struction is generally rapid in children and faster in adults. Autoantibodies against islet cells, insulin, glutamic acid decarboxylase-65 (GAD-65), and zinc transporter 8 (Zn T8) may be detected in the serum of such patients. These antibodies wane over time and do not have sufficient diagnostic accuracy to be used routinely for diagnosis, especially after the first year. With the progressive destruction of beta cells, there is little or no secretion of insulin. These patients are generally not obese. They are more prone to develop other autoimmune disorders such as Addison disease, Graves disease, Hashimoto thyroiditis, and celiac disease. A subset of T1DM not associated with insulin autoimmunity and not associated with the above HLA is termed idiopathic T1DM. It is more common in African and Asians and presents with episodic diabetic ketoacidosis (DKA).
T2DM is an insulin-resistance condition with associated beta-cell dysfunction. Initially, there is a compensatory increase in insulin secretion, which maintains glucose levels in the normal range. As the disease progresses, beta cells change, and insulin secretion is unable to maintain glucose homeostasis, producing hyperglycemia. Most of the patients with T2DM are obese or have a higher body fat percentage, distributed predominantly in the abdominal region. This adipose tissue itself promotes insulin resistance through various inflammatory mechanisms, including increased FFA release and adipokine dysregulation. Lack of physical activity, prior GDM in those with hypertension or dyslipidemia also increases the risk of developing T2DM. Evolving data suggest a role for adipokine dysregulation, inflammation, abnormal incretin biology with decreased incretins such as glucagon-like peptide-1 (GLP-I) or incretin resistance, hyperglucagonemia, increased renal glucose reabsorption, and abnormalities in gut microbiota.
History and Physical
Patients with diabetes mellitus most commonly present with increased thirst, increased urination, lack of energy and fatigue, bacterial and fungal infections, and delayed wound healing. Some patients can also complain of numbness or tingling in their hands or feet or with blurred vision.
These patients can have modest hyperglycemia, which can proceed to severe hyperglycemia or ketoacidosis due to infection or stress. T1DM patients can often present with ketoacidosis (DKA) coma as the first manifestation in about 30% of patients.
The height, weight, and body mass index (BMI) of patients with diabetes mellitus should be recorded. Retinopathy needs to be excluded in such patients by an ophthalmologist. All pulses should be palpated to examine for peripheral arterial disease. Neuropathy should be ruled out by physical examination and history.
Persons older than 40 years of age should be screened annually. More frequent screening is recommended for individuals with additional risk factors for diabetes.
- Certain races/ethnicities (Native American, African American, Hispanics, or Asian American, Pacific Islander),
- Overweight or obese persons with a BMI greater than or equal to 25 kg/m2 or 23 kg/m2 in Asian Americans,
- First-degree relative with diabetes mellitus
- History of cardiovascular disease or hypertension
- Low HDL-cholesterol or hypertriglyceridemia,
- Women with polycystic ovarian syndrome
- Physical inactivity
- Conditions associated with insulin resistance, for example, Acanthosis nigricans.
Women diagnosed with gestational diabetes mellitus (GDM) should have lifelong testing at least every three years. For all other patients, testing should begin at age 45 years, and if results are normal, patients should be tested at a minimum of every 3-years.
The same tests are used to both screen for and diagnose diabetes. These tests also detect individuals with prediabetes.
Diabetes can be diagnosed either by the hemoglobin A1C criteria or plasma glucose concentration (fasting or 2-hour plasma glucose).
Fasting Plasma Glucose (FPG)
A blood sample is taken after an 8 hour overnight fast. As per ADA, fasting plasma glucose (FPG) level of more than