Publication

Longitudinal analysis of varicella-zoster virus-specific antibodies in systemic lupus erythematosus: No association with subclinical viral reactivations or lupus disease activity

Rondaan, C., van Leer, C. C., van Assen, S., Bootsma, H., de Leeuw, K., Arends, S., Bos, N. A. & Westra, J., Jul-2018, In : Lupus. 27, 8, p. 1271-1278 8 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Rondaan, C., van Leer, C. C., van Assen, S., Bootsma, H., de Leeuw, K., Arends, S., ... Westra, J. (2018). Longitudinal analysis of varicella-zoster virus-specific antibodies in systemic lupus erythematosus: No association with subclinical viral reactivations or lupus disease activity. Lupus, 27(8), 1271-1278. https://doi.org/10.1177/0961203318770535

Author

Rondaan, C ; van Leer, C C ; van Assen, S ; Bootsma, H ; de Leeuw, K ; Arends, S ; Bos, N A ; Westra, J. / Longitudinal analysis of varicella-zoster virus-specific antibodies in systemic lupus erythematosus : No association with subclinical viral reactivations or lupus disease activity. In: Lupus. 2018 ; Vol. 27, No. 8. pp. 1271-1278.

Harvard

Rondaan, C, van Leer, CC, van Assen, S, Bootsma, H, de Leeuw, K, Arends, S, Bos, NA & Westra, J 2018, 'Longitudinal analysis of varicella-zoster virus-specific antibodies in systemic lupus erythematosus: No association with subclinical viral reactivations or lupus disease activity', Lupus, vol. 27, no. 8, pp. 1271-1278. https://doi.org/10.1177/0961203318770535

Standard

Longitudinal analysis of varicella-zoster virus-specific antibodies in systemic lupus erythematosus : No association with subclinical viral reactivations or lupus disease activity. / Rondaan, C; van Leer, C C; van Assen, S; Bootsma, H; de Leeuw, K; Arends, S; Bos, N A; Westra, J.

In: Lupus, Vol. 27, No. 8, 07.2018, p. 1271-1278.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Rondaan C, van Leer CC, van Assen S, Bootsma H, de Leeuw K, Arends S et al. Longitudinal analysis of varicella-zoster virus-specific antibodies in systemic lupus erythematosus: No association with subclinical viral reactivations or lupus disease activity. Lupus. 2018 Jul;27(8):1271-1278. https://doi.org/10.1177/0961203318770535


BibTeX

@article{3f47f4c4c11c47079af7a4891f8565fa,
title = "Longitudinal analysis of varicella-zoster virus-specific antibodies in systemic lupus erythematosus: No association with subclinical viral reactivations or lupus disease activity",
abstract = "Systemic lupus erythematosus (SLE) patients are at high risk of herpes zoster. Previously, we found increased immunoglobulin (Ig)G levels against varicella-zoster virus (VZV) in SLE patients compared to controls, while antibody levels against diphtheria and cellular immunity to VZV were decreased. We aimed to test our hypothesis that increased VZV-IgG levels in SLE result from subclinical VZV reactivations, caused by stress because of lupus disease activity or immunosuppressive drug use. Methods Antibody levels to VZV (IgG, IgA, IgM), total IgG and VZV-DNA were longitudinally determined in the serum of 34 SLE patients, using enzyme-linked immunosorbent assay and polymerase chain reaction. Clinical data were retrieved from medical records. Reactivation of VZV was defined as an at least fivefold rise in VZV-IgG or presence of VZV-IgM or VZV-DNA. Generalized estimating equations (GEE) were used to longitudinally analyse associations between antibody levels, lupus disease activity and medication use. Systemic Lupus Erythematosus Disease Activity Index, anti-double-stranded DNA and complement levels were used as indicators of lupus disease activity. Results A VZV reactivation was determined in 11 patients (33{\%}). In at least five of them, herpes zoster was clinically overt. No association between SLE disease activity or medication use and VZV-specific antibody levels was found. There was a weak association between total IgG and VZV-IgG. Conclusions Our results indicate that increased VZV-IgG levels in SLE do not result from frequent subclinical VZV reactivations, and are not associated with lupus disease activity. Increased VZV-IgG can only partially be explained by hypergammaglobulinaemia.",
author = "C Rondaan and {van Leer}, {C C} and {van Assen}, S and H Bootsma and {de Leeuw}, K and S Arends and Bos, {N A} and J Westra",
year = "2018",
month = "7",
doi = "10.1177/0961203318770535",
language = "English",
volume = "27",
pages = "1271--1278",
journal = "Lupus",
issn = "0961-2033",
publisher = "SAGE Publications Inc.",
number = "8",

}

RIS

TY - JOUR

T1 - Longitudinal analysis of varicella-zoster virus-specific antibodies in systemic lupus erythematosus

T2 - No association with subclinical viral reactivations or lupus disease activity

AU - Rondaan, C

AU - van Leer, C C

AU - van Assen, S

AU - Bootsma, H

AU - de Leeuw, K

AU - Arends, S

AU - Bos, N A

AU - Westra, J

PY - 2018/7

Y1 - 2018/7

N2 - Systemic lupus erythematosus (SLE) patients are at high risk of herpes zoster. Previously, we found increased immunoglobulin (Ig)G levels against varicella-zoster virus (VZV) in SLE patients compared to controls, while antibody levels against diphtheria and cellular immunity to VZV were decreased. We aimed to test our hypothesis that increased VZV-IgG levels in SLE result from subclinical VZV reactivations, caused by stress because of lupus disease activity or immunosuppressive drug use. Methods Antibody levels to VZV (IgG, IgA, IgM), total IgG and VZV-DNA were longitudinally determined in the serum of 34 SLE patients, using enzyme-linked immunosorbent assay and polymerase chain reaction. Clinical data were retrieved from medical records. Reactivation of VZV was defined as an at least fivefold rise in VZV-IgG or presence of VZV-IgM or VZV-DNA. Generalized estimating equations (GEE) were used to longitudinally analyse associations between antibody levels, lupus disease activity and medication use. Systemic Lupus Erythematosus Disease Activity Index, anti-double-stranded DNA and complement levels were used as indicators of lupus disease activity. Results A VZV reactivation was determined in 11 patients (33%). In at least five of them, herpes zoster was clinically overt. No association between SLE disease activity or medication use and VZV-specific antibody levels was found. There was a weak association between total IgG and VZV-IgG. Conclusions Our results indicate that increased VZV-IgG levels in SLE do not result from frequent subclinical VZV reactivations, and are not associated with lupus disease activity. Increased VZV-IgG can only partially be explained by hypergammaglobulinaemia.

AB - Systemic lupus erythematosus (SLE) patients are at high risk of herpes zoster. Previously, we found increased immunoglobulin (Ig)G levels against varicella-zoster virus (VZV) in SLE patients compared to controls, while antibody levels against diphtheria and cellular immunity to VZV were decreased. We aimed to test our hypothesis that increased VZV-IgG levels in SLE result from subclinical VZV reactivations, caused by stress because of lupus disease activity or immunosuppressive drug use. Methods Antibody levels to VZV (IgG, IgA, IgM), total IgG and VZV-DNA were longitudinally determined in the serum of 34 SLE patients, using enzyme-linked immunosorbent assay and polymerase chain reaction. Clinical data were retrieved from medical records. Reactivation of VZV was defined as an at least fivefold rise in VZV-IgG or presence of VZV-IgM or VZV-DNA. Generalized estimating equations (GEE) were used to longitudinally analyse associations between antibody levels, lupus disease activity and medication use. Systemic Lupus Erythematosus Disease Activity Index, anti-double-stranded DNA and complement levels were used as indicators of lupus disease activity. Results A VZV reactivation was determined in 11 patients (33%). In at least five of them, herpes zoster was clinically overt. No association between SLE disease activity or medication use and VZV-specific antibody levels was found. There was a weak association between total IgG and VZV-IgG. Conclusions Our results indicate that increased VZV-IgG levels in SLE do not result from frequent subclinical VZV reactivations, and are not associated with lupus disease activity. Increased VZV-IgG can only partially be explained by hypergammaglobulinaemia.

U2 - 10.1177/0961203318770535

DO - 10.1177/0961203318770535

M3 - Article

VL - 27

SP - 1271

EP - 1278

JO - Lupus

JF - Lupus

SN - 0961-2033

IS - 8

ER -

ID: 60951270