis.