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Diabetologia. 2017 Nov;60(11):2252-2255. doi: 10.1007/s00125-017-4403-3. Epub 2017 Aug 23.

Relapsing/remitting type 1 diabetes.

Author information

1
Department of Diabetes Immunology, Diabetes & Metabolism Research Institute, Beckman Research Institute at the City of Hope, 1500 E Duarte Rd, Duarte, CA, 91010, USA.
2
Department of Immunohaematology and Blood Transfusion, Leiden University Medical Center, Leiden, the Netherlands.
3
DeKinderkliniek, Children's Hospital, Almere, the Netherlands.
4
Flevo Hospital, Almere, the Netherlands.
5
Department of Pediatric Immunology and Rheumatology, Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht, the Netherlands.
6
Department of Diabetes Immunology, Diabetes & Metabolism Research Institute, Beckman Research Institute at the City of Hope, 1500 E Duarte Rd, Duarte, CA, 91010, USA. broep@coh.org.
7
Department of Immunohaematology and Blood Transfusion, Leiden University Medical Center, Leiden, the Netherlands. broep@coh.org.

Abstract

AIMS/HYPOTHESIS:

Type 1 diabetes is believed to be an autoimmune disease associated with irreversible loss of insulin secretory function that follows a chronic progressive course. However, it has been speculated that relapsing/remitting disease progression may occur in type 1 diabetes.

METHODS:

We report the case of an 18-year-old girl with Graves' disease, chronic inflammatory demyelinating polyneuropathy (CIDP) and multiple islet autoantibodies, presenting with relapsing/remitting hyperglycaemia. Peripheral blood mononuclear cells were analysed for islet autoimmunity.

RESULTS:

There were two instances of hyperglycaemia relapse during CIDP flare-ups that required insulin therapy and remitted after i.v. immunoglobulin (IVIG) therapy improving neurological symptoms. A diagnosis of type 1 diabetes was assigned on the basis of insulin need, HbA1c and islet autoantibodies. Insulin requirements disappeared following IVIG treatment and peaked during CIDP flare-ups. Pro- and anti-inflammatory cytokine responses were noted against islet autoantigens.

CONCLUSIONS/INTERPRETATION:

We provide clinical evidence of relapsing/remitting type 1 diabetes associated with IVIG treatment and the regulation of islet autoimmunity. Despite sufficient residual beta cell mass, individuals can experience episodes of impaired glycaemia control. This disconnect between beta cell mass and function highlighted by our case may have implications for the use of beta cell function as the primary endpoint for immune intervention trials aiming to protect beta cell mass rather than function. Immune modulation may restore beta cell function and glycaemic control.

KEYWORDS:

Autoimmune disease; Immune regulation; Immunotherapy; Type 1 diabetes

PMID:
28835984
DOI:
10.1007/s00125-017-4403-3
[Indexed for MEDLINE]

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