The cause of<unk>  is not fully understood, but many theories exist. Genetics Around one-third of people with<unk>  report a family history of the disease, and researchers have identified genetic loci associated with the condition. Identical twin studies suggest a 70% chance of a twin developing<unk>  if the other twin has the disorder. The risk is around 20% for nonidentical twins. These findings suggest both a genetic susceptibility and an environmental response in developing<unk> .<unk>  has a strong hereditary component, and many genes are associated with it, but how those genes work together is unclear. Most of the identified genes relate to the immune system, particularly the major histocompatibility complex (MHC) and T cells. Genetic studies are valuable due to their ability to identify molecular mechanisms and pathways for further study and potential medication targets. Classic genome-wide linkage analysis has identified nine loci on different chromosomes associated with<unk> . They are called<unk>  susceptibility 1 through 9 (PSORS1 through PSORS9). Within those loci are genes on pathways that lead to inflammation. Certain variations (mutations) of those genes are commonly found in<unk> . Genome-wide association scans have identified other genes that are altered to characteristic variants in<unk> . Some of these genes express inflammatory signal proteins, which affect cells in the immune system that are also involved in<unk> . Some of these genes are also involved in other autoimmune diseases. The major determinant is PSORS1, which probably accounts for 35–50% of<unk>  heritability. It controls genes that affect the immune system or encode skin proteins that are overabundant with<unk> . PSORS1 is located on chromosome 6 in the MHC, which controls important immune functions. Three genes in the PSORS1 locus have a strong association with<unk>  vulgaris: HLA-C variant HLA-Cw6, which encodes an MHC class I protein; CCHCR1, variant WWC, which encodes a coiled coil protein overexpressed in psoriatic epidermis; and CDSN, variant allele 5, which encodes corneodesmosin, a protein expressed in the granular and cornified layers of the epidermis and upregulated in<unk> . Two major immune system genes under investigation are interleukin-12 subunit beta (IL12B) on chromosome 5q, which expresses interleukin-12B; and IL23R on chromosome 1p, which expresses the interleukin-23 receptor, and is involved in T cell differentiation. Interleukin-23 receptor and IL12B have both been strongly linked with<unk> . T cells are involved in the inflammatory process that leads to<unk> . These genes are on the pathway that upregulate tumor necrosis factor-α and nuclear factor κB, two genes involved in inflammation. The first gene directly linked to<unk>  was identified as the CARD14 gene located in the PSORS2 locus. A rare mutation in the gene encoding for the CARD14-regulated protein plus an environmental trigger was enough to cause plaque<unk>  (the most common form of<unk> . Lifestyle Conditions reported as worsening the disease include chronic infections, stress, and changes in season and climate. Others factors that might worsen the condition include hot water, scratching<unk>  skin lesions, skin dryness, excessive alcohol consumption, cigarette smoking, and obesity. The effects of stopping cigarette smoking or alcohol misuse have yet to be studied as of 2019. HIV The rate of<unk>  in human immunodeficiency virus-positive (HIV) individuals is comparable to that of HIV-negative individuals, but<unk>  tends to be more severe in people infected with HIV. A much higher rate of psoriatic arthritis occurs in HIV-positive individuals with<unk>  than in those without the infection. The immune response in those infected with HIV is typically characterized by cellular signals from Th2 subset of CD4+ helper T cells, whereas the immune response in<unk>  vulgaris is characterized by a pattern of cellular signals typical of Th1 subset of CD4+ helper T cells and Th17 helper T cells. The diminished CD4+-T cell presence is thought to cause an overactivation of CD8+-T cells, which are responsible for the exacerbation of<unk>  in HIV-positive people.<unk>  in those with HIV/AIDS is often severe and may be untreatable with conventional therapy. In those with long-term, well-controlled<unk> , new HIV infection can trigger a severe flare-up of<unk>  and/or psoriatic arthritis. Microbes<unk>  has been described as occurring after strep throat, and may be worsened by skin or gut colonization with Staphylococcus aureus, Malassezia spp., and Candida albicans. Guttate<unk>  often affects children and adolescents and can be triggered by a recent group A streptococcal infection (tonsillitis or pharyngitis). Medications Drug-induced<unk>  may occur with beta blockers, lithium, antimalarial medications, nonsteroidal anti-inflammatory drugs, terbinafine, calcium channel blockers, captopril, glyburide, granulocyte colony-stimulating factor, interleukins, interferons, lipid-lowering medications, and paradoxically TNF inhibitors such as infliximab or adalimumab. Withdrawal of corticosteroids (topical steroid cream) can aggravate<unk>  due to the rebound effect.
Psoriasis
Onychomycosis
Parapsoriasis
Basal-cell carcinoma
Lupus vulgaris
Dermatitis
Vitiligo
Dandruff