ABSTRACT
Malaria is a major health concern in the developing world including India. Overdiagnosis and overprescribing of malaria may lead to increase morbidity, mortality and increases risk of resistance to antimalarial drugs and hence increase the economical burden to health care system. The present study was carried out to determine the actual cases of malaria and extent of chloroquine resistance at Civil Hospital Ahmedabad, a tertiary care teaching hospital in Gujarat, India. After Institutional Ethics Committee approval, adult patients of either gender, presenting with a history of fever at the Out Patient Department (OPD), diagnosed to be suffering from malaria and prescribed chloroquine were included in the study. Peripheral thick blood smear test and OptiMAL-rapid diagnostic test (RDT) were carried out. RDT was performed in these patients on day 0 before the start of chloroquine treatment and after completion of the 3 day chloroquine treatment. They were again subjected to RDT on day 4. The positive cases on RDTon day 4 were considered as resistant to chloroquine. During the study period of 12 months, out of the 250 clinically suspected cases of malaria who were prescribed chloroquine, 80 (31%) cases (35 cases of P. vivax and the 45 of P. falciparum ) were positive for malaria (by the peripheral smear and the Rapid Diagnostic Test (RDT) OptiMAL test). Thirty out of the 35 cases of P. vivax malaria, responded to the three- day chloroquine treatment. Out of the 45 cases of P. falciparum malaria, 30 responded to chloroquine while 15 patients (35%) continued to be OptiMAL positive on 4th day and required change of treatment. It suggests that an early diagnosis, definitive treatment and avoiding overprescribing could delay drug resistance and reduce the morbidity and mortality due the disease.
ABSTRACT
Spontaneous motor activity, rotarod test and observational rating of sedation were employed to study effect of nifedipine on sedation produced by reserpine, clonidine and propranolol. Reserpine (2 mg kg-1), clonidine (4 mg kg-1), and propranolol (40 mg kg-1) significantly reduced spontaneous motor activity and staying capacity of animals on accelerating rotarod (P < 0.01). Observational sedation was also caused significantly as indicated by a higher score in test. Nifedipine (2 mg kg-1) produced no sedation or excitation on its own. Reduction in spontaneous motor activity produced by reserpine and clonidine was partially reversed in animals treated with nifedipine (P < 0.01). A similar effect of nifedipine was also evident on the observational sedation induced by reserpine and clonidine. Effect of these drugs on rotarod times was nearly totally antagonised by nifedipine. Nifedipine did not oppose the sedation produced by propranolol which actually became significantly greater in the animals pretreated with nifedipine in all three tests. It is concluded that nifedipine antagonizes the sedation produced by reserpine and clonidine, probably by blocking central alpha 2-adrenoceptors. The sedative effect of propranolol can be potentiated by nifedipine possibly because of a pharmacokinetic interaction.