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Pediatr Diabetes. 2018 Mar;19(2):293-299. doi: 10.1111/pedi.12547. Epub 2017 Jun 9.

Early childhood infections precede development of beta-cell autoimmunity and type 1 diabetes in children with HLA-conferred disease risk.

Author information

1
Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
2
Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland.
3
Department of Pediatrics, University of Tartu and Tartu University Hospital, Tartu, Estonia.
4
Immunogenetics Laboratory, University of Turku and Turku University Hospital, Turku, Finland.
5
Department of Virology, School of Medicine, University of Tampere, Tampere, Finland.
6
Fimlab Laboratories, Pirkanmaa Hospital District, Tampere, Finland.
7
Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, Finland.
8
Tampere Center for Child Health Research, Tampere University Hospital, Tampere, Finland.

Abstract

BACKGROUND:

The etiology of type 1 diabetes (T1D) is largely unknown. Infections and microbial exposures are believed to play a role in the pathogenesis and in the development of islet autoimmunity in genetically susceptible individuals.

OBJECTIVE:

To assess the relationships between early childhood infections, islet autoimmunity, and progression to T1D in genetically predisposed children.

METHODS:

Children with human leukocyte antigen (HLA)-conferred disease susceptibility (N=790; 51.5% males) from Finland (n = 386), Estonia (n = 322), and Russian Karelia (n = 82) were observed from birth up to the age of 3 years. Children attended clinical visits at the age of 3, 6, 12, 18, 24, and 36 months. Serum samples for analyzing T1D-associated autoimmune markers were collected and health data recorded during the visits.

RESULTS:

Children developing islet autoimmunity (n = 46, 5.8%) had more infections during the first year of life (3.0 vs 3.0, mean rank 439.1 vs 336.2; P = .001) and their first infection occurred earlier (3.6 vs 5.0 months; P = .005) than children with no islet autoimmunity. By May 2016, 7 children (0.9%) had developed T1D (progressors). Compared with non-diabetic children, T1D progressors were younger at first infection (2.2 vs 4.9 months; P = .004) and had more infections during the first 2 years of life (during each year 6.0 vs 3.0; P = .001 and P = .027, respectively). By 3 years of age, the T1D progressors had twice as many infections as the other children (17.5 vs 9.0; P = .006).

CONCLUSIONS:

Early childhood infections may play an important role in the pathogenesis of T1D. Current findings may reflect either differences in microbial exposures or early immunological aberrations making diabetes-prone children more susceptible to infections.

KEYWORDS:

childhood infections; islet autoimmunity; respiratory tract infections; the hygiene hypothesis; type 1 diabetes

PMID:
28597957
DOI:
10.1111/pedi.12547
[Indexed for MEDLINE]

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