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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diagnostic tests that are hazardous or infeasible, or both, may become accepted before inadequacies are recognised; only multicentre trials can provide the necessary information for an unrestricted acceptance of any new diagnostic procedure. We prospectively studied the results obtained in 24 experienced echocardiography laboratories. 2949 tests were done in 2799 patients. In 341 tests (12% of the overall population, 21% of the negative tests) the test could not be completed because of complex ventricular tachyarrhythmias (134, 38% of all submaximal studies); nausea and/or headache (71, 20%); hypotension and/or bradycardia (62, 17%); supraventricular tachyarrhythmias (44, 12%); hypertension (24, 7%); and others (20, 6%). Dangerous events (life-threatening complications or side-effects requiring specific treatment and lasting more than 3 hours, or new hospital admission) occurred in 14 cases (1 every 210 tests)--9 cardiac (3 ventricular tachycardias; 2 ventricular fibrillations; 2 myocardial infarctions; 1 prolonged antidote-resistant myocardial ischaemia; 1 severe, persistent hypotension) and 5 extracardiac (atropine poisoning with hallucinations lasting several hours in the absence of either myocardial ischaemia or hypotension). Life-threatening and/or longlasting complications may occur during dobutamine/atropine stress echocardiography. The test is generally well tolerated, although may be interrupted by minor, self-limiting, usually symptomless side-effects.
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PMID:Safety and tolerability of dobutamine-atropine stress echocardiography: a prospective, multicentre study. Echo Dobutamine International Cooperative Study Group. 798 9

Industrial solvents mixed from thinner, used in paints, leathers, rubber, varnishes, have neurotoxic action. By laboral inhalation or spontaneously these are absorbed from the lungs, transported by blood and because of this high lipophilic section are retained within the lipid rich nervous system. Euphoric effects appear accompanied with visual and additive halucinations. In chronic abusers it produce schizophrenic-paranoid consequences with encephalic and peripheral neuronal and nervous fibers destruction, accompanied of blindness and paralysis. Cocaine is another neurotoxic drug. At first it produces euphoria, arterial hypertension and symptoms suggestive of underlying psychiatric diseases. The cocaine addicts often suffer depression, paranoia, hallucinations, seizures and suicidal ideation. The morphological base of the symptomatology is the encephalic and peripheral neuronal and nerve fibers destruction.
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PMID:[Clinico-pathologic correlation of dementia produced by thinner and cocaine]. 806 72

We describe severe sertraline intoxication in a child after accidental ingestion. Sertraline is a new antidepressant that has potent and selective inhibition of neuronal serotonin reuptake. Drug company-sponsored research has suggested little toxicity for this compound. Our patient exhibited prolonged tachycardia, hypertension, hallucinations, coma, hyperthermia, tremors of all extremities, and skin flushing. Clinicians should consider the possibility of serotonin syndrome among patients with similar clinical features and a recent history of sertraline or other serotonergic agent ingestion.
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PMID:Sertraline intoxication in a child. 819 16

Alcohol withdrawal syndrome (AWS) may result in nausea, vomiting, diarrhea, weakness, sweating, tremors, tachycardia, hypertension, agitation, delirium, hallucinations, seizures, and death beginning 6 hours after alcohol cessation in alcoholics. Benzodiazepines are cross-tolerant with ethanol and are considered first-line therapy for treating AWS. Chlordiazepoxide and diazepam are first metabolized by hepatic oxidation, then glucuronidation. Lorazepam and oxazepam undergo only hepatic glucuronidation. Benzodiazepine oxidation is decreased in persons with liver disease and the elderly. Accumulation with resultant excessive sedation and respiratory depression may be significant when administering chlordiazepoxide or diazepam to patients with impaired oxidative metabolism. Lorazepam and oxazepam metabolism is minimally affected by age and liver disease. Chlordiazepoxide and diazepam are erratically absorbed by the intramuscular route. Lorazepam is predictably absorbed by the intramuscular route. Oxazepam is not available in parenteral form. Lorazepam appears to be the safest empiric choice among the various benzodiazepines for treating AWS in the elderly and in patients with liver disease, or those who require therapy by the intramuscular route.
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PMID:Benzodiazepines for alcohol withdrawal in the elderly and in patients with liver disease. 870 Jul 92

Jimson weed (Datura stramonium, a member of the Belladonna alkyloid family) is a plant growing naturally in West Virginia and has been used as a home remedy since colonial times. Due to its easy availability and strong anticholinergic properties, teens are using Jimson weed as a drug. Plant parts can be brewed as a tea or chewed, and seed pods, commonly known as "pods" or "thorn apples," can be eaten. Side effects from ingesting jimson weed include tachycardia, dry mouth, dilated pupils, blurred vision, hallucinations, confusion, combative behavior, and difficulty urinating. Severe toxicity has been associated with coma and seizures, although death is rare. Treatment consists of activated charcoal and gastric lavage. Esmolol or other beta-blocker may be indicated to reduce severe sinus tachycardia. Seizures, severe hypertension, severe hallucinations, and life-threatening arrhythmias are indicators for the use of the anticholinesterase inhibitor, Physostigmine. This article reviews the cases of nine teenagers who were treated in hospitals in the Kanawha Valley after ingesting jimson weed. We hope this article will help alert primary care physicians about the abuse of jimson weed and inform health officials about the need to educate teens about the dangers of this plant.
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PMID:The dangers of jimson weed and its abuse by teenagers in the Kanawha Valley of West Virginia. 927 42

During the autumn of 1995, the National Poisons Information Centre was contacted about several cases of poisoning with Jimson weed (Datura stramonium). Five cases are described here. Upon admission to hospital the patients had moderate to severe anticholinergic symptoms, such as mydriasis, sinus tachycardia, agitation, dry mouth, urine retention, fever, hypertension, hallucinations and seizures. Owing to their agitated behaviour, gastrointestinal decontamination was impossible. Repeated doses of physostigmine (2-3 mg) administered intravenously reversed the anticholinergic features without side-effects. In the most severe case, physostigmine was needed for 18 hours (total dose; 25.5 mg). The patients recovered in a day or two, but mydriasis persisted in many cases.
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PMID:[Poisoning with Jimson weed. Five cases treated with physostigmine]. 932 14

A wealth of experimental evidence demonstrates that cerebral ischemia causes excessive release of glutamate and that glutamate contributes to ischemic injury. Glutamate antagonism by any of several mechanisms can ameliorate the extent of infarction. These antagonists comprise noncompetitive blockers of the ion channel associated with the N-methyl-D-aspartate (NMDA) receptor [e.g., aptiganel (Cerestat)], competitive antagonists of the glutamate recognition site of the NMDA receptor (e.g., selfotel) or of the glycine recognition site (e.g., ACEA 1021, GV150526), antagonists at the polyamine site (e.g., eliprodil), and drugs that may interfere with glutamate release by sodium channel blockade as well as having other actions (e.g., lubeluzole, 619C89). Clinical experience suggests that although some NMDA antagonists are poorly tolerated at putative neuroprotective doses (e.g., selfotel), potentially neuroprotective plasma concentrations can be achieved in humans with others (e.g., aptiganel), though tolerable adverse effects are frequently observed. These clinical effects include hypertension (which is probably preferable to the hypotension seen with nimodipine and lifarizine), sedation, confusion or hallucinations and, at high doses, catatonia. Glycine antagonists may be associated with fewer adverse effects, but preclinical studies suggest that brain penetration may be low. Although recent studies with selfotel and eliprodil have been discontinued because of insufficient evidence for a satisfactory risk/benefit ratio, encouraging experience with aptiganel, magnesium, and glycine antagonists has prompted continued clinical trials with these agents. To be of sufficient size to detect a clinically useful improvement in outcome, these trials need to be large (600-1,000 patients). Present trials with aptiganel (Cerestat) are comparing the efficacy and tolerability of two doses vs. placebo in patients treated within 6 hours of ischemic stroke. Outcome is assessed by the modified Rankin Scale at 3 months.
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PMID:Cerestat and other NMDA antagonists in ischemic stroke. 937 Nov 55

Selegiline (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B) is widely used in the treatment of Parkinson's disease. As the first MAO-B inhibitor approved for the treatment of Parkinson's disease, concerns were raised about the safety of the drug based on the adverse effect profiles of older, nonselective MAO inhibitors. Unlike the nonselective MAO inhibitors, selegiline does not significantly potentiate tyramine-induced hypertension (the 'cheese effect') at the dosages (5 to 10 mg daily) used for the treatment of Parkinson's disease. Selegiline has been well tolerated when given alone. The most frequent adverse events seen during monotherapy have been insomnia, nausea, benign cardiac arrhythmias, dizziness and headache. When combined with levodopa, selegiline can potentiate the typical adverse effects of levodopa, if the dose of levodopa is not reduced sufficiently. Thus, the most common adverse effects associated with this combination are nausea, dizziness, fatigue, constipation and insomnia. At the later stages of Parkinson's disease when fluctuations in disability occur, peak dose dyskinesias, psychiatric complications like hallucinations and insomnia, and orthostatic hypotension are further potentiated by selegiline. Mortality was recently reported to be increased when selegiline and levodopa were given together in comparison with treatment with levodopa alone, but a large meta-analysis of 5 long term studies and 4 separate studies did not support this conclusion. Selegiline seems to be generally well tolerated in combination with other drugs. However, when pethidine (meperidine) has been given to patients who are receiving selegiline therapy, severe adverse effects have been reported. Thus, the concomitant use of these drugs is not recommended. A low tyramine diet is recommended if selegiline is used together with nonselective MAO inhibitors or the selective, reversible MAO-A inhibitor, moclobemide. Several adverse effects have been reported when fluoxetine and selegiline have been used together. A recent survey revealed that the incidence of a true serotonin syndrome is, however, very low with this combination. Concomitant use of selegiline and other selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors (SSRIs) like citalopram, which have generally less interactions than fluoxetine, seems to be well tolerated. Nevertheless, caution is advised when combining a SSRI or a tricyclic antidepressant and selegiline.
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PMID:Safety of selegiline (deprenyl) in the treatment of Parkinson's disease. 967 55

Authors report a case of hallucinations related to clonidine treatment in an elderly man with hypertension and renal failure. The symptoms appeared shortly after treatment is starting. The hallucinations disappeared after clonidine withdrawal. Implications for clinical practice are evocated.
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PMID:[Clonidine hallucinations: description of a clinical case]. 1082 81

Between 10%-28% of patients who receive the immunosuppressant cyclosporine (CsA) experience some form of neurotoxic adverse event. Both sensorial motoric functions may be adversely affected, and thus patients present with a wide range of neurological and psychiatrical disorders. Mild symptoms are common and include tremor, neuralgia, and peripheral neuropathy. Severe symptoms affect up to 5 % of patients and include psychoses, hallucinations, blindness, seizures, cerebellar ataxia, motoric weakness, or leukoencephalopathy. Tacrolimus is associated with similar neurotoxic adverse events. Neurotoxicity may result in serious complications for some patients, particularly recipients of orthotopic liver transplants. Factors that may promote the development of serious complications include advanced liver failure, hypertension, hypocholesterolemia, elevated CsA or tacrolimus blood levels, hypomagnesemia, and methylprednisolone. Occipital white matter appears to be uniquely susceptible to the neurotoxic effects of CsA; injury to both the major and minor vasculature may cause hypoperfusion or ischemia and local secondary toxicity in the white matter. Calcineurin inhibition by CsA and tacrolimus alters sympathetic outflow, which may play a role in the mediation of neurotoxic and hypertensive adverse events. The symptoms of CsA- and tacrolimus-associated neurotoxicity may be reversed in most patients by substantially reducing the dosage of immunosuppressant or discontinuing these drugs. However, some patients have experienced permanent or even fatal neurological damage even after dose reduction or discontinuation. CsA-sparing and tacroli-mus-sparing drug regimens that use the immunosuppressant mycophenolate mofetil, which has no neurotoxic effects, may reduce the incidence and severity of neurotoxic adverse events while maintaining an adequate level of immunoisuppression.
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PMID:Neurotoxicity of calcineurin inhibitors: impact and clinical management. 1105 66


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