Literature DB >> 26833050

The effect of systemic corticosteroids on the innate and adaptive immune system in children with steroid responsive nephrotic syndrome.

Hatice Ezgi Baris1, Safa Baris2, Elif Karakoc-Aydiner1, Ibrahim Gokce3, Nurdan Yildiz3, Dilek Cicekkoku1, Ismail Ogulur1, Ahmet Ozen1, Harika Alpay3, Isil Barlan1.   

Abstract

UNLABELLED: The severity and duration of immunosuppression caused by corticosteroids (CSs) usage have not been extensively studied. We aimed to investigate the effects of CSs on the various compartments of immune system in relation to timing of initiation and persistence of therapy. Pediatric patients with idiopathic nephrotic syndrome (NS) treated with 2 mg/kg/day prednisolone and healthy control (HC) were enrolled. Blood samples were drawn for immunologic analyses at baseline and at the first and second weeks and first, second, and third months of CS therapy in addition to first and second weeks and first, second, and third months of discontinuation. Fourteen patients (M/F, 7/7) between 1 and 8 years old were evaluated. Untreated NS exhibited high absolute lymphocyte count (ALC)(p = 0.010), absolute CD3(+) T cells (p = 0.020) and absolute CD8(+) T cells (p = 0.006) compared to HC. Suppression in ALC was observed and nadir value was noted at first month of therapy compared to baseline (p = 0.002). The CD4(+) (p = 0.036) and CD8(+) T cell (p = 0.013) counts decreased significantly at the first week of treatment compared to baseline. While baseline B cell counts was indifferent from HC, gradually increased in 2 weeks of CS initiation and decreased during the treatment with a statistical significance compared to HC (p = 0.010). However, after cessation of CS, B cell counts continued to decline and found to be significantly different than baseline at first week (p = 0.008) and at third month (p = 0.040).
CONCLUSION: Apart from baseline lymphocyte subset changing observed in untreated NS patients, our data implies that T cells were suppressed very early in the CS treatment. Interestingly, depressed B cell counts were detected later but persisted even after CS cessation. Due to early decrease in T cells, it would be beneficial to assume the patients as immunosuppressed at the very beginning of CS treatment to avoid infections. WHAT IS KNOWN: • Corticosteroids (CSs) are widely used for a variety of diseases including nephrotic syndrome, which is related with complex immune disturbance including T and B cells dysfunctions. • CSs induce neutrophilic leukocytosis concomitant with lymphopenia and eosinopenia leading to immunosupression. What is New: • T cell subsets and proliferation are susceptible to CSs more than B cells; however, the reversibility is faster with dose reduction in CS. • The change of B cells and B cell subtypes (CD27 (+) memory) shows prolonged effect of CSs on B cells which may alter antibody production even after 3 months of CSs cessation.

Entities:  

Keywords:  Children; Corticosteroids; Immunosuppression; Lymphocytes; Nephrotic syndrome; Neutrophils

Mesh:

Substances:

Year:  2016        PMID: 26833050     DOI: 10.1007/s00431-016-2694-x

Source DB:  PubMed          Journal:  Eur J Pediatr        ISSN: 0340-6199            Impact factor:   3.183


  31 in total

Review 1.  Glucocorticoids in T cell development and function*.

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5.  Effects of long-term low-dose corticosteroid therapy on humoral immunity.

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Authors:  Rebecca M Lombel; Debbie S Gipson; Elisabeth M Hodson
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Review 2.  Targeting B Cells and Plasma Cells in Glomerular Diseases: Translational Perspectives.

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3.  Synaptopodin is upregulated by IL-13 in eosinophilic esophagitis and regulates esophageal epithelial cell motility and barrier integrity.

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8.  Pneumocystis jirovecii Pneumonia in Patients with Nephrotic Syndrome: Application of Lymphocyte Subset Analysis in Predicting Clinical Outcomes.

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9.  Mass Cytometry Studies of Patients With Autoimmune Endocrine Diseases Reveal Distinct Disease-Specific Alterations in Immune Cell Subsets.

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10.  The Inhaled Steroid Ciclesonide Blocks SARS-CoV-2 RNA Replication by Targeting the Viral Replication-Transcription Complex in Cultured Cells.

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