Psoriasis is a skin disease that causes itchy or sore patches of thick, red skin with silvery scales. You usually get them on your elbows, knees, scalp, back, face, palms and feet, but they can show up on other parts of your body.

Some people with psoriasis have psoriatic arthritis. It causes pain, stiffness, and swelling of the joints. It is often mild, but can sometimes be serious and affect many joints. The joint and skin problems don't always happen at the same time.

Your doctor will do a physical exam and imaging tests to diagnose psoriatic arthritis. There is no cure, but medicines can help control inflammation and pain. In rare cases, you might need surgery to repair or replace damaged joints.

Psoriatic arthritis is a condition involving joint inflammation (arthritis) that usually occurs in combination with a skin disorder called psoriasis. Psoriasis is a chronic inflammatory condition characterized by patches of red, irritated skin that are often covered by flaky white scales. People with psoriasis may also have changes in their fingernails and toenails, such as nails that become pitted or ridged, crumble, or separate from the nail beds.

Signs and symptoms of psoriatic arthritis include stiff, painful joints with redness, heat, and swelling in the surrounding tissues. When the hands and feet are affected, swelling and redness may result in a "sausage-like" appearance of the fingers or toes (dactylitis).

In most people with psoriatic arthritis, psoriasis appears before joint problems develop. Psoriasis typically begins during adolescence or young adulthood, and psoriatic arthritis usually occurs between the ages of 30 and 50. However, both conditions may occur at any age. In a small number of cases, psoriatic arthritis develops in the absence of noticeable skin changes.

Psoriatic arthritis may be difficult to distinguish from other forms of arthritis, particularly when skin changes are minimal or absent. Nail changes and dactylitis are two features that are characteristic of psoriatic arthritis, although they do not occur in all cases.

Psoriatic arthritis is categorized into five types: distal interphalangeal predominant, asymmetric oligoarticular, symmetric polyarthritis, spondylitis, and arthritis mutilans.

The distal interphalangeal predominant type affects mainly the ends of the fingers and toes. The distal interphalangeal joints are those closest to the nails. Nail changes are especially frequent with this form of psoriatic arthritis.

The asymmetric oligoarticular and symmetric polyarthritis types are the most common forms of psoriatic arthritis. The asymmetric oligoarticular type of psoriatic arthritis involves different joints on each side of the body, while the symmetric polyarthritis form affects the same joints on each side. Any joint in the body may be affected in these forms of the disorder, and symptoms range from mild to severe.

Some individuals with psoriatic arthritis have joint involvement that primarily involves spondylitis, which is inflammation in the joints between the vertebrae in the spine. Symptoms of this form of the disorder involve pain and stiffness in the back or neck, and movement is often impaired. Joints in the arms, legs, hands, and feet may also be involved.

The most severe and least common type of psoriatic arthritis is called arthritis mutilans. Fewer than 5 percent of individuals with psoriatic arthritis have this form of the disorder. Arthritis mutilans involves severe inflammation that damages the joints in the hands and feet, resulting in deformation and movement problems. Bone loss (osteolysis) at the joints may lead to shortening (telescoping) of the fingers and toes. Neck and back pain may also occur.

Psoriatic arthritis affects an estimated 24 in 10,000 people.

Between 5 and 10 percent of people with psoriasis develop psoriatic arthritis, according to most estimates. Some studies suggest a figure as high as 30 percent. Psoriasis itself is a common disorder, affecting approximately 2 to 3 percent of the population worldwide.

Anyone can get psoriatic arthritis, but it is most common in adults, affecting men and women equally. The large majority of people who get it already have psoriasis, and, on average, psoriatic arthritis develops about 7 to 10 years after the onset of skin symptoms. While it is not yet clear who will develop psoriatic arthritis, obesity and having severe psoriasis appear to be associated with a higher risk of arthritis among people with psoriasis. Sometimes stressful events, trauma to the joints or bones, or infections may trigger the disease.

The specific cause of psoriatic arthritis is unknown. Its signs and symptoms result from excessive inflammation in and around the joints. Inflammation occurs when the immune system sends signaling molecules and white blood cells to a site of injury or disease to fight microbial invaders and facilitate tissue repair. When this has been accomplished, the body ordinarily stops the inflammatory response to prevent damage to its own cells and tissues. Mechanical stress on the joints, such as occurs in movement, may result in an excessive inflammatory response in people with psoriatic arthritis. The reasons for this excessive inflammatory response are unclear.

Researchers have identified changes in several genes that may influence the risk of developing psoriatic arthritis. The most well-studied of these genes belong to a family of genes called the human leukocyte antigen (HLA) complex. The HLA complex helps the immune system distinguish the body's own proteins from proteins made by foreign invaders (such as viruses and bacteria). Each HLA gene has many different normal variations, allowing each person's immune system to react to a wide range of foreign proteins. Variations of several HLA genes seem to affect the risk of developing psoriatic arthritis, as well as the type, severity, and progression of the condition.

Variations in several other genes have also been associated with psoriatic arthritis. Many of these genes are thought to play roles in immune system function. However, variations in these genes probably make only a small contribution to the overall risk of developing psoriatic arthritis. Other genetic and environmental factors are also likely to influence a person's chances of developing this disorder.

Normal Function

The CARD14 gene provides instructions for making a protein that turns on (activates) a group of interacting proteins known as nuclear factor-kappa-B (NF-κB). The NF-κB protein complex regulates the activity of multiple genes, including genes that control the body's immune responses and inflammatory reactions. Inflammation is a normal immune system response to injury and foreign invaders (such as bacteria). The NF-κB protein complex also protects cells from certain signals that would otherwise cause them to self-destruct (undergo apoptosis).

The CARD14 protein is found in many of the body's tissues, but it is particularly abundant in the skin. NF-κB signaling appears to play important roles in regulating inflammatory reactions in the skin and in promoting the survival of skin cells.

Health Conditions Related to Genetic Changes

Generalized pustular psoriasis

At least three CARD14 gene mutations have been found in people with generalized pustular psoriasis (GPP), a rare and severe form of an inflammatory skin disorder called psoriasis. Individuals with GPP have repeated episodes in which large areas of skin become red and inflamed and develop small pus-filled blisters (pustules). The skin problems can be accompanied by fever and other signs of inflammation throughout the body (systemic inflammation). The episodes are thought to be triggered by infections, certain medications, pregnancy, or other stresses on the body. Most people with CARD14-associated GPP also have symptoms of the most common form of psoriasis called psoriasis vulgaris (PV), which is characterized by red, scaly patches of skin (plaques).

The CARD14 gene mutations associated with GPP (including GPP with PV) lead to production of an altered CARD14 protein that more readily turns on NF-κB. Overactive NF-κB signaling increases the activity of genes involved in the body's inflammatory response. The resulting abnormal inflammation contributes to the skin problems characteristic of GPP and PV.

CARD14 gene mutations increase the risk of developing GPP. Not everyone with a mutation in this gene has the characteristic problems with inflammation. This complex condition is thought to arise from a combination of genetic and environmental factors.

Familial pityriasis rubra pilaris

At least three mutations in the CARD14 gene have been identified in people with familial pityriasis rubra pilaris, a rare hereditary skin condition characterized by a patchy, salmon-colored skin rash covered in fine scales. These mutations lead to overactivation of NF-κB signaling, which triggers an abnormal inflammatory response in the skin. Researchers are working to determine how these changes lead to the specific features of familial pityriasis rubra pilaris.

Psoriatic arthritis

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Other disorders

Changes in the CARD14 gene may also contribute to other forms of psoriasis. At least two mutations have been identified in families with psoriasis. Several other rare variants of the CARD14 gene have been associated with an increased risk of psoriasis in people without a family history of the disorder. Studies suggest that these genetic changes enhance activation of NF-κB, resulting in abnormal inflammation, which is a characteristic feature of psoriasis. However, CARD14 gene mutations appear to be an uncommon risk factor for this condition. Additional factors in combination with the particular CARD14 gene mutation may help determine which form of skin inflammation develops.

Other Names for This Gene

• bcl10-interacting maguk protein 2
• BIMP2
• CAR14_HUMAN
• CARD-containing MAGUK protein 2
• card-maguk protein 2
• carma 2
• CARMA2
• caspase recruitment domain family, member 14
• caspase recruitment domain-containing protein 14

Genomic Location

Normal Function

The HLA-B gene provides instructions for making a protein that plays a critical role in the immune system. HLA-B is part of a family of genes called the human leukocyte antigen (HLA) complex. The HLA complex helps the immune system distinguish the body's own proteins from proteins made by foreign invaders such as viruses and bacteria.

HLA is the human version of the major histocompatibility complex (MHC), a gene family that occurs in many species. Genes in this complex are categorized into three basic groups: class I, class II, and class III. In humans, the HLA-B gene and two related genes, HLA-A and HLA-C, are the main genes in MHC class I.

MHC class I genes provide instructions for making proteins that are present on the surface of almost all cells. On the cell surface, these proteins are bound to protein fragments (peptides) that have been exported from within the cell. MHC class I proteins display these peptides to the immune system. If the immune system recognizes the peptides as foreign (such as viral or bacterial peptides), it responds by triggering the infected cell to self-destruct.

The HLA-B gene has many possible variations, that result in the production of proteins that differ by changes in at least one protein building block (amino acid). This variety allows each person's immune system to react to a wide range of foreign invaders. Most HLA-B gene alleles are rare, while others do not affect protein function or change the structure of the protein. Hundreds of versions (alleles) of the HLA-B gene are known, each of which is given a particular number (such as HLA-B27). Closely related alleles are categorized together; for example, more than 60 very similar alleles are subtypes of HLA-B27. These subtypes are designated as HLA-B*2701 to HLA-B*2763.

Health Conditions Related to Genetic Changes

Ankylosing spondylitis

Variants in the HLA-B gene, particularly a version called HLA-B27, significantly increase the risk of developing ankylosing spondylitis. This condition is a form of painful, ongoing joint inflammation (chronic inflammatory arthritis) that primarily affects the spine. It is uncertain how the HLA-B27 gene variant causes the increased risk. Researchers speculate that HLA-B27 may abnormally display peptides that trigger an immune reaction, resulting in the inflammatory process that causes arthritis. Other research suggests that the joint inflammation characteristic of this disorder may result from improper folding of the HLA-B27 protein or the presence of abnormal forms of the protein on the cell surface. It is possible that HLA-B27 may increase the risk of ankylosing spondylitis through more than one mechanism, or by different mechanisms in different individuals based on their genetic and environmental background.

Although many people with ankylosing spondylitis have the HLA-B27 variation, most people with this version of the HLA-B gene never develop the disorder. It is estimated that among those with the HLA-B27 allele, only one to five percent develop ankylosing spondylitis. Additional HLA-B alleles play a smaller role in disease risk: the HLA-B47 and HLA-B51 alleles can contribute to increased risk, whereas the HLA-B7 and HLA-B57 alleles might provide some small amount of protection against developing the condition. Other genetic and environmental factors, many of which are unknown, affect the chances of developing ankylosing spondylitis and influence its progression.

Behçet disease

Several versions of the HLA-B gene, particularly HLA-B51, are associated with an increased risk of developing Behçet disease, a chronic inflammatory condition that affects many parts of the body. This association is strongest in people from Japan, the Middle East, and other parts of Asia. Researchers do not know how HLA-B51 increases the risk of this disorder. Although many people with Behçet disease have the HLA-B51 variation, most people with this version of the HLA-B gene never develop the condition. It appears likely that other factors, such as viral or bacterial infections and changes in other genes, also influence the development of this complex disorder.

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Stevens-Johnson syndrome/toxic epidermal necrolysis

Several variations of the HLA-B gene have been studied as risk factors for Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN), a potentially life-threatening skin reaction most often triggered by medications. For example, the variation HLA-B*1502 increases the risk of SJS/TEN in people taking certain medications used to treat seizures, particularly a drug called carbamazepine. This version of the gene is most common among people of Han Chinese or southeast Asian descent. Another version of the gene, HLA-B*5801, increases the risk of SJS/TEN in people treated with allopurinol (a drug used to treat kidney stones and gout, which is a form of arthritis caused by a buildup of uric acid in the joints). This association has been confirmed in southeast Asians and in people of non-Asian ancestry, although HLA-B*5801 occurs less frequently in non-Asian populations.

Studies suggest that the HLA-B gene variations associated with SJS/TEN cause the immune system to react abnormally to some medications. In a process that is not well understood, the triggering drug causes immune cells called cytotoxic T cells and natural killer (NK) cells to release a substance called granulysin. This substance destroys cells in the skin and mucous membranes, including the lining of the mouth and the airways. The death of these cells causes severe blistering and peeling that can have life-threatening effects.

Most people who have variations in the HLA-B gene that are associated with an increased risk of SJS/TEN never develop the condition, even if they are exposed to drugs that can trigger it. Researchers believe that additional genetic and nongenetic factors, many of which are unknown, likely play a role in whether a particular individual develops SJS/TEN.

Other disorders

The HLA-B27 variant is associated with a group of inflammatory joint diseases related to ankylosing spondylitis. These conditions are known as spondyloarthropathies. Some of these disorders are associated with a common skin condition called psoriasis or with chronic disorders that cause inflammation of the intestinal walls (inflammatory bowel disease). One of the spondyloarthropathies, reactive arthritis, is typically triggered by bacterial infections of the gastrointestinal or genital tract. Following an infection, affected individuals may develop arthritis, back pain, and eye inflammation. Like ankylosing spondylitis, many factors probably contribute to the development of reactive arthritis and other spondyloarthropathies.

Among people with human immunodeficiency virus (HIV) infection, a version of the HLA-B gene designated HLA-B*5701 increases the risk of an adverse reaction (hypersensitivity) to the drug abacavir. This medication slows the spread of the HIV-1 virus in the body. People with abacavir hypersensitivity often develop a fever, chills, rash, upset stomach, and other symptoms when treated with this drug.

Several variations of the HLA-B gene appear to play a role in the progression of HIV infection to acquired immunodeficiency syndrome (AIDS). AIDS is a disease that damages the immune system, preventing it from effectively defending the body against infections. The signs and symptoms of AIDS may not appear until 10 or more years after infection with HIV. Studies suggest that people with HIV infection who have HLA-B27 or HLA-B57 tend to progress more slowly than usual to AIDS. On the other hand, researchers believe that HIV-positive individuals who have HLA-B35 tend to develop the signs and symptoms of AIDS more quickly than usual. Other factors also influence the progression of HIV infection to AIDS.

Another version of the HLA-B gene, HLA-B53, has been shown to help protect against severe malaria, a disease caused by a parasite that is carried by mosquitoes. HLA-B53 is most common in West African populations, where malaria is a frequent cause of death in children. Studies suggest that this version of the HLA-B gene may help the immune system respond more effectively to the parasite that causes malaria.

Other Names for This Gene

• 1B07_HUMAN
• HLA class I histocompatibility antigen, B alpha chain
• leukocyte antigen B
• MHC class I HLA-B heavy chain

Genomic Location

Normal Function

The HLA-DPB1 gene provides instructions for making a protein that plays a critical role in the immune system. The HLA-DPB1 gene is part of a family of genes called the human leukocyte antigen (HLA) complex. The HLA complex helps the immune system distinguish the body's own proteins from proteins made by foreign invaders such as viruses and bacteria.

The HLA complex is the human version of the major histocompatibility complex (MHC), a gene family that occurs in many species. The HLA-DPB1 gene belongs to a group of MHC genes called MHC class II. MHC class II genes provide instructions for making proteins that are present on the surface of certain immune system cells. These proteins attach to protein fragments (peptides) outside the cell. MHC class II proteins display these peptides to the immune system. If the immune system recognizes the peptides as foreign (such as viral or bacterial peptides), it triggers a response to attack the invading viruses or bacteria.

The protein produced from the HLA-DPB1 gene attaches (binds) to the protein produced from another MHC class II gene, HLA-DPA1. Together, they form a functional protein complex called an antigen-binding DPαβ heterodimer. This complex displays foreign peptides to the immune system to trigger the body's immune response.

Each MHC class II gene has many possible variations, allowing the immune system to react to a wide range of foreign invaders. Researchers have identified hundreds of different versions (alleles) of the HLA-DPB1 gene, each of which is given a particular number (such as HLA-DPB1*03:01).

Health Conditions Related to Genetic Changes

Granulomatosis with polyangiitis

At least one variant of the HLA-DPB1 gene has been associated with granulomatosis with polyangiitis (GPA). This condition occurs when the immune system malfunctions and attacks the body's own tissues and organs (autoimmunity), causing inflammation that affects the lungs, airways, and kidneys. The associated variant, called HLA-DPB1*0401, has been found more frequently in people with GPA than in those who do not have the condition; this variant is thought to increase the risk of developing GPA.

Because the HLA-DPB1 gene is involved in the immune system, changes in it might be related to the autoimmune response and inflammation that damage the lungs, kidneys, and other organs. However, it is unclear what specific role the HLA-DPB1 gene variant plays in development of this condition. It is likely that environmental factors trigger the condition in people who are genetically predisposed to it. Other genetic factors are also likely to be involved in GPA.

Juvenile idiopathic arthritis

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Other disorders

Variants of the HLA-DPB1 gene are associated with immune reactions to beryllium, a metallic element that can be toxic. Beryllium exposure can occur in manufacturing plants and the nuclear and aerospace industries. About 2 to 10 percent of people exposed to beryllium develop beryllium sensitization or chronic beryllium disease. Sensitization is an immune reaction that occurs in response to beryllium exposure; sensitization can cause an increase in the number of certain immune system cells in the blood, but it may not lead to any symptoms. In some people, sensitization leads to chronic beryllium disease, which is a lung disease characterized by the formation of small masses of inflammatory cells (granulomas). The lungs can become scarred and stiff and lose their ability to function. Having variants of the HLA-DPB1 gene that contain the protein building block (amino acid) glutamic acid at position 69 (written as E69) increases the risk of developing beryllium sensitization or chronic beryllium disease.

Other Names for This Gene

• beta1 domain MHC class II HLA DPB
• class II HLA beta chain
• DPB1
• DPB1_HUMAN
• HLA class II histocompatibility antigen, DP beta 1 chain
• HLA class II histocompatibility antigen, DP(W4) beta chain
• HLA DP14-beta chain
• HLA-DP
• HLA-DP histocompatibility type, beta-1 subunit
• HLA-DP1B
• HLA-DPB
• major histocompatibility complex class II antigen beta chain
• MHC class II antigen beta chain
• MHC class II antigen DP beta 1 chain
• MHC class II antigen DPB1
• MHC class II antigen DPbeta1
• MHC class II HLA-DP-beta-1
• MHC class II HLA-DRB1
• MHC HLA DPB1

Genomic Location

Normal Function

The IL23R gene provides instructions for making a protein called the interleukin 23 (IL-23) receptor. This protein is embedded in the outer membrane of several types of immune system cells, including T cells, natural killer (NK) cells, monocytes, and dendritic cells. These cells identify foreign substances and defend the body against infection and disease.

At the cell surface, the IL-23 receptor interacts with a protein called IL-23. These two proteins fit together like a lock and key. IL-23 is a cytokine, which is a type of protein that regulates the activity of immune cells. When IL-23 binds to its receptor, it triggers a series of chemical signals inside the cell. These signals promote inflammation and help coordinate the immune system's response to foreign invaders such as bacteria and viruses.

Health Conditions Related to Genetic Changes

Ankylosing spondylitis

Several variations (polymorphisms) in the IL23R gene have been found to influence the risk of ankylosing spondylitis. This condition is a form of painful, ongoing joint inflammation (chronic inflammatory arthritis) that primarily affects the spine.

One of these IL23R gene polymorphisms appears to reduce the likelihood of developing this disorder. This genetic change alters a single protein building block (amino acid) in the IL-23 receptor, replacing the amino acid arginine with the amino acid glutamine at protein position 381 (written as Arg381Gln or R381Q). Other IL23R variations appear to increase the risk of developing ankylosing spondylitis.

It is not fully known how these changes are related to a person's risk of developing this disorder, but studies suggest that the effects of IL23R variations are likely related to the IL-23 receptor's role in inflammation. Other genetic and environmental factors, many of which are unknown, also affect the chance of developing ankylosing spondylitis.

Crohn's disease

Several variants in or near the IL23R gene have been found to influence the risk of developing Crohn's disease. These associations have been reported primarily in people of northern European ancestry. For example, Arg381Gln, which is a protective factor for ankylosing spondylitis (described above), also appears to reduce the risk of developing Crohn's disease. Although it is unclear how this change protects against Crohn's disease, researchers believe that the receptor's role in triggering inflammation in the intestinal walls may underlie its connection with this disorder.

Psoriatic arthritis

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Other disorders

Variants in the IL23R gene have also been associated with the risk of several other immune system-related conditions, including a skin disorder called psoriasis. In people with light skin, this chronic inflammatory condition causes patches of red, irritated skin that are often covered by flaky white scales, but these patches are darker looking in people with darker skin. Psoriasis likely results from a malfunction of the immune system in which the body's immune response turns against itself, attacking healthy skin cells by mistake.

Each of the known IL23R variations changes a single amino acid in the IL-23 receptor. One of these variations, Arg381Gln, appears to reduce the risk of developing psoriasis. (This variation has also been shown to protect against ankylosing spondylitis and Crohn's disease, described above.) Other IL23R variations may increase the risk of developing psoriasis. Researchers suggest that changes in the IL23R gene may contribute to general problems with regulation of the immune system, which may help explain why these variations are related to several different disorders characterized by immune system dysfunction.

Other Names for This Gene

• IL-23R
• IL23R_HUMAN
• interleukin-23 receptor

Genomic Location

This condition has an unknown inheritance pattern. Approximately 40 percent of affected individuals have at least one close family member with psoriasis or psoriatic arthritis.

Symptoms of psoriatic arthritis vary greatly from person to person. They may include:

• Scaly, inflamed patches of skin characteristic of psoriasis, often on the scalp, elbows, or knees.
• Joint stiffness, pain, and swelling of one or more joints. The joints of the spine can be affected as well, leading to stiffness in the neck, lower back, and hips. Joint stiffness is often worse in the morning or after resting.
• Fatigue, or feeling tired often or having a lack of energy.
• Tenderness in entheses, areas where tendons or ligaments attach to bones. The back of the heel and sole of the foot are commonly affected spots.
• Painful, sausage-like swelling of a whole finger or toe.
• Nail changes, such as pitting (tiny dents) or crumbling. Nails can also separate from the nail bed.
• Eye inflammation, especially uveitis, inflammation of the middle layer of the eye. This condition can cause eye pain, redness, and blurry vision, and must be treated promptly to avoid vision loss.
• Inflammatory bowel disease, which causes inflammation in the digestive tract, occurs in some people.

Although there is no definitive test for psoriatic arthritis, your doctor may do the following to diagnose you with the condition:

• Ask if you have a family history of psoriasis or psoriatic arthritis.
• Talk to you about your symptoms and give you a physical exam. Swollen and tender joints, psoriasis skin lesions, and nail changes are telltale signs.
• Examine your skin for signs of psoriasis, if you have never been diagnosed with the condition.
• Take a blood sample to check for other conditions, such as rheumatoid arthritis.
• Order imaging tests such as x-rays, ultrasounds, or magnetic resonance imaging (MRI), which can reveal changes in joints, entheses, or the spine.

Treatment of psoriatic arthritis continues to improve, which can give many people relief from symptoms and improve their quality of life. Your treatment plan depends on the pattern of symptoms and their severity. You may need to try different medications to find one that works, or use a combination of them.

Milder forms of the disease may be treated by:

• Over-the-counter anti-inflammatory and pain medications, whichcan help treat pain and swelling.
• Injections of corticosteroids, strong inflammation-fighting drugs, into the affected joints. Because they are potent drugs, your doctor will prescribe the lowest dose possible to achieve the desired benefit.

More persistent or severe disease may be treated by:

• Disease-modifying anti-rheumatic drugs (DMARDs), oral therapies that suppress the immune system on a broad level and help to decrease signs and symptoms of the disease.
• Biologic response modifiers, which target specific immune messages and interrupt the signal, helping to decrease or stop inflammation and prevent future damage.

Health care providers who treat psoriatic arthritis include:

• Rheumatologists, who specialize in arthritis, including psoriatic arthritis, and other diseases of the bones, joints, and muscles.
• Dermatologists, who specialize in conditions of the skin, hair, and nails.
• Physiatrists (rehabilitation specialists) who supervise exercise programs.
• Occupational therapists, who teach ways to protect joints, lessen pain, perform activities of daily living, and conserve energy.
• Physical therapists, who help to improve joint function.
• Primary health care providers, including family doctors, internists, and pediatricians, who treat problems as they arise and coordinate care between the different specialized health care providers.
• Dietitians, who teach about nutrition and maintaining a healthy weight.

Having psoriatic arthritis can affect your day-to-day life, but there are ways to lessen its impact. In addition to going to your doctor regularly, here are some things you can try to help manage your symptoms:

• If you smoke, work with your doctor to make a plan to quit. Some studies have shown that the more a person smokes, the worse the symptoms tend to be.
• Maintain a healthy weight. This will place less strain on your joints and may help you respond better to medications.
• Try different exercise programs and find the best one for you. Low-impact activities such as walking, cycling, swimming, yoga, or tai chi may be especially helpful. Talk with your doctor before starting any exercise program.
• Protect your joints, such as by pushing open a door with your whole body instead of just your fingers.
• Reach out for support to help cope with the emotional and mental effects of psoriatic arthritis. Consider joining a support group or seek counseling, which can help you learn more about coping and living with the disease.

Participating in your care can help build confidence in your ability to perform day-to-day activities, allowing you to lead a full, active, and independent life.

The NIAMS supports translational and clinical research at universities and other organizations throughout the country that are studying psoriatic arthritis. Researchers are continuing work to understand what causes the disease, which may help them identify new treatment strategies. Following are some examples of the types of studies that are ongoing.

• Research has already uncovered many of the immune molecules involved in psoriasis and psoriatic arthritis. Investigators are using structural and biochemical methods to engineer inhibitors of these molecules, which may form the basis of new medicines.
• Using bioinformatics methods to mine patient records and gene activity datasets, scientists are seeking to identify new therapeutic targets.
• Scientists do not know why some people with psoriasis get psoriatic arthritis, while others do not. They are working to uncover ways to predict which patients will develop psoriatic arthritis so that those at risk can be closely monitored and treated if symptoms arise.
• Other researchers are investigating if treating patients who have psoriasis with biologic medications, which act throughout the body, can prevent the onset of psoriatic arthritis.
• Investigators suspect that internal factors besides a person’s genes may contribute to getting psoriatic arthritis. For example, they are studying the roles played by epigenetics (modifications to DNA that turn genes on and off) and the microbiome (the collection of all the microbes that inhabit the human body).
• People with psoriatic arthritis have a greater risk of certain diseases and conditions, such as obesity, diabetes, anxiety, depression, and cardiovascular problems. Scientists are seeking ways to decrease these risks.