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)

After a few days of prodromal illness with diarrhea and fever there was an abrupt onset of coma, seizures, severe shock, and hyperpyrexia in two infants; they than developed bleeding, pancytopenia, and impairment of liver and renal function. Both infants survived with major neurologic sequelae. The clinical symptoms and laboratory parameters were compatible with hemorrhagic shock and encephalopathy syndrome which was first described in 1983. The clinical course and biochemical features of this disease and its differential diagnoses are described, and etiology and pathogenesis are discussed. Furthermore it will be discussed, whether the hemorrhagic shock and encephalopathy syndrome is actually a "new" disease or just a new label for a known disorder.
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PMID:[Hemorrhagic shock and encephalopathy syndrome in infancy and childhood]. 203 47

Thirty-seven patients with acute leukemia in relapse were treated with a three-drug combination that included a 3- or 4-day course of AMSA with total doses ranging from 600 mg/m2 to 740 mg/m2 I.V., cytosine arabinoside 25 mg/m2 I.V. followed by 200 mg/m2 by continuous infusion daily for 5 days, and thioguanine 100 mg/m2 p.o. q 12h for 5 days. Eight of the 25 patients with acute nonlymphoblastic leukemia achieved a complete remission and 3 a partial remission. None of the five patients with acute lymphoblastic leukemia achieved a response and there was one partial remission in the seven patients with myelodysplastic syndrome or blastic CML. Reversible toxicity included nausea and vomiting (78%), alopecia (100%), pancytopenia (100%), mild stomatitis (63%), and hepatic dysfunction (24%). One patient developed seizures and cardiac arrhythmias. The activity of this combination in heavily treated patients with ANLL is comparable to that of the anthracycline-containing regimens, and its use in previously untreated patients with ANLL should now be explored.
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PMID:Treatment of acute leukemia in relapse with 4'(9-acridinylamino) methanesulfon-m-anisidide (AMSA) in combination with cytosine arabinoside and thioguanine. 689 90

A 31-year-old woman with systemic lupus erythematosus presented with respiratory and renal symptoms followed by abdominal pain and seizure. Clinical diagnoses of lupus pneumonitis, nephritis, vasculitis, and cerebritis were made. The patient had a progressively downhill course with pancytopenia and hemolysis treated with aggressive immunosuppressive therapy and extended plasmapheresis. Lupus pneumonitis leading to diffuse alveolar damage was the immediate cause of death. Diffuse proliferative lupus nephritis was seen in the biopsy, and the autopsy demonstrated thrombotic microangiopathy. Extra-renal complications of lupus and response to therapy are discussed in the format of a Tulane Clinicopathologic Conference.
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PMID:A 31-year-old woman with lupus erythematosus and fatal multisystem complications. 915 Jun 65

A wide range of adverse effects has been reported following prolonged use of anticonvulsant drugs. More commonly reported adverse effects for ethosuximide include gastric disturbances, psychiatric disorders and Systemic Lupus Erythematosus (SLE). Rare instances of leukopenia and pancytopenia have been noted. A case is presented of a 12 year old girl who developed generalized lymphadenopathy with progressive weight loss and leukopenia following prolonged use of ethosuximide for simple absence seizures. The enlarged lymph nodes regressed with withdrawal of the drug but re-appeared when the drug was recommenced. Sodium valproate was then introduced and ethosuximide discontinued. The seizures were successfully controlled with sodium valproate. Histopathology report of the lymphnode biopsy showed marked reactive lymphnode hyperplasia.
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PMID:Ethosuximide induced lymphadenopathy--a case report. 1196 53

A 13-yr-old female was admitted to our hospital with fever, seizure, and cervical lymphadenopathy. Laboratory data showed pancytopenia, elevation of serum transaminase, lactate dehydrogenase, triglyceride, and ferritin levels. Lymph node biopsy revealed features of Kikuchi's disease and there were signs of histiocytosis and hemophagocytic phenomenon in bone marrow. She recovered after treatment with intravenous immunoglobulin and corticosteroids therapy. Hemophagocytic syndrome can be associated with Kikuchi's disease especially in childhood and seems to have a less aggressive clinical course and better prognosis.
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PMID:Hemophagocytic syndrome associated with Kikuchi's disease. 1292 40

Anemia is common with connective tissue disorders, but pancytopenia is rare. We report a 22-year-old female who presented with menorrhagia, seizures, anemia, leukocytosis, thrombocytopenia, pericardial effusion, positive ANA, and evidence of vasculitis on CT head scan and was diagnosed with systemic lupus erythematosus (SLE). After 7 months of remission, she was readmitted with menorrhagia and pancytopenia. Investigations revealed aplastic anemia. She survived on transfusion support for 6 weeks, during which period she received methylprednisolone and cyclophosphamide pulses, and phenytoin was omitted but to no avail. Cyclosporine (300 mg/day) was started and the aplastic anemia responded. After 4 months of therapy, the cyclosporine was gradually tapered over the next 2 months. The patient has been on 10 mg/day of prednisolone for the last 6 months. Aplastic anemia is rare in SLE and the response to immunosuppressants is variable, but here is a success story.
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PMID:Aplastic anemia complicating systemic lupus erythematosus: successful management with cyclosporine. 1368 Jan 50

A 23-month-old boy with Wiskott-Aldrich syndrome (WAS) received human leukocyte antigen (HLA)-one locus mismatched, unmanipulated allogeneic bone marrow graft from his mother. An Epstein-Barr virus (EBV)-associated post-transplantation lymphoproliferative disorder (PTLD) of donor cell origin and hemophagocytosis syndrome with fever, lymphadenopathy, hepatosplenomegaly, seizures, involuntary movements and pancytopenia developed 52 days after transplantation. It was difficult to decide on the treatment strategy because the patient presented with B-cell hyperplasia that morphologically appeared malignant but was oligoclonal by heavy-chain analyses. Despite of donor leukocyte transfusion, low dose chemotherapy, and anti-B cell monoclonal antibody immunotherapy, the patient died 107 days after transplantation.
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PMID:Epstein-Barr virus associated post-transplantation lymphoproliferative disorder with hemophagocytosis in a child with Wiskott-Aldrich syndrome. 1554 18

In September 2000, a 22-year-old female was admitted to our hospital due to high grade fever, liver enzymes elevation and pancytopenia. Bone marrow aspiration was performed, and hemophagocytosis was present. Epstein-Barr virus (EBV) DNA was positive in her peripheral blood, and we diagnosed the case as EBV-associated hemophagocytic syndrome (EB-VAHS) after excluding other malignancies. The initial therapy including etoposide and dexamethasone was started. As severe leukocytopenia developed, etoposide was stopped and cyclosporin A (CsA) was administered continuously. Four days after administration of CsA, she developed convulsive seizures with loss of consciousness. An MRI demonstrated decreased signal with T1-weighting and high signal with T2-weighting in the subcortical white matter including the posterior lobe. We stopped CsA infusion, and glycerol was administered. Soon the symptom disappeared. When patients developed an episode of convulsive seizure, other diagnostic possibilities were central nervous system (CNS) involvement of hemophagocytosis, EBV encephalitis and acute disseminated encephalomyelitis (ADEM). CsA neurotoxicity must be considered even in the case of EB-VAHS with administration of CsA. As previously reported, Fluid-attenuated Inversion Recovery (FLAIR) imaging improved diagnostic confidence and conspicuity of the T2 hyper intense lesions of CsA neurotoxicity, as well as tacrolimus encephalopathy, typically in the subcortical white matter. Key words; Cyclosporin neurotoxicity; Epstein-Barr virus associated-Hemophagocytic syndrome; Magnetic Resonance Image (MRI).
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PMID:Cyclosporin neurotoxicity with Epstein-Barr virus-associated hemophagocytic syndrome. 1575 52

Systemic lupus erythematosus (SLE) has numerous manifestations. Haematology is the common system influenced by the disease. The antibody antiphospholipid syndrome, secondary hematology disorder in SLE, is related to high incidence of thrombosis. The thrombosis events like myocardial infarction and stroke are high in mortality. We reported a-36-year old woman treated for lung tuberculosis (TB) with secondary infection, nephritis lupus, and pancytopenia. The general condition has improved and the patient was planned to discharge while she suddenly fell down, unconscious and had seizure. The CT-scan showed an area of hypodensity on the left thalamus. Haematology results showed high level of fibrinogen and D-dimer as the signs of thrombosis. The anticardiolipin antibody was intermediately positive for IgG and IgM, but lupus anticoagulan was weakly positive. The serial test within 2 months still showed positive IgG. The patient received supportive treatment, heparinization, neurotropic drugs and anticonvulsant. She was discharged in good condition while continuing oral anticoagulant to prevent recurrent seizure.
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PMID:Cerebral thrombosis in systemic lupus erythematosus with the antibody antiphospholipid syndrome. 1748 92

Folate is essential for normal brain development. This report describes a 15-month-old boy who presented with generalized and focal seizures and a decline in mental status. Laboratory tests revealed low folate levels in blood (1.13 nmol/L) and cerebrospinal fluid, accompanied by pancytopenia. Bone marrow aspiration confirmed the presence of megaloblastic anemia. Treatment with high-dose intravenous folinic acid led to normalization of cerebrospinal folate levels. These findings apparently indicate a defect in folic acid transport to the central nervous system. A clinical picture of developmental arrest, seizures, somnolence, and megaloblastic anemia should alert physicians to the possibility of folate deficiency.
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PMID:Neurological manifestations of folate transport defect: case report and review of the literature. 1764 Dec 72


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