Correlations between caregiver psychiatric symptoms and offspring psychopathology in a low-resource setting

Objective: Associations between parental/caregiver depression and adverse child outcomes are well established and have been described through one or more mechanisms: child psychopathology following exposure to a depressed caregiver, child psychopathology exacerbating a caregiver's depression, and caregiver and offspring depression sharing the same etiology. Data from low and middle-income countries is scarce. We examined correlations between common symptoms of mental disorders in caregivers and their offspring's psychopathology in a Brazilian sample. Methods: In this cross-sectional study, adult caregivers were screened for depression during routine home visits by community health workers as part of the Brazilian Family Health Strategy. Caregivers with suspected depression were assessed using the Zung Self-Rating Depression Scale and the Self-Reporting Questionnaire (SRQ-20). Children's symptoms were evaluated using the Strengths and Difficulties Questionnaire (SDQ). Results: The sample included 68 primary caregivers and 110 children aged 6 to 15 years. Higher caregiver scores on the SRQ-20 correlated significantly with psychiatric symptoms in offspring. Conclusion: These results substantiate our hypothesis that child psychopathology correlates with caregivers' psychiatric symptoms. This paper adds to the growing literature on community mental health assessment and can help guide future strategies for reducing the burden of common mental disorders in caregivers and children alike in low and middle-income countries.Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2012/17485-4]Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)Instituto LemannNIMH [D43 TW009675, T32 MH096724, T32-MH19139, K01MH104514]Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)Columbia University Department of Psychiatry/New York State Psychiatric Institute [T32MH096724]Univ Fed Sao Paulo UNIFESP, Dept Psiquiatria, Sao Paulo, SP, BrazilNew York State Psychiat Inst & Hosp, Div Epidemiol, New York, NY 10032 USAColumbia Univ Coll Phys & Surg, Dept Psychiat, 722 W 168th St, New York, NY 10032 USANew York State Psychiat Inst & Hosp, Div Child Psychiat, New York, NY 10032 USAUniv Fed Sao Paulo UNIFESP, Dept Psiquiatria, Sao Paulo, SP, Brazil(FAPESP) [2012/17485-4]NIMH [D43 TW009675, T32 MH096724, T32-MH19139, K01MH104514]Columbia University Department of Psychiatry/New York State Psychiatric Institute [T32MH096724]Web of Scienc

Task shifting interpersonal counseling for depression: a pragmatic randomized controlled trial in primary care

Abstract Background Task shifting approaches (rational redistribution of tasks among health workforce teams) to train lay professionals to assist with integrating mental health treatment in primary care has been recommended to close the mental health treatment gap for depression in low- and middle-income countries. This study aims to examine the a new model for depression care in a low-resource environment compared to enhanced treatment at usual (E-TAU). Methods We trained non-specialist community health workers (local lay employees of the public health system) to provide Interpersonal Counseling (IPC) to treat depressive symptoms in the Brazilian, São Paulo city, family health strategy (FHS). We conducted a randomized controlled trial involving 86 patients with a current major depressive disorder or dysthymia (based on DSM-IV) recruited from an FHS clinic. Participants were randomized to IPC intervention (n = 43) or E-TAU (n = 43). Participants allocated to IPC received 3–4 sessions provided by community health workers; research psychologists followed the E-TAU participants to facilitate their referral to specialized mental health care within the public system. Reduction of depressive symptoms was assessed using the Hamilton Rating Scale (HDRS-17) and the Patient Health Questionnaire (PHQ-9); minor psychiatric symptomatology (including depression, anxiety and somatoform symptoms) were measured using the Self Reporting Questionnaire (SRQ); and functioning was measured by the Clinical Global Impression Scale over a 2-month period. Results Intention-to-treat analysis showed significant improvement on symptoms for both groups over 2 months, without significant differences between them. Per-protocol analysis showed significant better HDRS-17 outcomes for the IPC group. Conclusions Training non-specialist community health workers in low- and middle-income countries to provide IPC could be a successful strategy in reducing the burden of depression and also potentially a low-cost and effective alternative to specialist-led services that might not be possible in low income settings. Trial registration Brazilian Clinical Trials, number RBR-5qhmb5 (trial url: http://www.ensaiosclinicos.gov.br/rg/RBR-5qhmb5/) , retrospectively registered after May 1, 2013

Oral rivaroxaban for the treatment of symptomatic pulmonary embolism.

BACKGROUND: A fixed-dose regimen of rivaroxaban, an oral factor Xa inhibitor, has been shown to be as effective as standard anticoagulant therapy for the treatment of deep-vein thrombosis, without the need for laboratory monitoring. This approach may also simplify the treatment of pulmonary embolism. METHODS: In a randomized, open-label, event-driven, noninferiority trial involving 4832 patients who had acute symptomatic pulmonary embolism with or without deep-vein thrombosis, we compared rivaroxaban (15 mg twice daily for 3 weeks, followed by 20 mg once daily) with standard therapy with enoxaparin followed by an adjusted-dose vitamin K antagonist for 3, 6, or 12 months. The primary efficacy outcome was symptomatic recurrent venous thromboembolism. The principal safety outcome was major or clinically relevant nonmajor bleeding. RESULTS: Rivaroxaban was noninferior to standard therapy (noninferiority margin, 2.0; P=0.003) for the primary efficacy outcome, with 50 events in the rivaroxaban group (2.1%) versus 44 events in the standard-therapy group (1.8%) (hazard ratio, 1.12; 95% confidence interval [CI], 0.75 to 1.68). The principal safety outcome occurred in 10.3% of patients in the rivaroxaban group and 11.4% of those in the standard-therapy group (hazard ratio, 0.90; 95% CI, 0.76 to 1.07; P=0.23). Major bleeding was observed in 26 patients (1.1%) in the rivaroxaban group and 52 patients (2.2%) in the standard-therapy group (hazard ratio, 0.49; 95% CI, 0.31 to 0.79; P=0.003). Rates of other adverse events were similar in the two groups. CONCLUSIONS: A fixed-dose regimen of rivaroxaban alone was noninferior to standard therapy for the initial and long-term treatment of pulmonary embolism and had a potentially improved benefit-risk profile. (Funded by Bayer HealthCare and Janssen Pharmaceuticals; EINSTEIN-PE ClinicalTrials.gov number, NCT00439777.)

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)

Ezetimibe added to statin therapy after acute coronary syndromes

BACKGROUND: Statin therapy reduces low-density lipoprotein (LDL) cholesterol levels and the risk of cardiovascular events, but whether the addition of ezetimibe, a nonstatin drug that reduces intestinal cholesterol absorption, can reduce the rate of cardiovascular events further is not known. METHODS: We conducted a double-blind, randomized trial involving 18,144 patients who had been hospitalized for an acute coronary syndrome within the preceding 10 days and had LDL cholesterol levels of 50 to 100 mg per deciliter (1.3 to 2.6 mmol per liter) if they were receiving lipid-lowering therapy or 50 to 125 mg per deciliter (1.3 to 3.2 mmol per liter) if they were not receiving lipid-lowering therapy. The combination of simvastatin (40 mg) and ezetimibe (10 mg) (simvastatin-ezetimibe) was compared with simvastatin (40 mg) and placebo (simvastatin monotherapy). The primary end point was a composite of cardiovascular death, nonfatal myocardial infarction, unstable angina requiring rehospitalization, coronary revascularization ( 6530 days after randomization), or nonfatal stroke. The median follow-up was 6 years. RESULTS: The median time-weighted average LDL cholesterol level during the study was 53.7 mg per deciliter (1.4 mmol per liter) in the simvastatin-ezetimibe group, as compared with 69.5 mg per deciliter (1.8 mmol per liter) in the simvastatin-monotherapy group (P<0.001). The Kaplan-Meier event rate for the primary end point at 7 years was 32.7% in the simvastatin-ezetimibe group, as compared with 34.7% in the simvastatin-monotherapy group (absolute risk difference, 2.0 percentage points; hazard ratio, 0.936; 95% confidence interval, 0.89 to 0.99; P = 0.016). Rates of pre-specified muscle, gallbladder, and hepatic adverse effects and cancer were similar in the two groups. CONCLUSIONS: When added to statin therapy, ezetimibe resulted in incremental lowering of LDL cholesterol levels and improved cardiovascular outcomes. Moreover, lowering LDL cholesterol to levels below previous targets provided additional benefit