Psoriasis and obesity may share a common genetic cause, says research published by JAMA Dermatology, which suggests a link between psoriasis, type 2 diabetes, body mass index, and obesity. Researchers can learn a lot about shared causes of diseases by using twin studies. A genetic link is one theory for the possible association, researchers say. Wednesday, April 27, 2016 WEDNESDAY, April 27, 2016 (HealthDay News) — The chronic skin disease psoriasis may be linked to excess weight and type 2 diabetes, results of a new study suggest. This study can’t prove that psoriasis causes type 2 diabetes or obesity or vice versa, Lonnberg added. Some of this risk may be due to shared genetics between psoriasis and diabetes. This would suggest that genetic factors play a role in these variables. The contribution of HLA to familial clustering can also be estimated by measuring the expected proportion of affected sib-pairs that share zero haplotypes identical by descent (IBD) divided by the observed proportion s s/Ps (35).
Psoriasis is a long-lasting autoimmune disease characterized by patches of abnormal skin. 4 In twin studies, identical twins are three times more likely to both be affected compared to non-identical twins; this suggests that genetic factors predispose to psoriasis. Diagnosis is typically based on the signs and symptoms. IL-12 and IL-23 share a common domain, p40, which is the target of the recently FDA-approved ustekinumab. Genetic susceptibility factors affecting both the immune system and epidermis could predispose to disease. In this review, we detail the recent advances in the understanding of psoriasis pathogenesis, including the information regarding immunological factors, genetic aspects, and susceptibility genes shared with other autoimmune or inflammatory diseases. Psoriasis Linked To Type 2 Diabetes, Obesity; Research Suggests Genetic Link. Psoriasis may increase risk for obesity and type 1 diabetes. One possibility is that psoriasis predisposes individuals to a sedentary lifestyle, a risk factor for both obesity and diabetes. Most Shared.
The causes of psoriasis aren’t fully known. This means that a combination of things have to happen for you to develop psoriasis: you have to inherit the gene and be exposed to certain external aspects. Furthermore, we found evidence for interaction between the major risk allele, HLA-Cw6, and CARD15, CYLD, and TGM5 susceptibility alleles. Taken together, our data show that shared genetic factors may contribute to the etiology of both psoriasis and other skin or immune-mediated disorders. The pathophysiological overlaps between diverse autoimmune diseases and the co-occurrence of some of them in some families suggest the existence of common etiological mechanisms, and notably a shared genetic background. As in other complex disorders, the difficulty in identifying genes that predispose to psoriasis by linkage studies might be because of the involvement of several low-penetrance genes, which may interact with each other, with the major gene HLA-C, or with environmental factors. Genome-wide association studies (GWAS) have found genetic variants associated with increased risk of developing autoimmunity. Thus along with epidemiological and clinical evidence, this suggests that some genetic risk factors with their biologic effects may be shared across diseases. We have demonstrated that variants associated with these pathways change the strength of signal received from cytokine stimulation, thereby suggesting a predisposition to increased inflammation in susceptible individuals.
In order to better understand the genetic factors that explain this predisposition to autoimmunity, we performed a comprehensive evaluation of shared autoimmune genetic variants. Nevertheless, recent estimates suggest that these risk loci collectively explain between 8 15 of the genetic risk for SLE 3, 4, highlighting the fact that much of the heritable basis for SLE remains to be identified. (CelD), psoriasis (PS), psoriatic arthritis (PsA), juvenile idiopathic arthritis (JIA), Kawasaki disease (KA), systemic sclerosis (SScl), sarcoidosis (SA), vitiligo (VI), alopecia areata (AA) and Beh et’s disease (BeD). We have identified multiple risk variants that predispose to autoimmunity in children. These shared genetic and inflammatory pathways suggest biologic plausibility for an increased risk of diabetes in patients with psoriasis. Psoriasis and the risk of diabetes Relevance: Psoriasis is characterized by chronic red painful skin lesions and is caused by genetic factors and chronic inflammation which may predispose these patients to diabetes. A review of the investigation of PsA genetic susceptibility factors is, therefore, both controversial and complex. Another explanation is that psoriasis and PsA may share susceptibility factors, which may be genetic, environmental or both. The findings in this study suggest that occupational exposure to specific chemicals plays an important role in the development of NHL in Canada. Lymphoma Rates Are Low but Increased in Patients With Psoriasis: Results From a Population-Based Cohort Study in the United Kingdom. Variance decomposition showed that additive genetic factors accounted for 68 (95 CI, 60 -75 ) of the variance in the susceptibility to psoriasis, for 73 (95 CI, 58 -83 ) of the variance in susceptibility to type 2 diabetes mellitus, and for 74 (95 CI, 72 -76 ) of the variance in BMI. DZ twin pairs, who on average only share half of their genetic variants.
Psoriasis Risk Factors
With significant further advances in understanding the genetic risk factors and their biological mechanisms, the possibility of genetically tailored (or personalized ) therapy may be realized. Although all autoimmune diseases share similarities in the basic immunological mechanisms, in other aspects, such as clinical manifestation and age of onset, individual diseases vary widely. This suggests a substantial role of common genetic variation in susceptibility to autoimmune diseases, and contrasts with other multifactorial diseases, such as neurodegenerative disorders. Genetic susceptibility factors affecting both the immune system and epidermis could predispose to disease. In this review, we detail the recent advances in the understanding of psoriasis pathogenesis, including the information regarding immunological factors, genetic aspects, and susceptibility genes shared with other autoimmune or inflammatory diseases. Bowes et al confirmed the existence of PsA-specific genetic risk loci that had been predicted because PsA has a larger estimated heritability than psoriasis. 2 There is a strong genetic component for both psoriasis and PsA, and they share the majority of genetic susceptibility loci identified to date. Although much more work needs to be done to completely understand the molecular pathways leading to psoriasis and PsA, the work by Bowes et al offers genetic clues that may help researchers and clinicians make predictions about who is predisposed to developing PsA.1,6 Increased understanding of the genetic components of the diseases may also enable identification of new therapeutic targets and allow pharmacogenomic predictions about how specific patients will respond to different therapies.