Ca a inoe al. Diabe ol Me ab Synd (2020) 12:56
h ps://doi.o g/10.1186/s13098-020-00563-x
RESEARCH
Non-immune-media ed
e susimmune-media ed ype 1 diabe es:
diagnosis andlong- e m di e ences—
e ospec i e analysis
Diana Ca a ino1*†, Diana Sil a1*†, Joana Guioma 1, C is ina Ribei o1, Luísa Ruas1, Luís Ca doso1,2
and Isabel Pai a1
Abs ac
Backg ound: The Ame ican Diabe es Associa ion p oposed wo subca ego ies o ype 1 diabe es melli us: ype 1A
o immune-media ed diabe es (IDM) and ype 1B o idiopa hic diabe es. The absence o β-cell au oimmune ma k-
e s, pe manen insulinopenia and p one o ke oacidosis de ine he second ca ego y, whose pa hogenesis emains
unclea . Only a mino i y o pa ien s all in o his ca ego y, also designa ed non-immune-media ed (NIDM), which is
conside ed by se e al au ho s simila o ype 2 diabe es. The aim o his s udy is o e alua e di e ences a he diagno-
sis and 10 yea s la e o wo ca ego ies.
Me hods: Re ospec i e coho s udy o pa ien s wi h β-cell au oimmune ma ke s pe o med a diagnosis and
unde ec able c-pep ide. We e excluded pa ien s wi h suspicion o ano he speci ic ype o diabe es. We ob ained wo
g oups: IDM (≥ 1 posi i e an ibody) and NIDM (nega i e an ibodies). Age, amily his o y, an h opome y, du a ion o
symp oms, clinical p esen a ion, blood glucose a admission, A1C, lipid p o ile, a e ial hype ension, o al dia y insu-
lin dose (TDID), mic o ascula and mac o ascula complica ions we e e alua ed. Resul s we e conside ed s a is ically
signi ican wi h p < 0.05.
Resul s: 37 pa ien s, 29 wi h IDM and 8 pa ien s wi h NIDM. The age o diagnosis o IDM g oup (23 yea s) was
signi ican ly di e en (p = 0.004) om he NIDM g oup (38.1). The body mass index (BMI) a he diagnosis did no
di e signi ican ly (p = 0.435). The du a ion o symp oms was longe in he NIDM (p = 0.003). The disease p esen a-
ion (p = 0.744), blood glucose (p = 0.482) and HbA1c (p = 0.794) a admission and TDID a discha ge (p = 0.301) did
no di e signi ican ly. To al and LDL choles e ol le els we e highe in NIDM g oup bu did no di e signi ican ly
(p = 0.585 and p = 0.579, espec i ely). A e 10 yea s BMI did no di e be ween g oups (p = 0.079). Pa ien s wi h IDM
showed a signi ican ly highe HbA1c (p = 0.008) and TDID (p = 0.017). Rela i e o he lipid p o ile, he e was no signi i-
can di e ence, howe e he LDL choles e ol and iglyce ides we e highe on he NIDM g oup, as he pe cen age o
hype ension. Mic o ascula complica ions we e highe in he IDM g oup, bu no signi ican di e ence was ound.
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Open Access
Diabe ology &
Me abolic Synd ome
*Co espondence: [email p o ec ed]; diana [email p o ec ed]
†Diana Ca a ino and Diana Sil a con ibu ed equally o his wo k
1 Endoc inology, Diabe es and Me abolism Depa men , Cen o
Hospi ala e Uni e si á io de Coimb a EPE, P ace a P o . Mo a Pin o,
3000-075 Coimb a, Po ugal
Full lis o au ho in o ma ion is a ailable a he end o he a icle
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Ca a inoe al. Diabe ol Me ab Synd (2020) 12:56
Backg ound
In 1997, he Ame ican Diabe es Associa ion p oposed
wo subca ego ies o ype 1 diabe es melli us: ype 1A
o immune-media ed diabe es and ype 1B o idiopa hic
diabe es [1, 2].
The immune-media ed diabe es (IDM) esul s om a
cellula au oimmune des uc ion o he β-cells o he pan-
c eas, media ed by T-cells [3, 4]. Ma ke s o he immune
des uc ion o he β-cell include isle cell au oan ibodies,
insulin au oan ibodies, GAD (GAD65) au oan ibodies
and y osine phospha ase (IA2) au oan ibodies. The e is
li le o no insulin sec e ion, mani es ed by low o unde-
ec able le els o plasma C-pep ide [4], and exogenous
insulin is necessa y o p ese e li e. Insulin esis ance
does no play a majo ole in i s pa hogenesis [3]. The
disease has s ong HLA (human leukocy e an igen) hap-
lo ypes associa ions, wi h linkage o he DQA and DQB
genes. The IDM commonly occu s in childhood and
adolescence, bu i can occu a any age and pa ien s a e
a ely obese a he diagnosis [4].
The idiopa hic diabe es is cha ac e ized by absence o
β-cell au oimmune ma ke s, wi h pe manen insulinope-
nia and p one o ke oacidosis [1, 2, 4]. The au ho s o his
pape e oked his ype o diabe es by non-immune-medi-
a ed diabe es melli us (NIDM).
Only a mino i y o pa ien s wi h ype 1 diabe es mel-
li us all in o his subca ego y, howe e i is being ecog-
nized as an impo an clinical en i y [5].
NIDM has been mos ly desc ibed in A ican-Ame -
ican and Asian pa ien s, e en hough i has also been
desc ibed in na i e Ame icans and in Eu opean Medi e -
anean indi iduals [1–3].
Al hough pa ien s wi h NIDM ha e gene ally an onse
simila o ha o pa ien s wi h IDM, some di e ences a e
equen ly ound.
NIDM is cha ac e ized by acu e onse o se e e hype -
glycemia wi h ke oacidosis, equi ing hospi al admis-
sion and ea men wi h insulin and luid and elec oly e
eplacemen [5]. Insulin he apy is gene ally necessa y
o a pe iod going om 6 o 18mon hs, wi h subsequen
good con ol o disease jus wi h o al agen s and die [2].
Recu en ke oacidosis is unusual [5].
NIDM shows a di e en pheno ype, a e mo e o en
male, middle aged, o e weigh , o modes ly obese (obe-
si y class I). They ha e a amily his o y o ype 2 diabe-
es [2, 3, 5, 6]. Due o he p esence o some me abolic
ea u es o ype 2 diabe es, he NIDM has also been
e e ed in he li e a u e as a ypical diabe es, ype 1.5 dia-
be es, Fla bush diabe es and ke osis-p one diabe es [5,
7–9].
I s pa hogenesis is unknown, and he in o ma ion abou
his is sca e, bu is likely ela ed o insulin esis ance and
ansien β-cell dys unc ion, pe haps due o gluco oxic-
i y and lipo oxici y mechanisms [2, 3, 10]. HLA- ela ed
genes a e no belie ed o be in ol ed in i s pa hogenesis,
e en hough mu a ions in di e en genes om HLA ha e
been epo ed, sugges ing ha NIDM may ha e a speci ic
gene ic backg ound.
Recen ly, a he Classi ica ion o diabe es melli us 2019
o he Wo ld Heal h O ganiza ion, he NIDM was eclas-
si ied as ke osis-p one ype 2 diabe es [11].
Me hods
This s udy was app o ed by he local e hics e iew boa ds
(Coimb a Hospi al and Uni e si y Cen e ). All Pa ien s
signed an in o med consen o he scien i ic use o hei
da a.
Re ospec i e coho s udy, om Janua y 2003 o
Decembe 2008, based on clinical eco ds o pa ien s
wi h low C-pep ide (< 0.5ng/mL) and in which diabe-
es melli us- ela ed au oimmune ma ke s (an i GAD-65,
an i-isle s, an i-insulin, an i IA2) we e measu ed. Only
pa ien s whose assays we e pe o med a he ime o
diagnosis o diabe es melli us we e conside ed o ensu e
he inclusion o pa ien s wi h ype 1 DM. O hese, we
ob ained wo g oups: one wi h posi i e au oimmuni y—
IDM g oup (≥ 1 posi i e an ibody) and ano he wi h neg-
a i e au oimmuni y—NIDM g oup. Di e ences be ween
g oups a diagnosis we e e alua ed wi h ega d o age
o diagnosis, amily his o y, an h opome y, du a ion o
symp oms, clinical p esen a ion o disease, plasma glu-
cose a hospi al admission, HbA1c, lipid p o ile, a e ial
hype ension and o al daily insulin dose (TDID).
The au ho s also analyzed di e ences be ween he
g oups a long e m ollow-up- en yea s—wi h ega d
o an h opome y, HbA1c, lipid p o ile, a e ial hype -
ension, TDID, mic o ascula and mac o ascula
complica ions.
C-pep ide measu emen was pe o med a e co ec-
ion o ke osis o ke oacidosis and s abiliza ion o plasma
glucose le els. The lipid p o ile was ob ained in he i s
medical e alua ion a e discha ge.
Conclusion: Pa ien s wi h IDM had a poo me abolic con ol and highe insulin equi emen . Pa ien s wi h NIDM
we e olde and showed highe ca dio ascula isk, esembling a clinical pheno ype o ype 2 diabe es.
Keywo ds: Non-immune-media ed diabe es melli us, Immune-media ed diabe es melli us, Dyslipidemia, To al daily
insulin dose, Mic o ascula complica ions, mac o ascula complica ions
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Ca a inoe al. Diabe ol Me ab Synd (2020) 12:56
In his s udy, all pa ien s included we e ea ed wi h
con en ional basal-bolus he apy.
All pa ien s we e Caucasian.
Ca ego ical a iables a e p esen ed as equencies and
pe cen ages, and con inuous a iables as means and
s anda d de ia ions, o medians and in e qua ile anges
o a iables wi h skewed dis ibu ions. No mal dis i-
bu ion was checked using skewness and ku osis. All
epo ed p alues a e wo- ailed, wi h a p alue o 0.05
indica ing s a is ical signi icance.
The di e ences be ween g oups we e de ec ed by he
S uden ’s es o con inuous a iables wi h no mal dis-
ibu ion, by he Mann–Whi ney es and Wilcoxon es
o con inuous a iables wi hou no mal dis ibu ion and
by he χ2 es o ca ego ical a iables.
Analyses we e pe o med wi h he use o SPSS .25.
Resul s
Di e ences a diagnosis
A diagnosis, 29 pa ien s (78.4%) had posi i e au oim-
mune ma ke s and 8 had nega i e au oimmune ma k-
e s. In he g oup wi h posi i e au oimmuni y,15 pa ien s
we e emale (48.3%), while in he g oup wi h nega i e
au oimmuni y hey we e all male.
In he IDM g oup, he median age o pa ien s a diag-
nosis was 23.0 (9) yea s, and in he NIDM g oup he
mean age a diagnosis was 38.1 ± 12.8yea s, wi h a s a is-
ically signi ican di e ence (p = 0.004).
BMI a diagnosis did no di e signi ican ly (p = 0.435)
be ween he wo g oups (20.97kg/m2 in IDM s 20.37kg/
m2 in NIDM). The e was no s a is ically signi ican asso-
cia ion be ween g oups and amily his o y o ype 1 DM
(p = 0.999) o ype 2 DM (p = 0.999).
Symp oms du a ion in bo h pa ien g oups was s a-
is ically di e en (p = 0.003), wi h a du a ion o
21.8 ± 8.8days in he IDM g oup s 45.0 (60) days in he
NIDM g oup, bu he e was no s a is ically signi ican
associa ion be ween he g oups and he clinical p esen a-
ion o he disease (p = 0.744).
Plasma glucose a hospi al admission was no s a-
is ically di e en (25.47mmol/L in he IDM g oup s
23.92 mmol/L in he NIDM g oup) (p = 0.482), such
as HbA1c a diagnosis (11.3% s 11.8%, espec i ely)
(p = 0.794).
Wi h ega d o lipid p o ile, o al-choles e ol, LDL-C,
HDL-C and iglyce ides le els, hey did no di e sig-
ni ican ly be ween he wo g oups (p = 0.585, p = 0.579,
p = 0.833 and p = 0.555, espec i ely), al hough o al-
choles e ol and LDL-C le els we e highe in he NIDM
g oup. The pe cen age o pa ien s wi h dyslipidemia was
highe in he NIDM g oup (25% s 24.1%), howe e he
di e ence was no s a is ically signi ican (p = 0.999).
Wi h ega d o a e ialhype ension, he e was no signi -
ican di e ence be ween he g oups (p = 0.999).
The TDID a discha ge was no s a is ically di e en
(46.4 uni s s. 40.1 uni s) (p = 0.301) (Table1).
Di e ences a 10yea s o  ollow‑up
A en yea s e alua ion, BMI was no s a is ically di e -
en (p = 0.079) be ween he wo g oups (25.14kg/m2 in
IDM g oup s 22.58kg/m2 in NIDM).
Rela i e o HbA1c he e was s a is ically signi ican
di e ence be ween he g oups (p = 0.008), wi h 8.7% o
IDM g oup and 7.4% o NIDM g oup.
The insulin equi emen was also s a is ically di e -
en . The TDID o he IDM g oup was 52.35 uni s and he
NIDM g oup was 33.5 uni s (p = 0.017).
The pe cen age o pa ien s wi h dyslipidemia was
highe in he NIDM g oup (62.5% s 44.8%), howe e he
di e ence was no s a is ically signi ican (p = 0.999).
Wi h ega d o lipid p o ile, o al-choles e ol, LDL-C,
HDL-C and iglyce ides le els he e was no s a is ically
signi ican di e ence be ween he wo g oups (p = 0.728,
p = 0.571, p = 0.338, p = 0.648, espec i ely), howe e he
LDL-C and iglyce ides le els we e highe in he NIDM
g oup.
The pe cen age o pa ien s wi h hype ension was
highe in he NIDM g oup (25% s 17.2%), al hough
he e was no signi ican di e ence be ween he g oups
(p = 0.999).
Wi h ega d o mic o ascula complica ions, he e was
no s a is ically signi ican di e ence a he pe cen age o
e inopa hy, neu opa hy and neph opa hy be ween he
wo g oups (p = 0.550, p = 0.550, p = 0.550, espec i ely)
bu he pe cen age was highe in he IDM g oup. A
10yea s ollow-up, he NIDM g oup had no mic o as-
cula complica ions.
The e was no signi ican di e ence on he mac o ascu-
la disease oo (Table2).
Discussion andconclusions
Ou s udy sugges s ha he NIDM may be de ec ed
among subjec s o Caucasian e hnici y and in spi e o ini-
ial clinical p esen a ion compa ible wi h IDM, hey di e
a diagnosis in e ms o au oimmune ma ke s, sex, age o
pa ien s and symp oms du a ion.
All pa ien s in he NIDM g oup included in ou s udy
we e men, epo ing a male p edominance consis en
wi h o he s udies [1–3, 12] So a , he cause o his male
p edominance is unknown, howe e i is hough ha
ho monal ac o s may be in ol ed.
In he IDM g oup, he median age o pa ien s a diag-
nosis was highe , in ag eemen wi h o he s udies [1, 7,
13].
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Ca a inoe al. Diabe ol Me ab Synd (2020) 12:56
Symp oms du a ion in bo h pa ien g oups was s a-
is ically di e en , wi h a longe du a ion in he NIDM
g oup, unlike o he s udies, in which he e we e no di e -
ences be ween he wo g oups [1].
BMI a diagnosis did no di e signi ican ly be ween
he wo g oups. In mos p e ious s udies, pa ien s in he
NIDM g oup ha e a highe BMI wi h isce al obesi y,
esembling pa ien s wi h ype 2 diabe es [1, 2].
The e was no s a is ically signi ican associa ion in he
clinical p esen a ion o he disease, as in p e ious s ud-
ies [3, 7, 12], making some imes di icul o di e en ia e i
wi h he IDM g oup.
HbA1c a diagnosis and he TDID a discha ge we e
no s a is ically di e en be ween he wo g oups, which
is in ag eemen wi h o he wo ks [1, 2]. To al-choles-
e ol and LDL-C le els we e highe in he NIDM g oup,
as p e iously epo ed in o he s udies, whe e pa ien s
om his g oup ha e a mo e a he ogenic lipid p o ile, as
pa ien s wi h ype 2 diabe es [2].
A a long- e m e alua ion, ou s udy shows ha
pa ien s wi h IDM had a poo me abolic con ol, wi h
highe HbA1c and highe insulin equi emen , consis -
en wi h p e ious s udies [2]. On he o he hand, in he
NIDM g oup he e was a highe HbA1c educ ion wi h
lowe insulin equi emen .
In ac , o he s udies epo ed a se e e insulin sec e o y
de iciency only du ing he acu e ke o ic phase in pa ien s
wi h NIDM wi h a clinical emission phase co ela ed o
an insulin sec e ion eco e y [2].
Pa ien s wi h NIDM showed a lowe  endency o
mic o ascula complica ions, like ype 2 diabe es. Mic o-
ascula complica ions we e mo e equen in he IDM
g oup.
Pa ien s wi h NIDM showed, as a he diagnosis, a ypi-
cal a he ogenic lipid p o ile, cha ac e ized a 10yea s by
high LDL-choles e ol and iglyce ides le els. This g oup
also showed a highe p opo ion o a e ialhype ension
pa ien s. So, he au ho s concluded ha NIDM is associ-
a ed wi h highe ca dio ascula isk han IDM since he
diagnosis.
The e a e some limi a ions o his s udy, ha should be
men ioned, such as he sample size ha was condi ioned
by he e ospec i e na u e o he s udy. The au ho s we e
limi ed o pa ien s whose assays we e made a diagnosis
o a oid misdiagnosis.
In conclusion, ecogni ion o he NIDM ca ego y is
c i ical in clinical p ac ice because i may modi y he
he apeu ic app oach o hese pa ien s, in he mid and
long e m. This en i y was ini ially diagnosed in Asian
and A ican Ame ican popula ions, howe e , indi iduals
om o he e hnic g oups, namely Caucasian, ha e been
Table 1 Clinical andme abolic pa ame e s inpa ien s wi hIDM andNIDM a diagnosis
SD: s anda d de ia ion; IQR: in e qua ile ange
p* < 0.05: s a is ically signi ican di e ence
P esen a ion o he disease: diabe ic ke oacidosis; hype glycemic hype osmola synd ome; polyu ic polydipsic synd ome; diabe ic ke oacidosis wi h hype osmola i y;
seizu es
IDM g oup
(n = 29; 78.4%)
Mean ± SD
Median (IQR)
NIDM g oup
(n = 8; 21.6%)
Mean ± SD
Median (IQR)
p alue
Clinical pa ame e s
Age (yea s) 23.0 (9) 38.1 ± 12.8 0.004*
BMI (Kg/m2) 20.97 (3.5) 20.37 ± 2.7 0.435
Family his o y ype 1/2 DM (%) 17.2/37.9 12.5/37.5 0.999
Symp oms du a ion (days) 21.8 ± 8.8 45.0 (60) 0.003*
P esen a ion o he disease 0.744
A e ial hype ension (%) 6.9 0 0.999
Me abolic pa ame e s
Plasma glucose a admission (mmol/L) 25.47 (8.16) 23.92 (8.66) 0.482
HbA1c (%) 11.3 ± 2.2 11.8 (2.5) 0.794
TDID (U) 46.4 ± 15.3 40.1 ± 12.3 0.301
Dyslipidemia (%) 24.1 25.0 0.999
To al-C (mmol/L) 8.77 (2.61) 9.05 (2.72) 0.585
LDL-C (mmol/L) 5.57 ± 1.44 5.90 ± 1.47 0.579
HDL-C (mmol/L) 2.75 ± 0.83 2.80 (0.50) 0.833
T iglyce ides (mmol/L) 4.73 (1.37) 3.72 (2.05) 0.555
Page 5 o 6
Ca a inoe al. Diabe ol Me ab Synd (2020) 12:56
inc easingly iden i ied. The ini ial clinical p esen a ion
is simila o he IDM g oup, equi ing in ensi e ini ial
insulin he apy and luid and elec oly e eplacemen .
Howe e , behind he gluco oxici y and lipo oxici y phase,
he e is unc ional eco e y o he β cell a e se e al
weeks, which allows in mos pa ien s an app oach wi h
die alone o die plus o al medica ions.
The pa hophysiological mechanisms leading o he
acu e onse o se e e hype glycemia, wi h o wi h-
ou ke osis and ke oacidosis in suscep ible pa ien s a e
unknown; hence u he in es iga ion in his a ea is
needed.
The ecogni ion o NIDM pa ien s is also c ucial
because hey a e exposed o a highe ca dio ascula
isk needing adequa ed ea men o educe he long-
e mca dio ascula complica ions.
Abb e ia ions
DM: Diabe es melli us; NIDM: Non-immune-media ed diabe es melli us;
IDM: Immune-media ed diabe es melli us; TDID: To al daily insulin dose; HLA:
Human leukocy e an igen; GAD: Glu amic acid deca boxylase.
Acknowledgemen s
No applicable.
Au ho s’ con ibu ions
DC and DS has p oduced he epo and li e a u e e iew. CR, JG and LR
assis ed in he p oduc ion o he a icle and he li e a u e e iew. IP and LC
o e saw he c ea ion o he manusc ip . All au ho s ead and app o ed he
inal manusc ip .
Funding
This esea ch did no ecei e any speci ic g an om unding agencies in he
public, comme cial, o no - o -p o i sec o s.
A ailabili y o da a and ma e ials
All da a gene a ed o analysed du ing his s udy a e included in his published
a icle.
E hics app o al and consen o pa icipa e
This s udy was app o ed by he local e hics e iew boa ds (Coimb a Hospi al
and Uni e si y) and all pa icipan s signed he consen o use hei da a o
scien i ic pu pose.
Consen o publica ion
I was ob ained om all he pa icipan s included.
Compe ing in e es s
The au ho s decla e ha hey ha e no compe ing in e es s.
Au ho de ails
1 Endoc inology, Diabe es and Me abolism Depa men , Cen o Hospi ala
e Uni e si á io de Coimb a EPE, P ace a P o . Mo a Pin o, 3000-075 Coimb a,
Po ugal. 2 Medicine Facul y o Coimb a Uni e si y, Coimb a, Po ugal.
Recei ed: 30 Janua y 2020 Accep ed: 25 June 2020
Re e ences
1. Aguile a E, Casami jana R, E cilla G, e al. Adul -onse a ypical ( ype 1)
diabe es: addi ional insigh s and di e ences wi h ype 1A diabe es in a
Eu opean Medi e anean popula ion. Diabe es Ca e. 2004;27:1108–14.
2. Gua no a V, Vigne i E, Pilli e i G, e al. Highe ca diome abolic isk in
idiopa hic e sus au oimmune ype 1 diabe es: a e ospec i e analysis.
Diabe ol Me ab Synd . 2018;10:40.
3. Piñe o-Piloña A, A ilés-San a L, Lin onjua P, e al. Idiopa hic ype 1 diabe-
es in Dallas, Texas. Diabe es Ca e. 2001;24:1014–8.
Table 2 Clinical and me abolic pa ame e s in pa ien s
wi hIDM andNIDM a 10yea s o  ollow-up
SD: s anda d de ia ion; IQR: in e qua ile ange; NA: no applicable
p* < 0.05: s a is ically signi ican di e ence
We ound a educ ion in HbA1C a 10yea s o ollow-up in bo h g oups
[2.4 ± 2.6% in he IDM g oup; 3.9 (4.0) % in he NIDM g oup]. The HbA1C
educ ion was highe in he NIDM g oup, al hough i did no di e signi ican ly
(p = 0.109). Wi h ega d o he a ia ion o he TDID, he IDM g oup had a highe
need o insulin a 10yea s compa ed o he diagnosis (52.4 ± 16.7U a 10yea s
e sus 46.4 ± 15.3U a diagnosis), unlike he NIDM g oup [33, 5 (12) U a 10yea s
e sus 40.1 ± 12.3 U a diagnosis] (Table3)
IDM g oup
(n = 29; 78.4%)
Mean ± SD
Median (IQR)
NIDM g oup
(n = 8; 21.6%)
Mean ± SD
Median (IQR)
p alue
Clinical pa ame e s
BMI (Kg/m2) 25.1 (4.2) 22.6 ± 3.5 0.079
A e ial hype ension (%) 17.2 25.0 0.999
Me abolic pa ame e s
HbA1c (%) 8.7 (1.7) 7.4 (1.0) 0.008*
TDID (U) 52.4 ± 16.7 33.5 (12) 0.017*
Dyslipidemia (%) 44.8 62.5 0.999
To al-C (mmol/L) 185.7 ± 43.2 184 (112) 0.728
LDL-C (mmol/L) 108.5(51) 112 (89) 0.571
HDL-C (mmol/L) 58.1 ± 13.7 58.4 ± 13.0 0.338
T iglyce ides (mmol/L) 79(51) 83 (169) 0.648
Long e m complica ions
Mic o ascula complica-
ions
Re inopa hy 13.8 0 0.550
Neu opa hy 10.3 0 0.550
Neph opa hy 10.3 0 0.550
Mac o ascula complica-
ions
Co ona y disease 0 12.5 0.250
Ce eb o ascula disease 3.4 0 0.999
Pe iphe al a e ial
disease 0 0 NA
Table 3 O e - ime a ia ion o  HbA1c be ween IDM
andNIDM g oups
SD: s anda d de ia ion; IQR: in e qua ile ange
p* < 0.05: s a is ically signi ican di e ence
IDM g oup
(n = 29; 78.4%)
Mean ± SD
Median (IQR)
NIDM g oup
(n = 8; 21.6%)
Mean ± SD
Median (IQR)
p
HbA1c (%) 2.4 ± 2.6 3.9 ± 4.0 0.109

Page 6 o 6
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melli us. Diabe es Ca e. 2012;35:S64–71.
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