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January-March 2016 Volume 7 | Issue 1
Page Nos. 1-55
Online since Tuesday, March 29, 2016
Accessed 52,663 times.
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COMMENTARY |
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Abuse of topical corticosteroids in India: Concerns and the way forward  |
p. 1 |
Subodh Kumar, Aman Goyal, Yogendra Kumar Gupta DOI:10.4103/0976-500X.179364 PMID:27127387 |
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RESEARCH PAPERS |
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Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts |
p. 6 |
Elena Grossini, Carla Gramaglia, Serena Farruggio, Lara Camillo, David Mary, Giovanni Vacca, Patrizia Zeppegno DOI:10.4103/0976-500X.179358 PMID:27127388Objective: To examine the effects of asenapine on nitric oxide (NO) release and Ca2+ transients in H9C2 cell line, which were either subjected to peroxidation or not. Materials and Methods: H9C2 were treated with asenapine alone or in presence of intracellular kinase blockers, serotoninergic and dopaminergic antagonists, and voltage Ca2+ channels inhibitors. Experiments were also performed in H9C2 treated with hydrogen peroxide. NO release and intracellular Ca2+ were measured through specific probes. Results: In H9C2, asenapine differently modulated NO release and Ca2+ movements depending on peroxidative condition. The Ca2+ pool mobilized by asenapine mainly originated from the extracellular space and was slightly affected by thapsigargin. Moreover, the effects of asenapine were reduced or prevented by kinases blockers, dopaminergic and serotoninergic receptors inhibitors, and voltage Ca2+ channels blockers.Conclusions: On the basis of our findings, we can conclude that asenapine by interacting with its specific receptors, exerts dual effects on NO release and Ca2+ homeostasis in H9C2; this would be of particular clinical relevance when considering their role in cardiac function modulation. |
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Variability in plasma concentration of cefotaxime in critically ill patients in an Intensive Care Unit of India and its pharmacodynamic outcome: A nonrandomized, prospective, open-label, analytical study |
p. 15 |
B Abhilash, Chakra Dhar Tripathi, Anoop Raj Gogia, Girish Gulab Meshram, Manu Kumar, B Suraj DOI:10.4103/0976-500X.179356 PMID:27127389Background: Cefotaxime is a widely utilized cephalosporin in most intensive care units of India. However, no data are available about its pharmacokinetic/pharmacodynamic variability in critically ill patients of the Indian population. Aim: To investigate the variability in the plasma concentration and pharmacodynamic profile of intermittent dosing of cefotaxime in critically ill patients, according to their locus of infection and causative organism. Materials and Methods: Cefotaxime levels were determined using high-performance liquid chromatography by grouping patients according to their locus of infection as hepatobiliary, renal, pulmonary, and others. Patients with cefotaxime concentration below the minimum inhibitory concentration (MIC) and 5 times below the MIC for the isolated organism were determined. Results: The difference in the plasma cefotaxime concentration between the hepatobiliary and the nonhepatobiliary groups was significant at 1 h (P = 0.02) following drug dosing, while the difference was significant between the renal and nonrenal group at 1 h (P = 0.001), 4 h (P = 0.009), and 8 h (P = 0.02) after drug dosing. The pulmonary group showed significantly (P < 0.05) lower plasma cefotaxime levels than the nonpulmonary group at all-time points. The cefotaxime levels were below the MIC and below 5 times the MIC for the isolated organism in 16.67% and 43.33% of the patients, respectively. Conclusion: The concentration of cefotaxime differs according to the locus of an infection in critically ill patients. Use of another class of antibiotic or shifting to continuous dosing of cefotaxime, for organisms having MIC values above 1 mg/L, is advisable due to the fear of resistance. |
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RESEARCH LETTERS |
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Inhibition of astrocyte activation is involved in the prevention of postoperative latent pain sensitization by ketamine and gabapentin in mice |
p. 22 |
Elizabeth Romero-Alejo, Margarita M Puig, Asunción Romero DOI:10.4103/0976-500X.179357 PMID:27127390 |
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Effect of flumazenil on memory retrieval determined by trial-to-criteria inhibitory avoidance method in mice |
p. 24 |
Sanket B Raut, Somesh S Bolegave, Padmaja A Marathe DOI:10.4103/0976-500X.179354 PMID:27127391 |
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Nonsteroidal anti-inflammatory drugs causing local inflammation of tissue at the site of injection |
p. 26 |
Anton Aleksandrovich Kasatkin, Alexandr A Urakov, Ilya Aleksandrovich Lukoyanov DOI:10.4103/0976-500X.179359 PMID:27127392 |
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Incidence of metabolic syndrome in breast cancer survivors on adjuvant hormonal therapy |
p. 28 |
Anahita Kate, Dharanipragada Kadambari DOI:10.4103/0976-500X.179362 PMID:27127393 |
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Evaluation of inter-rater agreement between three causality assessment methods used in pharmacovigilance |
p. 31 |
Saket J Thaker, Rahul S Sinha, Nithya J Gogtay, Urmila M Thatte DOI:10.4103/0976-500X.179361 PMID:27127394 |
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CASE REPORTS |
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”Ping-pong gaze” secondary to monoamine oxidase inhibitor overdose |
p. 34 |
Amy Attaway, Laila Sroujieh, Tracey L Mersfelder, Christopher Butler, Daniel Ouellette DOI:10.4103/0976-500X.179360 PMID:27127395An infrequent manifestation of monoamine oxidase inhibitor (MAOI) toxicity is “ping-pong gaze” (PPG). We describe the case of a 26-year-old female who was found unresponsive after taking 40 tablets of phenelzine. On presentation to the hospital, her eyes were moving in characteristic “ping pong” fashion. After 6 hours her gaze terminated. The following day her neurologic exam was benign and she had no long-term sequelae. While the etiology of PPG is unknown, it is most often seen with irreversible structural brain damage. However, a detailed literature review revealed that previous cases of MAOI toxicity where the patient survived have all had complete neurologic recovery. |
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Tamoxifen-induced hypertriglyceridemia causing acute pancreatitis |
p. 38 |
Hemant Kumar Singh, Mahendranath S Prasad, Arun K Kandasamy, Kadambari Dharanipragada DOI:10.4103/0976-500X.179365 PMID:27127396Tamoxifen has both antagonistic and agonistic tissue-specific actions. It can have a paradoxical estrogenic effect on lipid metabolism resulting in elevated triglyceride and chylomicron levels. This can cause life-threatening complications like acute pancreatitis. To our knowledge, very few cases of tamoxifen-induced pancreatitis have been reported in the literature. We report a case of severe hypertriglyceridemia and acute pancreatitis following tamoxifen use. A 50-year-old diabetic lady was on tamoxifen (20mg/day) hormonal therapy for breast cancer. Within 3 months of starting therapy, she developed hypertriglyceridemia and acute pancreatitis. Laboratory values include: Serum amylase 778 IU/L, total cholesterol 785 mg/dL, triglycerides 4568 mg/dL and high-density lipoproteins (HDL) 12 mg/dL. Tamoxifen was substituted with letrozole and atorvastatin started. There was a prompt reversal of the adverse effects. Effects on lipid profile must be considered while initiating tamoxifen in predisposed individuals as the consequences are life threatening. |
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Pioglitazone-induced congestive heart failure and pulmonary edema in a patient with preserved ejection fraction |
p. 41 |
Vaneet Jearath, Rajan Vashisht, Vipul Rustagi, Sujeet Raina, Rajesh Sharma DOI:10.4103/0976-500X.179363 PMID:27127397Pioglitazone-induced heart failure is known in patients with underlying heart disease, but is not well documented in patients with normal left ventricular function. Pioglitazone has been very popular as it is an insulin sensitizer and insulin resistance is prevalent among Indians. Fluid retention exacerbates pre-existing heart failure or precipitates heart failure in a patient with underlying left ventricular dysfunction. However, pathogenesis of heart failure in a patient with normal left ventricular function is not known. Probably it is due to dose-related effect on pulmonary endothelial permeability, rather than alterations in left ventricular mass or ejection fraction. We report a patient who developed congestive heart failure and pulmonary edema with normal left ventricular function within 1 year of starting pioglitazone therapy. We have to be careful in monitoring all possible side effects during followup when patients are on pioglitazone therapy. |
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Acute compartment syndrome of hand resulting from radiographic contrast iohexol extravasation |
p. 44 |
Kolar Vishwanath Vinod, Rampelli Shravan, Radhakrishnan Shrivarthan, Pedapati Radhakrishna, Tarun Kumar Dutta DOI:10.4103/0976-500X.179353 PMID:27127398Intravenous (IV) administration of iodinated contrast agents (ICAs) is frequently employed for image enhancement while performing radiographic studies such as computed tomography and angiography. Complications related to IV administration of ICAs such as immediate hypersensitivity reactions and nephrotoxicity are well-known. However, severe skin and soft tissue injuries and acute compartment syndrome resulting from contrast extravasation are rare. This is especially so with small volume extravasation of a low osmolar, nonionic ICA such as iohexol. Here, we report a 63-year-old woman who developed acute compartment syndrome of left hand following iohexol extravasation and had swelling, blistering, cutaneous and soft tissue necrosis. She underwent fasciotomy for acute compartment syndrome of hand and later surgical debridement of necrotic skin and soft tissues was carried out. Clinical pharmacology of ICAs, extravasation injuries following their IV administration, their management and measures to reduce them are discussed in brief. |
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CORRESPONDENCE |
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Exercise-induced urticaria, cholinergic urticaria, and Kounis syndrome |
p. 48 |
Nicholas G Kounis, George N Kounis, George D Soufras DOI:10.4103/0976-500X.179355 PMID:27127399 |
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EDUCATIONAL FORUM |
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A closer look at the World Health Organization's prescribing indicators |
p. 51 |
Richard Ofori-Asenso DOI:10.4103/0976-500X.179352 PMID:27127400This communication focuses on the World Health Organization's prescribing indicators. It describes the methods for computing the indicators and highlights their applicability as well as limitations in evaluating the patterns of medicines usage. |
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BOOK REVIEW |
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Pathophysiology and pharmacology of cardiovascular disease |
p. 55 |
Raja J Selvaraj |
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