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Pharmacogenomics of Cytochrome P450 of Nimodipine Metabolism After Aneurysmal Subarachnoid Hemorrhage.
Peacock, SH, James, C, Turnbull, MT, Cowart, JB, Reid, JM, Freeman, WD
The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses. 2019;(5):238-242
Abstract
INTRODUCTION Aneurysmal subarachnoid hemorrhage (aSAH) is a type of stroke that is life threatening with high rates of mortality, and many survivors are left with permanent neurologic deficits. Nimodipine is the treatment of choice for aSAH with the goal of reduction of delayed cerebral ischemia. It is the only evidence-based medication that has been shown to have improved outcomes for delayed cerebral ischemia; therefore, it is important for neuroscience nurses to be knowledgeable of the pharmacology and pharmacogenomics properties of this medication, including cytochrome P450 (CYP450) enzymes. METHODS AND RESULTS This article reviews the CYP450 enzyme system including a review of the pharmacotherapy and pharmacogenomics of nimodipine for patients with aSAH illustrated with case study of a patient with abnormal drug metabolism. CONCLUSION CYP450 enzymes can be inhibited or induced by multiple medications resulting in clinically significant differences in drug metabolism. Food and Drug Administration-approved medication nimodipine is the only medication shown to improve outcomes in patients with aSAH. Hence, it is important to have awareness of potential drug-to-drug interactions and pharmacogenomics of nimodipine when caring for critically ill patients with aSAH.
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Gabapentin and pregabalin to treat aggressivity in dementia: a systematic review and illustrative case report.
Supasitthumrong, T, Bolea-Alamanac, BM, Asmer, S, Woo, VL, Abdool, PS, Davies, SJC
British journal of clinical pharmacology. 2019;(4):690-703
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Abstract
AIMS: The prevalence of dementia is rising as life expectancy increases globally. Behavioural and psychological symptoms of dementia (BPSD), including agitation and aggression, are common, presenting a challenge to clinicians and caregivers. METHODS Following PRISMA guidelines, we systematically reviewed evidence for gabapentin and pregabalin against BPSD symptoms of agitation or aggression in any dementia, using six databases (Pubmed, CINHL, PsychINFO, HealthStar, Embase, and Web of Science). Complementing this formal systematic review, an illustrative case of a patient with BPSD in mixed Alzheimer's/vascular dementia, who appeared to derive benefits in terms of symptom control and functioning from the introduction of gabapentin titrated up to 3600 mg day-1 alongside other interventions, is presented. RESULTS Twenty-four relevant articles were identified in the systematic review. There were no randomized trials. Fifteen papers were original case series/case reports of patients treated with these compounds, encompassing 87 patients given gabapentin and six given pregabalin. In 12 of 15 papers, drug treatment was effective in the majority of cases. The remaining nine papers were solely reviews, of which two were described as systematic but predated PRISMA guidelines. Preliminary low-grade evidence based on case series and case reviews suggests possible benefit of gabapentin and pregabalin in patients with BPSD in Alzheimer's disease. These benefits cannot be confirmed until well-powered randomized controlled trials are undertaken. Evidence in frontotemporal dementia is lacking. CONCLUSION Gabapentin and pregabalin could be considered for BPSD when medications having stronger evidence bases (risperidone, other antipsychotics, carbamazepine and citalopram) have been ineffective or present unacceptable risks of adverse outcomes.
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Non-cardiogenic pulmonary edema and life-threatening shock due to calcium channel blocker overdose: a case report and clinical review.
Siddiqi, TA, Hill, J, Huckleberry, Y, Parthasarathy, S
Respiratory care. 2014;(2):e15-21
Abstract
Calcium channel blockers (CCBs) overdose can be life-threatening when manifest as catastrophic shock and non-cardiogenic pulmonary edema. We describe a case of massive overdose of multiple medications, including sustained-release verapamil, which was resistant to conventional support. Initial treatment for CCB overdose is primarily supportive, and includes fluid resuscitation. The mechanism of non-cardiogenic pulmonary edema is not well known, and reported cases have been successfully treated with mechanical ventilation. Circulatory shock may fail to respond to atropine, glucagon, and calcium in severely poisoned patients, and vasopressors are usually required. Attempting to overcome calcium-channel antagonism with the supra-therapeutic doses of calcium salts is clinically indicated to reverse hypotension and bradycardia. There is evidence that hyperinsulinemia-euglycemia therapy is superior to other therapies for CCB poisoning, and the mechanism is thought to be the insulin-mediated active transport of glucose into the cells, which counters the CCB-induced intra-cellular carbohydrate-deficient state. Conventional decontamination measures are ineffective in accelerating clearance of CCB. Experience with intravenous lipid emulsion for lipophilic drug overdose, such as verapamil, is limited, but has been proposed as a rescue therapy and might improve cardiac inotropy through intravascular sequestration of the lipophilic CCB.
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Raynaud disease.
Butendieck, RR, Murray, PM
The Journal of hand surgery. 2014;(1):121-4
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Coronary artery spasm and ventricular arrhythmias.
Looi, KL, Grace, A, Agarwal, S
Postgraduate medical journal. 2012;(1042):465-71
Abstract
Coronary artery spasm (CAS) is characterised by chest pain at rest and transient ST segment elevation on the ECG. The natural history of variant angina is not fully understood. Patients with CAS are younger, mostly female subjects and usually do not have traditional cardiovascular risk factors other than cigarette smoking. Cardiac arrhythmias are known to be associated with CAS. Ventricular arrhythmia is a well-recognised complication and sudden cardiac death has also been documented. The most important diagnostic tool in CAS is coronary angiography. 24 h ECG Holter monitoring can be very useful in the diagnosis of ventricular arrhythmias caused by CAS. The mainstay therapy for CAS is calcium channel blockers and nitrates. The use of β-blockers, especially the non-selective group, can promote attacks or prolong vasospastic state. The indication for implantable cardioverter defibrillator (ICD) implantation in a patient with CAS is still not clearly established. The role of primary prevention with the use of ICD is controversial; however, ICD implantation should be considered in high risk patients despite optimal medical treatment.
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Amlodipine fatality in an infant with postmortem blood levels.
Spiller, HA, Milliner, BA, Bosse, GM
Journal of medical toxicology : official journal of the American College of Medical Toxicology. 2012;(2):179-82
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INTRODUCTION Amlodipine is a dihydropyridine calcium channel blocker used in the treatment of hypertension and angina pectoris. Toxic effects reported from amlodipine include hypotension, reflex tachycardia, metabolic acidosis, and pulmonary edema. We report a rare fatality in an infant after ingestion of amlodipine with benazepril, with postmortem blood concentrations. CASE REPORT An 11-month-old, 10.88-kg boy ingested 10 to 45 mg amlodipine with 40 to 180 mg benazepril. No action was taken initially because the parents believed only one or two capsules had been ingested. A later count revealed a maximum of nine capsules missing. The child was observed at home and vomited once with possible capsule fragments. Forty-five minutes post-ingestion, the child was noted to be suddenly unresponsive and was brought the local emergency department by a private vehicle. Upon arrival (90 min post-ingestion), the child was unresponsive with the following vital signs HR 133 bpm, BP 67/42 mmHg, respiratory rate 40/min, and temperature 97.5°F. Pertinent abnormal laboratory values were HCO(3) 13 mmol/l and glucose 302 mg/dl. The child was placed on oxygen via a non-rebreather mask and was intubated 45 min post-arrival. The patient became progressively bradycardic, and 55 min after arrival, the patient was in asystole with no palpable blood pressure. Resuscitation measures included chest compressions, epinephrine atropine, sodium bicarbonate, and calcium gluconate. Rescue insulin therapy was begun with 4 units IVP followed by 10 units per hour. Resuscitation efforts persisted for 1 h without success. An autopsy revealed pulmonary edema and no gross or microscopic evidence of natural disease. Stomach contents revealed food matter with small white fragments. Analysis of postmortem heart blood showed amlodipine 1,300 ng/ml (therapeutic <20 ng/ml). Benazepril levels were not available. DISCUSSION We believe this is the first reported fatality in an infant from amlodipine. While benazepril may have contributed, ACE inhibitors have not been previously associated with rapid cardiovascular collapse. CONCLUSION Small doses of amlodipine (0.9 to 4.1 mg/kg) may produce rapid and fatal cardiovascular collapse in an infant.
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Towards evidence-based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 3. Elevation of serum magnesium may improve clinical outcome after aneursymal subarachnoid haemorrhage.
Horner, D
Emergency medicine journal : EMJ. 2011;(2):166-8
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Coronary artery spasm: a 2009 update.
Stern, S, Bayes de Luna, A
Circulation. 2009;(18):2531-4
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[Infant botulism: case report and review].
Arriagada S, D, Wilhelm B, J, Donoso F, A
Revista chilena de infectologia : organo oficial de la Sociedad Chilena de Infectologia. 2009;(2):162-7
Abstract
Botulism is a rare disease in Chile and of the known clinical presentation, infant botulism is the most common. We report the case of a previously healthy seven month old male infant with a two weeks history of rinorrea, cough, fatigue, constipation and progressive weakness after the consumption of honey. Stool cultures were positive for Clostridium botulinum group 1 type A and electromyography was compatible with the diagnosis. The patient evolved with arterial hypertension, interpreted as secondary to autonomic dysfunction, which responded to calcium channel blockers. Muscle tone improved progressively during the following four weeks. Infant botulism is a potentially fatal disease; diagnosis can be difficult given the broad clinical manifestations. Prevention should focus on education of parents of infants as well as medical personnel.
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Calcium channel blocker-associated small bowel angioedema.
Turcu, AF, White, JA, Kulaga, ME, Skluth, M, Gruss, CB
Journal of clinical gastroenterology. 2009;(4):338-41
Abstract
INTRODUCTION Isolated angioedema of the small intestine is a rare entity. The cases described have been related with angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, or C1 esterase inhibitor deficiency. We present a case of small intestine angioedema caused by calcium channel blockers (CCBs) and a review of the literature. CASE REPORT Over the course of approximately 2 years, a 56-year-old African American woman presented to our hospital with 8 similar episodes of diffuse, intermittent abdominal pain, nausea, vomiting, and diarrhea. The diagnostic workup was extensive and included normal stool studies, anticardiolipin antibodies, antinuclear antibodies, antineutrophil cytoplasmic antibodies, cryoglobulin studies, complement levels, urinary 5-hydroxyindoleacetic acid, and serum markers for inflammatory bowel diseases. A computed tomographic angiogram was normal. Abdominal computed tomographic scans showed prominent mural thickening of different intestinal segments, always involving the ileum. An esophagogastroduodenoscopy showed patchy edematous, violaceous folds in the second portion of the duodenum. Colonoscopy revealed a markedly edematous and erythematous distal ileum. The recurrences subsided after CCBs were discontinued in this patient and reoccurred when they were incidentally restarted. CONCLUSIONS Our case demonstrates that CCBs can cause isolated intestinal angioedema with distinctive endoscopic findings. The discontinuation of the involved medication is the key for both diagnosis and treatment.