**3. Genetics**

The term Latent Autoimmune Diabetes in the Adult (LADA, Latent Autoimmune Diabetes of the Adult) by its abbreviations in English; it was coined by Tuomi et al. to describe patients with a slowly progressive form of autoimmune or type 1 DM who could be treated initially

Both diseases, both DM type 1 and LADA; present specific antibodies: anti-decarboxylase of glutamic acid (anti-GAD), anti-beta cells (ICA), anti-tyrosine phosphatase (IA-2) and anti-insulin, the first of which is the most prevalent, followed by ICA [5, 6]; in more than 10% of adults with presumed DM type 2 (DM2) [7, 8], so LADA is the most prevalent form of autoimmune diabetes in adults and probably also the most prevalent form of autoimmune diabetes in general [9].

Clinically, these patients are difficult to distinguish from type 2 diabetic subjects who are

The presence or absence of islet autoantibodies is one of the most direct ways to distinguish

And, although LADA is undoubtedly related to type 1 DM, its clinical presentation frequently features traits attributable to type 2 DM and is often misdiagnosed and treated for significant periods of time. This is helped by the fact that the current diagnostic criteria used to identify

Although the American Diabetes Association (ADA) currently does not recognize this disease as a specific type, there is increasing information about it, as well as groups dedicated to its study.

There is a big difference in the prevalence of type LADA DM among different population groups around the world. In North America it is estimated that 5–10% of new cases of DM in

In a UK Prospective Diabetes Study (UKPDS), about 10% of adults with suspected type 2 diabetes at the time of diagnosis had evidence of islet autoimmunity in the form of circulating ICA or GAD antibodies and most progressed to dependence on insulin in 6 years [12]. See **Table 1**. In Central America there are still no studies that describe the prevalence of LADA type Diabetes. In countries like Honduras, its diagnosis is based on the clinic; this reduces the credibility of the diagnosis, especially when there is not enough equipment to corroborate the

Given that an appreciable proportion of people with diabetes who do not require insulin have a high proportion of antibodies against glutamic acid decarboxylase (GAD), it has been concluded that the LADA type Diabetes is probably much more prevalent than the DM type 1 but less frequent than DM type 2 [24]. This in turn explains the reason for the use of Anti-GAD, in comparison with other antibodies, to detect type LADA DM among subjects diagnosed as

positive for the markers that characterize patients with type 1 diabetes.

this variant of diabetes are imprecise and subject to controversy.

adult patients could correspond to this pathology [11].

presence or absence of the antibodies described above.

between type 1 and type 2 diabetic patients [10].

without insulin [4].

24 Diabetes and Its Complications

**2. Epidemiology**

DM type 2 [13, 25].

Pathological studies have proposed that LADA and type 1 DM share physiopathological and genetic aspects; such as genes (HLA, INS VNTR and PTPN22) and with respect to DM type 2 (TCF7L2) [26], which suggest that it may represent a genetic admixture of the two types of diabetes, especially when non-insulin requiring.

It is known that LADA has a higher frequency of human histocompatibility antigens (HLA) characteristic of DM type 1: HLA-DR3 (28% of patients), DR4 (27%) and DR 3/4 (22%), in comparison with the general population [26, 27].

The dilemma persists in the fact whether this genetic mixture represents a totally different disease syndrome or is part of a continuum of an autoimmune process.

It is important to mention that in all the genome-wide association studies directed to the exome sequencing carried out until now or the sequencing of the whole genome exome, they have not yet been carried out in large cohorts of adult autoimmune patients.

As mentioned, both diseases have specific antibodies. Concomitantly, a decrease in the frequency and activation of "natural killer" cells in peripheral blood compared with healthy individuals has been demonstrated, which translates into a defect in the immune response [28].
