Autoimmunity destructive

Named after Thomas Addison who first described the clinical condition in the mid 1850s, Addison s disease is one of the commonest endocrinopathies. At one time, most cases of Addison s were due to infection, usually by tuberculosis, of the adrenal cortex but nowadays the likely cause is autoimmune destruction of the tissue, and may be associated with dysfunction of other endocrine glands. 

The etiology of type 1 diabetes is autoimmune destruction of the pancreatic beta cells, which is initiated by an event such as viral infection and progresses to the point of frank symptoms during childhood and the teenage years. 

IDDM is caused by T cell-mediated autoimmune destruction of the insulin-producing P-pancreatic islet cells in genetically predisposed individuals. This is probably due to the expression of a super antigen on the surface of the jS cells in such individuals, although the molecular detail of what extent factors trigger onset of the jS cell destruction remain to be elucidated. IDDM may, however, be controlled by parenteral administration of exogenous insulin preparations, usually by regular s.c. injection. 

The pathogenesis of type I diabetes is autoimmune destruction of the cells of the pancreas. The factor or factors that trigger this autoimmune response are unknown. Predisposing factors appear to include certain major histocompatibility complex haplotypes and autoantibodies to various islet cell antigens. The progression of the autoimmune response is characterized by lymphocytic infiltration and destruction of the pancreatic cells resulting in insulin deficiency. Type I diabetes mellitus constitutes about 10% of cases of diabetes mellitus. 

Corbett, J. A., and McDaniel, M. L. (1992). Does nitric oxide mediate autoimmune destruction of beta-cells Possible therapeutic interventions in IDDM. Diabetes 41, 897-903. 

Hashimoto s thyroiditis Autoimmune destruction of thyroid Present early, absent later Mild to severe... 

Insulin secretory capacity during onset of type 1 diabetes. [Note Rate of autoimmune destruction of P cells may be faster or slower than shown.]... 

Adrenal insufficiency can be associated with hypothyroidism (either by autoimmune destruction or due to hypophyseal disease) and carries the risk of acute Addisonian crisis if thyroid substitution precedes glucocorticoid therapy. The diagnostic problem presented by the fact that a few patients with central hypothyroidism have a moderately increased serum TSH should be kept in mind (62). 

Yoon JW, Jun HS. Autoimmune destruction of pancreatic beta cells. Am J Ther. 2005 12 580-591. 

TGF-/J and IL-10 Systemic delivery via rAAV protects from autoimmune diabetes, and protects transplanted islets from autoimmune destruction Islets Prevention of autoimmune diabetes Goudy et al. (2001) Zhang et al. (2003) Deng et al. (1997)... 

The development of type 1 diabetes is the culmination of a chronic autoimmune destruction of the pancreatic P-cells that occurs over many years. This process results in severe, and ultimately complete, insulin deficiency. In the absence of insulin, fasting hyperglycemia is... 

Diabetes mellitus ( sweet urine ) involves relative over-production of glucose by the liver and under-utilization by other organs. Diabetes is the most serious metabolic disease in terms of its social impact. Obesity and the indulgent Western diet correlates with mature age diabetes. Type 1 diabetes (juvenile diabetes) typically manifests at less than 20 years from autoimmune destruction of the insulin-producing pancreatic (3 cells. Type 1 diabetes is insulin-dependent diabetes mellitus (IDDM) and is fatal without exogenous insulin. Type 2 diabetes mellitus (mature age diabetes) occurs later in life and typically involves both deficient insulin production and insulin resistance , that is, the target cells are less responsive to insulin. Type 2 diabetes is initially non-insulin-dependent diabetes (NIDDM) but insulin therapy (in addition to oral antidiabetics) may eventually be required. Hyperglycaemia due... 

Qll There is both a genetic and environmental component in type 1 diabetes. The pathological basis of the condition is autoimmune destruction of the pancreatic islet cells, which is said to be associated with genetic and environmental factors such as viral infection. It has been shown that antibodies to islet cells and insulin autoantibody (IAA) can exist for years before the occurrence of symptoms, possibly as a result of the autoimmune processes the IAA may form during the process of active islet and /1-cell destruction. Both insulin and glucagon play a role in the development of hyperglycaemia and hyperketonaemia, since both a- and /1-cell functions are abnormal in diabetes. Both a lack of insulin and a relative excess of glucagon coexist in type 1 diabetes, and so the metabolic abnormalities that occur are likely to be caused by both hormones. 

D supplements are less at risk of developing the disease. It is not known how vitamin D protects against the development of diahetes, hut it may he hy modulation of the differentiation of lymphocytes involved in the autoimmune destruction of pancreatic -islet cells. The protective dose is above current reference intakes and indeed may he above the tolerable upper intake of 25 //g per day for infants (Harris, 2002). 

Isolated reports of Candida esophagitis or Pneumocystis proved Pneumocystis carinii) infections in immunocompetent patients and the possible decrease in CD4-I- T cells with or without opportunistic infections in several HIV-infected patients (SED-13,1097) (379) suggest that unexpected immunosuppressive effects of interferon alfa can occur. An autoimmune destruction of CD4 cells in patients with a particular HLA haplotype has been proposed as a possible mechanism (380). One patient also had an acute and fatal acute precipitation of infection with Entamoeba histolytica (SEDA-22, 403). However, the available evidence is still very limited and no firm conclusion can be drawn on a possible association between interferon alfa treatment and a fall in CD4 cell count or an immunosuppressive effect. 

Type 1 diabetes is characterized by a near-absolute insulin deficiency at diagnosis or soon thereafter. The beta cells of the pancreas are no longer able to secrete insulin due to autoimmune destruction. Therefore, people with type 1 diabetes require exogenous administration of insulin for survival. People with type 2 diabetes may require insulin therapy when diet, exercise, and the oral agents are no longer enough to provide adequate glucose control. 

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