Increased Risk of Autoimmune Disease in Families with Wegener’s Granulomatosis

2010 ◽  
Vol 37 (12) ◽  
pp. 2553-2558 ◽  
Author(s):  
ANN KNIGHT ◽  
SVEN SANDIN ◽  
JOHAN ASKLING
Keyword(s):  
Inflammatory Disease ◽  
Wegener’S Granulomatosis ◽  
Cox Regression ◽  
Disease Risk ◽  
Inflammatory Diseases ◽  
Population Level ◽  
Wegener's Granulomatosis ◽  
First Degree Relatives ◽  
Increased Risk ◽  
Autoimmune Inflammatory Disease

Objective.The etiology of Wegener’s granulomatosis (WG) is unknown. Susceptibility genes for WG that also affect the risks of other autoimmune/inflammatory diseases have been identified, indicating the existence of shared interdisease genetic susceptibilities. To determine the effect, on a population level, of shared susceptibility on disease risk, we assessed the occurrence of autoimmune/inflammatory disease in first-degree relatives of patients with WG.Methods.In the Swedish Hospital Discharge Register we identified 2288 individuals discharged with the diagnosis of WG between 1970 and 2003. Through linkage to the Swedish Multi-generation Register we identified 787 parents, 1212 siblings, and 3650 children of these patients. From the Register of Total Population we identified 10 controls for each patient with WG, and 65,000 of their first-degree relatives. Through linkage to the nationwide Outpatients Register, we identified autoimmune/inflammatory disease among all relatives. Relative risks were estimated as hazard ratio (HR) using Cox regression. The study period was 2001–2006.Results.Biological first-degree relatives of patients with WG were at a moderately increased risk of any autoimmune/inflammatory disease (HR 1.32, 95% CI 1.18–1.49), including specific associations with, for example, multiple sclerosis (HR 1.92, 95% CI 1.16–3.16), Sjögren’s syndrome (HR 2.00, 95% CI 1.07–3.73), and seropositive rheumatoid arthritis (HR 1.54, 95% CI 1.09–2.19).Conclusion.Relatives of patients with WG are at increased risk of being diagnosed with other autoimmune/inflammatory diseases, indicating shared susceptibility between WG and other auto-immune/inflammatory disease.

scholarly journals C-Reactive Protein and All-Cause Mortality in a Large Hospital-Based Cohort

2008 ◽  
Vol 54 (2) ◽  
pp. 343-349 ◽  
Author(s):  
Claudia Marsik ◽  
Lili Kazemi-Shirazi ◽  
Thomas Schickbauer ◽  
Stefan Winkler ◽  
Christian Joukhadar ◽  
...  
Keyword(s):  
Hospital Admission ◽  
Acute Phase ◽  
Cox Regression ◽  
Disease Risk ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Increased Risk ◽  
All Cause Mortality ◽  
Low Sensitivity

Abstract Background: C-reactive protein (CRP), an acute-phase protein, is a sensitive systemic marker of inflammation and acute-phase reactions. Testing CRP concentrations at hospital admission may provide information about disease risk and overall survival. Methods: All first-ever transmittals to the department of medical and chemical laboratory diagnostics for determination of low-sensitivity CRP (n = 274 515, 44.5% male, median age 51 years) between January 1991 and July 2003 were included [median follow-up time: 4.4 years (interquartile range, 2.3–7.4 years)]. The primary endpoint was all-cause mortality. Multivariate Cox regression adjusted for sex and age was applied for analysis. Results: Compared to individuals within the reference category (CRP <5 mg/L), hazard ratios (HR) for all-cause mortality increased from 1.4 (5–10 mg/L category) to 3.3 in the highest category (>80 mg/L, all P <0.001). CRP was associated with various causes of death. The relation of CRP to cancer death was stronger than to vascular death. Younger patients with increased CRP had relatively far worse outcome than older patients (maximal HR: ≤30 years: 6.7 vs >60 years: 1.7–3.7). Interestingly, both short- and long-term mortality were associated with increasing CRP concentrations (>80 mg/L: HR 22.8 vs 1.4). Conclusion: Measurement of low-sensitivity CRP at hospital admission allowed for the identification of patients at increased risk of unfavorable outcome. Our findings indicate that close attention should be paid to hospitalized patients with high CRP not only because of very substantial short-term risk, but also long-term excess risk, the basis for which needs to be determined.

scholarly journals Long term outcomes of patients with chronic inflammatory diseases after percutaneous coronary intervention

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
E Marcusohn ◽  
R Zukermann ◽  
A Roguin ◽  
O Kobo
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Cox Regression ◽  
Inflammatory Diseases ◽  
Tertiary Care ◽  
Coronary Intervention ◽  
Long Term Outcomes ◽  
Chronic Inflammatory Diseases ◽  
Increased Risk ◽  
Percutaneous Coronary

Abstract Introduction Patients with chronic inflammatory diseases are at increased risk for coronary artery disease. Aim We aimed to assess the long-term outcomes of patients with chronic inflammatory diseases who underwent percutaneous coronary intervention. Methods A Retrospective cohort study of all adult (>18 years) patients who underwent PCI in a large [1000 bed] tertiary care centerfrom January 2002 to August 2020. Results A total of 12,951 patients underwent PCI during the study period and were included in the cohort. The population of chronic inflammatory diseases includes 247/12,951 [1.9%]; 70 with IBD and 173 with AIRD. The composite endpoint of mortality, ACS or CHF admission was more frequent in the inflammatory disease group (77.5% in AIRD group, 72.9% in the IBD group and 59.6% in the non-inflammatory group, p<0.001). The adjusted cox regression model found a statistically significant increased risk of the composite primary endpoints of around 40% for patients both with AIRD and IBD. The increased risk for ACS was 61% for AIRD patients and 37% for IBD patients. Patients with inflammatory diseases were found to have a significant increased risk CHF admission, while both IBD and AIED patients had a non-significant increased risk for mortality. Conclusion Patients with AIRD and IBD are at higher risk for cardiovascular events also in long term follow up once diagnosed with CAD and treated with PCI. FUNDunding Acknowledgement Type of funding sources: None.

Abstract P150: Association of Cholesterol Measures With Coronary Heart Disease Risk in Blacks and Whites in the Reasons for Geographic and Racial Differences in Stroke Study (regards)

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Neil Zakai ◽  
Jessica Minnier ◽  
Monika M Safford ◽  
Lisandro Colantonio ◽  
Marguerite M Irvin ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Total Cholesterol ◽  
Racial Differences ◽  
Cox Regression ◽  
Disease Risk ◽  
Point Estimate ◽  
Chd Risk ◽  
Increased Risk ◽  
Blacks And Whites

Introduction: Abnormal plasma lipid levels associate with coronary heart disease (CHD) risk. Race interaction for these associations are not established. Hypothesis: We hypothesized that the association of HDL, LDL, and triglyceride with CHD is stronger in whites versus blacks. Methods: The REasons for Geographic and Racial Differences in Stroke (REGARDS) cohort recruited 30,283 black and white individuals aged 45+ from the contiguous U.S. from 2003-7. Participants were followed until December 31, 2016 for CHD events (i.e., myocardial infarction or CHD death), participants with history of CHD at baseline were excluded. Cox regression models were used to assess the association between baseline lipids and incident CHD events adjusting for traditional cardiovascular risk factors. Results: With 23,894 participants (57.8% white and 58.4% female, mean age 64.11± 9.32), over a median 9.9 years of follow-up, 1,487 CHD events occurred (615 among blacks). Overall, higher total Cholesterol, LDL cholesterol, and triglycerides were associated with increased risk of CHD in both blacks and whites with no evidence of a race interaction (Table 1). For HDL, the point estimate was more protective in whites (HR 0.90) than in blacks (HR 0.98), but the interaction was non-significant (p=0.15). However, when HDL was stratified into clinical categories (<40, 40-59, and ≥60), the reduction in point estimates was maintained among whites (HR 1.00, 0.88, and 0.74) but not among blacks (HR 1.00, 1.31, and 1.19) for HDL <40, 40-59, and ≥60 respectively, p-interaction 0.01. Conclusion: Total cholesterol, LDL, and triglycerides predict CHD risk equally in blacks and whites in the REGARDS study, however there is heterogeneity in the protective effect by race, especially when traditional clinical categories are used. In whites, higher HDL is associated with reduced risk, whereas in blacks the association is not maintained. These findings suggest that HDL levels are a more viable metric for white than blacks to predict CHD risk.

scholarly journals Methylation-Based Biological Age and Breast Cancer Risk

2019 ◽  
Vol 111 (10) ◽  
pp. 1051-1058 ◽  
Author(s):  
Jacob K Kresovich ◽  
Zongli Xu ◽  
Katie M O’Brien ◽  
Clarice R Weinberg ◽  
Dale P Sandler ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Cox Regression ◽  
Disease Risk ◽  
Statistical Tests ◽  
Biological Age ◽  
Cancer Case ◽  
Increased Risk

Abstract Background Age is one of the strongest predictors of cancer, chronic disease, and mortality, but biological responses to aging differ among people. Epigenetic DNA modifications have been used to estimate “biological age,” which may be a useful predictor of disease risk. We tested this hypothesis for breast cancer. Methods Using a case-cohort approach, we measured baseline blood DNA methylation of 2764 women enrolled in the Sister Study, 1566 of whom subsequently developed breast cancer after an average of 6 years. Using three previously established methylation-based “clocks” (Hannum, Horvath, and Levine), we defined biological age acceleration for each woman by comparing her estimated biological age with her chronological age. Hazard ratios and 95% confidence intervals for breast cancer risk were estimated using Cox regression models. All statistical tests were two-sided. Results Each of the three clocks showed that biological age acceleration was statistically significantly associated with increased risk of developing breast cancer (5-year age acceleration, Hannum’s clock: hazard ratio [HR] = 1.10, 95% confidence interval [CI] = 1.00 to 1.21, P = .04; Horvath’s clock: HR = 1.08, 95% CI = 1.00 to 1.17, P = .04; Levine’s clock: HR = 1.15, 95% CI = 1.07 to 1.23, P < .001). For Levine’s clock, each 5-year acceleration in biological age corresponded with a 15% increase in breast cancer risk. Although biological age may accelerate with menopausal transition, age acceleration in premenopausal women independently predicted breast cancer. Case-only analysis suggested that, among women who develop breast cancer, increased age acceleration is associated with invasive cancer (odds ratio for invasive = 1.09, 95% CI = 0.98 to 1.22, P = .10). Conclusions DNA methylation-based measures of biological age may be important predictors of breast cancer risk.

Cardiovascular disease risk in survivors of 20 adult cancers.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. 11571-11571
Author(s):  
Helen Strongman ◽  
Sarah Gadd ◽  
Anthony Matthews ◽  
Kathryn Mansfield ◽  
Susannah Jane Stanway ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Cancer Survivors ◽  
Cox Regression ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Cancer Site ◽  
Cvd Risk ◽  
Increased Risk ◽  
Wide Range

11571 Background: There are concerns about long-term cardiovascular disease (CVD) risk in cancer survivors, but few studies have quantified the risks for a wide range of cancers and specific CVD outcomes. Methods: Using UK electronic health records, we identified cohorts of adults alive one year after a cancer diagnosis at 20 different sites. Risks of a range of CVD outcomes were compared to age, sex and general practice matched cancer free controls using Cox regression; crude and adjusted models were compared to investigate the role of shared cancer/CVD risk factors (e.g. smoking and diabetes). Results: 126 120 cancer survivors and 603 144 controls were followed over a median (IQR) 4.6 (2.5-8.1) and 5.6 (3.2-9.2) years. Crude and adjusted hazard ratios (HRs) were similar. In adjusted models, there was strong evidence (p<0.01) of increased risk of CVDs among cancer survivors compared with controls: venous thromboembolism (VTE, 18 cancers), heart failure/cardiomyopathy (7 cancers), arrhythmia (4 cancers), and stroke (3 cancers). In stratified analyses HRs were higher in younger people and continued beyond 5 years post diagnosis. Conclusions: We found increased long term CVD risk among survivors of several cancers compared to the general population, which varied by cancer site and specific CVD outcome.[Table: see text]

Survival Predictors of Head and Neck Burkitt’s Lymphoma: An Analysis of the SEER Database

2021 ◽  
pp. 019459982110415
Author(s):  
Salma Ahsanuddin ◽  
Joshua B. Cadwell ◽  
Neel R. Sangal ◽  
Jordon G. Grube ◽  
Christina H. Fang ◽  
...  
Keyword(s):  
Head And Neck ◽  
Cox Regression ◽  
Medical Center ◽  
Academic Medical Center ◽  
Population Level ◽  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Seer Database ◽  
Increased Risk ◽  
Ann Arbor

Objective To analyze population-level data for Burkitt’s lymphoma of the head and neck. Study Design Retrospective study of a national cancer database. Setting Academic medical center. Methods The SEER database (Surveillance, Epidemiology, and End Results) identified all patients with primary Burkitt’s lymphoma of the head and neck from 1975 to 2015. Demographic, clinicopathologic, and treatment characteristics were analyzed. Multivariable Cox regressions analyzed factors associated with survival while controlling for baseline differences. Results A total of 920 patients with a mean (SD) age of 37.6 years (25.0) were identified. A majority of patients were White (82.8%) and male (72.3%). The most primary common sites included the lymph nodes (61.3%), pharynx (17.7%), and nasal cavity/paranasal sinuses (5.2%). The majority of patients received chemotherapy (90.5%), while fewer underwent surgery (42.1%) or radiotherapy (12.8%). Choice of treatment differed significantly among patients of different ages, year of diagnosis, primary site, nodal status, and Ann Arbor stage. Overall 10-year survival was 67.8%. On multivariable Cox regression, patients with older age (hazard ratio [HR], 1.05 per year; P < .001) and higher stage at presentation had increased risk of mortality ( P < .001). Furthermore, cases diagnosed between 2006 and 2015 (HR, 0.35; P < .001) and 1996 and 2005 (HR, 0.53; P = .001) had lower mortality when compared with those diagnosed between 1975 and 1995. Treatment including surgery and chemotherapy tended to have the best survival ( P < .001). Conclusion Burkitt’s lymphoma of the head and neck diagnosed in more recent years has had improved survival. Factors significantly associated with survival include age, Ann Arbor stage, and treatment regimen. Treatment including surgery and chemotherapy was associated with the highest survival.

Intermediate Renal Outcomes, Kidney Failure, and Mortality in Obese Kidney Donors

2021 ◽  
pp. ASN.2021040548
Author(s):  
Hassan N. Ibrahim ◽  
Dina N. Murad ◽  
Sean A. Hebert ◽  
Horacio E. Adrogue ◽  
Hana Nguyen ◽  
...  
Keyword(s):  
Kidney Failure ◽  
Cox Regression ◽  
Disease Risk ◽  
Absolute Risk ◽  
Kidney Donors ◽  
Risk Of Death ◽  
Increased Risk ◽  
Time Varying Covariates ◽  
Baseline Covariates

BackgroundObesity is associated with the two archetypal kidney disease risk factors: hypertension and diabetes. Concerns that the effects of diabetes and hypertension in obese kidney donors might be magnified in their remaining kidney have led to the exclusion of many obese candidates from kidney donation.MethodsWe compared mortality, diabetes, hypertension, proteinuria, reduced eGFR and its trajectory, and the development of kidney failure in 8583 kidney donors, according to body mass index (BMI). The study included 6822 individuals with a BMI of <30 kg/m2, 1338 with a BMI of 30–34.9 kg/m2, and 423 with a BMI of ≥35 kg/m2. We used Cox regression models, adjusting for baseline covariates only, and models adjusting for postdonation diabetes, hypertension, and kidney failure as time-varying covariates.ResultsObese donors were more likely than nonobese donors to develop diabetes, hypertension, and proteinuria. The increase in eGFR in obese versus nonobese donors was significantly higher in the first 10 years (3.5 ml/min per 1.73m2 per year versus 2.4 ml/min per 1.73m2 per year; P<0.001), but comparable thereafter. At a mean±SD follow-up of 19.3±10.3 years after donation, 31 (0.5%) nonobese and 12 (0.7%) obese donors developed ESKD. Of the 12 patients with ESKD in obese donors, 10 occurred in 1445 White donors who were related to the recipient (0.9%). Risk of death in obese donors was not significantly increased compared with nonobese donors.ConclusionsObesity in kidney donors, as in nondonors, is associated with increased risk of developing diabetes and hypertension. The absolute risk of ESKD is small and the risk of death is comparable to that of nonobese donors.

Shared genetic factors may not explain the raised risk of comorbid inflammatory diseases in multiple sclerosis

2012 ◽  
Vol 18 (10) ◽  
pp. 1430-1436 ◽  
Author(s):  
H Roshanisefat ◽  
S Bahmanyar ◽  
J Hillert ◽  
T Olsson ◽  
S Montgomery
Keyword(s):  
Multiple Sclerosis ◽  
Genetic Factors ◽  
Cox Regression ◽  
Disease Risk ◽  
Inflammatory Diseases ◽  
Inflammatory Conditions ◽  
Disease Characteristics ◽  
Immune Mediated ◽  
Risk Patients ◽  
Shared Genetic

Background: Comorbid inflammatory conditions in multiple sclerosis (MS) patients suggest shared risks with MS. Objective: To estimate if the risk of immune-mediated disease in MS patients and their parents is increased. Methods: Swedish register data were analysed using Cox regression to estimate immune-mediated disease risk among 11284 fathers and 12006 mothers of MS patients, compared with 123158 fathers and 129409 mothers of index subjects without MS. Similar analyses were conducted among 20276 index subjects with MS and 203951 without. Results: Parents of patients with MS did not have a significantly altered immune-mediated disease risk. Patients with MS had a consistently raised risk for several immune-mediated diseases: ulcerative colitis, Crohn’s disease, type 1 diabetes, psoriasis, polyarthritis nodosa and pemphigoid. The risk was more pronounced for diseases diagnosed subsequent to MS onset. Conclusion: The increased occurrence of other immune-mediated diseases in MS patients may not be due to shared genetic factors and surveillance bias is likely to be the main or possibly the entire explanation. If not entirely explained by surveillance bias, a modestly raised occurrence of comorbid diseases may be due to shared environmental risks or factors related to MS disease characteristics.

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