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Diabetes Mellitus Type I

(Insulin-Dependent Diabetes Mellitus, IDDM)

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Clinical Manifestations







*most predictive of IDDM; interrupted immunity to Glu decarboxylase prevents IDDM in mice

**theory: early exposure to cow milk may trigger their formation and the development of IDDM

***catalyzes the conversion of pro-insulin to insulin

****great homology with a virus related to congenita IDDM

- CD8 cells are the predominant cells in the islets

- antibodies against CD4 cells prevents IDDM in mice

- interleukin-1: inhibits insulin secretion; cytotoxic in large amounts

- interleukin-6: secereted by beta cells; enhances immune reactions

- interferon alpha: found in the pancreas of patients who die of diabetic ketoacidosis; attracts lymphocytes, induced by viruses, stimulates HLA molecule expression. Insulitis develops in mice who have intereferon alpha in their pancreas, but not in those who do not have it.

- cytokines may trigger the production of nitric oxide by beta cells; since beta cells lack SOD they can not get rid of NO or oxygen radicals, which may be lethal to them

- Viral infection theory: this theory holds that a viral infection triggers the production of antibodies that cross react with natural antigens of the beta cells. Viruses that have been implicated include: Cixsackie B4, CMV, rubella, mumps, hepatitis, EBV, and en encephalomyocarditis virus of mice.

- Environmental insult theory: a viral infection or the expression of a beta-cell superantigen causes the generation of cytokines that induce the expression of adhesion molecules on the pancreatic vascular endothelium. These adhesion molecules bind leukocytes that present antigens from the damaged beta cells to the helper T cells, thereby triggering the autoimmune reaction.

Clinical Manifestations

- the 3 P's: polyuria, polyphagia, polydipsia

- slender body habitus as a rule

- honeymoon period may precede frank diabetes

- weight loss

- may make a debut with diabetic ketoacidosis

- hyperglycemia

- insulinopenia

- positive autoantibody tests


Primary Preventive Therapy

- immunosuppressive therapy at the time of onset in diabetic patients (e.g. cyclosporine, azathioprine, anti-CD5 antibodies, antilymphocyte globulin, prednisone, intravenous immunoglobulin)

- immunosuppressive therapy before onset in high-risk subjects (see below)

- insulin administration (intravenous and/or subcutaneous)

- nicotinamide

- bacille Calmette-Gerin vaccine

- avoid cow's milk

Treatment of Diabetes Mellitus Type1

- insulin

- recommended: intensive therapy (Diabetic Complications Control Trial)

- will prevent or delay the onset and progression of complications

- goals of intensive therapy

- three or more injections of insulin SQ or by implanted pump

- adjustments as necessary for changes in diet, illnesses or predicted exercise

- HgbA1C less than 6.05%

- weekly glucose level at 3am of over 65 mg/dl

- fasting glucose level 70-120 mg/dl

- postpandrial glucose not over 180 mg/dl

- balanced diet

- education

- high surveillance intensity for complications (e.g. diabetic ketoacidosis, retinitis, etc)

- attention by multidisciplinary team including a diabetologist, nurse and nurse educator

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