About Psoriasis
What is it?
Psoriasis is a chronic, recurrent and universal inflammatory disorder, which can affect the skin, tendons, ligaments, and joints (Gottlieb, 2001; Gottlieb & Bos, 2002; Lebwohl, 2003).
Approximately 1.5 million Americans suffer from moderate to severe plaque psoriasis. Psoriasis is not contagious and it cannot spread by touch, sexual relation, kissing or fluid transmission from person to person. You have to born with Psoriasis to have it.
History
The first historical report on psoriasis was made by Celsus (25 AC- DC 45). Hippocrates (460 -375 AC) described lesions similar to psoriasis that he classified as "squamous eruptions" and named them lopoi (from lepo, desquamation). It was Galenus (DC 133-200) credited with the first use of the word psoriasis, from the Greek, psora, pruritus.
Prevalence / Statistics
Psoriasis rates range from 0.5% to 4.6% depending on the country and race (Lebwohl, 2003).
Psoriasis is considered a rare dermatosis in childhood and corresponds to about 4% of all dermatosis observed in patients below the age of 16 years of age. It is estimated that between 25 and 45% of the cases of Psoriasis may start their course before the age of 16 years and about 2% of them before the age of 2.
It is more commonly affecting Caucasians and patients living at higher latitudes (Lebwohl, 2003). Although it is not a life-threatening condition, it can lead to significant impairment, psychological stress and sometimes death. Patients who are severely afflicted can have up to 100% body surface area involvement.
Psoriasis may appear at any age, but there are two peak onset periods; during childhood / early adulthood (early onset psoriasis) and after age 40 (late onset).
Causes
Despite recent advances in genetic research, the cause of psoriasis remains unknown.
It is considered a chronic skin and joint inflammatory disease, immunomediated with polygenic predisposition characterized by complex modifications of growth and epidermal differentiation as well as multiple biochemical, immune and vascular abnormalities, in addition to the unexplained correlation with emotional episodes.
Psoriasis is believed to be a T-cell–mediated autoimmune disorder. The process is believed to begin with an environmental factor, perhaps a viral antigen, which induces T cells to produce cytokines. The cytokines stimulate keratinocyte proliferation and production of antigenic adhesion molecules in the dermal blood vessels. These adhesion molecules further stimulate T cells to produce cytokines, thus perpetuating the response. We know that many times the triggering mechanism may be psychological stress, certain medications (lithium, beta blockers, antimalarial drugs, nonsteroidal anti-inflammatory drugs, and oral steroid withdrawal) and an infection.
In the past, keratinocyte disorder was the etiopathogenic basis of Psoriasis; however, currently it is known that it is initially an immune affection mediated by type Th1 response
People affected with psoriasis often notice times when their skin gets worse. (these times are know as flares).
Things that can cause these flare-ups include a cold and dry climate, infections, stress, and dry skin. Also, certain medicines, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and medicines used to treat high blood pressure or certain mental illnesses, may trigger an outbreak or make your psoriasis worse. Although a link between psoriasis and stress seems to exist, evidence to support a causal relationship as of today is lacking.
Smoking, especially in women, makes you more likely to get psoriasis and can make it worse if you already have it.
Comorbidities
The most common co-morbidities include psoriatic arthritis and anxiety/depression disorders (Gisondi et al 2005; Kimball et al 2005) such as decreased self-esteem and general mood disorders.
People with psoriasis have significantly higher rates of obesity, diabetes, heart failure and high blood pressure than the general public. It is believe how substances produced in the fat (inflammatory markers) relate to the risk of heart disease in people with the metabolic syndrome and psoriasis.
People with metabolic syndrome have insulin resistance, increased waist size, high blood pressure, or high cholesterol.
There is strong evidence for a genetic predisposition to psoriasis, in particular to childhood psoriasis. It is estimated that 71% of patients with childhood psoriasis have a positive family history.
If one parent has psoriasis, children have a 10 percent chance of developing psoriasis. If both parents have psoriasis, children have a 50 percent chance
Psoriasis may disqualify a person from serving in the U.S. military. According to the Department of Defense (DOD) Directive 6130.3. Current or history of psoriasis (696.1) is disqualifying. The complete directive are available at our forum.
As of the end of 2011 a clear understanding of the pathogenesis of psoriasis does not yet exist. I will love to say that is becoming clearer and clearer every day. Regretfully almost daily new factors are discovered while an specific causation becomes more elusive.
Hyper proliferation of keratinocytes is a further characteristic feature. Studies have depicted that the epidermal cell cycle of psoriatic lesions is shortened by approximately eight-fold more than normal.
The lesions are classified as erythrosquamous, due to the erythema which develops as a result of involvement of the vasculature, and the involvement of the epidermis with scale formation.
Principal Types:
There are five principal types of psoriasis: plaque, guttate, inverse, pustular and erythrodermic. Plaque psoriasis is the most common form of psoriasis.
The diagnosis of psoriasis can usually be established on clinical grounds. If the clinician is in doubt, a small cutaneous punch biopsy and subsequent histopathological examination can be performed.
There is to date no permanent cure for psoriasis and eruptions often recur. However, most treatments are related to significant improvements in quality of life.
Therapies
There are multiple therapeutic options for psoriasis. First-line therapy for patients with moderate to severe psoriasis is the application of topical agents, followed by phototherapy (UVB) for more extensive disease. If extensive disease does not respond to UVB, second-line agents include psoralen plus UVA (PUVA), methotrexate, cyclosporine or other systemic agents, including novel biologic therapies.
New psoriasis treatment regimens have been developed and include combination, rotational and sequential therapy.
Total direct and indirect health care costs of psoriasis for patients are calculated at $11.25 billion annually, with work loss accounting for 40 percent of the cost burden. Approximately 60 percent of psoriasis patients missed an average of 26 days of work a year due to their illness.
In general, mild psoriasis can usually be treated effectively with topical medications, such as anthralin, topical corticosteroids, topical retinoids (Tazorac) and vitamin D derivatives (Taclonex, Vectical). Localized plaques may be treated with laser and small light therapies units.
Moderate psoriasis should be exclusively treated first with Phototherapy and if this was to fail for that particular patient (which happens in approximately 25% of patients) it may require the use of systemic treatments, such as methotrexate, cyclosporine, Soriatane, etc.
Psoriasis medications may be used in combination. Topical corticosteroids may be used in combination with vitamin D derivatives, and Biologics may be used in combination with methotrexate or phototherapy. There is plenty of research of Phototherapy helping Biologics effectiveness.
People with signs of psoriatic arthritis will benefit from treatments that help to control psoriasis as well as arthritis in order to minimize the chances of developing a long-term disability.
CREDITS
Travis, L., Weinberg, J.M. , eMedicineHealth, Gladman et al., Ann Rheum Dis, 2005 , Youn et al., J Dermatol, 1999; Henseler et al., J Am Acad Dermatol, 1985. , Morris et al., Pediatr Dermatol, 2001., Dermatology Nursing, Sampogna, Br J Dermatol, 2004,; Wolkenstein, JEADV, 2006. , Mallbris et al., J Invest Dermatol, 2005., Xtraclaser.com
