ABSTRACT
ABSTRACT Purpose: To evaluate the rate of cystoid macular edema development among cataract surgery patients on four different therapeutic regimens. Methods: The present study is a retrospective analysis of 5,380 eyes following uncomplicated phacoemulsification at Wake Forest University. The study period went from July 2007 to December 2012. Patients received one of four regimens, as follows: postoperative generic ketorolac 0.4% and prednisolone 1%, postoperative name-brand ketorolac 0.45% and prednisolone 1%, postoperative bromfenac 0.09% and prednisolone 1%, preoperative and postoperative bromfenac 0.09% alone. A statistical analysis was performed to assess the differences in rate of cystoid macular edema development among the four different therapeutic regimens. The diagnosis of cystoid macular edema required worsening of vision and evidence of increased macular thickness on optical coherence tomography. Results: The overall rate of cystoid macular edema was 0.82%. Treatment by postoperative generic ketorolac 0.45% and prednisolone 1% demonstrated the highest rate of cystoid macular edema development (2.20% of the cases). Postoperative name-brand ketorolac 0.45% and prednisolone 1% exhibited intermediate rates of cystoid macular edema development (0.90% of the cases). Postoperative administration of bromfenac 0.09% and prednisolone 1% exhibited intermediate rates of cystoid macular edema development (0.44% of the cases). Preoperative and postoperative bromfenac 0.09% alone resulted in the lowest rate of cystoid macular edema development (0.09% of the cases). The rate of cystoid macular edema was significantly lower when bromfenac was used alone vs. either regimen where ketorolac and prednisolone were used (OR 0.043, 95% CI 0.002 to 0.312; p<0.001). Conclusions: Post-cataract surgery cystoid macular edema developed less frequently following topical non-steroidal anti-inflammatory drugs regimen compared to the other therapies evaluated. Bromfenac, without corticosteroids, achieved lower rates of cystoid macular edema vs. various combinations of non-steroidal anti-inflammatory drugs with corticosteroids.
RESUMO Objetivo: Avaliar a taxa de desenvolvimento do edema macular cistóide em pacientes submetidos à cirurgia de catarata em quatro esquemas terapêuticos diferentes. Métodos: O presente estudo é uma análise retrospectiva de 5.380 olhos após facoemulsificação não complicada na Wake Forest University. O período do estudo foi entre julho de 2007 e dezembro de 2012. Os pacientes receberam um dos quatro esquemas: cetorolaco genérico pós-operatório 0,4% e prednisolona 1%, cetorolaco 0,45% pós-operatório e prednisolona 1%, bromfenac 0,09% e a prednisolona 1% pós-operatório, bromfenaco 0,09% no pré-operatório e isoladamente no pós-operatório. Uma análise estatística foi realizada para avaliar as diferenças na taxa de desenvolvimento do edema macular cistóide entre os quatro diferentes regimes terapêuticos. O diagnóstico de edema macular cistóide exigiu uma piora da visão e uma evidência de aumento da espessura macular na tomografia de coerência óptica. Resultados: A taxa global de edema macular cistóide foi de 0,82%. O tratamento com cetorolaco genérico pós-operatório 0,45% e prednisolona 1% demonstrou a maior taxa de desenvolvimento de edema macular cistóide (2,20% dos casos). O cetorolaco 0,45% e a prednisolona 1% no pós-operatório exibiram taxas intermediárias de desenvolvimento de edema macular cistóide (0,90% dos casos). A administração de bromofenac 0,09% e de prednisolona 1% no pós-operatório apresentou taxas intermediárias de desenvolvimento de edema macular cistóide (0,44% dos casos). O bromfenac 0,09% no pré e pós-operatório isoladamente resultou na menor taxa de desenvolvimento de edema macular cistóide (0,09% dos casos). A taxa de edema macular cistóide foi significativamente menor quando o bromfenac foi utilizado isoladamente em relação ao esquema onde cetorolaco e a prednisolona foram usados (OR 0,043, 95% CI 0,002 a 0,312; p<0,001). Conclusões: O edema macular cistóide pós-cirurgia de catarata desenvolveu-se com menor frequência após o tratamento tópico de medicamentos anti-inflamatórios não esteroidais, comparado às outras terapias avaliadas. Bromfenac, sem corticosteróides, alcançou taxas mais baixas de edema macular cistóide vs. Várias combinações em comparação com as várias combinações de drogas anti-inflamatórias não esteroidais com corticosteróides.
Subject(s)
Humans , Male , Female , Aged , Aged, 80 and over , Benzophenones/therapeutic use , Bromobenzenes/therapeutic use , Prednisolone/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Macular Edema/prevention & control , Phacoemulsification/adverse effects , Cataract , Macular Edema/etiology , Retrospective Studies , Drug Therapy, CombinationABSTRACT
Decabromodiphenylethane (DBDPE) has been widely used as an alternative flame retardant due to the restriction or phase-out of traditional polybrominated diphenyl ethers (PBDEs), and is of increasing concern regarding its ubiquity, persistence, and potential adverse effects. In the present study, the toxicological effects of DBDPE were evaluated using zebrafish as an in vivo model. Upon being exposed to DBDPE-polluted sediments for a short term, it was found that the mortality and malformation of zebrafish (including edema, bent notochord, and bent tail) were not affected even at the highest concentration tested (1000.0 µg/kg dry sediment). Regarding behavioral responses, it was found that zebrafish larvae of 48 hours post fertilization (hpf) in all groups escaped successfully with a touch to the dorsal fin. However, when exposed to the highest DBDPE concentration, the larvae of 120 hpf exhibited significantly smaller distances as compared to the control. Moreover, the results of the acetylcholinesterase (AChE) activity, the expression levels of two important nerve-related genes, and the cell apoptosis all indicated that DBDPE posed low neurotoxicity in embryo-larval zebrafish. The results in this study shed some light on the potential risks of DBDPE in the real environment and highlight the application of the sediment exposure route in the future.
Subject(s)
Animals , Abnormalities, Drug-Induced , Apoptosis , Behavior, Animal , Bromobenzenes , Toxicity , Geologic Sediments , Larva , Neurotoxicity Syndromes , Water Pollutants, Chemical , Toxicity , Zebrafish , EmbryologyABSTRACT
PURPOSE: To compare the additive effects of two types of non-steroidal anti-inflammatory drugs (NSAIDs), bromfenac 0.1% or ketorolac 0.45%, relative to topical steroid alone in cataract surgery. MATERIALS AND METHODS: A total 91 subjects scheduled to undergo cataract operation were randomized into three groups: Group 1, pre/postoperative bromfenac 0.1%; Group 2, pre/postoperative preservative-free ketorolac 0.45%; and Group 3, postoperative steroid only, as a control. Outcome measures included intraoperative change in pupil size, postoperative anterior chamber inflammation control, change in macular thickness and volume, and ocular surface status after operation. RESULTS: Both NSAID groups had smaller intraoperative pupil diameter changes compared to the control group (p<0.05). There was significantly less ocular inflammation 1 week and 1 month postoperatively in both NSAID groups than the control group. The changes in central foveal subfield thickness measured before the operation and at postoperative 1 month were 4.30+/-4.25, 4.87+/-6.03, and 12.47+/-12.24 microm in groups 1 to 3, respectively. In the control group, macular thickness and volume increased more in patients with diabetes mellitus (DM), compared to those without DM. In contrast, in both NSAID groups, NSAIDs significantly reduced macular changes in subgroups of patients with or without DM. Although three ocular surface parameters were worse in group 1 than in group 2, these differences were not significant. CONCLUSION: Adding preoperative and postoperative bromfenac 0.1% or ketorolac 0.45% to topical steroid can reduce intraoperative miosis, postoperative inflammation, and macular changes more effectively than postoperative steroid alone.
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Anti-Inflammatory Agents, Non-Steroidal/administration & dosage , Benzophenones/administration & dosage , Bromobenzenes/administration & dosage , Cataract , Cataract Extraction , Inflammation/prevention & control , Ketorolac/administration & dosage , Lens Implantation, Intraocular , Macular Edema/prevention & control , Miosis/prevention & control , Phacoemulsification , Postoperative Complications/drug therapy , Postoperative Period , Premedication , Treatment OutcomeABSTRACT
This study investigated the toxicity of commercial non-steroid anti-inflammatory drug (NSAID) eye solutions against corneal epithelial cells in vitro. The biologic effects of 1/100-, 1/50-, and 1/10-diluted bromfenac sodium, pranoprofen, diclofenac sodium, and the fluorometholone on corneal epithelial cells were evaluated after 1-, 4-, 12-, and 24-hr of exposure compared to corneal epithelial cell treated with balanced salt solution as control. Cellular metabolic activity, cellular damage, and morphology were assessed. Corneal epithelial cell migration was quantified by the scratch-wound assay. Compared to bromfenac and pranoprofen, the cellular metabolic activity of diclofenac and fluorometholone significantly decreased after 12-hr exposure, which was maintained for 24-hr compared to control. Especially, at 1/10-diluted eye solution for 24-hr exposure, the LDH titers of fluorometholone and diclofenac sodium markedly increased more than those of bromfenac and pranoprofen. In diclofenac sodium, the Na+ concentration was lower and amount of preservatives was higher than other NSAIDs eye solutions tested. However, the K+ and Cl- concentration, pH, and osmolarity were similar for all NSAIDs eye solutions. Bromfenac and pranoprofen significantly promoted cell migration, and restored wound gap after 48-hr exposure, compared with that of diclofenac or fluorometholone. At 1/50-diluted eye solution for 48-hr exposure, the corneal epithelial cellular morphology of diclofenac and fluorometholone induced more damage than that of bromfenac or pranoprofen. Overall, the corneal epithelial cells in bromfenac and pranoprofen NSAID eye solutions are less damaged compared to those in diclofenac, included fluorometholone as steroid eye solution.
Subject(s)
Humans , Anti-Inflammatory Agents, Non-Steroidal/administration & dosage , Benzophenones/administration & dosage , Benzopyrans/administration & dosage , Bromobenzenes/administration & dosage , Cell Movement/drug effects , Cells, Cultured , Diclofenac/administration & dosage , Epithelial Cells/drug effects , Epithelium, Corneal/cytology , Fluorometholone/administration & dosage , L-Lactate Dehydrogenase/metabolism , Microscopy, Electron, Transmission , Ophthalmic Solutions , Propionates/administration & dosageABSTRACT
<p><b>OBJECTIVE</b>The purpose of the present study was to evaluate the nephroprotective and antioxidant properties of Triphala against bromobenzene-induced nephrotoxicity in female Wistar albino rats.</p><p><b>METHODS</b>Animals were divided into five groups of six rats and treated as follows: Group I was a normal control and received no treatment, Group II received only bromobenzene (10 mmol/kg), Groups III and IV received bromobenzene and Triphala (250 and 500 mg/kg, respectively), Group V received Triphala alone (500 mg/kg), and Group VI received bromobenzene and silymarin (100 mg/kg). Antioxidant status and serum kidney functional markers were analyzed.</p><p><b>RESULTS</b>Bromobenzene treatment resulted in significant (P< 0.05) decreases in the activities of antioxidant enzymes such as catalase, superoxide dismutase, glutathione-S-transferase and glutathione peroxidase as well as total reduced glutathione. There was a significant (P< 0.05) increase in lipid peroxidation in kidney tissue homogenates. There were significant (P< 0.05) reductions in the levels of serum total protein and albumin as well as significant (P< 0.05) increases in serum creatinine, urea and uric acid. The oral administration of two different doses (250 and 500 mg/kg) of Triphala in bromobenzene-treated rats normalized the tested parameters. The histopathological examinations of kidney sections of the experimental rats support the biochemical observations.</p><p><b>CONCLUSION</b>Triphala treatment alleviated the nephrotoxic effects of bromobenzene by increasing the activities of antioxidant enzymes and reducing the levels of lipid peroxidation and kidney functional markers.</p>
Subject(s)
Animals , Female , Rats , Acute Kidney Injury , Diagnosis , Metabolism , Antioxidants , Pharmacology , Bromobenzenes , Pharmacology , Disease Models, Animal , Kidney , Metabolism , Pathology , Kidney Function Tests , Medicine, Ayurvedic , Phyllanthus emblica , Plant Preparations , Chemistry , Pharmacology , Plant Structures , Protective Agents , Pharmacology , Rats, Wistar , Silymarin , Pharmacology , Terminalia , Treatment OutcomeABSTRACT
Information regarding decabromodiphenyl ethane (DBDPE) effects on hepatotoxicity and metabolism is limited. In the present study, Wistar rats were given oral DBDPE at different doses. DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, 7-pentoxyresorufin O-depentylase (PROD) activity, and induced CYP3A2 mRNA, CYP3A2 protein, and luciferin benzylether debenzylase (LBD) activity. UDPGT activity increased with its increasing exposure levels, suggesting that oral DBDPE exposure induces drug-metabolizing enzymes in rats via the CAR/PXR signaling pathway. The induction of CYPs and co-regulated enzymes of phase II biotransformation may affect the homeostasis of endogenous substrates, including thyroid hormones, which may, in turn, alter glucose metabolism.
Subject(s)
Animals , Female , Male , Rats , Bromobenzenes , Toxicity , Chemical and Drug Induced Liver Injury , Flame Retardants , Toxicity , Liver , Metabolism , Random Allocation , Rats, Wistar , Toxicity TestsABSTRACT
<p><b>OBJECTIVE</b>To investigate the toxic effects of decabromodiphenyl ethane (DBDPE), used as an alternative to decabromodiphenyl ether in vitro.</p><p><b>METHODS</b>HepG2 cells were cultured in the presence of DBDPE at various concentrations (3.125-100.0 mg/L) for 24, 48, and 72 h respectively and the toxic effect of DBDPE was studied.</p><p><b>RESULTS</b>As evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and lactate dehydrogenase assays and nuclear morphological changes, DBDPE inhibited HepG2 viability in a time- and dose-dependent manner within a range of 12.5 mg/L to 100 mg/L and for 48 h and 72 h. Induction of apoptosis was detected at 12.5-100 mg/L at 48 h and 72 h by propidium iodide staining, accompanied with overproduction of reactive oxygen species (ROS). Furthermore, N-acetyl-L-cysteine, a widely used ROS scavenger, significantly reduced DBDPE-induced ROS levels and increased HepG2 cells viability.</p><p><b>CONCLUSION</b>DBDPE has cytotoxic and anti-proliferation effect and can induce apoptosis in which ROS plays an important role.</p>
Subject(s)
Humans , Apoptosis , Bromobenzenes , Toxicity , Cell Survival , Dose-Response Relationship, Drug , Environmental Pollutants , Toxicity , Hep G2 Cells , Reactive Oxygen Species , Time FactorsABSTRACT
The framework of iridoid monoterpene has been constructed in a photo-initiated three step sequence involving 1,3-cyclo-addition of bromobenzene to vinyl acetate, ring opening of the formed vinylcyclopropyl bromide with Ag[+]/H[2] O[2], and subsequent acid catalysed Hock-cleavage of the generated allylic hydro-peroxide
Subject(s)
Bromobenzenes , Bromides , AlkenesABSTRACT
In this study the hepatorenal protective effects of nifedipine and vitamin C were investigated in albino rats during acute and chronic bromobenzene [Br B] induced hepatorenal toxicity. Hepatotoxicity and hepatoprotective activities were monitored by estimating serum transaminase [SGPT and SGOT], alkaline phosphatase [ALP], total bilirubin [TB] and total proteins [TP]. Nephrotoxicity and nephroprotective activities were monitored by estimating blood urea nitrogen [BUN] and serum creatinine. Histopathological and histochemical studies of the livers and kidneys of experimental rats were also done. Administration of nifedipine and vitamin C concomitant with Br B to rats led to complete normalization of toxin induced alteration assessed by biochemical parameters and almost abolishing the toxin induced histopathological and histochemical changes in the rats livers and kidneys. A conclusion was made that infedipine and vitamin C have protected against bromobenzene induced hepatorenal toxicity