Presentation
Signs and symptoms of psoriasis may include the following [7]:
- Family history of similar skin condition
- Pruritus (mostly seen in eruptive, guttate psoriasis)
- Cutaneous erythematous plaques, pustules or small papules
- Erythema and scaling
- Joint pain
- Pain (mostly seen in erythrodermic psoriasis and in some instances of traumatized plaques or in the joints affected by psoriatic arthritis)
- Dystrophic nails
- Recent streptococcal throat infection, immunization, viral infection, use of antimalarial drug, or trauma
- Eye related findings are seen in around 10% of patients and conjunctivitis or blepharitis are the most common ocular symptoms.
Workup
The diagnosis of psoriasis is mostly clinical. Laboratory findings are useful in differentiating between psoriatic arthritis and rheumatoid arthritis and a typical laboratory finding showing psoriasis will produce the following results: [8].
- Negative test result for rheumatoid factor (RF)
- Normal Erythrocyte sedimentation rate (ESR) (except in pustular and erythrodermic psoriasis)
- Elevated Uric acid level may be in psoriasis (especially in pustular psoriasis)
- Fluid from pustules is sterile with neutrophilic infiltrate
In cases of hands and foot psoriasis where the use of topical steroids appear to be worsening the situation, fungal studies should also be performed.
Treatment
Management of psoriasis may involve drugs, light therapy, stress reduction, climatotherapy, and various adjuncts such as sunshine, moisturizers, and salicylic acid [9].
Expert dermatologists from across the globe released a consensus report on treatment optimization and transitioning for moderate-to-severe plaque psoriasis. The recommendations are covered below:
- Methotrexate may be used for as long as it remains effective and well-tolerated.
- Cyclosporine is generally used intermittently for inducing a clinical response with one or several courses over a 3–6 month period.
- Transition from conventional systemic therapy to a biological agent may be done directly or with an overlap if transitioning is needed because of lack of efficacy, or with a treatment-free interval if transitioning is needed for safety reasons.
- Combination therapy may be helpful.
- Continuous therapy for patients receiving biologicals is recommended.
Prognosis
Psoriasis is generally not life threatening in most cases but it causes some inconvenience [6]. It is a however, a chronic disease and may reoccur is some cases. The peeling, splitting of skins can bring about pain and self-esteem issues. Therefore, psoriasis affects a patient’s quality of life as the individual will have to deal with embarrassment about appearance and self-consciousness. This is not forgetting the cost of remedy.
Etiology
The major causes of keratinocyte turnover remain unknown till date. However, it has been proven that environmental, immunologic and genetic factors all seem to play different roles in the development of the condition [2].
Environmental factors
Stress has been postulated as a major cause but apart from this, other factors have equally been known to trigger the exacerbation of the condition. The factors include trauma, infections, alcohol and drug use. Evidence also exists towards the increased incidence of psoriasis in patients that have been diagnosed with chronic gingivitis. With treatment of the gingivitis came improved control of the psoriasis, however, the long term incidence was not affected. This gives further proof to the fact that there is a multifactorial and genetic influence as far as the disease etiology is concerned.
Genetic factors
The gene locus has been determined therefore, patients with psoriasis definitely have a genetic predisposition for the condition. It is not yet clear what the triggering event maybe for most cases but there is a high possibility that the event is immunologic. The first lesion arising from the condition is seen often after an upper respiratory infection.
This illness is closely linked with some human leukocyte antigen alleles (HLA alleles) especially the human leukocyte antigen Cw6 (HLA-Cw6). Psoriasis is an autosomal dominant trait in some families [3].
According to evidence, there is a high level of dermal and circulating TNF-α suggesting that Psoriasis is an autoimmune condition. This may be why treatment with TNF-α inhibitors has proven successful in some cases. The psoriatic lesions are linked with increased T-cell activity beneath the underlying skin area.
Another important factor to keep in mind is the fact that 2.5% of people with HIV see worsening cases of psoriasis as CD4 continues to decrease.
Epidemiology
There are 970-2300 cases of psoriasis for every 100,000 people around the world, an incidence of 1% to 3%.
Psoriasis can be seen at any age but it is most common in adults aged 20-30 years [4]. There is no sexual predilection and the condition is rarely seen in people of African descent. One out of 3 patients has a positive family history suggesting familial clustering. Risk of getting affected with the condition increases with a first degree relative being affected but the risk increases to 60% when both parents are either affected now or where affected in the past.
Pathophysiology
As pointed out earlier, psoriasis is multifactorial and complex and it appears to be influenced by immune mediated as well as genetic components. This is of course supported by the fact that psoriasis has been treated successfully in the past with biologic medications and immune mediating medications.
The pathogenesis of the disease is still open to debates till date. There are varying theories as to what causes the disease and thus far, traumatic insult, stressful life events and infection have been mooted. In many patients however, no obvious triggers exist. As soon as the condition is triggered, there is substantial leukocyte recruitment to the dermis and epidermis and this is what causes the rather characteristic psoriatic plaques.
Keratinocyte proliferation arises when the epidermis gets infiltrated by an increased number of activated T-cells [5]. This fact is supported by histologic examination and immunohistochemical staining of psoriatic plaques which have shown large T cell populations within psoriatic lesions.
Finally, a hyper-inflated deregulated inflammatory sequence begins, followed by a strong production of different kinds of cytokines.
Prevention
There is no way to prevent psoriasis.
Summary
Psoriasis is a chronic disorder that is relatively common. It is characterised by excessive proliferation of keratinocytes which lead to the forming of thickened skin, inflammation and scaly plaques [1]. These result in erythema and in some cases, pruritus.
If left untreated, acute erythrodermic psoriasis and generalised psoriasis may become life threatening. Affected patients often need examination by a dermatologist and may be admitted to the hospital in some cases. Due to the sporadic course of the disease, it is often difficult to treat.
Patient Information
Psoriasis is skin disorder that is relatively common. It is a condition that changes the life cycles of skin cells. In doing so, it makes the cells to build up faster than normal on the skin's surface. The extra skin cells formed produce thick scales that are itchy and dry. The red patches that form may be painful in some cases.
This disease is chronic (long lasting) and the symptoms fluctuate in appearance. The symptoms may get better at certain times and at other times it may worsen.
In treating the condition, the focus of the treatment is to stop the cells of the skin from growing rapidly. Although there is no cure for this condition treatment often offers significant relief.
Exposure to small amounts of sunlight and the use of cortisone and other nonprescription creams can also help in the improvement of symptoms.
References
- Catsarou-Catsari A, Katambus A, Theodorpoylos P. Ophthalmological manifestations in patients with psoriasis. In: Acta Derm Venereol (Stock). 64. 1984:557-559.
- Huynh N, Cervantes-Castaneda RA, Bhat P, Gallagher MJ, Foster CS. Biologic response modifier therapy for psoriatic ocular inflammatory disease. Ocul Immunol Inflamm. May-Jun 2008;16(3):89-93.
- Menter A, Korman NJ, Elmets CA, Feldman SR, Gelfand JM, Gordon KB, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 4. Guidelines of care for the management and treatment of psoriasis with traditional systemic agents. J Am Acad Dermatol. Sep 2009;61(3):451-85.
- Mrowietz U, de Jong EM, Kragballe K, Langley R, Nast A, Puig L, et al. A consensus report on appropriate treatment optimization and transitioning in the management of moderate-to-severe plaque psoriasis. J Eur Acad Dermatol Venereol. Feb 26 2013.
- Christophers E, Sterry W. Psoriasis. In: Fitzpatrick TB, Eisen AZ, Wolff K, eds. Dermatology in General Medicine. New York: McGraw Hill; 1993:489-511.
- Parisi R, Symmons DP, Griffiths CE, et al. Global epidemiology of psoriasis: a systematic review of incidence and prevalence. J Invest Dermatol 2013; 133:377.
- Rachakonda TD, Schupp CW, Armstrong AW. Psoriasis prevalence among adults in the United States. J Am Acad Dermatol 2014; 70:512.
- Icen M, Crowson CS, McEvoy MT, et al. Trends in incidence of adult-onset psoriasis over three decades: a population-based study. J Am Acad Dermatol 2009; 60:394.
- Tollefson MM, Crowson CS, McEvoy MT, Maradit Kremers H. Incidence of psoriasis in children: a population-based study. J Am Acad Dermatol 2010; 62:979.
- Armstrong AW, Harskamp CT, Dhillon JS, Armstrong EJ. Psoriasis and smoking: a systematic review and meta-analysis. Br J Dermatol 2014; 170:304.