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Paris Fears
Medical English 101
06/28/2011
Psoriasis: A Closer Look at the Other Skin
Introduction.
‘Scaly skin’ a term used to define most skin diseases since ancient Greek times. Today we use that common characteristic of any skin disease to describe Psoriasis, a chronic non-infectious immune-mediated skin condition that causes thick red and flaky patches of skin. For many years this skin condition was not able to be differentiated from other common skin diseases including eczema, leprosy, impetigo, and tubular lupus. Viennese dermatologist Ferdinand von Hebra, was able to assign the name psoriasis and studies about the phenomenon known as ‘scaly skin’ began to arise.
With over 5 types of psoriasis, the disease is thought to affect about 7.5 to 8.5 million people in the United States, and about 125 million worldwide. Recent studies have worked to access how Psoriasis affects the quality of life of those affected. Common signs and symptoms are normally limited to surface skin however; they can go as deep as joint pains. The median age of people affected is about 25 or 55, and there is an increased prevalence in Caucasian and Hispanic races compared to African Americans. Data has been shown that family history or genetics are thought to play a significant role in development of psoriasis, and even more so other risk factors include alcohol, stress, and weight (obesity). Another interesting contributor to psoriasis is the immune system. Over the last two decades studies for new treatments have been explored however, very few are making significant breakthroughs and organizations such as the National Psoriasis Foundation are still progressing. Through this review, readers will gain an understanding of the prevalence, pathogenic aspects, clinical and physiological factors, as well as new and developing treatments.
Clinical Classification.
In Greek the word ‘Psora’ means to itch. Psoriasis is described as silver white scales on raised red patches of skin. While one of the most common diseases is also very hard to treat because the disease can be controlled not cured. There are 7 types of Psoriasis, including plague, guttate, inverse, pustular, and erythrodermic. Other less diagnoses types include nail psoriasis and psoriasis arthritis. Plaque is the most common of the 7 which is the basic dry, itchy red skin patches in certain sites. Erythrodermic is a more aggressive type of plague psoriasis involving more pain and patches throughout the whole body. Pustular psoriasis occurs as it is irritated and small pus filled bumps can cover either the whole body or just hands and feet. Guttate proceeds after a strep throat infection, and manifest itself into numerous red, scaly bumps. Inverse psoriasis occurs in excess skin folds (i.e. genitals, armpits, fat folds, under breast) this type is susceptible to fungal infection. The other less diagnosed types including psoriasis arthritis and nail psoriasis can manifest in severe cases of psoriasis. The natural course of Psoriasis involves periods of outbreaks where your psoriasis is obvious and there are times of remission meaning the rash clears for a period of time. With continuous use of medication the disease can be treated however, if stopped or withdrawn from skin, the condition can worsen. Although Psoriasis can begin at any age, its common onset is between the ages of 20 to 30 and later between the ages of 50 to 60.
Background.
The History of Psoriasis goes back to the ages of the bible, and up until 150 years ago people mistook the common disease for leprosy. During the late 1700’s to early 1800’s two dermatologist, Robert Willan and Joseph Jacob Plenck were writing of a condition similar to psoriasis but still could not differentiate it as its own entity from leprosy. Joseph Jacob Plenck did not take the time to differentiate the condition from other skin diseases. Robert Willan however had recognized the disease and decided it was another category or phase of leprosy. His two phases were Leporasa Graecorum which was when the skin had scales and Psora Leprosa which was when the condition became eruptive (Babu). In 1841 Ferdinand von Hebra a Viennese dermatologist, using Robert Willans notes, was able to coin the name Psoriasis and describe the clinical picture of the condition as we see it today. Throughout the 19th century many dermatologist worked to make connections to pathology of internal organs, metabolism, and the nervous system. The prevalence of race and gender has been known to fluctuate globally for years however; it is present in races from African American to Middle Eastern, to Asian and Pacific Islanders. [Table 1] The New England Journal of Medicine suggests, “Ethnic factors also appear to influence the prevalence of psoriasis, which ranges from no cases in the Samoan population to 12 percent in Arctic Kasach'ye. The influence of ethnic factors is particularly evident when one compares prevalence rates within the United States. The prevalence among blacks (0.45 to 0.7 percent) is far lower than that in the remainder of the U.S. population (1.4 to 4.6 percent).”
Other studies show Caucasian and Hispanic infection rates are more prevalent than those of African American. Psoriasis is less common in Asian populations than in the European population and was rarely seen in Africa until the human immunodeficiency virus (HIV) pandemic. At the time the connection was made between HIV and psoriasis many people were still uncertain as of why. However in recent studies, dermatologists have identified similarities between the disease manifestations on the body’s immune system. Within genetic studies the markers for psoriasis have been found in chromosomes (1,3,4,6,8,10,16,17,18,19,20). [Table 2]. Table 2 shows the effected cytokines of psoriasis and identifies which loci and chromosomal location they are found. Studies have found that if the parents have psoriasis there is a 25% chance that the child may suffer from the skin disease. About 40% of patients with psoriasis have a family history of the disorder among first-degree (i.e. parents, offspring, siblings). Today around 7.5 to 8.5 million people in the United States and 125 million worldwide have Psoriasis. 150,000 new cases of psoriasis are reported annually. It has been found that around four hundred people die annually from psoriasis-related causes in the US. Throughout the 20th century the advances of genetic and environmental influences on the disease are increasing in significance. The most beneficial connection made was between life style factors influencing the body’s immune system speeding up growth of skin cells.
Physiology.
As stated psoriasis is an chronic “long term” inflammatory disorder of the immune system. The most important thing to understand is psoriasis is not contagious or infectious; you cannot contract this disease from touching, having sex, or swimming with someone who has psoriasis. Psoriasis Triggers are normally anything that can cause a deficiency in the immune system functions include but not limited to stressful events, different medications, cold/dry weather changes, alcohol use and/or withdrawal, to little sun, injury to skin (including cuts, burns, and insect bites), and Bacteria or viral infections (strep throat and upper respiratory infections). Drugs that have been known to worsen the symptoms of psoriasis include anti-malaria drugs, beta-blockers, lithium, as well as ACE inhibitors. A normal immune system protects the body against invaders and destroys bacteria and foreign protein. With a psoriasis patient the immune system sends faulty signals for rapid skin cell reproduction and growth causing the red and silvery white scaly skin. Normally, skin cells grow, mature, and are sloughed off over a period of about a month. The body eventually sheds these cells, revealing new skin cells. In people with psoriasis, however, the immune system is overactive and the skin cells reproduce in only 3 to 4 days. The body has no way to shed the skin cells fast enough, and they accumulate on the surface, forming raised, red patches or plaques (National Psoriasis Foundation). The accumulation of inflammatory cells in the epidermis and altered dermal vessels are major characteristics, and these changes are driven by release of cytokines and growth factors. Cytokines are signaling protein molecules that are mainly for intercellular communication, with more of these in the cell signaling for their cell surface receptor the skin thinks it’s time to grow skin cells when it hasn’t gone through is full cycle. Many investigations have shown that the process of epidermal differentiation in the lesion is aberrant or very abnormal from the regular process of the outer layer of skin. [Figure 1] Figure 1 proceeds to show the difference between the epidermis and the keratin layer of skin in normal skin cells and psoriasis skin cells.
Other ideas of the immune system importance relate to the T cells. T cells or lymphocytes also known as white blood cells one of the key types of immune system cells. As mentioned T cells are supposed to circulate through the body and fight invaders also known as antigens in body. Antigens activate the T cells, which causes initiation of the immune system to neutralize them. In Psoriasis the activated T cells with the virus/bacteria antigens rise to the skin surface and cause rapid skin cell growth that makes red skin and itchy silvery scales. Theories as to the immune systems role in diseases include its inability to rebuild itself. Once the skin T-cells begin depleting in psoriasis, just as in HIV form, the body has to work overtime to fight it which many times is not enough to return the skin back to normal.[Figure 2] Figure 2 demonstrates the antigens coming to activate the lymphocytes which reach the surface and release cytokines to fight the psoriasis plaque. Alongside this process macrophages are coming to aid the lymphocytes in the epidermis to kill the psoriasis effects from reaching the lymph nodes.
Throughout the history it has been said psoriasis wasn’t detected in the African populations until the epidemic of HIV an immunosuppressive disease. Studies show that psoriasis often has its initial presentation in advanced HIV infection, and it may even be the initial clinical manifestation of HIV infection. Psoriasis tends to become more severe as the HIV infection progresses, and there is even some correlation between low CD4 counts and the severity of psoriasis. CD4 is the glycoprotein that the HIV virus coat can bind to. Understanding the importance of CD4 and T4 cell counts affect the immune system help display the correlation as to why patients with HIV may contract psoriasis. While many authors and dermatologist try to make other connections aside from the CD4 count between psoriasis and HIV there are very few that aren’t contradictory or speculation. Unfortunately scientist and dermatologist have not been able to trace the antigens that cause psoriasis. Since normal symptoms of psoriasis include dry itchy crackling skin, it is not uncommon for people to mistake psoriasis as dry skin from the naked eye. They often to this and try different topical lotions for dry skin that later end up worsening the condition. Other symptoms are pink or reddish dot patches, nail discoloration and disfiguration, along with swollen or stiff joints. These spots are seen in soft tissue areas for example the mouth, genitals, under the breast, armpits. Also other common places all over the body include the knees, elbows, back, and stomach.
Psoriasis can usually be recognized with ease, but atypical or non-classic forms are more difficult to identify and treat. Diagnoses come from doctors doing basic skin observations. Most diagnostics of Psoriasis can be confirmed through family history and physical examination. Studies show that if joint pains are the only symptoms present it is common to have a skin biopsy performed. Skin biopsy is a procedure where a skin tissue sample is removed and examined. This is normally done for the very rare cases related to psoriasis however; it can be performed to find skin cancers.
Quality of Life.
Psoriasis is a serious condition strongly affecting the way a person sees him or herself and the way he is seen by others. It has tremendous economic and financial ramifications. According to the author of “The Burden of Skin Diseases”, the total annual cost for treating psoriasis is estimated to be in the range of $1.6 billion to $4.3 billion dollars. As stated earlier there are about 250,000 new cases observed annually of this non-curable disease, psoriasis. This disease was accounted for nearly 2.25 million visits to ambulatory care centers during 1996 in the US.
Since early diagnosis of psoriasis the quality of life has been very poor. In a survey by the National Psoriasis Foundation almost 75% of patients believed that psoriasis had moderate to large negative impact on their quality of life, with alterations in their daily activities. Many patients with psoriasis often have many psychosocial issues such as poor self image, low self esteem, and shame and embarrassment regarding their disease. Aside from the psychosocial quality of life traits there are many health related alterations to a person with psoriasis. [Table 3]
Studies have shown an increase in the comorbidity connections to psoriasis from other diseases. Some of the many comormidities include hypertension, obesity, cardiovascular disease, metabolic syndrome, inflammatory bowel disease, cancer and malignancy, and/or other immune-related diseases. A study in the UK worked to show that patients ages 18 years or older, with psoriasis have an increasing risk factor in having ischemic heart disease, myocardial infarcts, and cardiovascular disease. The study showed that patients with severe psoriasis have an increased risk of CV mortality. It showed that males with psoriasis were more likely to die of cardiovascular disease and contract CV risk, such as type 2 diabetes and hypertension, than other psoriasis patients and non-psoriasis patients. In a case-control study, patients with new onset psoriasis were more likely to be obese compared with patients visiting a dermatologist for a skin problem other than psoriasis. Some studies show correlation to body mass index (BMI) while others have conflicting factors.
The direct link between psoriasis and many of the possibly associated diseases is the presence of chronic inflammation and, in particular, elevated levels of the multifunctional cytokine tumor necrosis factor-α. Conversely, obesity and smoking may increase the risk of developing psoriasis, suggesting that these may be primary risk factors for several comorbidities and that psoriasis is no more than an innocent bystander. Most importantly, psoriasis patients are more likely to visit physicians because of their disease than ‘healthy’ people from the general population, which puts them at risk for being screened for and diagnosed with other diseases (Bhosle, Kulkarni, Feldman, and Balkrishnan).
Due to the fact that some psoriasis patients had a 30% increased risk of cancer compared to the general population malignancy, also known as cancerous cells spreading throughout the body to other sites, is seen more often in psoriasis patients. Many of the connections are unclear if they are due to the pathophysiology of psoriasis, related to the treatment of psoriasis, or simply psoriasis associated behavior such as drinking and smoking. Above all, Smoking, obesity, and alcohol consumption have been associated with psoriasis and/or the severity of psoriasis; however it is uncertain whether the association is causal. While physicians are not sure exactly how these diseases are connected it is still important to see correlation and connection to other diseases that are better understood so hopefully dermatologist and scientist can further their treatment regiments.
Treatments.
The treatments of psoriasis have been progressing over the years, as the knowledge of disease and its causes increase. The normal methods of treatment include but are not limited to topical treatments such as ointments and creams, systematic medications such as pills and oral anticoagulants, and/or light therapy. Over the past decade, the topical treatment of psoriasis has evolved from the age-old applications, such as coal tar, to the more acceptable and efficacious options containing topical corticosteroids, vitamin D analogues, and combined agents. The aim of the treatment is to interrupt or stop the rapid growth of skin cells and clear and smooth the skin scales. According to The British Journal of Dermatology studies show that some patients take anywhere from 2 to 5 medications daily to treat their psoriasis disease. Table 4 expresses the co-medications involved in a study of 1203 patients showed that of all patients 60·1% received regular systemic medication. In female patients 71·2% were taking medications on a regular basis. Of all patients 18·5% took only one drug, 11·6% took two different and 30% took three or more different systemic medications. Every seventh patient with psoriasis (14·8%) in this survey had a recorded intake of five or more different drugs. [Table 4] The medications listed in table 4 include but are not limited to diuretics, thyroid medication, angiotensin II receptors, antidepressants, and gastritis medication.