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Showing results for tags 'genetic susceptibility'.
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Celiac.com 10/23/2024 - Cardiovascular diseases, such as coronary artery disease and stroke, have long been connected with various immune-mediated disorders due to the role inflammation plays in both conditions. This study explores whether there is a genetic connection between cardiovascular diseases and specific immune-mediated diseases, with a particular focus on psoriasis. Psoriasis is a chronic inflammatory condition that has previously been associated with an increased risk of cardiovascular disease. However, it is unclear whether the genetic risk factors for cardiovascular disease are also linked to an increased risk of psoriasis and other immune-related conditions. Study Objectives The main goal of the study was to investigate whether genetic predispositions to coronary artery disease and stroke also increase the risk of developing psoriasis or other immune-mediated diseases. The researchers utilized a method called Mendelian randomization, which uses genetic data to determine whether there is a causal relationship between two traits, as opposed to just an observed association. By using large datasets from genome-wide association studies, the study aimed to uncover whether genetic predictors of cardiovascular disease are directly linked to immune-mediated diseases, such as psoriasis, rheumatoid arthritis, and inflammatory bowel disease. Methods and Data To conduct the analysis, the study used Mendelian randomization to evaluate the genetic links between cardiovascular disease and immune-mediated diseases. This approach is particularly effective in differentiating causality from correlation because it uses genetic markers as proxies for risk factors. The researchers analyzed summary data from genome-wide association studies for coronary artery disease, stroke, psoriasis, and nine other immune-mediated diseases. The data included a large sample of participants, with over 1.1 million individuals for cardiovascular disease traits and nearly 500,000 for psoriasis. The study specifically examined whether genetic markers associated with coronary artery disease and stroke were linked to an increased risk of developing psoriasis or any of the other immune-mediated diseases. Key Findings The results of the study revealed that genetic predictors for both coronary artery disease and stroke were significantly associated with an increased risk of psoriasis. In particular, genetic risk factors for coronary artery disease were found to increase the risk of developing psoriasis by about 7%, while genetic risk factors for stroke increased the risk by 22%. Interestingly, when adjustments were made for stroke risk, the association between coronary artery disease and psoriasis became statistically insignificant. This suggests that there may be a shared genetic component that links both cardiovascular diseases and psoriasis, rather than two separate pathways. On the other hand, the study found no significant genetic link between cardiovascular disease risk factors and other immune-mediated diseases, such as rheumatoid arthritis and inflammatory bowel disease. This finding was somewhat unexpected, as these diseases also involve inflammation, which is thought to be a common factor in both cardiovascular disease and immune-mediated disorders. Genetic Risk and Celiac Disease The study also explored the relationship between genetic predictors of cardiovascular disease and various immune-mediated diseases, including celiac disease. Data from 4,533 cases of celiac disease and 10,750 controls were included in the analysis. The results indicated no significant association between genetic risk factors for cardiovascular disease—such as coronary artery disease or stroke—and the risk of developing celiac disease. This finding suggests that while cardiovascular genetic factors may influence the risk of developing psoriasis, they do not appear to have the same effect on celiac disease or other immune-mediated conditions. Understanding the Relationship Between Psoriasis and Cardiovascular Disease The discovery that genetic risk factors for cardiovascular disease are linked specifically to psoriasis, but not to other immune-mediated diseases, points to the possibility of a unique shared biological mechanism. Psoriasis is a disease driven by inflammation, and inflammation is also a key factor in the development of cardiovascular diseases like coronary artery disease and stroke. However, the study’s findings suggest that this connection may not extend to all immune-mediated diseases, challenging previous assumptions about the broad relationship between cardiovascular disease and inflammation-driven conditions. One possible explanation for this connection could lie in the specific inflammatory pathways involved in both cardiovascular disease and psoriasis. Psoriasis is known to involve certain inflammatory cellular and cytokine pathways, and these same pathways may play a role in the development of cardiovascular disease. However, these pathways may not be as significant in other immune-mediated diseases, which could explain the lack of genetic association with conditions like rheumatoid arthritis and inflammatory bowel disease. Implications for Treatment and Future Research The findings of this study have several important implications. First, they highlight the need for further research into the shared genetic mechanisms underlying cardiovascular disease and psoriasis. Understanding these mechanisms could lead to the development of new treatments that target both conditions. For example, therapies that reduce inflammation in psoriasis patients could potentially help lower their risk of cardiovascular disease, and vice versa. Second, the study underscores the importance of personalized medicine. As more is learned about the genetic links between different diseases, it becomes increasingly possible to develop tailored treatments that address an individual's unique genetic risk factors. For patients with psoriasis who are also at risk for cardiovascular disease, this could mean more targeted interventions that address both conditions simultaneously. Implications for Those with Celiac Disease The study’s findings highlight the importance of understanding the genetic overlap between cardiovascular disease and psoriasis, but they also underline the distinction when it comes to celiac disease. For those with celiac disease, the results are reassuring as they show no genetic link between cardiovascular risks and the condition. This separation emphasizes that while shared inflammatory pathways may exist between certain immune-mediated diseases and cardiovascular disease, celiac disease does not appear to be influenced by these cardiovascular genetic factors. As such, this research may provide a better understanding of how different immune-mediated diseases interact with cardiovascular health, guiding future research and treatment strategies. Read more at: jamanetwork.com
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Celiac.com 05/06/2021 - Gluten neuropathy is the term used to describe peripheral neuropathy that occurs in patients with gluten sensitivity or celiac disease in the absence of other risk factors. A team of researchers recently set out to describe the neurophysiological progression rate of gluten neuropathy across time and look into the potential role of genetic susceptibility in its development. The research team included Panagiotis Zis, Ptolemaios Sarrigiannis, Artemios Artemiadis, David S. Sanders & Marios Hadjivassiliou. They are variously affiliated with the Academic Directorate of Neurosciences, and the Academic Unit of Gastroenterology at Sheffield Teaching Hospitals NHS Foundation Trust in Sheffield, UK, and with the Medical School, University of Cyprus in Nicosia, Cyprus. The team looked at a group of 45 patients with gluten neuropathy for an average follow-up period of 8 ± 5 years. They gathered clinical and neurophysiological data, along with HLA-DQ genotype information. Average patient age at diagnosis was 60 ± 12 years. More than 75% of patients had a length-dependent neuropathy, while the rest had sensory ganglionopathy. Sixty percent of patients with positive DQA1*02 suffered from sensory ganglionopathy compared to just under 14% of DQA1*02-negative patients. The team also noted a statistically significant detail regarding the DQB1*06 allele and the DQA1*01/DQB1*06 haplotype, which were found more frequently in patients with gluten neuropathy than in healthy control subjects. The team found a linear effect of time on the neurophysiological findings, with radial sensory nerve action potential decreasing nearly 2% annually, sural sensory nerve action potential decreasing 3%, and tibial nerve motor compound action potential decreasing 6.5%, independently of age or gender. Gluten neuropathy is a late manifestation of gluten sensitivity and celiac disease. The majority of patients with gluten neuropathy suffer from length-dependent neuropathy with a linear deterioration over time. To help spot patients at risk for developing sensory ganglionopathy, the team recommends HLA genotyping for patients with gluten sensitivity or celiac disease who present with neuropathic symptoms. Read the full report in the Journal of Neurology volume 268, pages199–205(2021)
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Celiac.com 01/03/2019 - Celiac disease is common in Saudi Arabia, affecting about 1.5% of the country's total population, according to a recent mass screening study. A team of researchers recently set out to determine the frequency of celiac disease-predisposing human leukocyte antigen (HLA)-DQ genotypes in the Saudi population. The research team included A Al-Hussaini, H Alharthi, A Osman, N Eltayeb-Elsheikh, and A Chentoufi. They are variously affiliated with the Division of Pediatric Gastroenterology, Children's Specialized Hospital, King Fahad Medical City; College of Medicine, Alfaisal University; Prince Abdullah bin Khalid Celiac Disease Research Chair, Department of Pediatrics, Faculty of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia; the Department of Pathology and Laboratory Medicine, Division of Immunology, King Fahad Medical City, Riyadh, Kingdom of Saudi Arabia; the Department of Immunology, University of Mohammed VI for health sciences, Casablanca, Morocco. For their cross-sectional population-based study, the team enrolled 192 randomly selected healthy school children, who all tested negative for tissue transglutaminase-IgA. The team then used polymerase chain reaction sequence-specific oligonucleotide probes to type the children for D QA1 and D QB1 genes. More than half of the children carried the high-risk celiac disease-associated HLA-DQ molecules at the following rates: homozygous DQ2.5 ( 2.6%), DQ2.5/DQ2.2 ( 4.7%), heterozygous DQ2.5 ( 28.15%), homozygous DQ8 ( 4.2%), DQ8/DQ2.2 ( 3.6%), and double dose DQ2.2 ( 9.4%). Another 13% had low-risk celiac disease-associated HLA-DQ molecules, single dose DQ2.2 and heterozygous DQ8. In the ultra low-risk groups, subjects without alleles that promote DQ2/DQ8 variants (33.5%), 13.5% carried only one of the alleles of the high-risk HLA-DQ2.5 heterodimer called "half-heterodimer" (HLA-DQA1*05 in 12% and HLA-DQB1* 02 in 1.5%), and 20.8% lacked all the susceptible alleles (DQX.x). The celiac disease-risk groups showed no important differences in gender distribution. More than half the healthy general Saudi population carries celiac disease-predisposing HLA-DQ genotypes, one of the highest general rates in the world; a fact that may help to explain the high rates of celiac disease in the Saudi population. Source: Saudi J Gastroenterol. 2018 Sep-Oct;24(5):268-273. doi: 10.4103/sjg.SJG_551_17
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