Evidence of an excessive gender gap in the risk of psychotic disorder among North African immigrants in Europe: a systematic review and meta-analysis.

PURPOSE: Epidemiological studies in the Netherlands have reported an excessive gender gap in the risk for non-affective psychotic disorder (NAPD) among immigrants from Morocco with a higher risk elevation in males compared to females. We examined the consistency of these findings and their generalizability to immigrants from the Maghreb (Mauritania, Morocco, Algeria, Tunisia and Libya) in other European countries. METHODS: Systematic review and meta-analysis. Medline, PsychINFO and EMBASE databases were searched for publications in the period from January 1970 to April 2014. We included incidence and prevalence studies of non-affective psychotic disorder (NAPD) among migrants from the Maghreb in Europe and studies of subclinical psychotic symptoms (SPS) in representative samples. A meta-analysis was performed on the subgroup of incidence studies. RESULTS: Five incidence and three prevalence studies of NAPD, and two prevalence studies of SPS, conducted in the Netherlands (n=7), Belgium (n=1), France (n=1) and Italy (n=1) met our inclusion criteria. Across all research designs, the risks of NAPD and SPS were consistently increased among male, not female immigrants from the Maghreb. The meta-analysis of incidence studies of NAPD yielded male-to-female risk ratios of 5.1 [95 % confidence interval (CI) 3.1-8.4] for migrants from the Maghreb, 2.0 (95 % CI 1.6-2.5) for other migrant groups, and 1.8 (95 % CI 1.3-2.5) for non-migrant Europeans. CONCLUSIONS: The marked gender gap in psychosis risk among migrants from the Maghreb appears a consistent finding, foremost among the Moroccan-Dutch. The small number of studies limits the strength of conclusions that can be drawn about countries other than the Netherlands. Achievement-expectation mismatch, social marginalization and an increased prevalence of illicit drug use are possible explanations.

A meta-analysis of the risk for psychotic disorders among first- and second-generation immigrants.

BACKGROUND: There is increasing acceptance of migration as a risk factor for schizophrenia and related disorders; however, the magnitude of the risk among second-generation immigrants (SGIs) remains unclear. Generational differences in the incidence of psychotic disorders among migrants might improve our understanding of the relationship between migration, ethnicity and psychotic disorders. This meta-analysis aimed at determining the risk of psychotic disorders among SGIs in comparison with non-migrants and first-generation immigrants (FGIs). METHOD: Medline, EMBASE and PsycINFO databases were searched systematically for population-based studies on migration and psychotic disorders published between 1977 and 2008. We also contacted experts, tracked citations and screened bibliographies. All potential publications were screened by two independent reviewers in a threefold process. Studies were included in the meta-analysis if they reported incidence data, differentiated FGIs from SGIs and provided age-adjusted data. Data extraction and quality assessment were conducted for each study. RESULTS: Twenty-one studies met all inclusion criteria. A meta-analysis of 61 effect sizes for FGIs and 28 for SGIs yielded mean-weighted incidence rate ratios (IRRs) of 2.3 [95% confidence interval (CI) 2.0-2.7] for FGIs and 2.1 (95% CI 1.8-2.5) for SGIs. There was no significant risk difference between generations, but there were significant differences according to ethno-racial status and host country. CONCLUSIONS: The increased risk of schizophrenia and related disorders among immigrants clearly persists into the second generation, suggesting that post-migration factors play a more important role than pre-migration factors or migration per se. The observed variability suggests that the risk is mediated by the social context.

Hemostatic markers in patients at risk of cerebral ischemia.

BACKGROUND: Increased levels of markers of hemostasis may assist in the determination of the extent of carotid occlusive disease and the identification of neurologically intact individuals at increased risk of ischemic events. METHODS: We conducted a prospective study of 304 subjects, including 82 with a recent (< or =7 days) transient ischemic attack (TIA), 157 asymptomatic individuals with a cervical bruit, and 65 control subjects. Baseline evaluation included a neurological assessment, ECG, cervical ultrasonography, and cerebral CT and/or MRI. Levels of markers of coagulation and fibrinolytic activity were also determined. Results were analyzed in relation to the degree of carotid disease and the subsequent occurrence of cerebral and cardiac ischemic events. RESULTS: Over a mean follow-up period of 2.8 years (SD, 1.3 years), 114 ischemic events occurred. Survival analyses showed that prothrombin fragment 1.2 (F(1.2)) was a predictor of time to cerebral and cardiac ischemic events in the combined TIA and asymptomatic bruit group (relative risk [RR], 1.46; 95% CI, 1.18 to 1.81) as well as in the asymptomatic bruit group separately (RR, 1.70; 95% CI, 1.14 to 2.53). In the TIA group, both F(1.2) (RR, 2.36; 95% CI, 1.19 to 4.68) and severe (> or =80%) carotid stenosis (RR, 3.53; 95% CI, 1.19 to 10.51) were predictive of time to ischemic stroke, myocardial infarction, or vascular death. CONCLUSIONS: In patients with TIAs and in asymptomatic individuals with cervical bruits, F(1.2) levels were found to be independent predictors of subsequent cerebral and cardiac ischemic events. Our results are consistent with an active role of the coagulation system through upregulation of thrombin in carotid disease progression and in the pathogenesis of ischemic events in patients at risk.

Outcome of asymptomatic patients with carotid disease. Asymptomatic Cervical Bruit Study Group.

Asymptomatic cervical atherosclerosis carries a variable risk of vascular events. We sought to identify patients with asymptomatic cervical bruits who may be at increased risk of developing ischemic events. We conducted a prospective multicenter cohort study of neurologically asymptomatic patients presenting a cervical bruit. Patients had biannual neurologic and carotid duplex evaluation. Association between ultrasonographic findings and vascular events, adjusting for common risk factors, was evaluated. Seven hundred fifteen patients were followed on average for 3.6 years. Mean age was 65 years. At initial visit, 357 subjects had a > or = 50% stenosis. Overall, 237 events occurred in 177 patients. Annual rate of all primary vascular events in patients with > or = 50% stenosis was 11.0% versus 4.2% in those with < 50% stenosis (p < 0.001). Annual rate of stroke and vascular death was 5.5% in the > or = 50% group compared with 1.9% in the < 50% group (p < 0.001). Yearly rate of unheralded ischemic stroke was 4.2% in subjects with > or = 80% stenosis and 1.4% in those with stenosis < 80% (p < 0.001). A stroke or TIA was ipsilateral to a > or = 80% stenosis in 66% of patients. Progression of carotid stenosis particularly to more than 80% was associated both with a higher rate of ipsilateral neurologic events and overall combined vascular events. Our data suggest that severity of carotid stenosis is the main risk factor predicting occurrence of neurologic and other vascular events. Yearly rate of ipsilateral stroke with > or = 50% carotid stenosis is low (1.4%) and most are nondisabling. Progression to > or = 80% or occlusion is associated with worse outcome.

Lack of effect of aspirin in asymptomatic patients with carotid bruits and substantial carotid narrowing. The Asymptomatic Cervical Bruit Study Group.

OBJECTIVE: To determine the effectiveness of aspirin in preventing ischemic events in patients with asymptomatic carotid stenosis. DESIGN: Double-blind, placebo-controlled trial. SETTING: University-affiliated hospitals. PATIENTS: 372 neurologically asymptomatic patients with carotid stenosis of 50% or more in at least one artery as determined by luminal diameter reduction on duplex ultrasonography. INTERVENTION: Patients were randomly assigned to receive either enteric coated aspirin, 325 mg/d, or identically appearing placebo. Duration of therapy was 2.0 years for the aspirin recipients and 1.9 years for the placebo recipients. OUTCOME MEASURES: Patients were scheduled for a clinical examination every 6 months for assessment of the occurrence of any clinical event in the composite end point, which consisted of transient ischemic attack, stroke, myocardial infarction, unstable angina, or death. RESULTS: At baseline, the 188 patients receiving aspirin and the 184 patients receiving placebo had similar demographic, ultrasonographic, and laboratory characteristics. The median duration of follow-up was 2.3 years. The annual rate of all ischemic events and death from any cause was 12.3% for the placebo group and 11.0% for the aspirin group (P = 0.61). The Cox proportional hazards analysis yielded an adjusted hazard ratio (aspirin-placebo) of 0.99 (95% CI, 0.67 to 1.46; P = 0.95). The annual rates for vascular events only were 11% for the placebo group and 10.7% for the aspirin group (P = 0.99). The multivariate analysis yielded a hazard ratio of 1.08 (CI, 0.72 to 1.62; P = 0.71). CONCLUSION: Aspirin did not have a significant long-term protective effect in asymptomatic patients with high-grade (> or = 50%) carotid stenosis.

Hemostatic markers in acute transient ischemic attacks.

BACKGROUND AND PURPOSE: Hemostatic abnormalities have been shown previously in stroke patients. The purpose of this study was to assess the activity of selected parameters of the coagulation system in acute reversible cerebral ischemia. METHODS: We measured fibrinopeptide A, thrombin-antithrombin III, and D-dimer in 36 patients in both the acute (< 7 days) and postacute stage (1 and 3 months) after a transient ischemic attack (TIA). The results were compared with those of 20 asymptomatic patients with a history of remote TIA and 65 age- and sex-matched controls. RESULTS: Mean fibrinopeptide A and thrombin-antithrombin III values were elevated in the acute stage after a TIA (P < .02) compared with levels at 1 month. In contrast, D-dimer was significantly increased at all three times points after the event when compared with remote TIA (P < .05) or control subjects (P < .001). No association could be found between marker levels and clinical outcome or the degree of cervical atherosclerosis as assessed by duplex ultrasonography. CONCLUSIONS: These findings suggest that after acute reversible cerebral ischemia, there is early transient activation of thrombogenesis and ongoing fibrinolysis.