Risk Factors of Pneumonia in Primary Antibody Deficiency Patients Receiving Immunoglobulin Therapy: Data from the US Immunodeficiency Network (USIDNET).


Journal

Journal of clinical immunology
ISSN: 1573-2592
Titre abrégé: J Clin Immunol
Pays: Netherlands
ID NLM: 8102137

Informations de publication

Date de publication:
10 2022
Historique:
received: 22 02 2022
accepted: 22 06 2022
pubmed: 3 7 2022
medline: 23 11 2022
entrez: 2 7 2022
Statut: ppublish

Résumé

Despite immunoglobulin replacement (IgRT) therapy, some patients with primary antibody deficiency (PAD) continue to develop respiratory infections. Recurrent and severe respiratory infections, particularly pneumonia, can lead to significant morbidity and mortality. Therefore, we sought to determine the risk factors of developing pneumonia in PAD patients, already receiving IgRT. We evaluated clinical and laboratory features of PAD patients enrolled in the US Immune Deficiency Network (USIDNET) registry by April 2017. Patients were included if they met the following criteria: (1) PAD diagnosis (common variable immunodeficiency (CVID), agammaglobulinemia, hypogammaglobinemia, and specific antibody deficiency (SAD) and (2) available data on infections before and after IgRT. Patients were excluded if they were not receiving IgRT, or if no pre/post infections data were available. Descriptive and multivariable logistic regression analyses were used to identify factors associated with pneumonia post-IgRT. A total of 1232 patients met the inclusion criteria. Following IgRT, 218 patients (17.7%) were reported to have at least one pneumonia episode. Using multivariate logistic regression analysis, we found a statistically significant increased risk of pneumonia in patients with asthma (OR: 2.55, 95% CI (1.69-3.85), p < 0.001) bronchiectasis (OR: 3.94, 95% CI (2.29-6.80), p < 0.001), interstitial lung disease (ILD) (OR: 3.28, 95%CI (1.43-7.56), p < 0.005), splenomegaly (OR: 2.02, 95%CI (1.08-3.76), p < 0.027), allergies (OR: 2.44, 95% CI [1.44-4.13], p = 0.001), and patients who were not on immunosuppressives (OR: 1.61; 95%CI [1.06-2.46]; p = 0.027). For every 50 unit increase in IgA, the odds of reporting pneumonia post IgRT decreased (OR: 0.86, 95% CI [0.73-1.02], p = 0.062). Infectious organisms were reported in 35 of 218 patients who reported pneumonia after IgRT. Haemophilus influenzae was the most frequently reported (n = 11, 31.43%), followed by Streptococcus pneumoniae (n = 7, 20.00%). Our findings suggest PAD patients with chronic and structural lung disease, splenomegaly, and allergies were associated with persistent pneumonia. However, our study is limited by the cross-sectional nature of the USIDNET database and limited longitudinal data. Further studies are warranted to identify susceptible causes and explore targeted solutions for prevention and associated morbidity and mortality. Patients with primary antibody deficiency with structural lung disease, allergies, and splenomegaly are associated with persistent pneumonia post-IgRT.

Sections du résumé

BACKGROUND
Despite immunoglobulin replacement (IgRT) therapy, some patients with primary antibody deficiency (PAD) continue to develop respiratory infections. Recurrent and severe respiratory infections, particularly pneumonia, can lead to significant morbidity and mortality. Therefore, we sought to determine the risk factors of developing pneumonia in PAD patients, already receiving IgRT.
METHODS
We evaluated clinical and laboratory features of PAD patients enrolled in the US Immune Deficiency Network (USIDNET) registry by April 2017. Patients were included if they met the following criteria: (1) PAD diagnosis (common variable immunodeficiency (CVID), agammaglobulinemia, hypogammaglobinemia, and specific antibody deficiency (SAD) and (2) available data on infections before and after IgRT. Patients were excluded if they were not receiving IgRT, or if no pre/post infections data were available. Descriptive and multivariable logistic regression analyses were used to identify factors associated with pneumonia post-IgRT.
RESULTS
A total of 1232 patients met the inclusion criteria. Following IgRT, 218 patients (17.7%) were reported to have at least one pneumonia episode. Using multivariate logistic regression analysis, we found a statistically significant increased risk of pneumonia in patients with asthma (OR: 2.55, 95% CI (1.69-3.85), p < 0.001) bronchiectasis (OR: 3.94, 95% CI (2.29-6.80), p < 0.001), interstitial lung disease (ILD) (OR: 3.28, 95%CI (1.43-7.56), p < 0.005), splenomegaly (OR: 2.02, 95%CI (1.08-3.76), p < 0.027), allergies (OR: 2.44, 95% CI [1.44-4.13], p = 0.001), and patients who were not on immunosuppressives (OR: 1.61; 95%CI [1.06-2.46]; p = 0.027). For every 50 unit increase in IgA, the odds of reporting pneumonia post IgRT decreased (OR: 0.86, 95% CI [0.73-1.02], p = 0.062). Infectious organisms were reported in 35 of 218 patients who reported pneumonia after IgRT. Haemophilus influenzae was the most frequently reported (n = 11, 31.43%), followed by Streptococcus pneumoniae (n = 7, 20.00%).
CONCLUSION
Our findings suggest PAD patients with chronic and structural lung disease, splenomegaly, and allergies were associated with persistent pneumonia. However, our study is limited by the cross-sectional nature of the USIDNET database and limited longitudinal data. Further studies are warranted to identify susceptible causes and explore targeted solutions for prevention and associated morbidity and mortality.
CLINICAL IMPLICATIONS
Patients with primary antibody deficiency with structural lung disease, allergies, and splenomegaly are associated with persistent pneumonia post-IgRT.

Identifiants

pubmed: 35779201
doi: 10.1007/s10875-022-01317-2
pii: 10.1007/s10875-022-01317-2
doi:

Substances chimiques

Immunoglobulins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1545-1552

Subventions

Organisme : BLRD VA
ID : I01 BX004633
Pays : United States
Organisme : CSRD VA
ID : I01 CX000104
Pays : United States

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Maha N Syed (MN)

The William T Shearer Center for Human Immunobiology at Texas Children's Hospital, Houston, TX, USA.
Department of Pediatrics, Section of Immunology, Allergy and Retrovirology, Baylor College of Medicine, Houston, TX, USA.

Carleigh Kutac (C)

Department of Pediatrics, Section of Immunology, Allergy and Retrovirology, Baylor College of Medicine, Houston, TX, USA.

Jennifer M Miller (JM)

Department of Pediatrics, Section of Immunology, Allergy and Retrovirology, Baylor College of Medicine, Houston, TX, USA.

Rebecca Marsh (R)

Division of Bone Marrow Transplantation and Immune Deficiency, Cincinnati Children's Hospital, and Department of Pediatrics, University of Cincinnati, Cincinnati, OH, USA.

Kathleen E Sullivan (KE)

Division of Allergy and Immunology, Children's Hospital of Philadelphia, Philadelphia, PA, USA.

Charlotte Cunningham-Rundles (C)

Departments of Medicine and Pediatrics, Division of Allergy and Clinical Immunology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Ramsay L Fuleihan (RL)

Division of Pediatric Allergy, Immunology and Rheumatology, Columbia University Medical Center, New York, NY, USA.

Farrah Kheradmand (F)

Biology of Inflammation Center, Baylor College of Medicine, TX, Houston, USA.
Center for Translational Research On Inflammatory Diseases (CTRID), Michael E. DeBakey Department of Veterans Affairs, TX, Houston, USA.

Joud Hajjar (J)

The William T Shearer Center for Human Immunobiology at Texas Children's Hospital, Houston, TX, USA. joud.hajjar@bcm.edu.
Department of Pediatrics, Section of Immunology, Allergy and Retrovirology, Baylor College of Medicine, Houston, TX, USA. joud.hajjar@bcm.edu.

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