Journal of Diabetes & Clinical Practice
Open Access

Description

Adults with latent autoimmune diabetes have clinical characteristics that are similar to both type 1 diabetes (T1D) and type 2 diabetes (T2D) (T2D). It's an autoimmune type of diabetes that's similar to T1D, but patients with LADA also have insulin resistance, which is similar to T2D, and they share certain risk factors for the disease. According to studies, LADA patients have antibodies against insulin-producing cells, and these cells avoid producing insulin at a slower rate than T1D patients. T1D and T2D tend to have genetic risk factors in common, but LADA is genetically distinct from both. There is genetic and phenotypic variation within the LADA patient population, with varying degrees of insulin resistance and autoimmunity. LADA can thus be defined as a hybrid type of T1D and T2D, with phenotypic and genotypic similarities to both, as well as variation within LADA in terms of autoimmunity and insulin resistance, based on current knowledge. Adults with latent autoimmune diabetes experience symptoms close to those of other types of diabetes, including polydipsia (excessive thirst and drinking), polyuria (excessive urination), and blurred vision. When compared to juvenile type 1 diabetes, the signs take longer to manifest, taking at least six months. Antibodies to glutamic acid decarboxylase are typically found in people with LADA, although these antibodies are more common in adults than children with type 1 diabetes. GAD antibodies tests are used for differential diagnosis of LADA and type2 diabetes, as well as risk prediction in immediate family members for type 1 diabetes. They can also be used to track prognosis of type 1 diabetes clinical progression. Dietary therapy for LADA is similar to that for type 1 diabetes. Obese LADA patients benefit from calorie restriction as well as increased physical activity. Glibenclamide has been labelled as a drug that can hasten the onset of autoimmune disease. In the nonobese diabetic (NOD) mouse, thiazolidinediones appear to inhibit diabetes. Human data, on the other hand, is scarce. Metformin is likely to be beneficial in obese LADA patients. Nonetheless, insulin therapy is the preferred option. According to our findings, -cell function is compromised in adult patients with autoimmune diabetes at the time of diagnosis, regardless of the clinical phenotype. As a result, there is no need to delay starting insulin therapy. Indeed, type 2 diabetics without islet antibodies who are treated primarily with insulin have greater -cell function two years after diagnosis than those who are treated primarily with glibenclamide. Patients with type 2 diabetes that are mostly treated with insulin have improved glycemic control. This highlights the importance of starting insulin treatment as soon as possible for patients with autoimmune diabetes. Autoimmune diabetes with a slow onset is common, occurring in 10% of phenotypic type 2 diabetic patients, and in 25% of those under the age of 35 at the time of diagnosis. Total -cell loss occurs in almost all of these patients, but it can take up to 12 years to establish, according to prospective follow-up of these patients. Type 2 diabetic patients with islet antibodies have impaired -cell function at diagnosis, despite not having insulin at the time of diagnosis. As a result, insulin therapy is recommended at the time of diagnosis. Insulin's effect in these patients is most likely antiglucose toxicity rather than immunomodulatory