Insulindependent Diabetes Mellitus

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A disease afflicting 0.2% of the population, insulin-dependent diabetes mellitus (IDDM) is caused by an autoimmune attack on the pancreas. The attack is directed against specialized insulin-producing cells (beta cells) that are located in spherical clusters, called the islets of Langerhans, scattered throughout the pancreas. The autoimmune attack destroys beta cells, resulting in decreased production of insulin and consequently increased levels of blood glucose. Several factors are important in the destruction of beta cells. First, activated CTLs migrate into an islet and begin to attack the insulin-producing cells. Local cytokine production during this

Goodpasture Renal Biopsy Fluorescence

FIGURE 20-2

Fluorescent anti-IgG staining of a kidney biopsy from a patient with Goodpasture's syndrome reveals linear deposits of auto-antibody along the basement membrane. [From Web Path, courtesy of E. C. Klatt, UJniversity of Utah.]

FIGURE 20-2

Fluorescent anti-IgG staining of a kidney biopsy from a patient with Goodpasture's syndrome reveals linear deposits of auto-antibody along the basement membrane. [From Web Path, courtesy of E. C. Klatt, UJniversity of Utah.]

Goodpastures

FIGURE 20-3

Photomicrographs of an islet of Langerhans (a) in pancreas from a normal mouse and (b) one in pancreas from a mouse with a disease resembling insulin-dependent diabetes mellitus. Note the lymphocyte infiltration into the islet (insulitis) in (b). [From M. A. Atkinson and N. K. Maclaren, 1990, Sci. Am. 263(1):62.]

FIGURE 20-3

Photomicrographs of an islet of Langerhans (a) in pancreas from a normal mouse and (b) one in pancreas from a mouse with a disease resembling insulin-dependent diabetes mellitus. Note the lymphocyte infiltration into the islet (insulitis) in (b). [From M. A. Atkinson and N. K. Maclaren, 1990, Sci. Am. 263(1):62.]

response includes IFN-7, TNF-a, and IL-1. Auto-antibody production can also be a contributing factor in IDDM. The first CTL infiltration and activation of macrophages, frequently referred to as insulitis (Figure 20-3), is followed by cytokine release and the presence of auto-antibodies, which leads to a cell-mediated DTH response. The subsequent beta-cell destruction is thought to be mediated by cytokines released during the DTH response and by lytic enzymes released from the activated macrophages. Auto-antibodies to beta cells may contribute to cell destruction by facilitating either antibody-plus-complement lysis or antibody-dependent cell-mediated cytotoxicity (ADCC).

The abnormalities in glucose metabolism that are caused by the destruction of islet beta cells result in serious metabolic problems that include ketoacidosis and increased urine production. The late stages of the disease are often characterized by atherosclerotic vascular lesions—which in turn cause gangrene of the extremities due to impeded vascular flow— renal failure, and blindness. If untreated, death can result. The most common therapy for diabetes is daily administration of insulin. This is quite helpful in managing the disease, but, because sporadic doses are not the same as metabolically regulated continuous and controlled release of the hormone, periodically injected doses of insulin do not totally alleviate the problems caused by the disease. Another complicating feature of diabetes is that the disorder can go undetected for several years, allowing irreparable loss of pancreatic tissue to occur before treatment begins.

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