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 author reviewed the complications of 700 heart catheterizations in infants and children performed between 1970 and 1978 with a frequency of 55 to 113 investigations per year. Arrhythmias occurred on 70 occasions (10%), death within 24 hours: 14 (2%), extravasation of contrast media: 11 (1,6%), perforation by catheter: 6 (0,9%), cyanotic spells 5 (0,7%), myocardial ischemia: 4 (0,6%), respiratory arrest: 4 (0,6%), convulsions: 2 (0,3%), wound infection: 2 (0,3%), icterus 2 (0.3%), lung atelactasis: 1 (0,15%), bacterial endocarditis: 1 (0,15%), pyrexia: 1 (0,15%), exanthema: 1 (0,15%), pulmonary edema: 1 (0,15%), meningitis purulenta and hepatitis as possible complications: 1 (0,15%) each. The mortality figue of 2% lies well within the range of rates reported by Ho and ass. (1972): 1,5%, Stanger and ass. (1974): 3,0%, Rowe (1978): 0,95%, and Graham (1978): 2,9%. Mortality mainly occurs in sick neonates and infants with complex cardiac malformations. It could be lowered by a more aggressive approach to diagnostic work-up of suspected cardiac disease, as well as by using more sophisticated catheterization techniques and material and by introducing intensive care principles on the infant ward. Catheter related mortality (e. g. by perforation, severe arrhythmia) could be reduced to zero during the last three years. Myocardial staining by contrast media and electrocardiographic alterations suggesting myocardial ischemia occurred comparatively often but were never followed by serious or long lasting sequelae. Their occurrence was not related to the diagnosis or to the age of the patient. Respiratory arrest and convulsions could only be observed in sick infants. The seizures were not directly related to angiocardiography. All other complications were incidental events. Arrhythmias and vascular complications are discussed in separate papers.
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PMID:[The risks involved in the heart catheter examination. A retrospective evaluation of the complications after 700 examinations. II. Complications (author's transl)]. 53 Jul 26

Systemic lupus erythematosus (SLE) developed in as 23-year-old woman with psoriasis during treatment with psoralen-ultraviolet-A (PUVA). The connective tissue disease was characterized by an erythematous rash, hair loss, nephritis, splenomegaly, seizures, and coma. Serum antinuclear antibodies were present in high titer, and hypocomplementemia developed. Antibodies to native or ultraviolet-irradiated DNA were not demonstrated. While the association of psoriasis and lupus may have been fortuitous, the temporal relationships suggest that PUVA treatment in this case may have been of pathogenetic importance in the development of the connective tissue disease.
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PMID:Systemic lupus erythematosus: association with psoralen--ultraviolet-A treatment of psoriasis. 76 Jun 58

Diphenylhydantoin sodium is a standard drug in the treatment of convulsive disorders. Numerous untoward reactions have been reported. Lymphadenopathy related to drug-induced hypersensitivity has occurred. A yound woman undergoing treatment for seizures developed a large, tender, localized neck mass, associated with trismus, spasmotic torticollis, fever, eosinophilia, and skin rash. She was thought to be suffering from a deep cervical fascial space abscess. Symptoms subsided rapidly after elimination of anticonvulsant medication.
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PMID:Localized cervical lymphadenopathy induced by diphenylhydantoin sodium. 80 90

A case of phenytoin (DPH) encephalopathy with increasing seizures and EEG and mental changes is described. Despite adequate oral dosage of DPH (5 mg/kg/daily) the plasma level was very low (2.8 microgramg/ml). The encephalopathy was probably an idiosyncratic and not toxic or allergic reaction. In fact the concentration of free DPH was normal, the patient presented a retarded morbilliform rash during DPH treatment, the protidogram was normal, and an intradermic DPH injection had no local effect. The authors conclude that in a patient starting DPH treatment an unexpected increase in seizures, with EEG and mental changes occurring simultaneously, should alert the physician to the possible need for eliminating DPH from the therapeutic regimen, even if plasma concentrations are low.
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PMID:Phenytoin encephalopathy as probable idiosyncratic reaction: case report. 89 94

Serum levels of mephenytoin (Mesantoin) and its metabolite nirvanol were correlated with effectiveness and side effects in 93 patients. Mean mephenytoin level was 8% of the combined mephenytoin plus nirvanol levels. "Total mephenytoin" level should be used clinically, as neither individual component is as well correlated with clinical phenomena. Serum levels of 25 to 40 mug/ml usually yield improvement in seizure control without discomfort, and three-quarters of patients had fewer seizures. Side effects frequently associated with phenytoin were absent, but drowsiness, an occasional rash, and a single, fatal case of aplastic anemia were found. Performance on psychological tests of cognitive-attentional skills showed a modest improvement during mephenytoin administration. The drug merits wider employment in refractory seizure problems, but vigilant follow-up is required.
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PMID:Mephenytoin: a reappraisal. 100 Dec 84

Neuropathologic findings in 2 cases of cerebral lymphomatoid granulomatosis with sequelae are presented. A 30-year old male with macular rash and pulmonary lymphomatoid granulomatosis responded to Prednisone terapy but developed acute intracranial hypertension with coma. A necrotizing hemorrhagic lesion was evident in the left putamen surrounded by diffuse and perivascular atypical lymphoplasmacytic infiltration. An 18-year old girl developed pulmonary lymphomatoid granulomatosis, diplopia, slurred speech and right hemiparesis. Brain scan, angiography and EEG suggested a left fronto-parietal mass assumed to represent lymphomatoid granulomatosis. She responded well to cerebral irradiation, intrathecal methotrexate and cytoxan but relapsed with seizures and increasing respiratory insufficiency. At autopsy, stigmata of cerebral lymphomatoid granulomatosis were absent but a parenchymatous degeneration consistent with disseminated necrotizing leukoencephalopathy following antileukemic therapy in children, was found.
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PMID:Cerebral lymphomatoid granulomatosis. A report of two cases, with disseminated necrotizing leukoencephalopathy in one. 100 3

Drug-induced systemic lupus erythematosus (SLE)-like syndromes in children are most commonly associated with the administration of ethosuximide, diphenylhydantoin, and trimethadione. Five children receiving ethosuximide who presented with syndromes suggestive of SLE were studied. Each and fever, malar rash, arthritis, and lymphadenopathy. Two children had pleural effusions and another developed myocarditis and pericarditis. Three patients had anti-DNA antibodies associated with low serum C3. In four of five children symptoms disappeared with the discontinuation of ethosuximide; two of these continue to have antinuclear antibodies (ANA). One child continues to have active SLE with nephritis. A group of 101 children from a seizure clinic were tested for the presence of ANA. ANA were found in 14 of 70 children receiving ethosuximide and/or diphenylhydantoin; 2 of 14 had anti-DNA antibodies. Serum ANA titers in the drug-induced SLE group did not differ significantly from those of the asymptomatic seizure patients. ANA were also present in 5 of 23 children receiving phenobarbital only. The induction of ANA by phenobarbital is a possible hypothesis. Quantitative immunoglobulins and C3 were not significantly altered in the asymptomatic children with ANA. Follow-up studies at ten months showed no asymptomatic child with ANA to have developed clinical with ANA to have developed clinical evidence of SLE. This study suggests that asymptomatic children who develop ANA should have careful observation, but need not have their anticonvulsants discontinued.
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PMID:Antinuclear antibodies and lupus-like syndromes in children receiving anticonvulsants. 108 1

A patient with a hereditary deficiency of the second component of complement and discoid lupus erythematosus with features of systemic lupus erythematosus was studied. The propositus had a 9-year history of rash and arthralgia. Transient renal disease had completely resolved; there was a history of seizures. Examination of his serum disclosed antinuclear antibodies but no total haemolytic complement activity. C2 was absent. Serum concentrations of C1s, C3, C5 and C9 were elevated; other complement components were present in normal concentration, including C3 pro-activator. The patient's C3 pro-activator was electrophoretically converted by inulin and four of five lipopolysaccharides, but was poorly converted by aggregated human IgG. Two separate turnover studies with radiolabelled C3 showed fractional catabolic rates of 3-03 and 2-48% of the remaining plasma pool/hr (range of three normals: 1-62-2-18%/hr); and estimated C3 synthetic rates of 2-74 and 2-31 mg/kg/hr (range of three normals: 0-89-1-40 mg/kg/hr). Serum complement profiles of the patient's family demonstrated that the C2 deficiency was inherited as an autosomal codominant. One sibling, homozygous for C2 deficiency, and three other siblings, both parents and one daughter, all heterozygous for C2 deficiency, are in good health. Immunofluorescent studies of the patient's diseased skin exhibited substantial deposits of IgG, IgM, C1q, and C4 but not of later acting complement components, properdin, or C3 proactivator. These studies do not support the notion that inflammation in C3-deficient individuals with lupus erythematosus is mediated by the alternative complement pathway.
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PMID:C3 metabolism in a patient with deficiency of the second component of complement (C2) and discoid lupus erythematosus. 108 39

Hypersensitivity to carbamazepine is a well-known phenomenon. The involvement of several organ systems including liver, kidney, bone marrow and other organs have been described. We have observed a 7-year-old boy who had been treated with carbamazepine for seizures. After 10 days of treatment he developed a severe illness with skin rash, high fever, lymphadenopathy, hepatosplenomegaly and lymphopenia. Only slightly decreased complement components and increased complement split products but no circulating immune complexes were demonstrable on admission. Anti-carbamazepine antibodies, T-cell-activation and a significant T-cell reactivity against carbamazepine were found, indicating specific hypersensitivity. Complete recovery was observed after discontinuation of the drug and steroid treatment.
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PMID:Severe adverse reaction to carbamazepine: significance of humoral and cellular reactions to the drug. 145 49

A previously healthy man presented with a five day history of high fever and headache, later followed by rash and the appearance of jaundice. On the second hospital day, he suddenly developed seizures, lapsed into a coma, and died. Polymerase chain reaction (PCR) amplification revealed a 434 base pairs DNA fragment common to the genome of typhus and spotted fever group rickettsiae in the patient's blood (estimated at about 1 x 10(2) organisms/ml), and to a lesser degree in the cerebrospinal fluid. However, serological tests for rickettsiae remained negative. PCR techniques may confirm the diagnosis at an early stage, even though the rickettsemia may be minimal and the patient seronegative.
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PMID:Case report: fatal seronegative rickettsial infection diagnosed by the polymerase chain reaction. 160 68


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