Type 1 diabetes (T1DM) is an autoimmune disease caused by the destruction of β-cells in the pancreas. In autoimmune diseases, the body’s immune system mistakes normal cells for pathogens and attacks them. Healthy β-cells synthesize and release insulin which controls glucose levels in the blood. When these β-cells are destroyed, the body can no longer synthesize insulin. In the absence of insulin, glucose cannot get into the cells and its level in the blood becomes too high, a condition known as hyperglycemia.

T1DM is the second most common type of diabetes after type 2 diabetes mellitus but the most common type in childhood. T1DM is considered a genetic disease that occurs when the person carrying predisposing genes is exposed to certain environmental conditions. The incidence is highest in the Scandinavian countries.

Symptoms

The symptoms of T1DM seem mild at first but they exacerbate rapidly if left unchecked. T1DM is  caused by unavailability of glucose for the cells, as well as  the electrolyte imbalance caused by the accumulation of glucose in the blood. Some common symptoms are:

• Polyuria (frequent urination)

• Polydipsia (increased thirst)

• Polyphagia (excessive eating)

• Sudden weight loss

• Diabetic ketoacidosis (DKA)

• Fatigue

• Headache

• Blurred vision

• Frequent infections

• Constipation and diarrhea

Of all the above-mentioned symptoms, DKA requires immediate medical attention. It manifests as deep breathing, nausea, vomiting, tiredness, dryness of mouth, fruity-smelling breath, headache, and muscle stiffness.

Moreover, T1DM causes a variety of complications that cause damage to the eyes, peripheral nerves, kidneys, and cardiovascular disease. These complications deteriorate the quality of life of the patients and are the major cause of morbidity and mortality associated with T1DM.

Diagnosis

The mean age of diagnosis for T1DM is 12 to 14 years but it can occur at any age. Most cases are diagnosed upon the presentation of polydipsia, polyphagia, and polyuria but some are diagnosed when admitted to the hospital following a DKA emergency. The first clinical indicator is raised glucose level. This is detected by a glucose tolerance test. In this test, the overnight fasted subject is given sugary water and their blood samples are taken after 30 min intervals for 2 hours. If the blood glucose level is 200 mg/dL or higher, it means the person has diabetes.

Following this, some diagnostic tests, such as C-peptide test and autoantibodies test, are performed to determine which type of diabetes the patient is suffering from. C-peptide test provides information about the body’s ability to synthesize insulin. A C-peptide level of less than 0.2 nmol/l indicates T1DM. Whereas, the autoantibodies test confirms T1DM by detecting specific antibodies that are destroying pancreatic β-cells.

Management

Since the body cannot make insulin in T1DM, exogenous insulin is given to the patients to control their blood glucose. Exogenous insulin allows the cells to take up glucose thus enabling them to make energy and clear glucose from the blood. One major challenge in insulin therapy is that it should be synchronized with the body’s natural need for it. If the dose of insulin is high, hypoglycemia occurs, which causes loss of consciousness and seizures. And if the insulin dose is low, hyperglycemia occurs, which causes DKA and long-term complications. The insulin pump, a delivery system for insulin, has solved some of these problems. It automatically injects insulin depending upon the body’s basal requirement. Despite this, a lot of patients struggle to achieve optimal glycemic control.

New therapeutic interventions are being developed that replace the destroyed β-cells with stem cells or target the immune system to preserve the function of β-cells early in the disease progression. These interventions have the potential to replace lifelong insulin therapy and improve the quality of life of patients suffering from T1DM.