Richard F Clark, Saralyn R Williams, Frederick Fung, Aaron B Schneir, Binh T Ly, David A Tanen, Stephen W Munday
{"title":"A reassessment of topical organic phosphorus insecticide exposures and permanent paralysis.","authors":"Richard F Clark, Saralyn R Williams, Frederick Fung, Aaron B Schneir, Binh T Ly, David A Tanen, Stephen W Munday","doi":"10.1081/clt-200041851","DOIUrl":"https://doi.org/10.1081/clt-200041851","url":null,"abstract":"","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 7","pages":"991-2"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200041851","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24897191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A near-fatal overdose of carisoprodol (SOMA): case report.","authors":"Munawar Siddiqi, Constance A Jennings","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 2","pages":"239-40"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24581181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Unlabelled: Lead exposure is a preventable environmental health concern. Young children between the ages of 1 to 6 are most susceptible to its clinical effects. This article reports the results of lead level determinations in the drinking water of Philadelphia's public school buildings and remediation efforts aimed at dealing with this public health concern.
Methods: Water samples were collected from drinking sources in 292 school buildings in Philadelphia from May 2000 through January 2001. These samples were collected and sent to reference laboratories for determination of lead levels.
Results: A total of 42.5% (124) of schools had water lead levels not exceeding the action level of 20 ppb, of which 3.1% had nondetectable levels or levels less than 5 ppb. A total of 28.7% of buildings had water lead levels ranging from 20 to 50 ppb, 11.6% had levels between 50-100 ppb, and 17.1% had water lead levels of 100 ppb or more.
Conclusion: A total of 57.4% of Philadelphia's public school buildings had water lead levels exceeding the Environmental Protection Agencies (EPA) action level of 20 ppb, and 28.7% of school buildings had water with mean lead levels in excess of 50 ppb. Depending on the volume of water consumed, drinking water from school buildings may be a significant source of lead exposure for children in their formative years of development. Although Philadelphia's public school buildings were evaluated, lead-contaminated drinking water in schools is not only an urban concern. School buildings in suburban and rural areas may have similar water lead levels, and testing programs are desirable.
{"title":"Lead-contaminated drinking waters in the public schools of Philadelphia.","authors":"S D Bryant","doi":"10.1081/clt-120037429","DOIUrl":"https://doi.org/10.1081/clt-120037429","url":null,"abstract":"<p><strong>Unlabelled: </strong>Lead exposure is a preventable environmental health concern. Young children between the ages of 1 to 6 are most susceptible to its clinical effects. This article reports the results of lead level determinations in the drinking water of Philadelphia's public school buildings and remediation efforts aimed at dealing with this public health concern.</p><p><strong>Methods: </strong>Water samples were collected from drinking sources in 292 school buildings in Philadelphia from May 2000 through January 2001. These samples were collected and sent to reference laboratories for determination of lead levels.</p><p><strong>Results: </strong>A total of 42.5% (124) of schools had water lead levels not exceeding the action level of 20 ppb, of which 3.1% had nondetectable levels or levels less than 5 ppb. A total of 28.7% of buildings had water lead levels ranging from 20 to 50 ppb, 11.6% had levels between 50-100 ppb, and 17.1% had water lead levels of 100 ppb or more.</p><p><strong>Conclusion: </strong>A total of 57.4% of Philadelphia's public school buildings had water lead levels exceeding the Environmental Protection Agencies (EPA) action level of 20 ppb, and 28.7% of school buildings had water with mean lead levels in excess of 50 ppb. Depending on the volume of water consumed, drinking water from school buildings may be a significant source of lead exposure for children in their formative years of development. Although Philadelphia's public school buildings were evaluated, lead-contaminated drinking water in schools is not only an urban concern. School buildings in suburban and rural areas may have similar water lead levels, and testing programs are desirable.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"287-94"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120037429","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24678089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fertilizers are used to promote the survival and growth of plants and crops and have a good safety record when used properly. The basic elements in fertilizer include phosphorus, nitrite, and potassium. In addition, there are additive agents that vary for different crops and which may include some metals. Acute intoxication by ingesting fertilizer includes damage to various organ systems as well as severe cardiovascular or respiratory distress. We report the case of a 64-year-old man who ingested about 700 mL of fertilizer and suffered acute renal failure, hyperkalemia, and mild methemoglobinemia. After supportive care and emergent hemodialysis for hemodynamic instability due to hyperkalemia, the renal function of the patient recovered in four days.
{"title":"Acute renal failure following ingestion of manganese-containing fertilizer.","authors":"Wen-Hung Huang, Ja-Liang Lin","doi":"10.1081/clt-120037433","DOIUrl":"https://doi.org/10.1081/clt-120037433","url":null,"abstract":"<p><p>Fertilizers are used to promote the survival and growth of plants and crops and have a good safety record when used properly. The basic elements in fertilizer include phosphorus, nitrite, and potassium. In addition, there are additive agents that vary for different crops and which may include some metals. Acute intoxication by ingesting fertilizer includes damage to various organ systems as well as severe cardiovascular or respiratory distress. We report the case of a 64-year-old man who ingested about 700 mL of fertilizer and suffered acute renal failure, hyperkalemia, and mild methemoglobinemia. After supportive care and emergent hemodialysis for hemodynamic instability due to hyperkalemia, the renal function of the patient recovered in four days.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"305-7"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120037433","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24678092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Robert S Hoffman, Joseph L Kaplan, Oliver L Hung, Lewis R Goldfrank
Background: Plasma cholinesterase (PChE) metabolizes cocaine to ecgonine methyl ester (EME). Limited data demonstrate that EME is a mild vasodilator. Exogenous PChE protects against cocaine-induced seizures and lethality. It is unclear whether this protective effect results from enhanced degradation of cocaine, the loss of active metabolites (benzoylecgonine, norcocaine), or the production of a beneficial metabolite (EME). This study was designed to further investigate the pharmacologic effects of EME.
Methods: All experiments used female ICR Swiss albino mice weighing 20-30 grams. Mice were acclimated to 12 h alternating light-dark cycles and given food and water ad libitum. Using a randomized, blinded protocol, 80 mice were then pretreated with either IP EME (50 mg/kg) in a 0.9% sodium chloride solution or an equal volume of 0.9% sodium chloride solution as control. Five minutes later, all animals received 126 mg/kg of cocaine IP and were observed for seizures and death. Fatality was compared using a Fisher's exact test, and the time to seizures and death were compared using a Mann-Whitney U statistic.
Results: Pretreatment with EME increased survival following cocaine (9/40 vs. 2/40, for EME vs. control, respectively, p<0.05). The median times to seizure and death for both groups were 2.0 vs. 1.5 min (p>0.05), and 4.5 vs. 4.6 min (p>0.05) (EME vs. control for seizures and death, respectively).
Conclusion: In this animal model, EME is protective against cocaine lethality. This effect is consistent with the previously described vasodilatory effects of EME. Further studies are indicated to determine whether the increase in EME produced by exogenous PChE administration contributes to the benefits that occur when PChE is given to cocaine-poisoned animals.
背景:血浆胆碱酯酶(PChE)将可卡因代谢为ecgonine methyl ester (EME)。有限的数据表明,EME是一种温和的血管扩张剂。外源性PChE可防止可卡因引起的癫痫发作和致死。目前尚不清楚这种保护作用是由于可卡因的降解增强、活性代谢物(苯甲酰茶碱、去甲可卡因)的丧失,还是有益代谢物(EME)的产生。本研究旨在进一步探讨EME的药理作用。方法:所有实验均选用体重20 ~ 30 g的ICR瑞士白化雌性小鼠。小鼠适应12小时的明暗交替循环,并随意给予食物和水。采用随机盲法,80只小鼠分别在0.9%氯化钠溶液中注射50 mg/kg的IP EME或等量0.9%氯化钠溶液作为对照。5分钟后,所有动物接受126 mg/kg的可卡因IP,观察癫痫发作和死亡情况。死亡率用Fisher精确检验比较,发病时间和死亡时间用Mann-Whitney U统计比较。结果:EME预处理增加了可卡因后患者的生存时间(EME与对照组分别为9/40 vs 2/40, p0.05),癫痫发作和死亡时间分别为4.5 vs 4.6 min (EME与对照组分别为p>0.05)。结论:在该动物模型中,EME对可卡因致死性有保护作用。这种作用与先前描述的EME的血管舒张作用一致。进一步的研究表明,外源性PChE给药所产生的EME的增加是否有助于给可卡因中毒的动物服用PChE时产生的益处。
{"title":"Ecgonine methyl ester protects against cocaine lethality in mice.","authors":"Robert S Hoffman, Joseph L Kaplan, Oliver L Hung, Lewis R Goldfrank","doi":"10.1081/clt-120039540","DOIUrl":"https://doi.org/10.1081/clt-120039540","url":null,"abstract":"<p><strong>Background: </strong>Plasma cholinesterase (PChE) metabolizes cocaine to ecgonine methyl ester (EME). Limited data demonstrate that EME is a mild vasodilator. Exogenous PChE protects against cocaine-induced seizures and lethality. It is unclear whether this protective effect results from enhanced degradation of cocaine, the loss of active metabolites (benzoylecgonine, norcocaine), or the production of a beneficial metabolite (EME). This study was designed to further investigate the pharmacologic effects of EME.</p><p><strong>Methods: </strong>All experiments used female ICR Swiss albino mice weighing 20-30 grams. Mice were acclimated to 12 h alternating light-dark cycles and given food and water ad libitum. Using a randomized, blinded protocol, 80 mice were then pretreated with either IP EME (50 mg/kg) in a 0.9% sodium chloride solution or an equal volume of 0.9% sodium chloride solution as control. Five minutes later, all animals received 126 mg/kg of cocaine IP and were observed for seizures and death. Fatality was compared using a Fisher's exact test, and the time to seizures and death were compared using a Mann-Whitney U statistic.</p><p><strong>Results: </strong>Pretreatment with EME increased survival following cocaine (9/40 vs. 2/40, for EME vs. control, respectively, p<0.05). The median times to seizure and death for both groups were 2.0 vs. 1.5 min (p>0.05), and 4.5 vs. 4.6 min (p>0.05) (EME vs. control for seizures and death, respectively).</p><p><strong>Conclusion: </strong>In this animal model, EME is protective against cocaine lethality. This effect is consistent with the previously described vasodilatory effects of EME. Further studies are indicated to determine whether the increase in EME produced by exogenous PChE administration contributes to the benefits that occur when PChE is given to cocaine-poisoned animals.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 4","pages":"349-54"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120039540","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40899269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aruna Dewan, Vijay K Bhatnagar, Murli L Mathur, Tapas Chakma, Rekha Kashyap, Harsiddha G Sadhu, Sukesh N Sinha, Habibullah N Saiyed
Introduction: A number of families in a rural area of Jabalpur District (Madhya Pradesh), India, were affected by repeated episodes of convulsive illness over a period of three weeks. The aim of this investigation was to determine the cause of the illness.
Methods: The investigation included a house-to-house survey, interviews of affected families, discussions with treating physicians, and examination of hospital records. Endosulfan poisoning was suspected as many villagers were using empty pesticide containers for food storage. To confirm this, our team collected blood and food samples, which were transported to the laboratory and analyzed with GC-ECD.
Results: Thirty-six persons of all age groups had illness of varying severity over a period of three weeks. In the first week, due to superstitions and lack of treatment, three children died. In the second week, symptomatic treatment of affected persons in a district hospital led to recovery but recurrence of convulsive episodes occurred after the return home. In the third week, 10 people were again hospitalized in a teaching hospital. Investigations carried out in this hospital ruled out infective etiology but no facilities were available for chemical analysis. All persons responded to symptomatic treatment. The blood and food samples analyzed by our team showed presence of endosulfan, which was confirmed by GCMS. One of the food items (Laddu) prepared from wheat flour was found to contain 676 ppm of alpha-endosulfan.
Conclusions: Contamination of wheat grains or flour with endosulfan and its consumption over a period of time was the most likely cause of repeated episodes of convulsions, but the exact reason for this contamination could not be determined. This report highlights the unsafe disposal of pesticide containers by illiterate farm workers, superstitions leading to delay in treatment, and susceptibility of children to endosulfan.
{"title":"Repeated episodes of endosulfan poisoning.","authors":"Aruna Dewan, Vijay K Bhatnagar, Murli L Mathur, Tapas Chakma, Rekha Kashyap, Harsiddha G Sadhu, Sukesh N Sinha, Habibullah N Saiyed","doi":"10.1081/clt-120039542","DOIUrl":"https://doi.org/10.1081/clt-120039542","url":null,"abstract":"<p><strong>Introduction: </strong>A number of families in a rural area of Jabalpur District (Madhya Pradesh), India, were affected by repeated episodes of convulsive illness over a period of three weeks. The aim of this investigation was to determine the cause of the illness.</p><p><strong>Methods: </strong>The investigation included a house-to-house survey, interviews of affected families, discussions with treating physicians, and examination of hospital records. Endosulfan poisoning was suspected as many villagers were using empty pesticide containers for food storage. To confirm this, our team collected blood and food samples, which were transported to the laboratory and analyzed with GC-ECD.</p><p><strong>Results: </strong>Thirty-six persons of all age groups had illness of varying severity over a period of three weeks. In the first week, due to superstitions and lack of treatment, three children died. In the second week, symptomatic treatment of affected persons in a district hospital led to recovery but recurrence of convulsive episodes occurred after the return home. In the third week, 10 people were again hospitalized in a teaching hospital. Investigations carried out in this hospital ruled out infective etiology but no facilities were available for chemical analysis. All persons responded to symptomatic treatment. The blood and food samples analyzed by our team showed presence of endosulfan, which was confirmed by GCMS. One of the food items (Laddu) prepared from wheat flour was found to contain 676 ppm of alpha-endosulfan.</p><p><strong>Conclusions: </strong>Contamination of wheat grains or flour with endosulfan and its consumption over a period of time was the most likely cause of repeated episodes of convulsions, but the exact reason for this contamination could not be determined. This report highlights the unsafe disposal of pesticide containers by illiterate farm workers, superstitions leading to delay in treatment, and susceptibility of children to endosulfan.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 4","pages":"363-9"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120039542","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40899271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Although accurate determination of body weight is important in the management of the poisoned patient, many patients have their weight estimated rather than formally measured.
Objective: To determine how good medical staff are at estimating patients*** body weights.
Methods: Medical staff were asked to estimate the weight of six patients on a poisons ward. Estimated and actual patient weights were statistically compared.
Results: Medical staff produced a large range of estimated weights for all patients. Patient weight was incorrectly estimated by greater than 10% in 61% of individual estimations. There was poor statistical correlation between actual and estimated weight.
Conclusions: All patients administered medication based on body weight and those treated following an overdose of any substance should have formal body weight determined as part of their standard management.
{"title":"Doctors and nurses estimation of the weight of patients: A preventable source of systematic error.","authors":"Shaun Greene, Paul Dargan, G Y Shin, A I Jones","doi":"10.1081/clt-200026969","DOIUrl":"https://doi.org/10.1081/clt-200026969","url":null,"abstract":"<p><strong>Background: </strong>Although accurate determination of body weight is important in the management of the poisoned patient, many patients have their weight estimated rather than formally measured.</p><p><strong>Objective: </strong>To determine how good medical staff are at estimating patients*** body weights.</p><p><strong>Methods: </strong>Medical staff were asked to estimate the weight of six patients on a poisons ward. Estimated and actual patient weights were statistically compared.</p><p><strong>Results: </strong>Medical staff produced a large range of estimated weights for all patients. Patient weight was incorrectly estimated by greater than 10% in 61% of individual estimations. There was poor statistical correlation between actual and estimated weight.</p><p><strong>Conclusions: </strong>All patients administered medication based on body weight and those treated following an overdose of any substance should have formal body weight determined as part of their standard management.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 5","pages":"611-5"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200026969","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40901019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Christopher P Holstege, Jeffrey D Ferguson, Carl E Wolf, Alexander B Baer, Alphonse Poklis
Objectives: In the past, some moonshine products contained potentially toxic contaminants. Although moonshine production continues in the United States, no studies have analyzed the content of moonshine since the early 1960s. We hypothesize that moonshine continues to contain potentially toxic concentrations of contaminants.
Methods: Forty-eight samples of illicitly distilled moonshine were obtained from law enforcement agencies. An independent laboratory, blinded to both the moonshine source and a control sample of ethanol, conducted the analysis. Lead content was determined using atomic absorption spectrophotometry with a graphite tube atomizer. Alcohol content, including ethanol, acetone, isopropanol, methanol, and ethylene glycol, was determined using gas liquid chromatography with flame ionization detection.
Results: Ethanol content ranged from 10.5% to 66.0% with a mean value of 41.2%. Lead was found in measurable quantities in 43 of 48 samples with values ranging from 5 to 599 parts per billion (ppb) with a mean value of 80.7 ppb. A total of 29 of 48 (60%) of samples contained lead concentrations above or equal to the EPA water guideline of 15 ppb. Methanol was found in only one sample at a concentration of 0.11%. No samples contained detectable concentrations of acetone, isopropanol, or ethylene glycol.
Conclusions: Many moonshine samples contain detectable concentrations of lead. Extrapolations based on the described moonshine lead content suggest that chronic consumers of moonshine may develop elevated lead concentrations. Physicians should consider lead toxicity in the differential diagnosis when evaluating patients consuming moonshine.
{"title":"Analysis of moonshine for contaminants.","authors":"Christopher P Holstege, Jeffrey D Ferguson, Carl E Wolf, Alexander B Baer, Alphonse Poklis","doi":"10.1081/clt-200026976","DOIUrl":"https://doi.org/10.1081/clt-200026976","url":null,"abstract":"<p><strong>Objectives: </strong>In the past, some moonshine products contained potentially toxic contaminants. Although moonshine production continues in the United States, no studies have analyzed the content of moonshine since the early 1960s. We hypothesize that moonshine continues to contain potentially toxic concentrations of contaminants.</p><p><strong>Methods: </strong>Forty-eight samples of illicitly distilled moonshine were obtained from law enforcement agencies. An independent laboratory, blinded to both the moonshine source and a control sample of ethanol, conducted the analysis. Lead content was determined using atomic absorption spectrophotometry with a graphite tube atomizer. Alcohol content, including ethanol, acetone, isopropanol, methanol, and ethylene glycol, was determined using gas liquid chromatography with flame ionization detection.</p><p><strong>Results: </strong>Ethanol content ranged from 10.5% to 66.0% with a mean value of 41.2%. Lead was found in measurable quantities in 43 of 48 samples with values ranging from 5 to 599 parts per billion (ppb) with a mean value of 80.7 ppb. A total of 29 of 48 (60%) of samples contained lead concentrations above or equal to the EPA water guideline of 15 ppb. Methanol was found in only one sample at a concentration of 0.11%. No samples contained detectable concentrations of acetone, isopropanol, or ethylene glycol.</p><p><strong>Conclusions: </strong>Many moonshine samples contain detectable concentrations of lead. Extrapolations based on the described moonshine lead content suggest that chronic consumers of moonshine may develop elevated lead concentrations. Physicians should consider lead toxicity in the differential diagnosis when evaluating patients consuming moonshine.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 5","pages":"597-601"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200026976","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40978930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Patients taking multiple medications may suffer from unpredictable and complex drug-drug interactions resulting in significant morbidity and mortality. There are few reports in the literature of hypoglycemia with concurrent administration of an oral hyperglycemic agent and a fluoroquinolone antibiotic. We present a case of a diabetic patient taking glyburide who was prescribed ciprofloxacin and developed prolonged hypoglycemia, which persisted for over 24 hours. The mechanisms by which these agents interact to produce prolonged hypoglycemia are complex and probably multifactorial. Patients stabilized on glyburide who are started on a fluoroquinolone should have their glucose levels monitored closely.
{"title":"Refractory hypoglycemia from ciprofloxacin and glyburide interaction.","authors":"George Lin, Daniel P Hays, Linda Spillane","doi":"10.1081/clt-120037431","DOIUrl":"https://doi.org/10.1081/clt-120037431","url":null,"abstract":"<p><p>Patients taking multiple medications may suffer from unpredictable and complex drug-drug interactions resulting in significant morbidity and mortality. There are few reports in the literature of hypoglycemia with concurrent administration of an oral hyperglycemic agent and a fluoroquinolone antibiotic. We present a case of a diabetic patient taking glyburide who was prescribed ciprofloxacin and developed prolonged hypoglycemia, which persisted for over 24 hours. The mechanisms by which these agents interact to produce prolonged hypoglycemia are complex and probably multifactorial. Patients stabilized on glyburide who are started on a fluoroquinolone should have their glucose levels monitored closely.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"295-7"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120037431","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24678090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Traditionally, horse-serum-based antivenom has been used in the United States for North American crotaline snake evenomation. Crotalidae polyvalent immune Fab (ovine) was approved in 2000 for use in mild to moderate envenomations. The manufacture recommends use within 6 h of envenomation. Published postmarketing retrospective reports describe its use up to 9 h after envenomation. We describe a case of effective use of FabAV 52 h after envenomation with resultant correction of coagulopathy and mild improvement of local symptoms.
{"title":"Effectiveness of delayed use of crotalidae polyvalent immune Fab (ovine) antivenom.","authors":"Vikhyat Bebarta, Richard C Dart","doi":"10.1081/clt-120037454","DOIUrl":"https://doi.org/10.1081/clt-120037454","url":null,"abstract":"<p><p>Traditionally, horse-serum-based antivenom has been used in the United States for North American crotaline snake evenomation. Crotalidae polyvalent immune Fab (ovine) was approved in 2000 for use in mild to moderate envenomations. The manufacture recommends use within 6 h of envenomation. Published postmarketing retrospective reports describe its use up to 9 h after envenomation. We describe a case of effective use of FabAV 52 h after envenomation with resultant correction of coagulopathy and mild improvement of local symptoms.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"321-4"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120037454","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24678096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}