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APC resistance in neonates and infants

Standard

APC resistance in neonates and infants : adjustment of the APTT-based method. / Nowak-Göttl, U; Kohlhase, B; Vielhaber, H; Aschka, I; Schneppenheim, R; Jürgens, H.

in: THROMB RES, Jahrgang 81, Nr. 6, 15.03.1996, S. 665-70.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Nowak-Göttl, U, Kohlhase, B, Vielhaber, H, Aschka, I, Schneppenheim, R & Jürgens, H 1996, 'APC resistance in neonates and infants: adjustment of the APTT-based method', THROMB RES, Jg. 81, Nr. 6, S. 665-70.

APA

Nowak-Göttl, U., Kohlhase, B., Vielhaber, H., Aschka, I., Schneppenheim, R., & Jürgens, H. (1996). APC resistance in neonates and infants: adjustment of the APTT-based method. THROMB RES, 81(6), 665-70.

Vancouver

Nowak-Göttl U, Kohlhase B, Vielhaber H, Aschka I, Schneppenheim R, Jürgens H. APC resistance in neonates and infants: adjustment of the APTT-based method. THROMB RES. 1996 Mär 15;81(6):665-70.

Bibtex

@article{10f7f6c00b59474f84cb99267cad33f9,
title = "APC resistance in neonates and infants: adjustment of the APTT-based method",
abstract = "Resistance to activated protein C (APCR) has emerged as the most important hereditary cause of venous thromboembolism. Using an aPTT-based method together with DNA technique we investigated 120 healthy neonates and infants < 12 months of age and 24 infants with septicaemia for the presence of this mutation. In addition, data of 11 neonates with vascular occlusion, heterozygous (+/-) for the Arg 506 Gln mutation were included. Results of an aPTT-based method (clotting time using the APC/CaCl2 solution obtained in an undiluted, 1:5 and 1:11 dilution with factor V deficient plasma divided by clotting time with CaCl2 in the same plasma dilution) are shown: Whereas 7 (5.5%) out of 120 healthy neonates were (+/-) carriers for the factor V Arg 506 Gln mutation, concordance with the aPTT-based method (cut-off defined as ratio < 2) was found only when using the 1:11 plasma dilution. Six (four) out of 24 infants with sepsis, not carrying the factor V mutation, would have been classified as APC resistant when using the 1:1 (1:5) plasma dilution. Four (two) out of 18 patients, (+/-) for the Arg 506 Gln mutation showed APC ratios > 2 in the 1:1(1:5) plasma dilution.",
keywords = "Case-Control Studies, Drug Resistance, Humans, Infant, Infant, Newborn, Mutation, Partial Thromboplastin Time, Protein C, Sepsis, Thromboembolism",
author = "U Nowak-G{\"o}ttl and B Kohlhase and H Vielhaber and I Aschka and R Schneppenheim and H J{\"u}rgens",
year = "1996",
month = mar,
day = "15",
language = "English",
volume = "81",
pages = "665--70",
journal = "THROMB RES",
issn = "0049-3848",
publisher = "Elsevier Limited",
number = "6",

}

RIS

TY - JOUR

T1 - APC resistance in neonates and infants

T2 - adjustment of the APTT-based method

AU - Nowak-Göttl, U

AU - Kohlhase, B

AU - Vielhaber, H

AU - Aschka, I

AU - Schneppenheim, R

AU - Jürgens, H

PY - 1996/3/15

Y1 - 1996/3/15

N2 - Resistance to activated protein C (APCR) has emerged as the most important hereditary cause of venous thromboembolism. Using an aPTT-based method together with DNA technique we investigated 120 healthy neonates and infants < 12 months of age and 24 infants with septicaemia for the presence of this mutation. In addition, data of 11 neonates with vascular occlusion, heterozygous (+/-) for the Arg 506 Gln mutation were included. Results of an aPTT-based method (clotting time using the APC/CaCl2 solution obtained in an undiluted, 1:5 and 1:11 dilution with factor V deficient plasma divided by clotting time with CaCl2 in the same plasma dilution) are shown: Whereas 7 (5.5%) out of 120 healthy neonates were (+/-) carriers for the factor V Arg 506 Gln mutation, concordance with the aPTT-based method (cut-off defined as ratio < 2) was found only when using the 1:11 plasma dilution. Six (four) out of 24 infants with sepsis, not carrying the factor V mutation, would have been classified as APC resistant when using the 1:1 (1:5) plasma dilution. Four (two) out of 18 patients, (+/-) for the Arg 506 Gln mutation showed APC ratios > 2 in the 1:1(1:5) plasma dilution.

AB - Resistance to activated protein C (APCR) has emerged as the most important hereditary cause of venous thromboembolism. Using an aPTT-based method together with DNA technique we investigated 120 healthy neonates and infants < 12 months of age and 24 infants with septicaemia for the presence of this mutation. In addition, data of 11 neonates with vascular occlusion, heterozygous (+/-) for the Arg 506 Gln mutation were included. Results of an aPTT-based method (clotting time using the APC/CaCl2 solution obtained in an undiluted, 1:5 and 1:11 dilution with factor V deficient plasma divided by clotting time with CaCl2 in the same plasma dilution) are shown: Whereas 7 (5.5%) out of 120 healthy neonates were (+/-) carriers for the factor V Arg 506 Gln mutation, concordance with the aPTT-based method (cut-off defined as ratio < 2) was found only when using the 1:11 plasma dilution. Six (four) out of 24 infants with sepsis, not carrying the factor V mutation, would have been classified as APC resistant when using the 1:1 (1:5) plasma dilution. Four (two) out of 18 patients, (+/-) for the Arg 506 Gln mutation showed APC ratios > 2 in the 1:1(1:5) plasma dilution.

KW - Case-Control Studies

KW - Drug Resistance

KW - Humans

KW - Infant

KW - Infant, Newborn

KW - Mutation

KW - Partial Thromboplastin Time

KW - Protein C

KW - Sepsis

KW - Thromboembolism

M3 - SCORING: Journal article

C2 - 8868517

VL - 81

SP - 665

EP - 670

JO - THROMB RES

JF - THROMB RES

SN - 0049-3848

IS - 6

ER -