Abatacept is a co-stimulation blocker that inhibits T-cell activation and interrupts the process leading to inflammation in rheumatoid arthritis. Patients with severe arthritis who took abatacept with at least one other disease-modifying antirheumatic drug in six and 12-month clinical trials demonstrated statistically significant improvement in tender, swollen joints and other clinical measures compared with placebo. Mild to moderate adverse events included headache, nasopharyngitis, hypertension and back pain. The adverse events were similar to those seen in placebo groups. Abatacept should not be used in combination with other biologic agents because of reported increased rates of serious adverse events, including serious infections. With its different mechanism of action, abatacept may be an alternative add-on therapy for patients with an inadequate response to other arthritis therapies.
OBJECTIVES: To determine if young adults with a history of typical absence epilepsy (AE) in childhood have a greater risk of accidental injury than controls with juvenile rheumatoid arthritis (JRA). To assess the nature and severity of these injuries. METHODS: All patients with AE or JRA diagnosed between 1977 and 1985, who were 18 years or older at the onset of the study, were identified from review of pediatric electroencephalographic records for the province of Nova Scotia (AE) or review of the medical records database at the only tertiary care pediatric center for the province (JRA). Fifty-nine (86%) of 69 patients with AE and 61 (80%) of 76 patients with JRA participated in an interview in 1994 or 1995, assessing nature, severity, and treatment of prior accidental injuries. Patients with AE were further questioned about injuries sustained during an absence seizure. RESULTS: Sixteen (27%) of 59 patients with AE reported accidental injury during an absence seizure, with risk of injury being 9% per person-year of AE. Most injuries (81%) occurred during anti-epileptic drug therapy. Although the majority of injuries did not require treatment, 2 (13%) of 16 patients required minor treatment and 2 (13%) of 16 were admitted to hospital. The risk of accidental injury resulting from an absence seizure in person-years at risk was highest in juvenile myoclonic epilepsy (45%), moderate in juvenile AE (14%), and lowest in childhood AE (3%). Patients with AE had a greater number of overall accidental injuries than those with JRA (P
A functional dichotomy between Th1- and Th2-type immune responses has been suggested. This study was performed to investigate whether rheumatoid arthritis (RA), a disease with indications of Th1-deviated immune activation, is inversly related to atopic conditions which are Th2-mediated. Two hundred and sixty-three adult cases of RA, fulfilling the American Rheumatism Association (ARA) 1987 Revised Classification Criteria for RA, were identified in 1995 and compared with 541 randomly selected population referents. The presence of atopic manifestations was established through a postal questionnaire and by demonstrating circulating IgE antibodies to common allergens. RA was inversely associated with certain manifestations of rhinitis, which were regarded as the most reliable indicators of atopic disease in the present study. However, no negative association was seen between RA and asthma and eczema, respectively. The main results give some support for an inverse relationship between RA and rhinitis. The prevalence of circulating IgE antibodies was however similar in cases and controls, suggesting that the T-cell commitment mainly occurs in the affected organs.
Virtually all studies dealing with the occurrence of amyloidosis in subjects with rheumatoid arthritis (RA) have been based on selected series collected from university clinics. The purpose of the study was to obtain information on the true prevalence of amyloidosis and the role of amyloidosis as a cause of death.
The study included all 1666 subjects (480 men and 1186 women) who had died in 1989 and had been entitled under the national sickness insurance scheme to receive specially reimbursed medication for RA.
Amyloidosis was regarded as an immediate cause or an intervening antecedent cause of death in 64 cases (3.8%) and as a contributory cause of death in 33 cases (2%), corresponding to a prevalence of 5.8%. Amyloidosis had been diagnosed during life in 89 instances and was detected at autopsy in eight instances. Twenty-three (4.8%) of the subjects were men and 74 (6.2%) were women (P = 0.25). Compared with the remaining subjects in the study series, the lifespan of the subjects with amyloidosis was shortened by 7.7 yr.
The prevalence of amyloidosis was lower than apparent from most earlier studies. Monitoring information derived from the Finnish sickness insurance system is a useful way of following trends in the occurrence of amyloidosis complicating RA.
Prevalence of AA amyloid in rheumatoid arthritis (RA) is still unclear. The objective of this retrospective study was whether dedicated re-examination of autopsy tissues from RA patients increases the detection rate of amyloid compared to routine examination. Amyloid was re-examined in tissue samples and detection rate compared with original reports of 369 consecutively autopsied RA patients and 370 non-RA patients matched for sex, age, and year of autopsy between 1952 and 1991. Re-examination of 90% of the 739 cases showed doubling of the prevalence of amyloid compared with the original reports: from 18 to 30% in RA and from 2 to 4% in non-RA patients. In RA patients, cardiac amyloid was as frequent as renal amyloid. In RA patients with amyloid at re-examination, amyloidosis had been diagnosed before autopsy in 37%, and these patients had more inflammation and longer disease duration than RA patients without amyloid. Only 56% of RA patients with renal amyloid were known to have proteinuria. In conclusion, this autopsy study shows that amyloid in RA is a common finding which remains frequently undetected. In patients with active and long-lasting RA, a systematic search for amyloid may enable early diagnosis of amyloidosis, which will require effective suppression of inflammation.
OBJECTIVE: Anemia of chronic disease (ACD) is the most common extraarticular manifestation of rheumatoid arthritis (RA), but there is limited information on the cause and consequences of ACD. We investigated the prevalence, relation with proinflammatory cytokines, and effect on disease outcome of ACD in patients with RA. METHODS: The presence of anemia was analyzed in a cohort of 111 consecutive patients with early RA. Anemia was related to markers of erythropoiesis and inflammation [clinically and by levels of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and serum interleukin 1beta (IL-1beta), IL-2, IL-6, IL-8, and tumor necrosis factor-alpha]. The frequency of various disease outcomes during the mean followup of 74 months was compared between ACD and nonanemic patients. RESULTS: ACD was present in 25% during the first year of disease. ACD was associated with higher CRP (45 vs 22 g/l; p = 0.04) and ESR levels (54 vs 33 mm/h; p = 0.002). Hemoglobin levels were inversely correlated with serum erythropoietin (p = 0.003) in univariate analysis, but in multivariate analysis only ESR (p = 0.005) and IL-6 (p = 0.056) remained as independent predictors of hemoglobin levels. Presence of ACD was not associated with later development of disease manifestations or mortality. CONCLUSION: While ACD affected 25% of patients with RA early in the disease course, this had no influence on disease outcome including mortality during the following 6 years. The association between IL-6 and ACD suggests that IL-6-mediated bone marrow suppression is the main mechanism for development of ACD in RA.