No abstract

The primary endpoints in this study were the remission rates [final Hamilton Rating Scale for Anxiety (HAM-A) total score < or =7] and reduction from baseline in the HAM-A total score in patients with generalized anxiety disorder (GAD) and no associated depression. Patients with GAD (DSM-IV and HAM-A total score >18) were randomly assigned to treatment with venlafaxine XR or placebo for 8 weeks. A 1-week placebo run-in period preceded the double-blind phase. Patients with a >20% drop in their total HAM-A score during the run-in period, were excluded from the double-blind phase. All patients started therapy with 75 mg/day venlafaxine XR or matched placebo. Patients with less than 30% decrease in their HAM-A total score at the end of the second week, doubled their dose. Patients on the 150 mg/day dose underwent a 1-week taper period. Of the 24 patients in the venlafaxine XR group, 62.5% achieved remission versus 9.1% in the placebo group (P=0.0006). The mean decrease from baseline in HAM-A total score was 19.2 points for the venlafaxine XR group and 10.8 points for the placebo group (P<0.001). Eleven placebo-treated patients and seven venlafaxine XR treated patients doubled their dose at the end of the second week of double-blind treatment. No patient interrupted therapy because of side-effects. No changes in systolic or diastolic blood pressure were observed. Venlafaxine XR 75-150 mg/day was well tolerated. The remission rates achieved with venlafaxine 75-150 mg/day in non-depressed GAD patients were high with good tolerability.

Forty-three schizophrenic patients participating in this study were serotyped for human leukocyte antigens (HLA-A, -B, -C, -DR, -DQ antigens). Thirty-six of them were hospitalised in two state mental hospitals and 7 in our general hospital, psychiatric unit. The patients from our unit were typed for HLA before commencing clozapine treatment whereas the patients from state hospitals were typed after commencing treatment. Three out of 43 patients developed agranulocytosis. One had a combination of both ‘high-risk’ haplotypes (HLA-B16(38,39), DR4, DQ3 and HLA-DR2, DQ1), another had HLA-DR2, DQ1, whereas the last had a totally different haplotype. Between non-agranulocytic patients 1 was found to carry the HLA-B16(38,39), DR4, DQ3 haplotype and 14 (out of 40) had the HLA-DR2, DQ1. Taking into account other factors supposed to be involved (a noxious metabolite, and the presence of a humoral cytotoxic factor) we must admit that despite the finding of a high-risk haplotye in Jewish populations there are other aspects of this question awaiting clarification.

No abstract

No abstract