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Overview

Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion and / or insulin action. Chronic hyperglycemia is associated with long-term damage, dysfunction and failure of various organs especially the eyes, kidneys, nerves, heart and blood vessels.
CLASSIFICATION
In 1997 the American Diabetes Association (ADA) proposed a classification that is current. It includes four categories of patients and a 5th group of individuals who have abnormal glucose levels at high risk of developing diabetes (also at increased cardiovascular risk):

  1. Type 1 Diabetes Mellitus
  2. Type 2 Diabetes Mellitus
  3. Other specific types of diabetes
  4. Gestational diabetes
  5. The glucose intolerance y fasting glucose altered

Pathogenesis
The diabetic syndrome, although it has made common (hyperglycemia and its consequences) is heterogeneous in its pathogenesis. Moreover, there are differences in their primary categories of type 1 and 2 in terms of hereditary and environmental factors that trigger the metabolic disorder.
Etiopathogenesis of type 1 diabetes:
We observed a higher prevalence of this form in subjects with clinical certain antigens of the major histocompatibility complex HLA (Human LeucocyteAntigen) located on chromosome 6 and that control the immune response. The association of type 1 diabetes mellitus with HLA DR3, 4 DR, DQA Arg 50 and Asp DBQ No 57, would reflect a greater suceptibilidada developing the disease. For this to happen it requires of other environmental factors such as viruses, toxic or other immunogenic. This explains why only 50% of identical twins are concordant in laaparici?n of this type of diabetes.
The susceptible individuals, against ambient conditions, expressed in beta cells of the pancreas of type II antigens of histocompatibility abnormal, which are unknown by the immunocompetence of the subject system. This starts a process autoinmunoagresi?n, variable speed, bearing in months or years to a critical reduction of beta cell mass and expression of disease.
At present, the process can be detected in its pre-clinical phase (prediabetes) through the detection of islet cell antibodies (ICA) and antiGAD, which at high concentrations and persistent, with a deterioration in the phase response insulin secretion quick predict the onset of the disease. While the phenomenon of autoinmunoagresi?n is progressive and ends with the almost total destruction of beta cells, the disease can be written before that happens, to be associated with a stressful situation that transiently inhibits insulin secretory capacity of the cells Treatment.
In the clinical stage may be a partial recovery of insulin secretion that lasts a few months ("honeymoon"), and then have a insulinopenia irreversible evolution can be demonstrated by low C-peptide levels (<1 ng / ml) . Patients will then depend on the administration of exogenous insulin to sustain life and not develop ketoacidosis.
Etiopathogenesis of Type 2 Diabetes:
Its genetic nature has been suggested by the high concordance of this clinical form in identical twins and their family transmission. While it has been recognized specific genetic errors that explain the pathogenesis of some cases, in most defect is unknown, and most likely that multiple genetic alterations (polygenic). The first event in this sequence leading to diabetes is insulin resistance leading to increased insulin secretion and synthesis, and compensatory hyperinsulinemia, able to maintain metabolic homeostasis by year. Once it breaks the balance between insulin resistance and secretion, expression starts biochemistry (IGT) and subsequently diabetescl?nica. Individuals with impaired glucose tolerance and diabetes trends are short hiperinsulin?micosy this disease is a frequent component in the syndrome called insulin resistance or metabolic syndrome. Other components of this table and related to insulin-resistance and / or hiperinsulinemiason hypertension, dyslipidemia, obesity thoraco-abdominal (visceral), gout, increased prothrombotic factors, defective fibrinolysis and atherosclerosis. Therefore, these subjects have increased cardiovascular risk. Obesity and a sedentary lifestyle are factors which increase insulin resistance. The visceral obesidadpredominantemente, through increased secretion of free fatty acids and of adipocytokines (tumor necrosis factor, interleukins 1 and 6) and decrease of adiponectin, induces insulin resistance. If coexists with genetic resistance, produces a greater demand on the pancreas and explains most precocious onset of type 2 DM is observed even in children. To start the disease that has irreversible in most cases, should be associated with insulin resistance-a defect in beta cells. Several hypotheses have been postulated: depletion of the insulin secretion capacity versus time, coexistence of a genetic defect that interferes with the synthesis and secretion of insulin, interference of insulin secretion due to drugs and even by the relative increase the levels of glucose and fatty acid in the blood (glucolipotoxicidad).
Type 2 diabetes is a progressive disease that as the years pass metabolic control of product worsening insulin resistance and further deterioration of its secretion.
PREVALENCE
The prevalence (proportion of the population suffering from the disease) is variable in different communities, still very high in some ethnic groups as North American Indians and Polynesians (eg Pima Native Americans: 25% have type 2 diabetes). In Chile, it is estimated that the prevalence of diabetes reaches 1.2% of the general population (1970) and 6.3% of the population over 17 years (2003). However, there are notable differences with age. The prevalence is low in children: 0.024% (mainly DM type 1), rising noticeably in over 40 years, when it becomes more common type 2 DM. If in adults older than 40 years, diabetes has a prevalence of around 6%, the glucose intolerant is estimated at 15%. 90% of diabetics are type 2, 8% type 1, and the rest are imprecise classification or are secondary to other diseases. The vast majority of type 2 diabetics are obese.

  

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