The effect of short-term intensive chemotherapy on reactivation of tuberculosis.

BACKGROUND: Various malignancies and cytotoxic chemotherapy have been proposed to increase the risk of reactivation of tuberculosis. Available literature to support this observation is still conflicting. There is scarcity of data from countries with rampant tubercular infection, such as India, in this regard. DESIGN AND METHODS: In the present retrospective analysis, patients with high-grade non-Hodgkin's lymphoma with past history of tuberculosis and have had adequate antitubercular therapy were identified from a Lymphoma Group study. These patients were followed up during cytotoxic chemotherapy and later to assess the risk of reactivation. RESULTS: A cohort of eight patients with past history of tuberculosis was selected from 141 patients of high-grade non-Hodgkin's lymphoma. The median age was 33.5 years (range, 24-53 years). Median duration between completion of antitubercular treatment and diagnosis of lymphoma was 5 years (range, 1.5-10 years). All patients received cyclical cytotoxic chemotherapy. The median duration of follow up after completion of chemotherapy was 5 years (range, 10 months to 5 years). None of these patients developed reactivation of tuberculosis. CONCLUSION: Cyclical chemotherapy for non-Hodgkin's lymphoma does not lead to reactivation of tuberculosis.     

Antagonism of phencyclidine-induced deficits in prepulse inhibition by the putative atypical antipsychotic olanzapine

Prepulse inhibition (PPI) of the startle reflex provides an operational measure of sensorimotor gating. Deficits in PPI are observed in schizophrenia patients and can be modelled in animals by administration of noncompetitive NMDA antagonists such as phencyclidine (PCP) or dizocilpine (MK-801). Previous studies indicate that the atypical antipsychotic clozapine restores PPI in PCP-treated animals while the typical antipsychotic haloperidol does not. Olanzapine (LY170053) is a novel putative atypical antipsychotic that shares many pharmacological and behavioral properties with clozapine. The present study assessed the ability of olanzapine (0, 1.25, 2.5, 5.0 or 10.0 mg/kg) to antagonize deficits in PPI produced by PCP (1.5 mg/kg) and dizocilpine (0.1 mg/kg). At the two highest doses, olanzapine significantly increased PPI in PCP- and dizocilpine-treated animals without affecting PPI or baseline startle reactivity by itself. These results support the notion that olanzapine is functionally similar to clozapine and may have utility as an atypical antipsychotic agent.