Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042571 (vertigo)
 7,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A double-blind trial has been carried out to compare the effects of monobutazone and phenylbutazone in ambulant outpatients with rheumatoid arthritis.One patient developed urticaria, vertigo, weakness, tinnitus and blurred vision during monobutazone administration.Side effects occurring in other patients were for the most part trivial.Untoward symptoms were less frequent in patients taking monobutazone than among those on phenylbutazone.The subjects showed neither improvement nor deterioration during administration of ASA, monophenylbutazone or phenylbutazone.Nevertheless, statistical analysis demonstrated differences between the effects of treatment with monobutazone and phenylbutazone which indicated that phenylbutazone is more effective than monobutazone.
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PMID:Rheumatoid arthritis: comparison of treatment with monophenylbutazone and phenylbutazone. 490 91

In 37 pregnancy women preterm labour was inhibited with intravenous administration of ASA. 20 patients (Group I) had a combined treatment of ASA and Fenoterol. 7 pregnant women (Group II) without successful labour inhibition under Fenoterol were treated with ASA subsequently. In a third group of 10 women we administered ASA alone. The treatment was considered as successful if signs of preterm labour stopped and pregnancy maintained for 7 days or more. In the first group 16, in the second group all patients had been treated successfully. In group III we succeeded in labour inhibiting for more than 7 days in 6 cases. An initial loading dose of 5.5 to 7.0 mn/min ASA had been infused for 24 hours. If preterm labour was stopped, the dosage had been reduced. In all patients dose related but reversible symptoms of vertigo, tinnitus, headache and hyperventilation were seen. Furthermore we found a non-dose-dependent prolongation ( by 30% or normal) of bleeding time. In the fetus respectively the newborn an affection by this ASA treatment could be excluded. We propose inhibition of preterm labour by i.v. ASA administration in all pregnant women if beta-mimetic drugs are not successful or an intolerance is diagnosed. Contraindications for ASA therapy are mentioned.
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PMID:[Clinical study of the labour inhibiting effects an side effects of acetylsalicylic acid (ASA) (author's transl)]. 690 69

One of the most frequently performed surgical procedures in pediatrics is myringotomy and tube placement. Analgesia is often difficult to achieve and children may be uncontrollable, distressing both parents and nursing staff. We designed this investigation to determine if topical lidocaine instilled in the ear canal after myringotomy and tube placement could improve postoperative analgesia. This prospective, randomized, double-blind clinical trial compared topical 4% lidocaine combined with antibiotic drops to placebo and antibiotic drops placed in the external auditory canal following completion of myringotomy and tube placement. One hundred twenty-two ASA class I or II patients were enrolled and completed this investigation. Primary outcome measure was relief of pain based on pain scores and the need for acetaminophen. Patients who received 4% lidocaine with gentamicin had better pain scores (2.81; P = 0.002) than those receiving placebo (4.77). Twenty-seven patients (45%) in the control group received acetaminophen for treatment of postoperative pain compared to eight (13%) in the lidocaine group (P < 0.001). No reports or complaints of vertigo or tinnitus were noted in any patient. The application of 4% lidocaine in antibiotic drops significantly improves postoperative analgesia in patients undergoing myringotomy and tube insertion under general anesthesia. Utilizing this technique should help improve analgesia, specifically in the early postoperative period, and decrease the presence of stress following surgery.
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PMID:Topical lidocaine for postoperative analgesia following myringotomy and tube placement. 888 5

Adverse reactions to acetylsalicylic acid (aspirin, ASA) and other non-steroidal anti-inflammatory drugs (NSAIDs) are the second most important cause of adverse drug reactions (ARDs) after beta-lactams. They produce various clinical manifestations and can affect different organs. Gastrointestinal reactions (pyrosis, vomiting, gastralgia), neurological reactions (tinnitus, deafness, vertigo), blood dyscrasias, and nephrotoxic and hepatotoxic reactions are well known.NSAIDs are the drugs of choice in the treatment of chronic arthropathies and other childhood connective-tissue diseases and are also commonly used in the treatment of febrile and acute inflammatory processes. Not all NAIDs are authorized for use in the pediatric population but their spectrum of use varies according to the entity for which they are indicated and the legislation of the country. Published studies on the prevalence of aspirin intolerance in patients with bronchial asthma show a fair amount of disagreement. This may be due to (i) the method of selecting asthmatic patients for the study, which differs according to whether all asthmatic patients are included or only those dependent on corticoids; (ii) the diagnostic method used, whether based on clinical criteria or oral provocation tests, which will affect the number of patients with a diagnosis of intolerance. In children aged less than 10 years, including children with asthma, the prevalence is low, while among children and young adults aged 10-20 years old, the prevalence is estimated at 10 %. Some hypotheses attempt to explain the mechanisms through which adverse reactions to NAIDs take place. One hypothesis attributes the reaction to a reaginic immunological mechanism but this hypothesis has only been confirmed in exceptional cases. The theory of the cyclooxygenase pathway, currently the most widely accepted, is based on the ability of NSAIDs to inhibit the cyclooxygenase pathway of arachidonic acid metabolism, leading to prostaglandin depletion and an increase in leukotrienes. The discovery of two isoforms of the cyclooxygenase enzymes, COX-1 and COX-2, has represented a great advance in our understanding of the mechanism of action of NSAIDs and has also elucidated the problem of cross-reactivities. According to the theory of viral infection, aspirin-induced asthma could be caused by chronic viral infection since, after initial exposure to the virus, cytotoxic lymphocytes are produced. Their activity is inhibited by prostaglandin E2 (PGE2); aspirin and other NSAIDs block PGE2 production and allow cytotoxic lymphocytes to attack and eliminate the respiratory tract cells infected by the virus. During this reaction lysosomal enzymes and mediators are released, which could precipitate an asthmatic crisis.Clinically, five types of reaction have been identified: 1. Respiratory illness with aspirin sensitivity. 2. Aspirin-induced urticarial disease. 3. Allergic reactions to NSAIDs and aspirin. 4 and 5. Aseptic meningitis and pneumonitis due to hypersensitivity. The latter are exceptional and are published as case reports. They have never been associated with aspirin or acetaminophen and usually occur in patients undergoing prolonged treatment. Diagnosis is based on a detailed history. Skin tests are not valid and in vitro tests are not widely used. Provocation tests with aspirin and NSAIDs definitively identify sensitized patients but their indications and limitations should be kept in mind. In children, certain features of adverse reactions to NSAIDs are observed in relation to their incidence and clinical manifestations. Acetaminophen is considered the drug of choice but further studies of other alternatives in children are required.
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PMID:[Special features of NSAID intolerance in children]. 1278 61