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1.  Breast Cancer in Systemic Lupus Erythematosus 
Oncology  2013;85(2):117-121.
Objective
Evidence points to a decreased breast cancer risk in systemic lupus erythematosus (SLE). We analyzed data from a large multisite SLE cohort, linked to cancer registries.
Methods
Information on age, SLE duration, cancer date, and histology was available. We analyzed information on histological type and performed multivariate logistic regression analyses of histological types according to age, SLE duration, and calendar year.
Results
We studied 180 breast cancers in the SLE cohort. Of the 155 cases with histology information, 11 were referred to simply as ‘carcinoma not otherwise specified’. In the remaining 144 breast cancers, the most common histological type was ductal carcinoma (n = 95; 66%) followed by lobular adenocarcinoma (n = 11; 8%), 15 cancers were of mixed histology, and the remaining ones were special types. In our regression analyses, the independent risk factors for lobular versus ductal carcinoma was age [odds ratio (OR) 1.07, 95% confidence interval (CI) 1.01–1.14] and for the ‘special’ subtypes it was age (OR 1.06, 95% CI 1.01–1.10) and SLE duration (OR 1.05, 95% CI 1.00–1.11).
Conclusions
Generally, up to 80% of breast cancers are ductal carcinomas. Though our results are not definitive, in the breast cancers that occur in SLE, there may be a slight decrease in the ductal histological type. In our analyses, age and SLE duration were independent predictors of histological status.
doi:10.1159/000353138
PMCID: PMC3934367  PMID: 23887245
Breast cancer; Systemic lupus erythematosus; Histopathology; Epidemiology
5.  The MHC2TA –168A/G polymorphism and risk for rheumatoid arthritis: a meta-analysis of 6861 patients and 9270 controls reveals no evidence for association 
Annals of the rheumatic diseases  2007;67(7):933-936.
Background
An association between major histocompatibility complex (MHC) genes, particularly those within the class II HLA region, and rheumatoid arthritis (RA) is well established, and accounts for an estimated 30% of the genetic component in RA. The MHC class II transactivator gene (MHC2TA) on chromosome 16p13 has recently emerged as the most important transcription factor regulating genes required for class II MHC-restricted antigen presentation. Previous studies of a promoter region polymorphism (–168A/G, rs3087456) in the MHC2TA gene and RA have yielded conflicting results.
Objective
To assess the association of the MHC2TA –168A/G polymorphism (rs3087456) and risk for RA by meta-analysis.
Methods
Meta-analysis was performed for 6861 patients with RA and 9270 controls from 10 case–control studies. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated for each study. Summary ORs and 95% CIs were calculated for random effects models.
Results
No effect was observed for the G risk allele (OR 1.02, 95% CI 0.93 to 1.12, p=0.70) or the GG risk genotype (OR 1.14, 95% CI 0.95 to 1.36, p=0.16).
Conclusions
Our results indicate that the MHC2TA –168A/G polymorphism (rs3087456) is not associated with RA yet underscore the importance of including shared epitope allele carrier status, secondary phenotypes and more complete characterisation of MHC2TA variation in future studies.
doi:10.1136/ard.2007.077099
PMCID: PMC2951320  PMID: 17875550
6.  Risk and protective factors for thrombosis in systemic lupus erythematosus 
Annals of the rheumatic diseases  2008;68(2):238-241.
Objectives
Few studies have examined thrombosis in systemic lupus erythematosus (SLE), none have included Asian-Americans, and most have had small sample sizes. We analysed risk factors for thrombosis in a large, multiethnic SLE cohort.
Methods
We studied 1930 SLE subjects, including Caucasians, African-Americans, Asian-Americans and Hispanics. Data were derived from questionnaires and medical records. Documented history of thrombosis was the primary outcome. Explanatory variables included age at SLE diagnosis, gender, ethnicity, disease duration, smoking, antiphospholipid antibody (aPL) status, nephritis and specific medications.
Results
Smoking (OR 1.26, p = 0.011), longer disease duration (OR 1.26 per 5 years p = 0.027×10-7), nephritis (OR 1.35, p = 0.036), aPL positivity (OR 3.22, p<10-9) and immunomodulating medication use (OR 1.40, p = 0.011) were statistically significant risk factors for thrombosis. Younger age at SLE onset was protective (OR 0.52 for age ≤20, p = 0.001). After adjusting for disease severity and incorporating propensity scores, hydroxychloroquine use remained significantly protective for thrombosis (OR 0.62, p = 4.91×10-4).
Conclusions
This study confirms that older age at onset, longer disease duration, smoking, aPL positivity, history of nephritis and immunomodulating medication use are risk factors for thrombosis in SLE. These data are the first to confirm in a large and ethnically diverse SLE cohort that hydroxychloroquine use is protective for thrombosis.
doi:10.1136/ard.2008.093013
PMCID: PMC2875136  PMID: 18782792
7.  Smoking interacts with genetic risk factors in the development of rheumatoid arthritis among older Caucasian women 
Annals of the Rheumatic Diseases  2006;65(9):1163-1167.
Objective
To determine whether the impact of tobacco exposure on rheumatoid arthritis (RA) risk is influenced by polymorphisms at the HLA‐DRB1 and glutathione S‐transferase M1 (GSTM1) loci.
Methods
Subjects were participants from a case‐control study nested within the Iowa Women's Health Study, a population based, prospective cohort study of postmenopausal women. Incident RA cases (n = 115) were identified and medical records reviewed to confirm RA diagnosis. Controls without RA (n = 466) were matched with RA cases by age and ethnic background. HLA‐DRB1 typing classified subjects according to the presence of alleles encoding the RA “shared epitope” (SE) sequence. GSTM1 was genotyped using a multiplex polymerase chain reaction assay. Conditional logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals.
Results
Strong positive associations of smoking (OR = 6.0, p = 0.004), SE positivity (OR = 4.6, p = 0.0006), and GSTM1 null genotype (OR = 3.4, p = 0.007) with risk of RA, and significant gene‐environment interactions (smoking by SE interaction p = 0.034; smoking by GSTM1 interaction p = 0.047) were observed. Stratified analyses indicated that exposure to tobacco smoke primarily increased the risk of RA among subjects who lacked genetic risk factors for the disease (that is, SE negative or GSTM1 present).
Conclusions
Although these findings require confirmation in other groups, the results support the importance of considering both genetic and environmental factors, and also their interaction, in studies of complex diseases like RA.
doi:10.1136/ard.2005.049676
PMCID: PMC1798304  PMID: 16887863
rheumatoid arthritis; tobacco smoke; HLA‐DRB1; genetics;  GSTM1
8.  Association of smoking with dsDNA autoantibody production in systemic lupus erythematosus 
Annals of the Rheumatic Diseases  2005;65(5):581-584.
Objective
To determine whether exposure to tobacco smoke is associated with double stranded DNA (dsDNA) seropositivity in patients with systemic lupus erythematosus (SLE).
Methods
Medical record review was used to confirm the diagnosis of SLE and evaluate dsDNA antibody status. Smoking status at the time of autoantibody testing was assessed by patients' questionnaire responses. Multivariate regression analysis was used to determine whether exposure to tobacco smoke is associated with dsDNA seropositivity, while controlling for sex and age at SLE diagnosis.
Results
A significantly higher risk of dsDNA seropositivity in current smokers than never smokers (odds ratio (OR) = 4.0, 95% confidence interval (CI) 1.6 to 10.4) was shown by multivariate analysis. Current smokers were found to be at higher risk for dsDNA seropositivity than former smokers (OR = 3.0, 95% CI 1.3 to 7.1). The association between current smoking and dsDNA seropositivity remained significant after adjustment for sex, age at SLE diagnosis, amount smoked, age when smoking began, and the duration of smoking cessation (for former smokers).
Conclusion
The association of smoking with dsDNA seropositivity provides insight into the potential mechanisms underlying autoantibody formation. This information may also serve as a possible point of intervention to prevent disease or target treatment.
doi:10.1136/ard.2005.039438
PMCID: PMC1798144  PMID: 16150789
dsDNA; autoantibody production; smoking; systemic lupus erythematosus
9.  Mortality risk associated with rheumatoid arthritis in a prospective cohort of older women: results from the Iowa Women's Health Study 
Annals of the Rheumatic Diseases  2002;61(11):994-999.
Objective: To determine whether rheumatoid arthritis (RA) is associated with excess mortality among older women.
Methods: RA associated mortality was examined in a prospective cohort study that was started in 1986, and included 31 336 women aged 55–69 years without a history of RA at baseline. Up to 1997, 158 cases of RA were identified and validated against medical records. The relative risk (RR) and 95% confidence interval (CI) were calculated as measures of association between RA onset and subsequent mortality (overall and cause-specific) using Cox proportional hazards regression.
Results: Compared with non-cases, women developing RA during follow up had a significantly increased mortality risk (RR=1.52; 95% CI 1.05 to 2.20). Mortality was higher among rheumatoid factor (RF) positive cases (RR=1.90; 95% CI 1.24 to 2.92) than among RF negative cases (RR=1.00; 95% CI 0.45 to 1.99). There were trends towards increased proportions of RA related deaths from infection (RR=3.61; 95% CI 0.89–14.69) and circulatory disease (RR=1.46; 95% CI 0.76 to 2.81) but not malignancy (RR=0.97; 95% CI 0.46 to 2.04).
Conclusions: RA was associated with significantly increased mortality in a cohort of older women, and the association appeared to be restricted to those with RF positive disease.
doi:10.1136/ard.61.11.994
PMCID: PMC1753931  PMID: 12379522
10.  Transfer of P1 inserts into a yeast-bacteria shuttle vector by co-transformation mediated homologous recombination. 
Nucleic Acids Research  1998;26(15):3611-3613.
Manipulation of genomic inserts cloned into the bacteriophage P1 vector is hindered by the large size of the inserts. We have used co-transformation mediated recombination between the yeast-bacteria shuttle vector, pClasper, and various P1 clones to transfer the entire insert from the P1 into pClasper. This results in the insert being stably maintained in yeast, facilitating mutagenesis by homologous recombination. The recombinant plasmid can subsequently be transferred to and stably maintained in bacteria for efficient plasmid preparation. This method can also be applied to inserts from P1 artificial chromosome or bacterial artificial chromosome vectors.
PMCID: PMC147739  PMID: 9671827
12.  Tryptophan-induced eosinophilia-myalgia syndrome. 
Western Journal of Medicine  1990;153(3):269-274.
Eight patients who became ill while taking tryptophan had myalgia, fatigue, rash, fever, edema, alopecia, arthralgias, diminished joint motion, skin tightening, muscle cramping, and distal paresthesias. Three had shortness of breath, and one had pulmonary hypertension. Laboratory abnormalities included peripheral eosinophilia, leukocytosis, thrombocytosis, raised erythrocyte sedimentation rate, and elevated serum levels of aldolase, lactate dehydrogenase, and liver enzymes. Of 4 chest radiographs, 3 were abnormal. Of 5 skin and muscle biopsies, 4 showed sclerosis or mixed inflammatory cell infiltration of the dermis, subcutis, and fascia. Eosinophils were often present, but vasculitis was absent. Muscle inflammation was minimal. We conclude that the "eosinophilia-myalgia syndrome" is related to the ingestion of tryptophan and that abnormalities in the secretion of lymphokines may be important in its pathogenesis.
PMCID: PMC1002528  PMID: 2219890

Results 1-12 (12)