Doran MF, Crowson CS, Pond GR, O'Fallon WM, Gabriel SE. Frequency of infection in patients with rheumatoid arthritis compared with controls: a population-based study

Mayo Clinic, Rochester, Minnesota 55905, USA.
Arthritis & Rheumatology (Impact Factor: 7.76). 09/2002; 46(9):2287-93. DOI: 10.1002/art.10524
Source: PubMed


A high frequency of infections complicating rheumatoid arthritis (RA) has been described in reports of case series. This retrospective longitudinal cohort study was undertaken to compare the frequency of infections in a population-based incidence cohort of RA patients with that in a group of individuals without RA from the same population.
RA patients included all members of an incidence cohort of Rochester, Minnesota residents ages >or=18 years who were first diagnosed as having RA between 1955 and 1994. One age- and sex-matched subject without RA was selected for each patient with RA. Study subjects were followed up by review of their entire medical record until death, migration from the area, or study end (January 1, 2000), and details of all documented infections, along with information on potential risk factors for infection, were recorded. Hazard ratios for infections were estimated using stratified Andersen-Gill proportional hazards models, with adjustment for potential confounders.
The 609 RA patients and 609 non-RA study subjects (mean age 58.0 years; 73.1% female) were followed up for a mean of 12.7 years and 15.0 years, respectively, reflecting higher mortality among the group with RA. Hazards ratios for objectively confirmed infections, infections requiring hospitalization, and any documented infection in patients with RA were 1.70 (95% confidence interval [95% CI] 1.42-2.03), 1.83 (95% CI 1.52-2.21), and 1.45 (95% CI 1.29-1.64), respectively, after adjustment for age, sex, smoking status, leukopenia, corticosteroid use, and diabetes mellitus. Sites of infection with the highest risk ratios were bone, joints, skin, soft tissues, and the respiratory tract.
In this study, patients with RA were at increased risk of developing infections compared with non-RA subjects. This may be due to immunomodulatory effects of RA, or to agents with immunosuppressive effects used in its treatment.

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    • "of RA[10,12,13]. Co-morbid conditions that are over-represented in RA patients compared with the general population include cardiovascular disease (CVD)[3,14151617, interstitial lung disease181920, infections[21,22], gastrointestinal disease[12,23]and osteoporosis[24,25]. There are no convincing data for evidence of greater risk of malignancy, although a slight increase in overall risk has been reported[26]. "
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    ABSTRACT: Patients with rheumatoid arthritis (RA) suffer from co-morbidities that contribute to a shortened lifespan. Inflammation is important for the development of cardiovascular disease, but little is known on its relationship with other co-morbidities. We investigated the role of inflammation for the development of new comorbidities in early RA. Since 1995, all patients with early RA in Northern Sweden are included in a prospective study on co-morbidities, with a total of 950 patients being included. At the time for this study, 726 had been ill for ≥5 years. Data on co-morbidities, clinical and laboratory disease activity and pharmacological therapy were collected from patient records and further validated using a questionnaire at RA onset (T0) and after 5 years (T5). Of the patients, 53.2 % of the patients had one or more co-morbidity at onset, the commonest being: hypertension (27.3 %), obstructive pulmonary disease (13.9 %), diabetes (8.0 %), hypothyroidism (6.3 %) and malignancy (5.0 %). After 5 years, 41.0 % had developed at least one new co-morbidity, the most common being: hypertension (15.1 %), malignancy (7.6 %), stroke/transient ischemic accident (5.1 %), myocardial infarction (4.3 %) and osteoporosis (3.7 %). Age at disease onset, a raised erythrocyte sedimentation rate (ESR) at inclusion, previous treatment with glucocorticoids (GC; p < 0.001 for all), extra-articular RA (Ex-RA; p < 0.01), DAS28 (area under the curve) at 24 months (p < 0.05), previous smoking at inclusion (p = 0.058) and male gender (p < 0.01) were associated with a new co-morbidity overall at T5. Treatment with biologics (p < 0.05) reduced the risk. In multiple logistic regression modelling, ESR (p = 0.036) at inclusion was associated with a new co-morbidity after 5 years, adjusted for age, sex, smoking and GC treatment. In a similar model, Ex-RA (p < 0.05) was associated with a new co-morbidity at T5. In a third model, adjusted for age and sex, a new pulmonary co-morbidity was associated with a smoking history at inclusion (p < 0.01), but not with ESR. There was substantial co-morbidity among early RA patients already at disease onset, with considerable new co-morbidity being added during the first five years. Measures of disease activity were associated with the occurrence of a new co-morbidity indicating that the inflammation is of importance in this context.
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    • "Patients with rheumatoid arthritis (RA) are reported to have an increased susceptibility to infection [1]. Studies of a specific * Corresponding author. "
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    ABSTRACT: Patients with rheumatoid arthritis (RA) have increased susceptibility to infection. The risk of acquiring infection including tuberculosis (TB) in RA may be increased in patients receiving any immuno-suppressive medication including anti-TNF therapy, which is used successfully for treating patients with rheumatoid arthritis. The aim of this work was to assess the risk of TB in RA patients on anti-TNF therapy compared to conventional disease modifying anti rheumatic drugs when screening for latent TB and TB chemoprophylaxis was applied.
    Full-text · Article · Dec 2014
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    • "The higher rate of infectious events may result from an increased risk of infection inherent to RA (Doran et al., 2002a) (though this appears to have reduced over the last 50 years (Ni Mhuircheartaigh et al., 2013), which is thought to be secondary to immune disturbance associated with disease pathogenesis and the use of immune-modulators to control the condition (Doran et al., 2002a,b). An inherent risk of infection makes establishing a causal link between biologic DMARDs and infections more difficult. "
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