Can we predict suicide and non-fatal self-harm with the Beck Hopelessness Scale? A meta-analysis.

BACKGROUND: Hopelessness is considered a pre-eminent risk factor for suicide and non-fatal self-harm. We aimed to quantify the ability of the Beck Hopelessness Scale (BHS) to predict these two outcomes. METHOD: Medline, Embase, PsycINFO and Cinahl were searched to January 2006. We included cohort studies in which the BHS was applied and patients were followed-up to establish subsequent suicide or non-fatal self-harm. Four studies provided usable data on suicide, and six studies provided data on non-fatal self-harm. Summary sensitivity, specificity, likelihood ratios and diagnostic odds ratios (DORs) were calculated for each study. Random effects meta-analytic pooling across studies at the standard cut-off point (> or =9) was undertaken and summary receiver operating characteristic (ROC) curves constructed. RESULTS: For suicide, pooled sensitivity was 0.80 [95% confidence interval (CI) 0.68-0.90], pooled specificity was 0.42 (95% CI 0.41-0.44), and the pooled DOR was 3.39 (95% CI 1.29-8.88). For non-fatal self-harm, pooled sensitivity was 0.78 (95% CI 0.74-0.82), pooled specificity was 0.42 (95% CI 0.38-0.45), and the pooled DOR was 2.27 (95% CI 1.53-3.37). CONCLUSION: The standard cut-off point on the BHS identifies a high-risk group for potential suicide, but the magnitude of the risk is lower than previously reported estimates. The standard cut-off point is also capable of identifying those who are at risk of future self-harm, but the low specificity rate means it is unlikely to be of use in targeting treatment designed to lower the rate of repetition.

Preoperative gefitinib versus gefitinib and anastrozole in postmenopausal patients with oestrogen-receptor positive and epidermal-growth-factor-receptor-positive primary breast cancer: a double-blind placebo-controlled phase II randomised trial.

BACKGROUND: Some oestrogen-receptor (ER) positive breast cancers express epidermal growth factor receptor (EGFR), but whether inhibition of EGFR can suppress proliferation of breast cancer cells and ER function is not known. METHODS: In a double-blind, placebo-controlled randomised trial of 56 postmenopausal patients with ER-positive and EGFR-positive primary breast cancer, 27 women were randomly assigned to the tyrosine-kinase inhibitor of EGFR gefitinib (250 mg given orally once a day) and the aromatase inhibitor anastrozole (1 mg given orally once a day), and 29 women to gefitinib (250 mg given orally once a day) and placebo of identical appearance to anastrozole given orally once a day, all given for 4-6 weeks before surgery. Primary outcome was inhibition of tumour-cell proliferation, as measured by Ki67 antigen labelling index. Secondary outcomes were reduction in EGFR phosphorylation at Tyr 845, reduction in ER phosphorylation at Ser 118, tumour size, and toxic effects. Analyses were by intention to treat. FINDINGS: Patients assigned gefitinib and anastrozole had a greater reduction from pretreatment values in proliferation-related Ki67 labelling index than did those assigned gefitinib alone (mean % reduction 98.0 [95% CI 96.1-98.9] vs 92.4 [85.1-96.1]; difference between groups 5.6% [5.1-6.0], p=0.0054). Tumour size was reduced by 30-99% (partial response) in 14 of 28 patients assigned gefitinib and [corrected]in 12 of 22 assigned gefitinib, as assessed by ultrasonography. Reduction in phosphorylation of ER at Ser 118 was similar for both groups. Treatment was well tolerated and much the same for both groups. INTERPRETATION: Single-agent gefitinib and gefitinib combined with anastrozole are well-tolerated and effective treatments for reducing the size of breast tumours and levels of ER phosphorylation when given as neoadjuvant therapy.