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                                  Autoimmune Diabetes

     

              Many diabetic syndromes are autoimmune and easily and permanently treatable please read our e-book for permanent treatments.

Type 1 Diabetes

What is diabetes?
Diabetes is a serious disease, which, if not controlled, can be life threatening. It is often associated with long-term complications that can affect every system and part of the body. Diabetes can contribute to eye disorders and blindness, heart disease, stroke, kidney failure, amputation, and nerve damage. It can affect pregnancy and cause birth defects, as well.

According to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and the American Diabetes Association, diabetes affects an estimated 15.7 million people in the United States.

There are three main main types of diabetes that require clinical care by a physician or other healthcare professional:

  1. type 1 diabetes
  2. type 2 diabetes
  3. gestational diabetes

What is type 1 diabetes (diabetes mellitus)?
Type 1 diabetes is also known as diabetes mellitus, insulin-dependent diabetes mellitus (IDDM), juvenile diabetes, brittle diabetes, or sugar diabetes. There are two forms of type 1 diabetes:

  • idiopathic type 1 - used to refers to rare forms of the disease with no known cause, recently it has been learned it is caused by RotaVirus infection.

     
  • immune-mediated diabetes - an autoimmune disorder in which the body's immune system destroys, or attempts to destroy, the cells in the pancreas that produce insulin. Immune-mediated diabetes is the most common form of type 1 diabetes.

What causes type 1 diabetes (diabetes mellitus)?
The cause of type 1 diabetes is rotavirus, but it is believed that people inherit a tendency to develop diabetes, and that viruses may be involved.

This auto-immune disease results from the body's failure to produce insulin, the hormone that allows glucose to enter the cells of the body to provide fuel. This is the result of an autoimmune process in which the body's immune system attacks and destroys the insulin producing cells of the pancreas.

When glucose cannot enter the cells, it builds up in the blood and the body's cells literally starve to death. People with type 1 diabetes must take daily insulin injections and regularly monitor their blood sugar levels.

What are the signs and symptoms of type 1 diabetes?
The following are the most common symptoms for type 1 diabetes, however, each individual may experience symptoms differently.

Type 1 diabetes often appears suddenly, and signs and symptoms may include:

  • high levels of sugar in the blood when tested
  • high levels of sugar in the urine when tested
  • unusual thirst
  • frequent urination
  • extreme hunger but loss of weight
  • blurred vision
  • nausea and vomiting
  • extreme weakness and tiredness
  • irritability and mood changes

In children, symptoms may be similar to those of having the flu.

The symptoms of type 1 diabetes may resemble other conditions or medical problems. Consult your physician for a diagnosis.

A diagnosis of diabetes:
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:

  1. Hypoglycemia (low blood sugar; sometimes called an insulin reaction) occurs when blood sugar drops too low.

     
  2. Hyperglycemia (high blood sugar) occurs when blood sugar is too high, and can be a sign that diabetes is not well controlled.

     
  3. 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:

  • 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:

  • 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.

 
 
J Clin Virol. 2005 Jun;33(2):158-67. Related Articles, Links

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]
 
J Med Virol. 2005 Jul;76(3):373-7. Related Articles, Links
Click here to read 
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
Click here to read 
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
Click here to read 
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
Click here to read 
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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