Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The toxicities of antimalarial drugs vary because of the differences in the chemical structures of these compounds. Quinine, the oldest antimalarial, has been used for 300 years. Of the 200 to 300 compounds synthesised since the first synthetic antimalarial, primaquine in 1926, 15 to 20 are currently used for malaria treatment, most of which are quinoline derivatives. Quinoline derivatives, particularly quinine and chloroquine, are highly toxic in overdose. The toxic effects are related to their quinidine-like actions on the heart and include circulatory arrest, cardiogenic shock, conduction disturbances and ventricular arrhythmias. Additional clinical features are obnubilation, coma, convulsions, respiratory depression. Blindness is a frequent complication in quinine overdose. Hypokalaemia is consistently present, although apparently self-correcting, in severe chloroquine poisoning and is a good index of severity. Recent toxicokinetic studies of quinine and chloroquine showed good correlations between dose ingested, serum concentrations and clinical features, and confirmed the inefficacy of haemodialysis, haemoperfusion and peritoneal dialysis for enhancing drug removal. The other quinoline derivatives appear to be less toxic. Amodiaquine may induce side effects such as gastrointestinal symptoms, agranulocytosis and hepatitis. The main feature of primaquine overdose is methaemoglobinaemia. No cases of mefloquine and piperaquine overdose have been reported. Overdose with quinacrine, an acridine derivative, may result in nausea, vomiting, confusion, convulsion and acute psychosis. The dehydrofolate reductase inhibitors used in malaria treatment are sulfadoxine, dapsone, proguanil (chloroguanide), trimethoprim and pyrimethamine. Most of these drugs are given in combination. Proguanil is one of the safest antimalarials. Convulsion, coma and blindness have been reported in pyrimethamine overdose. Sulfadoxine can induce Lyell and Stevens-Johnson syndromes. The main feature of dapsone poisoning is severe methaemoglobinaemia which is related to dapsone and to its metabolites. Recent toxicokinetic studies confirmed the efficacy of oral activated charcoal, haemodialysis and haemoperfusion in enhancing removal of dapsone and its metabolites. No overdose has been reported with artemesinine, a new antimalarial tested in the People's Republic of China. The general management of antimalarial overdose include gastric lavage and symptomatic treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and management of poisoning due to antimalarial drugs. 330 66

Sixty patients with acute disseminated epidermal necrosis (ADEN) were hospitalized and carefully studied. They included thirty-nine patients with drug-associated Stevens-Johnson syndrome, five patients with drug-associated Lyell's syndrome, and sixteen patients with transitional ADEN. On the basis of growing evidence of an association between erythema multiforme major and drugs and between Lyell's syndrome and drugs, and because of the existence of transitional cases, a unitary hypothesis for this group of cases is proposed. Considering the lack of precise definitions and the confusing current terminology, we define and propose the following terms: ADEN type 1 for drug-associated Stevens-Johnson syndrome, ADEN type 2 for drug-associated transitional cases, and ADEN type 3 for drug-associated toxic epidermal necrolysis, or Lyell's syndrome. The most frequent underlying diseases in our patients were seizures, and the most frequently suspected cause of ADEN was the use of anticonvulsants. All our patients were treated with supportive therapy; none received corticosteroids. The general mortality rate was 15%. The recognition of ADEN type 2 (transitional) has important prognostic and therapeutic implications.
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PMID:Acute disseminated epidermal necrosis types 1, 2, and 3: study of sixty cases. 407 51

In this study, the clinical findings and management of allergic skin reactions induced by the most used antiepileptic drugs, Lamotrigine (LMT) and Carbamazepine (CBZ), were evaluated. Lamotrigine is an antiepileptic drug recently released in several countries; it is effective for a variety of seizure types in adults and children, both as an add-on agent and in monotherapy, and it is generally well tolerated. Clinical and epidemiologic evidence suggest serious cutaneous reactions to antiepileptic drugs are more likely to occur during the first 8 weeks and they appear to increase when drugs are administered with other anticonvulsants, such as Valproate (VPA). We selected 10 patients who presented an idiosyncratic skin rash when treated with carbamazepine (8 patients) and lamotrigine (2 patients) administered as monotherapy, and we followed up on these patients for several years. Seven reactions were mild/severe cutaneous eruptions; one Toxic Epidermal Necrolysis, a case of Stevens-Johnson and a case of Hypersensitivity Syndrome. All severe skin drug reactions were induced by Carbamazepine. In five patients the AEDs were ceased abruptly (sometimes with the administration of a different molecule), tapered in four and continued unchanged in one. We conclude that the discontinuation of the drug with substitution with another is the most effective treatment and that corticosteroids are helpful in mild cutaneous reactions, while in severe skin reactions, such as Toxic Epidermal Necrolysis, corticosteroids are only a complementary therapy since intravenous immunoglobulins are the first choice treatment.
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PMID:Skin reactions due to anti-epileptic drugs: several case-reports with long-term follow-up. 1257 37

Toxic epidermal necrolysis (TEN) is an infrequent disease but with a high mortality rate. It is a mucocutaneous reaction resulting from hypersensitivity to a variety of agents including most anticonvulsants. Many patients with primary or metastatic intracranial tumours receive anticonvulsants for seizure prophylaxis despite their efficacy not having been clearly demonstrated. Moreover, several cases have been reported in the literature in which serious adverse drug reactions such as TEN and Stevens-Johnson syndrome (SJS) have occurred following anticonvulsants exposure. In some of these cases the effect of radiation therapy and the tapering of steroid dose on the pathogenesis of these reactions have been highlighted. We report, here, a case of TEN that appeared in a patient receiving phenytoin, and shortly after the end of cranial and thoracic irradiation therapy for brain metastases of non-small cell lung cancer. Clinical considerations about diagnosis of SJS and TEN are presented. The use of prophylactic anticonvulsants is also discussed as well as a review of the literature.
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PMID:Toxic epidermal necrolysis in patients receiving anticonvulsants and cranial irradiation: a risk to consider. 1501 67

Toxic epidermal necrolysis (TEN) is a severe mucocutaneous syndrome that can be occasionally caused by anticonvulsant drugs. In some cases, cranial irradiation may act as a precipitating factor. Thus, in cancer patients who suffer from brain metastases and are administered antiepileptic drugs for seizure prophylaxis, the risk of developing TEN after receiving palliative brain radiotherapy cannot be ignored. We is reported. The case of a young patient with non-small cell lung cancer (NSCLC) treated with prophylactic phenobarbital who developed TEN within a few days of completing cranial radiotherapy for brain metastases is reported. To minimize the risk of TEN in patients undergoing brain radiotherapy, prophylactic anticonvulsant therapy is recommended only after an accurate measurement of the true benefits. Alternatively, discontinuation of antiepileptic treatment before the initiation of brain radiotherapy, or the use of anticonvulsants associated with a lower risk of developing cutaneous reactions might be considered.
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PMID:Brain radiotherapy during treatment with anticonvulsant therapy as a trigger for toxic epidermal necrolysis. 1746 58

Besides its use for the control of seizures, carbamazepine is being increasingly prescribed for neuropathic pain and depression, and this may explain the increased incidence of cutaneous drug reactions, namely Setevens-Johnson Syndrome (SJS)/Toxic Epidermal Necrolysis associated with this drug. We report a case of a 42-year-old woman, medicated with levotyroxin for years and carbamazepine for fifteen days due to a depressive state. A mucous and cutaneous eruption suddenly appeared and the diagnosis of SSJ was made. Skin biopsy confirmed the clinical diagnosis and patch testing and intradermal test were negative. The remaining laboratory findings were normal. Supportive measures and a course of oral predisolone (started at 1.5 mg/Kg) with progressive tapering were introduced and carbamazepine was immediately stopped, with a complete clinical resolution within two weeks.
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PMID:[Cutaneous adverse reaction to carbamazepine: unusual presentation]. 2047 Apr 76

Toxic epidermal necrolysis is a life-threatening disease. It may be induced by many kinds of drugs especially anti-epileptics such as lamotrigine, but less sun-exposure related. Lamotrigine has been effective for partial complex seizure and bipolar disorder and caused serious side effects such as Stevens-Johnson syndrome or toxic epidermal necrolysis. We reported a case of the patient who developed the manic episode and received lamotrigine and chlorpromazine drugs. After combination of lamotrigine and chlorpromazine, the patient developed skin rash to toxic epidermal necrolysis after sun-exposure. We had discontinued both drugs, given supportive treatment, and let him prevent sun-exposure greatly. The disease process got subsided nearly 4 weeks later. Clinicians should carefully prescribe mood stabilizer and photo-toxic or photosensitivity medications with higher drug-eruption rate.
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PMID:Toxic epidermal necrolysis after sun-exposure probably due to lamotrigine and chlorpromazine. 2305 Aug 97

Lyell's syndrome or toxic epidermal necrolysis (TEN) is a rare dermatological disease that causes serious morbidity and mortality. It is most commonly drug induced. The authors report the case of a 57-year-old woman who was admitted to our hospital with severe rash all over the body. She had been previously submitted to brain surgery for total resection of a large meningioma and medicated with phenytoin for seizures prophylaxis. During this treatment, erythematous lesions and blisters were observed first on her face and trunk and then spreading to the entire body. Detachment of the skin, as well as mucous involvement especially of mouth and conjunctiva, was also observed. TEN was diagnosed, and phenytoin was discontinued. Intravenous fluids, systemic steroids and tightened infection control measures were implemented. After 10 days, skin recovery and re-epithelialisation were established, temperature decreased and mucosal complications stabilised. The patient was discharged after 1 month of hospitalisation.
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PMID:Phenytoin-induced Lyell's syndrome. 2323 Feb 58

Toxic epidermal necrolysis (TEN) is a serious, life-threatening skin reaction characterized by severe exfoliation and destruction of the epidermis of the skin. In most TEN cases, drugs are believed to be the causative agent; antipsychotics, antiepileptics, and other medications such as sulfonamides are among the most common causes of drug-induced TEN. Phenytoin, a commonly prescribed medication for seizure, was found to cause TEN. Evidence-based treatment guidelines are lacking, so the best strategy is to identify and avoid potential risk factors and to provide intensive supportive care. The aim of this literature review is to focus on phenytoin-induced TEN, to explore the risk factors, and to highlight the possible treatment options once phenytoin-induced TEN is confirmed.
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PMID:Phenytoin-induced toxic epidermal necrolysis: Review and recommendations. 2765 8

This report highlights zonisamide as a potential cause of serious cutaneous reactions as well as its cross-reactivity with other sulfonamides. Here, we present a case of SJS-TEN due to zonisamide, which was effectively treated with IVIg. Subsequently, the patient was transitioned to levetiracetam for seizure control.
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PMID:Stevens-Johnson syndrome/toxic epidermal necrolysis associated with zonisamide. 2944 58


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