Psoriasis is an immune-mediated disease (a disease with an unclear cause that is characterized by inflammation caused by dysfunction of the immune system) that causes inflammation in the body. There may be visible signs of inflammation such as raised plaques (plaques may look different for different skin types) and scales on the skin.
This occurs because the overactive immune system speeds up skin cell growth. Normal skin cells completely grow and shed (fall off) in a month. With psoriasis, skin cells do this in only three or four days. Instead of shedding, the skin cells pile up on the surface of the skin. Some people report that psoriasis plaques itch, burn, and sting. Plaques and scales may appear on any part of the body, although they are commonly found on the elbows, knees, and scalp.
Inflammation caused by psoriasis can impact other organs and tissues in the body. People with psoriasis may also experience other health conditions.
One in three peoples may also develop psoriatic arthritis. Signs of PsA include swelling, stiffness, and pain in the joints and areas surrounding the joints. PsA often goes undiagnosed, particularly in its milder forms. However, it’s important to treat PsA early on to help avoid permanent joint damage.
Psoriasis locations can be anywhere on the body. Common psoriasis locations:
Plaques can be a few small patches or can affect large areas. It’s possible to have psoriasis plaques and scales in more than one location on the body at a time. Psoriasis on certain locations, called high-impact sites, can have an increased negative impact on quality of life, regardless of the total area affected by psoriasis.
While scientists do not know what exactly causes psoriasis, we do know that the immune system and genetics play major roles in its development. One thing we do know: psoriasis is not contagious. You cannot catch psoriasis from another person. Usually, something triggers psoriasis, causing symptoms to appear or worsen. Triggers vary from person to person.
The link between psoriasis and Metabolic Syndrome (MetS) has been observed, but it's not clear which one comes first or causes the other. Being overweight and having abnormal levels of fats in the blood increase the chances of getting psoriasis.
People with MetS have higher levels of inflammation markers, which might make them more likely to get psoriasis. MetS and psoriasis both involve inflammation, which affects the body's immune system. Also, certain proteins involved in inflammation are linked to both psoriasis and problems with regulating fats in the blood.
When people are overweight, their body fat releases substances that cause inflammation, which could contribute to psoriasis. Some researchers think there might be shared genetic factors between psoriasis and MetS.
Treating Metabolic Syndrome could help in reducing severity and symptoms of Psoriasis.
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Overlapping inflammatory pathways and genetic predisposition may link the pathophysiology of Metabolic Syndrome and psoriasis. Given this overlap, it is reasonable to infer that the conditions are related and that activity in one may be accompanied by activity in the other; likewise, effective treatment of one condition may result in improvement of the other. Adequate control of MetS through medication or lifestyle changes may lead to improvement in the signs and symptoms of psoriasis.
Diabetes and psoriasis are prevalent conditions with a spectrum of serious adverse outcomes. Both diseases are common comorbidities for each other, and diabetes is considered as a risk factor for psoriasis and vice versa. However, it is our contention that these diseases are not merely comorbidities of each other but rather share common underlying pathophysiologies (ie, genes and epigenetic changes, inflammation, abnormal environment, and insulin resistance) that drive disease.
Long term, low dose methotrexate is associated with insidious development of hepatic fibrosis in at least 5% of patients, which in some instances leads to cirrhosis and liver decompensation. The absence of serum enzyme elevations accompanying this progressive fibrosis makes it difficult to monitor patients short of performing routine surveillance liver biopsies at 1 to 2 year intervals. As shown in this example, even surveillance liver biopsies may not adequately reflect the severity of the liver injury and allow for stopping therapy before onset of serious fibrosis.