Publications
378 results found
Garralda E, Rangel L, Levin M, et al., 1999, Psychiatric adjustment in adolescents with a history of chronic fatigue syndrome, JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY, Vol: 38, Pages: 1515-1521, ISSN: 0890-8567
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- Citations: 53
Kondaveeti S, Hibberd ML, Booy R, et al., 1999, Effect of the Factor V Leiden mutation on the severity of meningococcal disease, PEDIATRIC INFECTIOUS DISEASE JOURNAL, Vol: 18, Pages: 893-896, ISSN: 0891-3668
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- Citations: 64
Ison CA, Anwar N, Cole MJ, et al., 1999, Assessment of immune response to meningococcal disease: comparison of a whole-blood assay and the serum bactericidal assay, MICROBIAL PATHOGENESIS, Vol: 27, Pages: 207-214, ISSN: 0882-4010
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- Citations: 30
Newport M, Levin M, 1999, Genetic susceptibility to tuberculosis, JOURNAL OF INFECTION, Vol: 39, Pages: 117-121, ISSN: 0163-4453
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- Citations: 14
Hermans PWM, Hibberd ML, Booy R, et al., 1999, <i>4G</i>/<i>5G</i> promoter polymorphism in the plasminogen-activator-inhibitor-1 gene and outcome of meningococcal disease, LANCET, Vol: 354, Pages: 556-560, ISSN: 0140-6736
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- Citations: 220
Hermans PW, Hibberd ML, Booy R, et al., 1999, 4G/5G promoter polymorphism in the plasminogen-activator-inhibitor-1 gene and outcome of meningococcal disease. Meningococcal Research Group., Lancet, Vol: 354, Pages: 556-560, ISSN: 0140-6736
BACKGROUND: Intravascular coagulation with infarction of skin, digits, and limbs is a characteristic feature of meningococcal sepsis. Children with meningococcal sepsis have higher than normal concentrations of plasminogen activator inhibitor 1 (PAI-1) in plasma. Combined with the widespread venous thrombosis, this finding suggests an impairment of fibrinolysis. A common functional insertion/deletion (4G/5G) polymorphism exists in the promoter region of the PAI-1 gene. We tested the hypothesis that children with the 4G/4G genotype produce higher concentrations of PAI-1, develop more severe coagulopathy, and are at greater risk of death during meningococcal sepsis. METHODS: The relation between meningococcal disease outcome, PAI-1 concentration, and PAI-1 genotype was investigated in 175 children with meningococcal disease (37 from Rotterdam, the Netherlands, and 138 from London, UK) and 226 controls (137 from Rotterdam, 89 from London). PAI-1 concentrations in plasma were measured by ELISA, and the 4G/5G PAI-1 polymorphism was detected by PCR and hybridisation. FINDINGS: Concentrations of PAI-1 on admission correlated with presentation (sepsis or meningitis) and outcome. The median PAI-1 concentration in children who died was substantially higher than that in survivors (2448 [IQR 1115-3191] vs 370 [146-914] ng/mL; p<0.0001). Patients with the 4G/4G genotype had significantly higher PAI-1 concentrations than those with the 4G/5G or 5G/5G genotype (1051 [550-2440] vs 436 [198-1225] ng/mL; p=0.03), and had an increased risk of death (relative risk 2.0 [1.0-3.8] for the two cohorts combined, and 4.8 [1.8-13] for the London cohort). INTERPRETATION: A genetic predisposition to produce high concentrations of PAI-1 is associated with poor outcome of meningococcal sepsis. This finding suggests that impaired fibrinolysis is an important factor in the pathophysiology of meningococcal sepsis.
Hibberd ML, Sumiya M, Summerfield JA, et al., 1999, Mannose-binding lectin and meningococcal disease, LANCET, Vol: 354, Pages: 337-337, ISSN: 0140-6736
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- Citations: 1
Kondaveeti S, Hibberd ML, Levin M, 1999, The insertion/deletion polymorphism in the t-PA gene does not significantly affect outcome of meningococcal disease, THROMBOSIS AND HAEMOSTASIS, Vol: 82, Pages: 161-162, ISSN: 0340-6245
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- Citations: 7
Finn A, Booy R, Levin M, et al., 1999, Infectious purpura fulminans: Caution needed in the use of protein C, BRITISH JOURNAL OF HAEMATOLOGY, Vol: 106, Pages: 253-253, ISSN: 0007-1048
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- Citations: 3
Pollard AJ, Galassini R, van der Voort EMR, et al., 1999, Cellular immune responses to <i>Neisseria meningitidis</i> in children, INFECTION AND IMMUNITY, Vol: 67, Pages: 2452-2463, ISSN: 0019-9567
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- Citations: 27
Pollard AJ, Galassini R, van der Voort EMR, et al., 1999, Humoral immune responses to <i>Neisseria meningitidis</i> in children, INFECTION AND IMMUNITY, Vol: 67, Pages: 2441-2451, ISSN: 0019-9567
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- Citations: 38
Eling M, Stephens AC, Oragui EE, et al., 1999, Tissue factor pathway inhibitor levels in children with meningococcal disease, PEDIATRIC RESEARCH, Vol: 45, Pages: 765-765, ISSN: 0031-3998
Heyderman RS, Ison CA, Peakman M, et al., 1999, Neutrophil response to <i>Neisseria meningitidis</i>:: Inhibition of adhesion molecule expression and phagocytosis by recombinant bactericidal permeability-increasing protein (rBPI<sub>21</sub>), JOURNAL OF INFECTIOUS DISEASES, Vol: 179, Pages: 1288-1292, ISSN: 0022-1899
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- Citations: 24
Derkx B, Wittes J, McCloskey R, 1999, Randomized, placebo-controlled trial of HA-1A, a human monoclonal antibody to endotoxin, in children with meningococcal septic shock, CLINICAL INFECTIOUS DISEASES, Vol: 28, Pages: 770-777, ISSN: 1058-4838
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- Citations: 92
Hibberd ML, Sumiya M, Summerfield JA, et al., 1999, Association of variants of the gene for mannose-binding lectin with susceptibility to meningococcal disease, LANCET, Vol: 353, Pages: 1049-1053, ISSN: 0140-6736
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- Citations: 289
Hibberd ML, Sumiya M, Summerfield JA, et al., 1999, Association of variants of the gene for mannose-binding lectin with susceptibility to meningococcal disease. Meningococcal Research Group., Lancet, Vol: 353, Pages: 1049-1053, ISSN: 0140-6736
BACKGROUND: The reasons why meningococcal disease develops in only a small proportion of individuals carrying the causative bacteria are unknown. Differences in host responses to bacterial colonisation are thought to be involved, since people with deficiencies in the terminal components of the complement pathway, or of properdin, are susceptible to meningococcal disease. We postulate that genetic variants of mannose-binding lectin (MBL), a plasma opsonin that initiates another pathway of complement activation, might similarly cause susceptibility to meningococcal disease. METHODS: The frequency of variants of the MBL gene was ascertained in children with meningococcal disease and controls from two independent studies; one hospital-based (194 patients and 272 controls [patients with non-infectious disorders]), and one community-based (72 patients and 110 controls [healthy individuals]), by means of PCR and restriction-enzyme digestion, with confirmation by DNA sequencing. FINDINGS: The proportion of people homozygous for MBL-variant alleles was higher in patients with meningococcal disease than in controls in the hospital study (15 [7.7%] vs four [1.5%]; odds ratio 6.5 [95% CI 2.0-27.2]) and in the community study (six [8.3%] vs three [2.7%]; 4.5 [0.9-29.1]). The population attributable fraction of cases attributable to MBL variants (homozygous and heterozygous) was 32%. INTERPRETATION: The MBL pathway is a critical determinant of meningococcal-disease susceptibility, and genetic variants of MBL might account for a third of all disease cases.
Pollard AJ, Britto J, Nadel S, et al., 1999, Emergency management of meningococcal disease, ARCHIVES OF DISEASE IN CHILDHOOD, Vol: 80, Pages: 290-296, ISSN: 0003-9888
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- Citations: 118
Nadel S, Marriage S, De Munter C, et al., 1998, Human albumin administration in critically ill patients - Review did not provide recommendations for alternative treatment, BRITISH MEDICAL JOURNAL, Vol: 317, Pages: 882-883, ISSN: 0959-8138
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- Citations: 5
Nadel S, Britto J, Booy R, et al., 1998, Avoidable deficiencies in the delivery of health care to children with meningococcal disease, JOURNAL OF ACCIDENT & EMERGENCY MEDICINE, Vol: 15, Pages: 298-303, ISSN: 1351-0622
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- Citations: 56
Festa M, Nadel S, Levin M, et al., 1998, Microvascular changes in meningococcal disease, JOURNAL OF VASCULAR RESEARCH, Vol: 35, Pages: 91-91, ISSN: 1018-1172
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- Citations: 1
Levin M, 1998, Experimental treatments of meningococcal sepsis, CURRENT OPINION IN INFECTIOUS DISEASES, Vol: 11, Pages: 309-311, ISSN: 0951-7375
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- Citations: 1
Curtis N, Levin M, 1998, Kawasaki disease thirty years on., Curr Opin Pediatr, Vol: 10, Pages: 24-33, ISSN: 1040-8703
This year marks the 30th anniversary of the first description of Kawasaki disease. The disease has emerged as an important cause of acquired heart disease in children. The cause of Kawasaki disease remains unknown and this presents many problems in the diagnosis and management of the disease. This paper reviews recent publications on the pathogenesis, diagnosis, and the short- and long-term management of Kawasaki disease.
Pollard AJ, Faust SN, Levin M, 1998, Meningitis and meningococcal septicaemia., J R Coll Physicians Lond, Vol: 32, Pages: 319-328, ISSN: 0035-8819
Nadel S, De Munter C, Britto J, et al., 1998, Albumin: saint or sinner?, Archives of Disease in Childhood, Vol: 79
Jouanguy E, Lamhamedi-Cherradi S, Altare F, et al., 1997, Partial interferon-γ receptor 1 deficiency in a child with tuberculoid bacillus Calmette-Guerin infection and a sibling with clinical tuberculosis, JOURNAL OF CLINICAL INVESTIGATION, Vol: 100, Pages: 2658-2664, ISSN: 0021-9738
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- Citations: 297
Pollard AJ, DeMunter C, Nadel S, et al., 1997, Abandoning empirical antibiotics for febrile children, LANCET, Vol: 350, Pages: 811-812, ISSN: 0140-6736
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- Citations: 7
Altare F, Jouanguy E, Newport M, et al., 1997, IFNgR1, a human mycobacterial susceptibility candidate gene, BULLETIN DE L INSTITUT PASTEUR, Vol: 95, Pages: 143-146, ISSN: 0020-2452
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- Citations: 12
Heyderman RS, Ison CA, Peters M, et al., 1997, Characterisation of platelet activation in an ex-vivo whole blood model of meningococcal bacteraemia, THROMBOSIS AND HAEMOSTASIS, Pages: P2512-P2512, ISSN: 0340-6245
Levin M, 1997, Paediatric and neonatal infections, CURRENT OPINION IN INFECTIOUS DISEASES, Vol: 10, Pages: 209-212, ISSN: 0951-7375
DeMunter C, Nadel S, Britto J, et al., 1997, ECMO for refractory cardiorespiratory failure due to meningococcal disease, LANCET, Vol: 349, Pages: 1398-1398, ISSN: 0140-6736
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- Citations: 8
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