Evidence map›Paper›PMID 41324804›Full record

ReviewClinical reviews in allergy & immunology2025

Common Variable Immunodeficiency Disorders: A perspective from New Zealand.

Rohan Ameratunga, Hilary J Longhurst, Klaus Lehnert, Euphemia Leung, Richard Steele, See-Tarn Woon

Abstract readReview
In one paragraph

Review in Clinical reviews in allergy & immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Rohan AmeratungaDepartment of Clinical Immunology, Auckland Hospital, Park Rd, Grafton, 1010, Auckland, New Zealand. rohana@adhb.govt.nz.
Hilary J LonghurstDepartment of Clinical Immunology, Auckland Hospital, Park Rd, Grafton, 1010, Auckland, New Zealand.
Klaus LehnertMaurice Wilkins Centre, University of Auckland, Symonds St, Auckland, New Zealand.
Euphemia LeungMaurice Wilkins Centre, University of Auckland, Symonds St, Auckland, New Zealand.
Richard SteeleDepartment of Clinical Immunology, Auckland Hospital, Park Rd, Grafton, 1010, Auckland, New Zealand.
See-Tarn WoonDepartment of Virology and Immunology, Auckland Hospital, Park Rd, Grafton, 1010, Auckland, New Zealand.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Common Variable Immunodeficiency Disorders (CVID) are the most frequent symptomatic Primary Immunodeficiency (PID) in adults and children. Patients with CVID present with predominant antibody deficiency with varying degrees of impaired cellular immunity. CVID was previously a diagnosis of exclusion, which led to considerable uncertainty about which patients would qualify for subcutaneous or intravenous immunoglobulin (SCIG/IVIG) replacement. Over the last twelve years, several sets of diagnostic criteria have been published which identify these disorders with greater precision. These new CVID diagnostic criteria assist with decisions on treatment, particularly SCIG/IVIG replacement. With the advent of massively parallel genome sequencing technologies, it has become apparent that a significant proportion of individuals with a CVID phenotype have an underlying causative genetic defect. If such a pathogenic variant is identified, these individuals are removed from the overarching diagnosis of CVID and are deemed to have a CVID-like disorder caused by a specific Inborn Error of Immunity (IEI). New Zealand has had a long-standing customized PID genetic testing program. Two novel autosomal dominant pathogenic variants causing CVID-like disorders, consequent to haploinsufficiency of Nuclear Factor kappa-light-chain-enhancer of activated B cells (NFKB1) and Transcription Factor 3 (TCF3), were identified in New Zealand families. The latter pathogenic variant was shown to have an epistatic interaction with TNFRSF13B (TACI) in a patient with a digenic CVID-like disorder. Epistasis is the synergistic, non-linear interaction between two or more genetic loci, leading to much more severe (or much milder) disease. This perspective reviews the current understanding of these disorders with contributions from three New Zealand-based studies: The Prospective NZ CVID and the NZ hypogammaglobulinemia sub-studies as well as a large retrospective case series of Transient Hypogammaglobulinemia of Infancy (THI). These clinical and genomic studies have offered insights into the complexities of these rare PIDs. This review examines current areas of uncertainty in the diagnosis of of these disorders.

Indexed as

Common Variable ImmunodeficiencyGenetic TestingHumansImmunoglobulins, IntravenousNew ZealandPhenotypeImmunoglobulins, IntravenousCommon Variable Immunodeficiency DisordersEpistasisHypogammaglobulinemiaSCIG/IVIGTransient Hypogammaglobulinemia of InfancyVaccine Challenge Responses

Identifiers

PMID41324804
PMCPMC12669308

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.