Causes:

The precise causes of psoriasis are unknown. It is generally believed to be due to damage in factors in the immune system, enzymes, and other materials that control skin cell division. This prompts an abnormal immune response, which causes rapid production of immature skin cells and inflammation.

Inflammatory Response and Autoimmunity

The Normal Immune System Response. The inflammatory process is the result of the body's immune response, which fights infection and heals wounds and injuries:

• When an injury or infection occurs, white blood cells are mobilized to rid the body of any foreign invaders, such as bacteria or viruses.
• The masses of blood cells that gather at the injured or infected site produce factors to repair wounds, clot the blood, and fight infections.
• In the process, the surrounding area becomes inflamed (red and swollen), and some healthy tissue is injured.

The Infection Fighters. The primary infection-fighting units are two types of white blood cells: lymphocytes and leukocytes.

Lymphocytes are a type of white blood cell designed to recognize foreign substances (antigens) and launch an offensive or defensive action against them. Lymphocytes include two subtypes known as T cells and B cells:

• B cells produce antibodies, which are designed to attack the antigens. Antibodies can either ride along with a B cell or travel on their own.
• T cells have special receptors attached to their surface that recognize the specific antigen.

A type of T cell called a helper T cell stimulates B cells and other white blood cells to attack a foreign substance. In psoriasis, however, the helper T cell appears to direct the B cells to produce autoantibodies ("self" antibodies), which attack skin cells. In psoriatic arthritis, cells in the joints also come under attack.

In psoriasis, helper T cells also release or stimulate the production of powerful immune factors called cytokines. In small amounts, cytokines are very important for healing. However, the high level of these cytokines that occurs in psoriasis can cause serious damage, including inflammation and injury during the psoriasis disease process.

Genetic Factors

A combination of genes is involved with increasing a person's susceptibility to the conditions leading to psoriasis. However, researchers are still unsure as to exactly how the disease is inherited.

HLA Molecules. The processes leading to all autoimmune diseases involve the human leukocyte antigen (HLA) system. Most immune disorders are associated with problems with this system. However, other genetic and environmental factors are required to actually trigger the disease.

Four key genes (named PSOR 1 - 4) seem to be involved with psoriasis. Seven recently identified DNA variations also may increase the risk of psoriasis. The variations are located in an area that helps the body distinguish its own cells from foreign invaders. These same DNA variations linked to psoriasis and psoriatic arthritis were also associated with four autoimmune diseases: type 1 diabetes, Grave's disease, celiac disease, and rheumatoid arthritis, suggesting that all of these diseases have the same genetic basis.

Triggers

Weather, stress, injury, infection, and medications, while not direct causes, are often important in triggering the disease process leading to the start and worsening of psoriasis.

Weather. Cold, dry weather is a common trigger of psoriasis flare-ups. Hot, damp, sunny weather helps relieve the problem in most patients. However, some people have photosensitive psoriasis, which actually improves in winter and worsens in summer when skin is exposed to sunlight.

Stress and Strong Emotions. Stress, unexpressed anger, and emotional disorders, including depression and anxiety, are strongly associated with psoriasis flare-ups. Research has suggested that stress can trigger specific immune factors associated with psoriasis flares.

Infection. Infections caused by viruses or bacteria can trigger some cases of psoriasis. For example:

• Streptococcal infections in the upper respiratory tract, such as tonsillitis, sinusitis, and strep throat, are known to trigger guttate psoriasis in children and young adults. The infections may make ordinary plaque psoriasis worse.
• Human immunodeficiency virus (HIV) is also associated with psoriasis.
• An uncommon form of human papillomaviruses (HPV) called EV-HPV has been associated with psoriasis. Although EV-HPV is probably not a direct cause, it may play a role in the continuation of psoriasis. This HPV form is not the virus associated with cervical cancer and genital warts.

Skin Injuries and the Koebner Response. The Koebner response is a delayed response to skin injuries, in which psoriasis develops later on at the site of the injury. In some cases, even mild abrasions can cause an eruption, which may be a factor in the frequency of psoriasis on the elbows or knees. It should be noted that psoriasis can develop in areas with no history of skin injury.

Medications. Drugs that can trigger the onset of the disease, worsen symptoms, or cause a flare-up include:

• Angiotensin-converting enzyme (ACE) inhibitors, drugs used to treat high blood pressure and heart problems
• Beta-blockers, drugs used to treat high blood pressure and heart problems
• Chloroquine, a medicine used to treat malaria
• Lithium for bipolar disorder treatment
• Indomethacin, a nonsteroidal anti-inflammatory drug (NSAID) -- Note: Other NSAIDs, such as meclofenamate, may actually improve the condition.
• Progesterone, used in female hormone therapies

Severe flare-ups may occur in people with psoriasis who stop taking their steroid pills by mouth, or who discontinue use of very strong steroid ointments that cover wide skin areas. The flare-ups may be of various psoriatic forms, including guttate, pustular, and erythrodermic psoriasis. Because these drugs are also used to treat psoriasis, this rebound effect is of particular concern.

Medications that cause rashes (a side effect of many drugs) can trigger psoriasis as part of the Koebner response.