DIABETICMedicine

DOI: 10.1111/j.1464-5491.2011.03287.x

Short Report: Genetics

Islet autoantibodies can discriminate maturity-onset
diabetes of the young (MODY) from Type 1 diabetes
T. J. McDonald*, K. Colclough, R. Brown, B. Shields*, M. Shepherd*, P. Bingley,
A. Williams, A. T. Hattersley* and Sian Ellard*
*Institute of Biomedical and Clinical Science, Peninsula Medical School, University of Exeter, Department of Clinical Chemistry and Immunology, Department of
Molecular Genetics, Royal Devon and Exeter NHS Foundation Trust, Institute of Health Services Research, Peninsula Medical School, University of Exeter, Exeter
and Diabetes and Metabolism, School of Clinical Sciences, University of Bristol, Bristol, UK
Accepted 2 March 2011

Abstract
Maturity-onset diabetes of the young is a monogenic form of familial, young-onset diabetes. It is rare (1% diabetes) and
may be misdiagnosed as Type 1 diabetes and inappropriately treated with insulin. Type 1 diabetes is characterized by the
presence of islet autoantibodies, including glutamate decarboxylase (GAD) and islet antigen-2 (IA-2) antibodies. The prevalence
of islet autoantibodies is unknown in maturity-onset diabetes of the young and may have the potential to differentiate this form
of diabetes from Type 1 diabetes. The aim of this study was to determine the prevalence of GAD and IA-2 antibodies in patients
with maturity-onset diabetes of the young and Type 1 diabetes.

Aim

Methods We measured plasma GAD and IA-2 antibodies in 508 patients with the most common forms of maturity-onset
diabetes of the young (GCK: n = 227; HNF1A: n = 229; HNF4A: n = 52) and 98 patients with newly diagnosed Type 1
diabetes (diagnosed < 6 months). Autoantibodies were considered positive if 99th centile of 500 adult control subjects.

GAD and or IA-2 antibodies were present in 80 98 (82%) patients with Type 1 diabetes and 5 508 (< 1%) patients
with maturity-onset diabetes of the young. In the cohort with Type 1 diabetes, both GAD and IA-2 antibodies were detected in
37.8% of patients, GAD only in 24.5% and IA-2 only in 19.4%. All five patients with maturity-onset diabetes of the young with
detectable antibodies had GAD antibodies and none had detectable IA-2 antibodies.

Results

The prevalence of GAD and IA-2 antibodies in maturity-onset diabetes of the young is the same as in control
subjects (< 1%). The finding of islet autoantibodies, especially IA-2 antibodies, makes the diagnosis of maturity-onset diabetes
of the young very unlikely and genetic testing should only be performed if other clinical characteristics strongly suggest this form
of diabetes rather than Type 1 diabetes. This supports routine islet autoantibody testing before proceeding to more expensive
molecular genetic testing.

Conclusion

Diabet. Med. 28, 10281033 (2011)

Keywords autoantibodies, GAD antibodies, GAD65, IA-2 antibodies, maturity-onset diabetes of the young
Abbreviation MODY, maturity-onset diabetes of the young

Introduction
Maturity-onset diabetes of the young (MODY) is caused by
highly penetrant single gene mutations that result in non-insulin
dependent diabetes typically presenting in lean young adults.
MODY accounts for approximately 1% of diabetes and may be
misdiagnosed as Type 1 diabetes [1,2]. A molecular genetic

Correspondence to: Professor Andrew T. Hattersley, Peninsula Medical

School, Barrack Road, Exeter, Devon, EX2 5DW, UK.
Email: Andrew.Hattersley@pms.ac.uk

1028

diagnosis is important because the treatment differs from Type 1

diabetes; patients with GCK mutations usually require no
treatment, whilst those with HNF1A and HNF4A mutations
are initially well controlled on sulphonylurea tablets [3].
Molecular genetic testing is expensive, labour intensive and it
should be limited to those who are most likely to have MODY.
This selection is made on the basis of clinical characteristics such
as young onset of diabetes, autosomal dominant inheritance,
non-insulin dependence and normal BMI. Laboratory tests also
assist the selection of patients; for example, serum C-peptide is

2011 The Authors.

Diabetic Medicine 2011 Diabetes UK

Original article

detectable in patients with MODY [1], but not in Type 1 diabetes

outside the initial honeymoon period.
Close to diagnosis, the most helpful investigation to
differentiate MODY from Type 1 diabetes might be islet
autoantibodies, as Type 1 diabetes results from an
autoimmune mediated destruction of the insulin-producing
pancreatic B-cells [4]. Testing for the pancreatic islet cell
autoantibody is labour intensive, technically demanding and
poorly standardized [57]. Unique islet antigens contributing to
the heterogeneous islet cell autoantibody immunofluorescence
staining include the GAD65 isoform of glutamate decarboxylase
[8], tyrosine phosphatase-related protein islet antigen 2 (IA-2)
[9,10], (pro)insulin [11] and, more recently, the zinc
transporter 8 (ZnT8) [12]. Most patients with Type 1 diabetes
will have multiple islet cell autoantibodies detectable in their
blood at diagnosis and less than 10% will have only one
detectable antibody when assessed using a combination of islet
cell autoantibody and antibodies to GAD65 (GAD antibodies),
IA-2 (IA-2 antibodies) and insulin [13,14]. The addition of ZnT8
autoantibodies (ZnT8A) may raise this autoimmunity detection
rate to 98% [12].
The prevalence of islet autoantibodies is unknown in MODY.
Several studies suggest that these patients are islet antibody
negative [2,15,16], but there are reports of individual cases with
several islet autoantibodies [1720]. Recently, Schober et al.
reported a pancreatic antibody prevalence of 17% in a registrybased German cohort with MODY, but their study did not use a
standardized approach to defining MODY or antibody testing
[21]. The true prevalence of islet autoantibodies in MODY is
difficult to predict, as the absence of antibodies is often part of the
selection strategy for identifying patients for genetic testing [22
25]. This could potentially lead to an underestimation of the true
prevalence of antibodies in MODY.
The aim of this study was to determine the prevalence of GAD
and IA-2 autoantibodies in a large cohort of patients with a
confirmed genetic diagnosis of HNF1A, HNF4A and GCK
MODY and to establish if islet autoantibodies can be used to
discriminate between Type 1 diabetes and MODY.

Patients and methods

Materials

Serum was prepared by adding 6.4 ll of 1 m calcium chloride

(CaCl2) solution and 10 ll of 400 IU thrombin to 250 ll of
EDTA plasma (stored at 80 C) to initiate clotting [26]. The
supernatant was removed for analysis after 7-min centrifugation
at 6000 g.
GAD and IA-2 antibody analysis was performed using
commercial ELISA assays (RSR Ltd., Cardiff, UK) and a
Dynex DSX automated ELISA system (Launch Diagnostics,
Longfield, UK) [27]. Both methods are highly specific and
sensitive (GAD antibodies 98% and 84% and IA-2 antibodies
99% and 74%, respectively) [28,29]. The laboratory participates
in the Diabetes Autoantibody Standardization Programme.

2011 The Authors.

Diabetic Medicine 2011 Diabetes UK

DIABETICMedicine

Study participants

To establish an antibody titre cut-off for GAD and IA-2

antibodies, we tested 500 routine clinical samples of patients
aged between 18 and 75 years without a clinical history of
diabetes and an HbA1c level of less than 6.0% (42 mmol mol).
Antibody status was investigated in serum from 508 patients
with a confirmed genetic diagnosis of MODY (263 probands
and 245 family members): 227 GCK, 229 HNF1A and 52
HNF4A. All clinical characteristics were taken from genetic test
request forms. The median age for HNF1A 4A MODY was
37 years (interquartile range 2550 years) and duration of
diabetes of 15 years (interquartile range 425 years). The
median age for GCK MODY was 34 years (interquartile range
1847.5 years) and duration of diabetes of 4 years (interquartile
range 212 years). Autoantibodies had been analysed prior to
genetic testing in 95 of 263 probands, with positive results
obtained for two of the 95. In addition, serum from 98 patients
(median age of 15 years; interquartile range 1225 years)
diagnosed with Type 1 diabetes within the past 6 months was
analysed. Fifty samples were from the Barts-Oxford (BOX)
family study and 48 from the Diabetes Autoantibody
Standardization Programme.

Results
GAD and IA-2 autoantibody assay cut-offs

The 99th percentile titre for GAD antibodies in 500 adults

without diabetes was calculated as 64 WHO units ml. The 99th
percentile for IA-2 antibodies was equivalent to the lowest
calibrator (RSR Ltd) at 15 WHO units ml, as no subjects had a
titre greater than the detection limit of the assay. All further
antibody results are considered positive if exceeding the 99th
centile for the assay.

Autoantibody prevalence

GAD and or IA-2 antibodies were present in 80 98 (82%)

patients with Type 1 diabetes and 5 508 (< 1%) patients with
MODY (Fig. 1). In patients with Type 1 diabetes, GAD
antibodies were more commonly detected than IA-2
antibodies, with 37 98 (37.8%) of patients positive for both
GAD and IA-2 antibodies, 24 98 (24.5%) having only GAD
antibodies detected and 19 98 (19.4%) having IA-2 antibodies
only. In the five patients with MODY (< 1%) with detectable
antibodies, all had GAD antibody titres and none had IA-2
antibodies. Sub-analysis in 168 of the 263 probands who had not
had previous antibody testing prior to genetic testing showed that
the antibody positive rate was 0.6%.

Discriminating MODY from Type 1 diabetes

Making no allowance for time of testing, out of the 508 patients

with MODY, 503 were GAD antibody negative, so that a

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DIABETICMedicine

Pancreatic autoantibodies can discriminate MODY from Type 1 diabetes T. J. McDonald et al.

90
IA-2 antibodies only
GAD antibodies only

80

IA-2 and GAD antibodies

Per cent detectable

70

60

50

40

30

20

10

0
Type 1 diabetes

MODY

FIGURE 1 GAD and IA-2 antibody prevalence in Type 1 diabetes and

maturity-onset diabetes of the young (MODY). Samples from 98 patients
with newly diagnosed Type 1 diabetes and 508 patients with MODY (GCK
n = 227, HNF1A n = 229, HNF4A n = 52). Data are presented as per cent
positive for IA-2 antibodies only, GAD antibodies only and positive for both
GAD and IA-2 antibodies.

negative GAD antibody test gave a sensitivity of 99% and

specificity of 62% at discriminating MODY from Type 1
diabetes. A negative IA-2 antibody test alone had a sensitivity
of 100% and a slightly lower specificity of 57%. The best
discrimination is achieved using combined antibody testing, with
one antibody positive result giving a discriminative sensitivity of
99% and a specificity of 82%.
This equates to a positive likelihood ratio for identifying
MODY from Type 1 diabetes of 5.4 for two negative results
and a negative likelihood ratio of 0.01 and < 0.003 for one
and two detectable autoantibodies, respectively. Assuming the
prevalence of MODY is approximately 1% in patients with
diabetes diagnosed before the age of 35 years, this result
would decrease the probability to approximately 1:8200, and
two positive antibodies would decrease it to less than
1:3.1 million.

MODY antibody-positive patients

The prevalence of autoantibodies in the cohort with MODY was

the same as in the control subjects used to define the population
cut-offs. The clinical characteristics of 4 5 mutation carriers with
positive autoantibodies are consistent with a clinical diagnosis of
MODY (Table 1), but the presentation and subsequent clinical
course of patient 5 is consistent with Type 1 diabetes.

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Discussion
We have shown that the prevalence of GAD and or IA-2
antibodies is less than 1% in HNF1A, GCK and HNF4A
MODY, equivalent to the prevalence in control subjects. This
confirms previous studies suggesting that autoantibodies are rare
in monogenic forms of diabetes [1720]. The few isolated case
reports describing a MODY antibody-positive patient do not
reflect an increase in the overall humoral islet autoimmunity in
patients with MODY [2,15,16]. A registry-based German and
Austrian cohort with MODY reported a 17% prevalence of islet
autoantibodies, although this was based on results reported from
a wide variety of laboratories throughout Germany and Austria.
No details were provided on the autoantibody assays used in
their study, including performance or definition and
comparability of thresholds between laboratories. Interestingly,
the positive rate in patients with Type 2 diabetes using the same
testing protocol was surprisingly high at 34% [21]. It is possible
some of the antibody-positive patients had Type 1 diabetes and
not MODY, as a diagnosis of MODY was not confirmed by
genetic testing in 20% of the patients.
The difference in prevalence between MODY and Type 1
diabetes makes antibody tests clinically useful in guiding genetic
testing. The greatest value is to use the presence of
autoantibodies to demonstrate that diagnosis of MODY is
unlikely. We suggest the finding of an elevated GAD antibody
titre should advocate further clinical evaluation before
continuing with testing, but if two antibodies are present
genetic testing should not be performed. In contrast, it is hard to
base genetic testing solely on the basis of two negative
antibodies, as this would only increase the probability of
MODY to 1:19 patients and other clinical characteristics
should be considered in these cases.
The five patients with a positive GAD antibody and a
confirmed genetic diagnosis of MODY may represent the 12%
of the population with detectable islet antibodies with no
associated pathogenesis. Alternatively, it may signify a
concomitant diagnosis of MODY and Type 1 diabetes, such
as that observed in one of the five patients. This highlights the
need to assess islet antibody results in light of both clinical
features and other non-genetic tests, such as serum or urine
C-peptide and HbA1c, when deciding whether to undertake
genetic testing.
There are several limitations to this study. Only the three
common MODY subtypes were investigated and may not reflect
antibody prevalence in other genetic aetiologies. The duration of
diabetes in MODY was relatively long (median 9 years)
compared with the patients with Type 1 diabetes who were
tested within 6 months of diagnosis. When we analysed the 71
patients with MODY (14%), for whom testing occurred within
1 year of diagnosis, there were no patients with GAD or IA-2
antibodies, suggesting that the difference in duration is not a
major reason for the difference in prevalence rates. An advantage
of GAD IA-2 antibodies over traditional islet cell autoantibody
testing is that they remain detectable for many years, with 70% of

2011 The Authors.

Diabetic Medicine 2011 Diabetes UK

 2011 The Authors.

Diabetic Medicine 2011 Diabetes UK

HNF1A
R272H

HNF1A
R203H

HNF1A
H577D

GCK
V182M

GCK
deletion
exons
5 and 6

8.1%

7.9%

6.7%

7.4%

7.2%

> 250

> 250

234

> 250

> 250

GAD
antibodies
(WHO-units ml)

29

14

32

31

Age at
diagnosis
(years)

47

39

Duration
(years)

Insulin

Diet OHA

Insulin

Insulin

Diet

Treatment at
diagnosis

Height 98 cm,
weight 15.9 kg

26.0

25.0

26.9

22.6

BMI

Insulin pump with

novorapid total
daily dose 12 units

Mixed insulin total

daily dose 16 units

Insulin basal bolus

regimen total daily
dose 30 units

Insulin basal bolus

regimen

Repaglinide (0.5 mg)

after every meal

Current treatment

ICA, islet cell autoantibody; N A, not applicable; OGTT, oral glucose tolerance test; OHA, oral hypoglycaemic agent.

Mutation

Patient

HbA1c
(%)

Table 1 Clinical characteristics of MODY antibody-positive patients

At diagnosis

At diagnosis
(1 month off
insulin in
first year)
37 years

At diagnosis
(unwilling to try
sulphonylurea)

NA

Time to insulin

Asymptomatic
detected at
army medical
Acute presentation,
HbA1c 13%, ICA
positive, ketosis

Gestational diabetes
(OGTT 4.6 to
> 11.7 mmol l)
Raised glucose
detected after
urinary tract
infection
Acute presentation,
polyuria, polydipsia,
lethargic

Presentation

Three-generation
family history

Two-generation
family history

Three- generation
family history

Three-generation
family history

Three-generation
family history

Family History

Original article
DIABETICMedicine

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DIABETICMedicine

Pancreatic autoantibodies can discriminate MODY from Type 1 diabetes T. J. McDonald et al.

patients with Type 1 diabetes having GAD and or IA-2

antibodies 11 years after diagnosis [30]. We did not have a
comparison group with a longer duration. Only two antibodies
were analysed and a higher sensitivity and specificity may be
achieved if more antibodies are used. Finally, we cannot exclude
that patients were not referred to the genetic laboratory because
they had been pre-screened for autoantibodies, which would lead
to a falsely low prevalence in our study group. However, as, in the
168 out of 263 probands (64%) who had not had previous
antibody testing, the positive rate was only 0.6%, this suggests
this is not a major cause of bias.
In conclusion, we have shown that the prevalence of GAD
IA-2 autoantibodies is less than 1% in HNF1A, GCK and
HNF4A MODY. Islet autoantibody testing close to diagnosis
gives very good discrimination of Type 1 diabetes from MODY.
This supports routine autoantibody testing before proceeding to
expensive molecular genetic testing.

Competing interests
Nothing to declare.

Acknowledgments

This study was funded by the European Community FP7

program CEED3 (HEALTH-F2-2008-223211) and the Health
Innovation Challenge Fund, a parallel funding partnership
between the Wellcome Trust and the Department of Health
(091985/HICF 1009-041). SE, MS, BS and ATH are supported
by the NIHR Peninsula Clinical Research Facility, University of
Exeter. MS is also supported by an NIHR postdoctoral
fellowship. We would to thank the Barts-Oxford (BOX)
family study and the Diabetes Antibody Standardisation
Program (DASP 2009) for providing type 1 patient samples.
Thanks to Mr Edward Jones and Miss Katherine Carr for their
assistance with the study.

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