Aim:To study the adverse drug reaction (ADR) pattern in a pediatric population in a tertiary care hospital.Materials and Methods:An observational study was done in the department of pediatrics in a tertiary care hospital. The ADRs occurring in the inpatient wards and outpatient department of pediatrics were actively monitored. The collected reports were analyzed for ADR pattern, drug groups, demographic profile, causality, severity, and preventability of the ADR.Results:A total of 30 ADRs were documented during the mid period of 2009 among pediatric patients. Most of the ADRs (60%) occurred below the age of 1 year. Antibiotics comprised the major group of drugs causing ADRs (67%). Rashes and urticaria were the most common type of ADR (37%) followed by fever, anaphylactic shock, vomiting, chills, and rigors. A single case of death had been reported in the study period. There were more occurrences of ADRs with multiple drugs compared to single drug therapy. About 80% of the ADRs were of probable causality and 87% were of probable preventability. There were no mild reactions, with 77% of reactions being moderate and 23% of reactions being severe in the severity scale.Conclusions:ADRs occur more among infants and antibiotics were more commonly implicated. Most of the reactions were of moderate severity. This indicates the need for a rigid ADR monitoring among pediatric patients to ensure safety of drug therapy.

Objectives: Cleistanthins A and B are the active compounds isolated from Cleistanthus collinus leaves. The hypotensive activity of both cleistanthins A and B and the leaf extract has been previously demonstrated, but the exact mechanism of action is not clear. So, this study was designed to test the vasorelaxant property of cleistanthins A and B and delineate its mechanism of action. Methods: Variable force transducers were used to record the force of contraction from the aortic rings of 24 male guinea pigs. The effect of cleistanthin A, cleistanthin B, prazosin and vehicle on the phenylephrine-induced contractions and potassium chloride-induced contractions was demonstrated and compared. Results: Cleistanthin B inhibited the phenylephrine-induced contractions in a dose-dependent manner and demonstrated potency (pIC 50 = 6.8 ± 1.06) comparable to prazosin (pIC 50 = 5.7 ± 0.7). Cleistanthin A potency could not be calculated. Both cleistanthin A (4 µg) and cleistanthin B (40 µg) caused a reduction of the maximal response of phenylephrine demonstrating irreversible blockade. They did not affect the potassium chloride-induced contractions. This illustrates that cleistanthins A and B are noncompetitive α 1 adrenergic blockers and the potency of cleistanthin B is comparable to prazosin. Conclusion: Both cleistanthins A and B have vasodilatory action on guinea pig aorta. The action is through non-competitive α 1 adrenergic receptor inhibition and calcium channel blockade does not contribute to the inhibition.

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