{"id":10448,"date":"2020-05-11T14:06:41","date_gmt":"2020-05-11T07:06:41","guid":{"rendered":"https:\/\/www.rescennt.com\/?p=10448"},"modified":"2022-02-12T14:56:53","modified_gmt":"2022-02-12T07:56:53","slug":"%e1%9e%87%e1%9e%98%e1%9f%92%e1%9e%84%e1%9e%ba%e1%9e%91%e1%9e%b9%e1%9e%80%e1%9e%93%e1%9f%84%e1%9e%98%e1%9e%95%e1%9f%92%e1%9e%a2%e1%9f%82%e1%9e%98","status":"publish","type":"post","link":"https:\/\/demo.rescennt.com\/km\/%e1%9e%87%e1%9e%98%e1%9f%92%e1%9e%84%e1%9e%ba%e1%9e%91%e1%9e%b9%e1%9e%80%e1%9e%93%e1%9f%84%e1%9e%98%e1%9e%95%e1%9f%92%e1%9e%a2%e1%9f%82%e1%9e%98\/","title":{"rendered":"Diabetes Mellitus"},"content":{"rendered":"

Diabetes Mellitus<\/span><\/h1>\n

Introduction<\/span><\/h2>\n

\"Type<\/a><\/p>\n

Type 2 diabetes accounts for over 90 percent of cases of diabetes in the United States, Canada, and Europe; type 1 diabetes accounts for another 5 to 10 percent, with the remainder due to other causes (table 1<\/a>). New information has led to increased understanding of genetic defects related to diabetes. Monogenic causes of type 2 diabetes (eg, those causing maturity onset diabetes of the young) represent only a small fraction of cases, and commonly inherited polymorphisms individually contribute only small degrees of risk for, or protection from, diabetes. Most of the genetic risk for type 2 diabetes results from complex polygenic risk factors.<\/span><\/p>\n

This article we will focus mainly on type 1, type 2 diabetes and gestational diabetes.<\/span><\/p>\n

Type 2 diabetes<\/span><\/h4>\n

Type 1 diabetes is characterized by destruction of the pancreatic beta cells, leading to absolute insulin deficiency. This is usually due to autoimmune destruction of the beta cells (type 1A). Testing for islet cell antibodies (ICA) or other islet autoantibodies (antibodies to glutamic acid decarboxylase [GAD] 65; insulin; the tyrosine phosphatases, insulinoma-associated protein 2 [IA-2] and IA-2 beta; and zinc transporter ZnT8) in serum may be helpful if establishing the diagnosis is important; a positive result is indicative of immune-mediated or type 1A diabetes [1<\/a>]. However, the absence of pancreatic autoantibodies does not rule out the possibility of type 1 diabetes. Some patients with absolute insulin deficiency have no evidence of autoimmunity and have no other known cause for beta cell destruction. They are said to have idiopathic or type 1B diabetes mellitus.<\/span><\/p>\n

Type 2 diabetes<\/span><\/h4>\n

Type 2 diabetes is by far the most common type of diabetes in adults and is characterized by hyperglycemia and variable degrees of insulin deficiency and resistance. It is a common disorder whose prevalence rises markedly with increasing degrees of obesity. Insulin resistance and insulin deficiency can arise through genetic or environmental influences, making it difficult to determine the exact cause in an individual patient. In addition, hyperglycemia itself can impair pancreatic beta cell function and exacerbate insulin resistance.<\/span><\/p>\n

Distinguishing type 1 from type 2 diabetes<\/span><\/h4>\n

It is occasionally difficult to distinguish between type 1 and atypical presentations of type 2 diabetes. Patients with type 1 diabetes have an absolute requirement for insulin therapy. However, many patients with type 2 diabetes lose beta cell function over time and require insulin for glucose control. Thus, need for insulin per se does not distinguish between type 1 and type 2 diabetes. While it is known that diabetic ketoacidosis (DKA) can occur in the presence of complete insulin deficiency and it is not a typical feature of type 2 diabetes, some patients with type 2 diabetes develop DKA under certain circumstances (usually severe infection or other illness). Thus, ketoacidosis cannot be relied upon as an absolute indicator that the patient has type 1 diabetes or that long-term insulin therapy will be required.<\/span><\/p>\n

We measure autoantibodies when the diagnosis of type 1 or type 2 diabetes is uncertain by clinical presentation:<\/span><\/p>\n