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Type 1 Diabetes
Written by Jeffrey R. Waggoner, MD   

Type 1 diabetes is caused by a progressive autoimmune destruction of the beta cells. It most commonly affects children, appearing in an acute fashion. Recently, the ability to detect antibodies has identified another population of adult patients who have latent autoimmune diabetes of the adult (LADA). All type 1 diabetics are dependent on exogenous insulin because the pathophysiology involves a destruction of the body’s ability to produce insulin, not a resistance to it because of obesity.

Genetic predisposition for Type 1 diabetes

The genetic predisposition to Type 1 diabetes is demonstrated by studies in identical twins. These studies show that when one twin develops Type 1 diabetes, islet cell and insulin antibodies are present in the second, initially nondiabetic twin for years before the development of overt diabetes. [1]

Prevention methods not proven

Because of the ability to identify at risk populations, it has been proposed that Type 1 diabetes might be prevented by the administration of low dose insulin prior to the onset of the disease. Studies to this point have not substantiated this theory. [2]

Clinical Presentation

Type 1 diabetes differs from Type 2 diabetes in that type 1 diabetics may develop ketosis and ketoacidosis. This form of diabetic crisis is diabetes’ most acute, life-threatening complication. It also has an influence on the manner in which the typical type 1 diabetic patient will present.

Hyperglycemia

The symptoms seen in such a presentation are secondary to hyperglycemia, glycosuria, and ketoacidosis (KA). Hyperglycemia apart from its associated glycosuria causes general symptoms—fatigue, malaise, irritability, and headache. Glycosuria causes increased urinary frequency as well as increased urinary volume (polyuria), and nocturia. In younger children, this may be reflected as enuresis in a previously continent child.

Polydypsia

Eventually, patients develop polydypsia — an unquenchable thirst because of the osmotic diuresis that causes dehydration.

Failure to thrive

Insulin deficiency creates an uninhibited gluconeogenesis. This creates a breakdown of protein and fat that leads to weight loss. This occurs in children who are eating a nutritionally stable diet. Thus failure to thrive and growth retardation may be the first signs of Type 1 diabetes. This may precede frank hyperglycemia. [3]

Ketosis and Ketoacidosis

Pathophysiology

One of insulin’s roles is an inhibition of the lypolytic action of cortisol and growth hormone. Consequently, diabetics experience increased levels of circulating levels of fatty acids. These fatty acids are oxidized in the liver through a process that eventually produces acetone. There is a resulting metabolic acidosis secondary to circulating ketone bodies (as well as a degree of excessive fatty acids and lactic acidosis). It is this process that is responsible for ketosis and ketoacidosis.

Clinical symptoms and progression

Clinical symptoms of ketoacidosis include severe dehydration; ketotic breath; acidotic breathing, i.e. so called Kussmaul respiration, which may masquerade as respiratory distress; abdominal pain; vomiting; drowsiness; and coma. [4]

When the body can no longer compensate for this metabolic acidosis by hyperventilation, along with the accompanying dehydration, the eventually uncompensated acidosis produces a state of renal failure and circulatory collapse, coma and death. [5]

Treatment of Type 1 diabetes

Guidelines for Pediatric Population

The complexities associated with diagnosis and treatment of Type 1 diabetes in the pediatric population may be appreciated by looking at the volume of recommendations made by various organizations that are internally incompatible. This is not so much a reflection of scientific or philosophic disagreement as it is a product of the acknowledgment that different patients require different approaches. [6]

However, consistent throughout the guidelines is the philosophy that the most successful treatments for pediatric Type 1 diabetes is best done through the use of a multi-disciplinary team that is experienced in this field; that aggressive control of hyperglycemic episodes is crucial to prevent sequelae; that equal attention must be given to episodes of hypoglycemia, in particular those that are difficult to recognize such as episodes that take place during sleep; and that the psychological impact of the disease cannot be overstated since noncompliance plays a greater role in diabetic crises than any other single factor. [7]

Treatment Philosophy

The specifics of treatment are too variable to describe in any greater detail other than to say that they may involve a variety of different kinds of insulin — although almost all are now human analogues; that a mix of insulin types is often used; and that insulin pumps now play a role in some patients’ treatment.

Pancreatic transplants and genetic manipulation are two treatment avenues being explored, but neither appears to be an option in the near future.

Other Information

Metformin is a biguanide with antihyperglycemic activity. Metformin hydrochloride exerts its action by improving hepatic sensitivity to insulin.

 
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