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Objective: To find out incidence of adverse drug reactions (ADR) in patients of internal medicine wards and study various aspects of ADR, e.g., causality, mortality, drugs commonly causing ADR in internal medicine wards of Guru Gobind Singh Hospital, Jamnagar, a tertiary care hospital. Materials and Methods: This was prospective, observational study carried out at Department of Medicine, Shri Meghji Pethraj Shah Medical College attached with Guru Gobind Singh Hospital, a tertiary care teaching hospital, Jamnagar, Gujarat over a period of 6 months. For statistical analysis, ADR were analyzed by using Chi-square test. Results: Out of total 860 patients admitted, 830 were analyzed as they met the inclusion criteria. A total of 45 (5.42%) patients developed 47 ADR. Among them, 27 (3.25 %) (95% CI, 2.03%, 4.47%) patients due to ADR required hospital admission in medicine ward (ADR Ad), 18 (2.17%) (95% CI, 1.17%-3.17%) patients developed ADR while already hospitalized in medicine ward (ADR In). Most of the fatal and life-threatening reactions occurred due to chemotherapeutic agents. Majority of patients discontinued suspected drug and recovered from ADR. Conclusion: Fatal and life-threatening adverse reactions reported in the present as well as other studies underline the importance of such studies and need for creating awareness among health professionals about looking for and reporting such reactions.

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Objectives: To identify the ADRs due to NSAIDs and to know how to monitor the drug's effect. Materials and Methods: A descriptive study was undertaken in the Orthopedic Outpatients Department of a tertiary care teaching hospital. Hundred patients were enrolled in this study to observe the risk of adverse drug reactions (ADRs) due to NSAIDs. All the ADRs were further analyzed in relation to age and sex, type of drug and its pattern. Probability scale was used for the causality assessment of the ADRs. Results: 26% of the 100 patients developed ADR due to NSAIDs. There was not much of a difference in the number of the ADRs in relation to the gender. Diclofenac was the highest prescribed drug (65 patients), followed by paracetamol (12), nimesulide (10), ibuprofen (6), piroxicam (5) and Etoricoxib (2). Diclofenac accounted for the maximum number (73%) of ADRs, followed by nimesulide (16%), paracetamol (7%), and Etoricoxib (4%). Conclusion: Pharmacovigilance improves recognition of ADRs by the medical students. It allows the treating physician to identify the ADR associated with drugs, in particular, with the ones considered relatively safe and with those commonly prescribed by the medical and non-health professionals.

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Objective: To evaluate the nootropic and neuroprotective effects of aspirin in Sprague Dawley rats. Materials and Methods: Retention of conditioned avoidance response (CAR) and central 5-HT-mediated behavior (lithium-induced head twitches) were assessed using repeated electroconvulsive shock (ECS) in rats. Rats were divided into eight groups: control (pretreated with distilled water), scopolamine (0.5 mg/kg i.p.), ECS (150 V, 50 Hz sinusoidal with intensity of 210 mA for 0.5 s) pretreated, aspirin (6.75 mg/kg orally) pretreated, combined scopolamine and aspirin pretreated, ondansetron (0.36 mg/kg orally) pretreated, combined ECS and ondansetron pretreated and combined ECS and aspirin pretreated groups. Data was analyzed by the chi-square test and ANOVA. Results: Findings show that administration of single ECS daily for consecutive 8 days results in enhancement of 5-HT-mediated behavior (lithium-induced head twitches) and in disruption of the retention of CAR. Aspirin and ondansetron administration significantly increased the retention of conditioned avoidance response compared to control. Ondansetron and aspirin significantly prevented ECS-induced attenuation of the retention of conditioned avoidance response also. On the other hand, ondansetron and aspirin significantly retarded the ECS-induced enhancement of 5-HT-mediated behavior. Conclusion: Inhibition of the serotonergic transmission by aspirin is responsible for its nootropic and neuroprotective actions.

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Aims: To find out the pharmacokinetic and pharmacodynamic drug interaction of carbamazepine, a protype drug used to treat painful diabetic neuropathy with glibenclamide in healthy albino Wistar rats following single and multiple dosage treatment. Materials and Methods: Therapeutic doses (TD) of glibenclamide and TD of carbamazepine were administered to the animals. The blood glucose levels were estimated by GOD/POD method and the plasma glibenclamide concentrations were estimated by a sensitive RP HPLC method to calculate pharmacokinetic parameters. Results: In single dose study the percentage reduction of blood glucose levels and glibenclamide concentrations of rats treated with both carbamazepine and glibenclamide were significantly increased when compared with glibenclamide alone treated rats and the mechanism behind this interaction may be due to inhibition of P-glycoprotein mediated transport of glibenclamide by carbamazepine, but in multiple dose study the percentage reduction of blood glucose levels and glibenclamide concentrations were reduced and it may be due to inhibition of P-glycoprotein mediated transport and induction of CYP2C9, the enzyme through which glibenclamide is metabolised. Conclusions: In the present study there is a pharmacokinetic and pharmacodynamic interaction between carbamazepine and glibenclamide was observed. The possible interaction involves both P-gp and CYP enzymes. To investigate this type of interactions pre-clinically are helpful to avoid drug-drug interactions in clinical situation.

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Objective: To study the anti-inflammatory activity of fluoxetine and escitalopram in newly diagnosed patients of depression and also to evaluate the association between depression and inflammation. Materials and Methods: Ninety-eight newly diagnosed patients of depression were recruited as cases. From these, 48 had started treatment with fluoxetine (20 mg/day) and 50 had started treatment with escitalopram (20 mg/day). After 2 months of treatment of these patients, Hamilton rating scale for depression (HRSD scale), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and white blood cell (WBC) count were measured and compared to their respective baseline values before starting treatment. One hundred healthy volunteers were recruited as controls and their baseline of CRP, ESR and WBC count were measured and compared with their respective baseline values of cases. Severity of depression was measured by HRSD scale and anti-inflammatory activity was measured by reduction CRP, ESR and WBC count. Results: On baseline comparison between cases and controls, there were significant increases in the levels of CRP (P = 0.014), ESR (P = 0.023) and WBC count (P = 0.020) in cases. In fluoxetine (20 mg/day) treatment group, there was a significant reduction in the levels of CRP (P = 0.046), ESR (P = 0.043) and WBC count (P = 0.021) after 2 months of treatment but no significant reduction in HRSD scale (P = 0.190). Similarly, in escitalopram treatment group, there was a significant reduction in CRP (P = 0.041), ESR (P = 0.030) and WBC count (P = 0.017) after 2 months of treatment but no significant reduction in HRSD scale (P = 0.169). Conclusion: In newly diagnosed patients of depression, inflammatory markers such as CRP, ESR and WBC count were significantly raised and Selective serotonin reuptake inhibitors SSRIs such as fluoxetine and escitalopram reduced them independent of their antidepressant effect. So, SSRIs have some anti-inflammatory activity independent of their antidepressant action.

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Objective: To assess and evaluate the frequency, severity and classification of drug-related problems (DRP) resulting in hospitalization in an internal medicine department of a large tertiary care hospital and to identify any patient, prescriber, drug, and system factors associated with these events. Materials and Methods: A prospective and descriptive study carried out in Department of Medicine, Government Medical College, Jagdalpur. The DRP and relevant data were recorded on the personal record of every individual patient, filled during the course of treatment. Result: A total of 3560 patient's records were analyzed. Among them118 admissions were due to DRP. The most common DRP noted was noncompliance in part of patient's i.e 55 (46.6%). Statistically significant correlations were found in the number of prescribed drugs and over the counter drugs (OTC) used by patients. Conclusion: The DRP that attributed to hospital admission are mostly avoidable through proper patient education and strengthening the need of pharmacovigilance with little more vigilance in patient care.

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Objective: To investigate pharmacologically whether CaSRs are involved in the Ca ²⁺ antagonist-induced [Ca ²⁺]i elevation in gingival fibroblasts. Materials and Methods: Gin-1 cells, normal human gingival fibroblasts, were used as the material. The [Ca ²⁺ ]i was measured with fura-2/AM, a Ca ²⁺ -sensitive fluorescent dye. Results: At first, we confirmed the existence of CaSRs in these cells by showing that [Ca ²⁺ ]i was elevated by high concentrations of extracellular Ca ²⁺ and by prototypic agonists of the CaSR such as gentamicin. The action of gentamicin was antagonized by inhibitors of phospholipase C (PLC), inositol trisphosphate (IP ₃ ) receptors, NSCCs, and, importantly, by the CaSR antagonist, NPS2390. Furthermore, the action of gentamicin was potentiated by activators of PLC and protein kinase C (PKC). This confirmed the pathway components mediating Ca ²⁺ responses to a known agonist of the CaSR. We then investigated whether nifedipine (an L-type Ca ²⁺ channel blocker) stimulates CaSRs to elevate [Ca ²⁺ ]i via a similar mechanism. Nifedipine Ca ²⁺ responses were dose-dependently blocked by NPS2390 and by the same inhibitors of PLC, IP ₃ receptors, and NSCCs that disrupted the action of gentamicin. Calphostin C (a PKC inhibitor) and TMB-8 (an inhibitor of Ca²⁺ release from stores) also inhibited the nifedipine-induced [Ca²⁺ ]i elevation. Conclusion: These findings suggest that CaSRs are involved in the nifedipine-induced [Ca ²⁺ ]i elevation in gingival fibroblasts.

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Atorvastatin-induced acute pancreatitis (AP) is one of the rare adverse effects available in the literature. We report a case of 53-year-old patient developed AP after treatment with atorvastatin monotherapy which resolved after drug withdrawal. Extensive workup on AP failed to reveal any other etiology for it. To our knowledge, this is one of the rare case reports of AP caused due to atorvastatin monotherapy and it further strengthens the fact that statins may cause AP. There is need of continued reporting of such a rare adverse effect of atorvastatin for increasing awareness and to manage and avoid the same.

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