Concomitant Ro/SSA and La/SSB antibodies are biomarkers for the risk of venous thromboembolism and cerebral infarction in primary Sjögren's syndrome.

BACKGROUND: To assess the risk of incident cardiovascular disease in patients with primary Sjögren's syndrome, overall and stratified by Ro/SSA and La/SSB autoantibody status. METHODS: A cohort of patients with primary Sjögren's syndrome in Sweden (n = 960) and matched controls from the general population (n = 9035) were included, and data extracted from the National Patient Register to identify events of myocardial infarction, cerebral infarction and venous thromboembolism. Hazard ratios were estimated using cox proportional hazard regressions. RESULTS: During a median follow-up of 9.5 years, the overall hazard ratio (HR) was 1.6 (95% CI 1.2-2.1) for myocardial infarction, 1.2 (95% CI 0.9-1.7) for cerebral infarction and 2.1 (95% CI 1.6-2.9) for venous thromboembolism. Patients positive for both Ro/SSA and La/SSB autoantibodies had a substantially higher risk of cerebral infarction (HR 1.7, 95% CI 1.0-2.9) and venous thromboembolism (HR 3.1, 95% CI 1.9-4.8) than the general population. These risks were not significantly increased in Ro/SSA- and La/SSB-negative patients. Among autoantibody-positive patients, the highest HR of cerebral infarction was seen after ≥10 years disease duration (HR 2.8, 95% CI 1.4-5.4), while the HR for venous thromboembolism was highest 0-5 years after disease diagnosis (HR 4.7, 95% CI 2.3-9.3) and remained high throughout disease duration. CONCLUSIONS: Primary Sjögren's syndrome is associated with a markedly increased risk of cardiovascular disease and the presence of Ro/SSA and La/SSB autoantibodies identify the subgroup of patients carrying the highest risk. These findings suggest that monitoring and prevention of cardiovascular disease in this patient group should be considered.

Infections increase the risk of developing Sjögren's syndrome.

OBJECTIVE: Environmental factors have been suggested in the pathogenesis of rheumatic diseases. We here investigated whether infections increase the risk of developing primary Sjögren's syndrome (pSS). METHODS: Patients with pSS in Sweden (n = 945) and matched controls from the general population (n = 9048) were included, and data extracted from the National Patient Register to identify infections occurring before pSS diagnosis during a mean observational time of 16.0 years. Data were analysed using conditional logistic regression models. Sensitivity analyses were performed by varying exposure definition and adjusting for previous health care consumption. RESULTS: A history of infection associated with an increased risk of pSS (OR 1.9, 95% CI 1.6-2.3). Infections were more prominently associated with the development of SSA/SSB autoantibody-positive pSS (OR 2.7, 95% CI 2.0-3.5). When stratifying the analysis by organ system infected, respiratory infections increased the risk of developing pSS, both in patients with (OR 2.9, 95% CI 1.8-4.7) and without autoantibodies (OR 2.1, 95% CI 1.1-3.8), whilst skin and urogenital infections only significantly associated with the development of autoantibody-positive pSS (OR 3.2, 95% CI 1.8-5.5 and OR 2.7, 95% CI 1.7-4.2). Furthermore, a dose-response relationship was observed for infections and a risk to develop pSS with Ro/SSA and La/SSB antibodies. Gastrointestinal infections were not significantly associated with a risk of pSS. CONCLUSIONS: Infections increase the risk of developing pSS, most prominently SSA/SSB autoantibody-positive disease, suggesting that microbial triggers of immunity may partake in the pathogenetic process of pSS.

Cardiovascular response to spinal anaesthesia in elderly men: effects of head-up tilt and dihydroergotamine administration.

In nine elderly (mean age 60, rang 42-74 years) cardiovascular pressures and cardiac output have been measured by catheterization of the pulmonary and brachial artery during spinal anaesthesia without and with dihydroergotamine (DHE) and during an added slight head-up (10-15 degrees). Spinal anaesthesia lowered arterial pressure and also stroke volume. After DHE arterial pressures as well as stroke volume were normalized. Tilting before spinal anaesthesia lowered stroke volume but arterial pressures were maintained. During spinal anaesthesia, tilting lowered arterial pressures as well as filling pressures of the heart. After administration of DHE during spinal anaesthesia the pressures were unaffected by tilting. It is concluded that in elderly men, unlike the young men previously studied, spinal anaesthesia decreases arterial blood pressures by a combination of reduced peripheral resistance and decreased stroke volume. The decreases in stroke volume and cardiac output were most pronounced in those patients with a reduced blood volume. DHE also prevents arterial pressure fall with head-up tilt during spinal anaesthesia.

Blood circulation in the kidney of the cat under methoxyflurane (penthrane) anaesthesia.

In order to establish whether methoxyflurane causes any change in renal vascular resistance, the renal venous flow was measured by means of a drop recording technique in six cats under methoxyflurane anaesthesia. Arterial pressure was recorded simultaneously, and the renal vascular resistance was calculated. Methoxyflurane caused a significant reduction of the renal vascular resistance to about 85% of control value at an anaesthetic depth characterised by loss of the corneal reflex. At a deeper anaesthetic stage characterised by steady state circulation and absence of any reflexes, no further significant fall in renal vascular resistance occurred. Autoregulation and depression of the sympathetic activity are assumed to explain the reduction of the renal vascular resistance.