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Type 1 Diabetes
What is diabetes?
A diagnosis of diabetes:
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A diagnosis of diabetes is made when any three of these
tests is positive, followed by a second positive test on
a different day:
- Fasting plasma glucose of greater than or equal
to 126 mg/dl with symptoms of diabetes.
- Casual plasma glucose (taken at any time of the
day) of greater than or equal to 200 mg/dl with the
symptoms of diabetes.
- Oral glucose tolerance test (OGTT) value of
greater than or equal to 200 mg/dl measured at a
two-hour interval. The OGTT is given over a
three-hour timespan.
What complications may be associated with type 1
diabetes?
Type 1 diabetes can cause different problems, but there
are three key complications:
- Hypoglycemia (low blood sugar; sometimes
called an insulin reaction) occurs when blood sugar
drops too low.
- Hyperglycemia (high blood sugar) occurs
when blood sugar is too high, and can be a sign that
diabetes is not well controlled.
- Ketoacidosis (diabetic coma) is loss of
consciousness due to untreated or under-treated
diabetes.
Treatment for type 1 diabetes:
Specific treatment will be determined by your
physician(s) based on:
First get rid of the virus see the hydrogen peroxide or
electronic section for a guide on how to do that at home.
- your age, overall health, and medical history
- extent of the disease
- your tolerance for specific medications,
procedures, or therapies
- expectations for the course of the disease
- your opinion or preference
People with type 1 diabetes must have daily
injections of insulin to keep the blood sugar level
within normal ranges. Other parts of the treatment
protocol may include:
Foods like cloves
and cinnamon
stimulate the production of Insulin. Use these twice a day.
- appropriate foods to manage blood sugar level.
- exercise to lower and help the body use blood
sugar.
- regular blood testing for blood-sugar levels.
- regular urine testing for ketone levels.
We consider diabetes a autoimmune disease. Caused by
antibodies against the insulin producing beta
islet cells.
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J Clin Virol. 2005 Jun;33(2):158-67. |
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Simultaneous type 1 diabetes onset in
mother and son coincident with an enteroviral infection.
Maria H, Elshebani A, Anders O, Torsten T, Gun F.
Microbiology and Tumor Biology Center, Karolinska
Institutet, Stockholm, Sweden.
Enterovirus (EV) infections have been implicated in the
development of type 1 diabetes. (T1D). They may cause
beta-cell destruction either by cytolytic infection of
the cells or indirectly by triggering the autoimmune
response. Virus was isolated from a woman at diagnosis
of T1D (Tuvemo 1) and in addition, virus was isolated
from her son at diagnosis of T1D at the same day (Tuvemo
2). None of the isolates could initially be serotyped by
conventional methods. The Tuvemo 1 virus was genotyped
and after sub-cultivation it was also serotyped as
Coxsackievirus B5. The mother revealed antibodies
against GAD65. The boy and the father both revealed a
significant increase in neutralization antibody titre
against two strains of CBV-4, clearly indicating a
recent or ongoing EV infection. In addition, the brother
showed such a titre rise against another CBV-4 strain
(E2) and against a CBV-5 strain (4429). These results
show that the whole family had a proven EV infection at
the time of T1D diagnosis of the mother and the
10-years-old boy, indicating that the infection might
cause or accelerate the T1D.
PMID: 15911432 [PubMed - in process]
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Med Virol. 2005 Jul;76(3):373-7. |
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Islet cell related antibodies and
type 1 diabetes associated with echovirus 30 epidemic: A
case report.
Cabrera-Rode E, Sarmiento L, Molina G, Perez C,
Arranz C, Galvan JA, Prieto M, Barrios J, Palomera R,
Fonseca M, Mas P, Diaz-Diaz O, Diaz-Horta O.
Department of Immunology of Diabetes, National Institute
of Endocrinology, Havana, Cuba.
Type 1 diabetes associated genes account for less than
50% of disease susceptibility. Human enteroviruses have
been implicated as environmental factors that might
trigger and/or accelerate this autoimmune disorder. We
now report of a 12-year-old girl that developed
pancreatic autoimmunity and type 1 diabetes after
enteroviral infection. Diabetes-associated autoimmunity
was evaluated by measurement of several islet cell
related autoantibodies. Neutralizing antibodies to
different enteroviruses were determined in the case and
eight children suffering from aseptic meningitis during
a large scale epidemic. Several types of
diabetes-associated antibodies were detected
post-infection in the adolescent with newly diagnosed
type 1 diabetes, including islet cell antibodies (ICA)
and tyrosine phosphatase antibodies (IA2A). ICA but not
IA2A appeared in the non-diabetic enterovirus-infected
subjects. Based on virological studies, type 1 diabetes
pathogenesis process could have been triggered by
echovirus 30 infections. This study provides the first
evidence of an association between echovirus 30
infection with the presence of pancreatic autoimmunity
and type 1 diabetes. Our data suggest that echovirus 30
Cuban strain could be considered a potentially
diabetogenic enteroviral variant. J. Med. Virol.
76:373-377, 2005. (c) 2005 Wiley-Liss, Inc.
PMID: 15902705 [PubMed - in process]
Studies on diabetic polyneuropathy patients with IVIg
Muscle Nerve. 2003 Apr;27(4):465-70.
Related Articles, Links
Chronic inflammatory demyelinating polyradiculoneuropathy in
diabetic patients.
Haq RU, Pendlebury WW, Fries TJ, Tandan R.
Department of Neurology, C 225 Given Building, University of Vermont
College of Medicine, Burlington 05405, USA.
This retrospective analysis was undertaken to determine whether a
subset of diabetic patients with demyelinating polyneuropathy were
similar to patients with chronic inflammatory demyelinating
polyradiculoneuropathy (CIDP). Ten patients meeting the clinical
criteria for idiopathic CIDP were compared to nine patients with
diabetes and demyelinating polyneuropathy. The diabetic patients
with demyelinating polyneuropathy displayed clinical,
electrophysiologic, and histologic features that were similar to
those in CIDP patients. All six patients with diabetes and
demyelinating polyneuropathy who were treated with immunomodulatory
therapy showed a favorable response. Our study highlights the
importance of investigating diabetic patients with polyneuropathy in
an attempt to identify patients with demyelinating polyneuropathy,
because of the likelihood of benefit in these patients from
immunomodulatory treatment.
PMID: 12661048 [PubMed - indexed for MEDLINE]
J Neurol. 2002 Jun;249(6):719-22.
Related Articles, Links
Intravenous immunoglobulin as first treatment in diabetics with
concomitant distal symmetric axonal polyneuropathy and CIDP.
Cocito D, Ciaramitaro P, Isoardo G, Barbero P, Migliaretti G,
Pipieri A, Proto G, Quadri R, Bergamasco B, Durelli L.
U. O. A. D. U. Neurologia I, Dipartimento di Neuroscienze,
Universita di Torino, Via Cherasco 15, 10126 Turin, Italy.
dariococito@yahoo.it
The authors investigated the impact of IVIg as first line treatment
of diabetic patients suffering from chronic inflammatory
demyelinating polyneuropathy (CIDP) concomitant with distal
symmetric axonal polyneuropathy. Nine patients with these clinical
and electrophysiological features were treated with IVIg (0.4
g/Kg/day for 5 days). Clinical and electrophysiological evaluations
were performed before and after treatment. Following IVIg treatment
there was no significant improvement in clinical deficit. However,
there was a significant and persistent decrease in the Rankin scale
score and an improvement in the demyelinating feature on nerve
conduction studies. Our findings suggest that IVIg had small but
detectable beneficial effects on diabetic patients with CIDP and a
high degree of axonal damage.
PMID: 12111305 [PubMed - indexed for MEDLINE]
World J Gastroenterol. 2005 May 21;11(19):2900-5.
Related Articles, Links
Six-year follow-up of pancreatic beta cell function in adults
with latent autoimmune diabetes.
Yang L, Zhou ZG, Huang G, Ouyang LL, Li X, Yan X.
Institute of Metabolism and Endocrinology, the Second Xiangya
Hospital, Central South University, Changsha 410011, Hunan Province,
China. zhouzg@hotmail.com.
AIM: To investigate the characteristics of the progression of islet
beta cell function in Chinese latent autoimmune diabetes in adult (LADA)
patients with glutamic acid decarboxylase antibody (GAD-Ab)
positivity, and to explore the prognostic factors for beta cell
function. METHODS: Forty-five LADA patients with GAD-Ab positivity
screened from phenotypic type 2 diabetic (T2DM) patients and 45 T2DM
patients without GAD-Ab matched as controls were followed-up every 6
mo. Sixteen patients in LADA1 and T2DM1 groups respectively have
been followed-up for 6 years, while 29 patients in LADA2 and T2DM2
groups respectively for only 1.5 years. GAD-Ab was determined by
radioligand assay, and C-peptides (CP) by radioimmune assay.
RESULTS: The percentage of patients whose fasting CP (FCP) decreased
more than 50% compared with the baseline reached to 25.0% at 1.5(th)
year in LADA1 group, and FCP level decreased (395.8+/-71.5 vs
572.8+/-72.3 pmol/L, P<0.05) at 2.5(th) year and continuously went
down to the end of follow-up. No significant changes of the above
parameters were found in T2DM1 group. The average decreased
percentages of FCP per year in LADA and T2DM patients were 15.8%
(4.0-91.0%) and 5.2% (-3.5 to 35.5%, P = 0.000) respectively. The
index of GAD-Ab was negatively correlated with the FCP in LADA
patients (r(s) = -0.483, P = 0.000). The decreased percentage of FCP
per year in LADA patients were correlated with GAD-Ab index, body
mass index (BMI) and age at onset (r(s) = 0.408, -0.301 and -0.523
respectively, P<0.05). Moreover, GAD-Ab was the only risk factor for
predicting beta cell failure in LADA patients (B = 1.455, EXP (B) =
4.283, P = 0.023). CONCLUSION: The decreasing rate of islet beta
cell function in LADA, being highly heterogeneous, is three times
that of T2DM patients. The titer of GAD-Ab is an important predictor
for the progression of islet beta cell function, and age at onset
and BMI could also act as the predictors.
PMID: 15902725 [PubMed - in process]
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