How is type 1 diabetes diagnosed and treated?
People living with type 2 DM are more vulnerable to various forms of both short- and long-term complications, which often lead to their premature death. This tendency of increased morbidity and mortality is seen in patients with type 2 DM because of the commonness of this type of DM, its insidious onset and late recognition, especially in resource-poor developing countries like Africa.7 Type 1 diabetes, also known as insulin-dependent diabetes and juvenile diabetes, involves the immune system. It can occur at any age but most often happens in children and young adults. It is also more severe than type 2. Type 1 diabetes often develops suddenly and can produce symptoms such as polydipsia, polyuria, enuresis, lack of energy, extreme tiredness, polyphagia, sudden weight loss, slow-healing wounds, recurrent infections and blurred vision[27] with severe dehydration and diabetic ketoacidosis in children and adolescents. The symptoms are more severe in children compared to adults. These autoimmune type 1 diabetes patients are also prone to other autoimmune disorders such as Graves disease, Hashimotos thyroiditis, Addisons disease, vitiligo, celiac sprue, autoimmune hepatitis, myasthenia gravis, and pernicious anemia[1]. The complete dependence on insulin of type 1 diabetes patients may be interrupted by a honeymoon phase which lasts weeks to months or in some cases 2-3 years. In some children, the requirement for insulin therapy may drop to a point where insulin therapy could be withdrawn temporarily without detectable hyperglycemia[44].
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Papers on diabetes - Diabetes mellitus is the epidemic of the century and without effective diagnostic methods at an early stage, diabetes will continue to rise. This review focuses on the types of diabetes and the effective diagnostic methods and criteria to be used for diagnosis of diabetes and prediabetes. Evidently, diabetes is a complex disease with a large pool of genes that are involved in its development. The precise identification of the genetic bases of diabetes potentially provides an essential tool to improve diagnoses, therapy (more towards individualized patient targeted therapy) and better effective genetic counseling. Furthermore, our advanced knowledge of the association between medical genetics and the chronic complications of diabetes, will provide an additional advantage to delay or eradicate these complications that impose an immense pressure on patients quality of life and the significantly rising cost of health-care services.
Damage of the β cells of the pancreas due to diffused injury of the pancreas can cause diabetes. This damage could be due to pancreatic carcinoma, pancreatitis, infection, pancreatectomy, and trauma[1]. Atrophy of the exocrine pancreas leads to progressive loss of the β cells[84]. Accumulation of fat in the pancreas or pancreatic steatosis could lead to diabetes due to decreased insulin secretion but may require a long time before the damage to β cells occurs[85]. In most cases, extensive damage of the pancreas is required before diabetes occurs and the exocrine function of the pancreas is decreased in these patients[86]. Cirrhosis in cystic fibrosis may contribute to insulin resistance and diabetes[2]. A rare form of type 1 diabetes of unknown origin (idiopathic), less severe than autoimmune type 1 diabetes and is not due to autoimmunity has been reported. Most patients with this type are of African or Asian descent and suffer from varying degrees of insulin deficiency and episodic ketoacidosis[45]. Diagnosis of type 2 diabetes before or during pregnancy is based on criteria mentioned before. Fasting plasma glucose 126 mg/dL (7. 0 mmol/L) or 2-h plasma glucose 200 mg/dL (11. 1 mmol/L) after a 75 g oral glucose load.
However, gestational diabetes has been diagnosed at 24-28 wk of gestation in women not previously diagnosed with diabetes using two approaches: the first approach is based on the one-step International Association of the Diabetes and Pregnancy Study Groups (IADPSG) consensus[128] and recently adopted by WHO[129]. Gestational diabetes is diagnosed using this method by FPG 92 mg/dL (5. 1 mmol/L), 1-h plasma glucose after a 75 g glucose load 180 mg/dL (10. 0 mmol/L) or 2-h plasma glucose after a 75 g glucose load 153 mg/dL (8. 5 mmol/L). This criteria is derived from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study[127] even though the HAPO study showed a continuous relationship between hyperglycemia and adverse short-term pregnancy outcome with no threshold reported[130]. The second approach is used in the United States and is based on the two-step NIH consensus[131]. In the first step 1-h plasma glucose after a 50 g glucose load under nonfasting state 140 mg/dL (7. 8 mmol/L) is followed by a second step under fasting conditions after a 100 g glucose load for those who screened abnormal in the first step.
There are two types of diabetes - type 1 and type 2. Type 2 (also known as adult-onset diabetes) usually develops after age 40 but can appear in children, particularly if they are obese. With type 2, the pancreas produces insulin, but either there is not enough or the body cant use it effectively. Insulin treatment isnt always necessary, as it is with type 1. A majority of individuals suffering from type 2 DM are obese, with central visceral adiposity. Therefore, the adipose tissue plays a crucial role in the pathogenesis of type 2 DM. Although the predominant theory used to explain this link is the portal/visceral hypothesis giving a key role in elevated non-esterified fatty acid concentrations, two new emerging theories are the ectopic fat storage syndrome (deposition of triglycerides in muscle, liver and pancreatic cells). These two hypotheses constitute the framework for the study of the interplay between insulin resistance and beta-cell dysfunction in type 2 DM as well as between our obesogenic environment and DM risk in the next In addition to diabetes, insulin resistance has many manifestations that include obesity, nephropathy, essential hypertension, dyslipidemia (hypertriglyceridemia, low HDL, decreased LDL particle diameter, enhanced postprandial lipemia and remnant lipoprotein accumulation), ovarian hyperandrogenism and premature adrenarche, non-alcoholic fatty liver disease and systemic inflammation[6,54]. The presence of type 2 diabetes in children and adolescence who are not obese[59-61], the occasional severe dehydration and the presence of ketoacidosis in some pediatric patients with type 2 diabetes[55] had led to the misclassification of type 2 to type 1 diabetes.