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)

Between December 1996 and September 1998, 13 patients with advanced recurrent malignant brain tumors (9 with glioblastoma multiforme, 1 with gliosarcoma, and 3 with anaplastic astrocytoma) were treated with a single intratumoral injection of 2 x 10(9), 2 x 10(10), 2 x 10(11), or 2 x 10(12) vector particles (VP) of a replication-defective adenoviral vector bearing the herpes simplex virus thymidine kinase gene driven by the Rous sarcoma virus promoter (Adv.RSVtk), followed by ganciclovir (GCV) treatment. The VP to infectious unit ratio was 20:1. Our primary objective was to determine the safety of this treatment. Injection of Adv.RSVtk in doses <==2 x 10(11) VP, followed by GCV, was safely tolerated. Patients treated with the highest dose, 2 x 10(12) VP, exhibited central nervous system toxicity with confusion, hyponatremia, and seizures. One patient is living and stable 29.2 months after treatment. Two patients survived >25 months before succumbing to tumor progression. Ten patients died within 10 months of treatment, 9 from tumor progression and 1 with sepsis and endocarditis. Neuropathologic examination of postmortem tissue demonstrated cavitation at the injection site, intratumoral foci of coagulative necrosis, and variable infiltration of the residual tumor with macrophages and lymphocytes.
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PMID:Phase I study of adenoviral delivery of the HSV-tk gene and ganciclovir administration in patients with current malignant brain tumors. 1093 31

Recently, new broad spectrum carbapenem has been investigated on a world-wide scale for the treatment of moderate to severe infections. In the neonatal intensive care units the extensive use of third generation cephalosporins for therapy of neonatal sepsis may lead to rapid emergence of multiresistant gram-negative organisms. We report the use of meropenem in 35 infants with severe infections due to Acinetobacter baumanii and Klebsiella pneumoniae. All gram negative bacteria were resistant to ampicillin, amoxicillin, ticarcilin, cefazoline, cefotaxime, ceftazidime, ceftriaxone and aminoglycosides. Eighty two percent of the cases (29/35) were born prematurely. Assisted ventilation was needed in 85.7% (30/35). All infants deteriorated during their conventional treatment and were changed to meropenem monotherapy. Six percent (2/35) died. The incidence of drug-related adverse events (mostly a slight increase in liver enzymes) was 8.5%. No adverse effects such as diarrhea, vomiting, rash, glossitis, oral or diaper area moniliasis, thrombocytosis, thrombocytopenia, eosinophilia and seizures were observed. At the end of therapy, overall satisfactory clinical and bacterial response was obtained in 33/35 (94.3%) of the newborns treated with meropenem. Clinical and bacterial response rates for meropenem were 100% for sepsis and 87.5% for nosocomial pneumonia. This report suggests that meropenem may be a useful antimicrobial agent in neonatal infections caused by multiresistant gram negative bacilli. Further studies are needed to confirm these results: Meropenem, newborn, sepsis and nosocomial infection.
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PMID:Meropenem in neonatal severe infections due to multiresistant gram-negative bacteria. 1123 30

Most of the information on predisposing factors and mortality in status epilepticus (SE) arises from data obtained from patients presenting to the casualty department. However, another population which is frequently seen by consultative neurologists are medically ill patients who develop SE while in hospital. These patients are often notoriously difficult to treat once SE arises. We sought to characterize patients at risk for SE arising when they are hospitalized for other reasons. By doing this, risk factors for developing SE and prognostic indicators might be determined. We retrospectively reviewed records from three urban hospitals in the United States to identify hospitalized patients developing SE over a 1 year period. SE was defined as a clinical seizure lasting 30 minutes or longer, or repeated seizures without recovery. Patients who were admitted in SE or for an epilepsy-related problem, or who were less than 1 year old were excluded from the study. Forty-one patients with in-hospital SE were identified. There were 28 males and 13 females with an age range from 1 to 91 years (mean: 60 years, median: 65 years). The mean interval from hospital admission to the onset of status epilepticus was 26 days. Nineteen (46%) patients had a prior history of either epilepsy or symptomatic seizures, and of these, 10 were inadequately treated as judged by serum anticonvulsant levels at the time SE developed. Focal brain abnormality was present in 26 (63%) patients, the most common of which was stroke (17 patients ). Major metabolic derangements including hypoxia, electrolyte imbalance, hepatic encephalopathy, and sepsis were present in 23 (56%) patients. Eleven (27%) patients were being treated with theophylline preparations at the time SE developed. Mortality in this group of patients with in-hospital SE was 61% (25 deaths), with about one-third dying while in status, and two-thirds dying subsequently in hospital. In this retrospective study, there was no clear relationship between mortality and the duration of SE in this group of patients. In-hospital development of SE is usually related to underlying focal brain abnormality, especially stroke, in combination with systemic metabolic derangement. Prognosis is poor, and appears to be more related to underlying conditions rather than to status duration. More accurate prospective studies are warranted.
Seizure 2001 Mar
PMID:Status epilepticus arising de novo in hospitalized patients: an analysis of 41 patients. 1140 54

The importance of an acute encephalopathy associated with nontyphoidal salmonellosis has recently been recognized, but the disease entity has been poorly established. In this study, we describe two encephalopathic patients associated with nontyphoidal salmonellosis. The patients exhibited a rapid evolution of coma after the onset of lethargy or seizure. Fever and diarrhea due to salmonellosis preceded these events. Secondary factors inducing encephalopathies, such as severe dehydration, sepsis, meningitis, electrolyte or metabolic disturbances, acute renal failure, and multiple organ failure, were excluded in the differential diagnosis at the onset of encephalopathic features. These clinical findings and rapid development of encephalopathic features from localized intestinal infection without any significant abnormalities in a variety of blood tests may suggest a toxic etiology. However, endotoxin was not found in serum from both patients. From these results, we conclude that nontyphoidal salmonellosis can cause a toxic encephalopathy syndrome, like shigellosis or verocytotoxin-producing Escherichia coli infection.
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PMID:Acute encephalopathy associated with nontyphoidal salmonellosis. 1145 56

The absence of fetal pulmonary maturity in patients with preterm premature rupture of the membranes (PPROM) is often considered an indication for conservative management. The purpose of this study was to examine the value of biochemical pulmonary maturity assessment for the prediction of neonatal outcome in patients with PPROM between 32 and 34 weeks' gestation. Pregnancies complicated by PPROM at 32 to 34 weeks' gestation that delivered from January 1995 to May 2000 and had biochemical pulmonary maturity assessment were reviewed. Patients with medical disorders, multiple gestations, fetal growth restriction or structural anomalies, or evidence of intra-amniotic infection were excluded. Neonatal outcome measures were compared between patients with mature and immature pulmonary indices. During this time period, 244 patients with PPROM at 32-34 weeks' gestation were delivered; 78 patients met inclusion criteria (n = 41 patients with mature indices and n = 37 patients with immature indices). There were no cases of perinatal death or sepsis. There was no difference in major neonatal morbidities including need for mechanical ventilation, grade 2 or 3 necrotizing enterocolitis, grade 3 or 4 intraventricular hemorrhage, or seizures. After controlling for confounding factors including gestational age at PPROM and delivery, latency period, group B streptococcus (GBS) vaginal colonization, corticosteroid therapy, neonatal sex, mode of delivery, fetal indications for delivery, and umbilical cord pH, biochemical pulmonary maturity was not predictive of major neonatal morbidity. In our population, biochemical pulmonary maturity status does not appear to be predictive of neonatal morbidity in pregnancies complicated by PPROM at 32-34 weeks' gestation.
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PMID:Relationship between fetal pulmonary maturity assessment and neonatal outcome in premature rupture of the membranes at 32-34 weeks' gestation. 1173 61

Thirty-one cases of human listeriosis seen from 1971-1999 were reviewed. cases were grouped as follows: Group I composed of 14 patients were studied in the period 1971-1984; and group II composed of 17 cases studied in the period 1985-1999. We tried to assess changes in the incidence, clinical findings and outcome in both periods. The incidence of listeriosis remained constant along the years, 1.2 cases/20,000 discharges. The mean age of the patients significantly increased along the years (55 11 years versus 68 12 years; p 0.002). 77% of cases had one or more underlying diseases predisposing to listeriosis. We observed an increasing number of listeriosis in patients without chronic diseases in recent years. Listeriosis presented as meningitis or primary sepsis. Mortality was 61% and was strictly associated with the severity of the underlying disease. Patients with meningoencephalitis and seizures had a worse prognosis. We did not observe differences in mortality of patients who were treated with beta-lactam monotherapy in comparison with those who were treated with beta-lactam/aminoglucoside combination. Cotrimoxazole was uniformly successful treatment of human listeriosis in this series.
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PMID:[Listeria monocytogenes infections in the adult. Clinical and microbiological issues of a changing disease]. 1174 87

The detection of neurodegenerative and neurometabolic diseases in children relies on a high index of suspicion as most will present as common paediatric problems such as recurrent vomiting, feeding problem, failure to thrive, sepsis, or developmental delay. Alternatively, children may present with an acute encephalopathy or with a chronic progressive encephalopathy. Clinical clues suggestive of neurometabolic disorders include encephalopathic features such as microcephaly, macrocephaly, developmental regression, developmental arrest, change in sensorium, seizures, hypotonia, hypertonia, abnormal eye signs; also extrapyramidal or cerebellar signs and systemic features like abnormal respiration, hepatosplenomegaly, abnormal hair, liver dysfunction, renal tubular dysfunction, cardiomyopathy, and feeding difficulties or growth problems. Initial screening include tests for acidosis, ketosis, hyperlacticemia, and hyperammonemia. Further investigations should amino acid chromatography, assays of organic acids, specific enzyme assay of white cell or fibroblast culture, and histopatholgy of cell and tissue biopsy (white blood cell, skin, muscle, conjunctiva, bone marrow, liver, rectum, or brain). The correct diagnosis holds implications for targeted therapeutic intervention, genetic counselling, and possibly, prenatal diagnosis.
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PMID:Neurodegenerative diseases in children. 1184 61

Late onset epilepsy is increasing in incidence. These patients often have significant underlying morbidity. This retrospective study in a tertiary referral centre identified 68 patients aged 65 years or older, with new onset seizures over a four-year period. 81% of patients (n = 55) were followed up at an average of 2.7 years post diagnosis. 38% of patients had evidence of cerebrovascular disease (CT visualised focal infarction, haemorrhage or small vessel ischaemia in 32%, clinical diagnosis with normal CT brain in 6%). No patient was found to have a space-occupying lesion. Of the 55 patients followed up, 45% of these had died at a mean age of 82 years old and 1.9 years post diagnosis (range 12 hours to 5 years). Three patients died as a direct result of seizures (trauma and sepsis). 14 patients died of clearly unrelated causes. Eight patients died from underlying vascular disease or Alzheimer's dementia. Patients who died during follow-up were on average 3.4 years older at the time of diagnosis than survivors (p< 0.05). Patients with atrial fibrillation at the time of diagnosis, had increased mortality (relative risk 2.53; 95% C.I. 1.19 - 5.36), but they were older than those without atrial fibrillation. At the time of follow up, 92% of those taking anti-convulsants were maintained seizure free on anticonvulsant monotherapy.
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PMID:New onset seizures in the elderly: aetiology and prognosis. 1198 47

Data regarding first-time seizures in children <or=6 months of age is limited. This retrospective study, therefore, reviews the presentation, management, and outcome of children <or=6 months of age presenting to a pediatric tertiary care facility with a first-time seizure. Charts for 31 patients were identified and reviewed. Nineteen patients (61%) received sepsis work-ups. Two of the 31 (7%) had infectious etiologies. One of these infants, a 3-month-old who presented with only a history of fever and eyes rolling back but otherwise appeared well on initial presentation, had pneumococcal meningitis. Neuroimaging studies were performed in 22 (71%) patients with 12 of 22 (54%) having abnormal findings. Electroencephalogram (EEGs) were performed on 22 patients (71%) with 11 (50%) showing seizure activity. Electrolytes were checked on 19 patients (61%) with 5 being clinically significant. Etiologies included idiopathic (32%), congenital anomalies (26%), inborn errors of metabolism (16%), electrolyte abnormalities (16%), infection (7%), and trauma (3%). In conclusion, unlike children >6 months of age in whom febrile seizures and idiopathic seizure disorders are most common, a large percentage of children <or=6 months of age presenting with first-time seizures have significant underlying pathology. This pathology often includes immediately life-threatening conditions in these children who may look deceptively well on initial evaluation.
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PMID:Infant seizures not so infantile: first-time seizures in children under six months of age presenting to the ED. 1236 24

Urea Cycle Disorders (UCD) is an inborn error of urea synthesis in which ammonium and other nitrogenous precursors of urea accumulate leading to episodic coma and a high mortality rate. Therapy with peritoneal dialysis, essential amino acids or their nitrogen-free analogues has increased survival. The authors report 5 cases of urea cycle disorders, all of whom developed and were rescued from hyperammonemic coma. However, the eventual outcome was quite variable. Argininosuccinate lyase deficiency (ALD) Case 1. A 2 month old male infant, a product of a consanguineous marriage (Suphanburi province); developed poor feeding on day 7, lethargy, convulsion, hepatomegaly and respiratory alkalosis leading to respiratory failure and coma. Hyperammonemia, elevation of glutamic acid and argininosuccinic acid and its anhydrides confirmed the diagnosis of ALD. He is now 9 years old and severely retarded. Case 2. A male infant with history of lethargy, poor feeding on day 3, treated as sepsis and required respiratory support for 6 days; subsequently readmitted at age 2 weeks with vomitting, lethargy, seizure activity and hyperammonemia, and was treated by a local pediatrician in Songkhla province. There was a history of parental consanguinity and he was referred to Siriraj Hospital on day 64 with severe essential amino acid deficiency and acrodermatitis enteropathica with markedly elevated plasma citrulline level. In spite of aggressive treatment; the patient developed sepsis and he expired on day 78. Ornithine transcarbamylase deficiency (OTC) Case 3. An eleven-month-old male infant, the product of a non-consanguineous marriage, developed neonatal onset of hyperammonemia on day 5 after poor feeding, lethargy, hypothermia, seizure, apnea and coma. He was rescued from neonatal hyperammonemic coma on day 9 after aggressive treatment, but expired at eleven months of age after overwhelming sepsis. Case 4. A male infant, sibling of case 3 was referred to Siriraj Hospital on day 8 with hyperammonemia and coma. In spite of intensive genetic counseling given after the birth of their first child with OTC, the couple chose to have another baby without informing any physician. The baby developed vomiting and lethargy on day 2; subsequently hyperammonemia was noted. In spite of aggressive treatment given; hepatic dysfunction, renal failure and disseminated intravascular coagulation defects occurred on day 15. He expired on day 18 after parental permission for discontinuation of all treatment. Argininosuccinate synthetase deficiency (ASS) or Citrullinemia. Case 5. A seven week old female infant, the product of a consanguineous marriage and of Pakistani ethnic origin; developed intermittent vomiting from day 6. Initial diagnoses included ruminations, sepsis and pyloric stenosis for which she was operated on (day 30); however, vomiting continued; subsequently seizures, hyperammonemic coma developed and she was rescued from hyperammonemic coma within 30 hours. Significant elevations of citrulline and L-glutamine were demonstrated. She was discharged in excellent condition to her home in Dubai, the United Arab Emirates.
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PMID:Urea cycle disorders in Thai infants: a report of 5 cases. 1240 52


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