46 Year Old Patient Diagnosed with Latent Autoimmune Diabetes in the Adult (LADA).
Cesar A López, MD; Mohan Vinuta M.D.
Introduction:
Latent Autoimmune Diabetes in Adults (LADA) also named slowly progressing insulin dependent diabetes or type 1.5 diabetes, is a type of diabetes with a prevalence approximately of 10% non-insulin-requiring diabetics, and is characterized by the presence of a type 2 diabetic phenotype combined with islet antibodies. Diagnosis is made by 3 features: Diagnosis of diabetes in a patient who is more than 30 years old, the presence of diabetes-associated autoantibodies and not treated with insulin during the first 6 months of diagnosis of hyperglycemia. ß-cell dysfunction is rapidly progressing depending on concentration and number of diabetes-associated autoantibodies, characterized by immeasurable fasting C-peptide and the requirement of insulin with in 3-6 years. The following case report shows a typical case of a 46 year old patient diagnosed 2 years earlier with diabetes type 1 after he had multiple admissions due to hyperglycemia. Phenotype was of a type 1 diabetes, but age of diagnosis and the presence of hyperglycemia with out DKA or HHS prior to diagnosis was consistent more with a type 2 diagnosis.
Case Report:
Discussion:
In 1986, was reported a subgroup of type 2 diabetic patients who, despite having islet autoantibodies, showed preserved ß-cell function. The type of diabetes in these patients was referred to as latent type 1 diabetes, showing clearly different features from classic type 1 and classic type 2 diabetes. Later was launched the term latent autoimmune diabetes in adults (LADA) for this slowly progressive form of autoimmune diabetes initially managed with diet and oral hypoglycemic agents before becoming insulin requiring. This form of diabetes has also been called slowly progressing insulin dependent diabetes or type 1.5 diabetes.
LADA is the defined as a type 2 diabetic phenotype combined with islet antibodies diagnosed by three features including: adult age at diagnosis (>30 years of age), the presence of diabetes-associated autoantibodies (at least one of the four antibodies commonly found in type 1 diabetic patients: ICAs, autoantibodies to GAD65, IA-2, and insulin), and not treated with insulin within the first 6 months after diagnosis to manage hyperglycemia.
Although LADA patients by definition are not insulin requiring at and during the first time after diagnosis of diabetes, within 6 years, ß-cell function is severely impaired, leading to insulin dependency. Nevertheless, ß-cell failure, defined as immeasurable fasting C-peptide, may take up to 12 years until it occurs in patients with islet antibodies.
High concentrations of islet antibodies predict future ß-cell failure or destructive process, whereas a low number of islet antibodies, particularly lack of ICAs, is associated with lack of progression to ß-cell failure, hence it shows that the presence of two or three islet antibodies at diagnosis predicts severe deterioration in ß-cell function within 5 years and the presence of only ICAs or only GADAs is associated with severe deterioration within 12 years. Progression to insulin dependence in LADA patients is more rapid in those aged younger than 45 yr than in older cases.
The natural course of these patients shows that C peptide will decrease with time in parallel with the curve for C peptide as in classical type 1 diabetic patients, and most of the LADA patients will require insulin within three years.
It is suggested that insulin deficiency as well as insulin resistance both participate in the course of LADA, because the frequency of metabolic syndrome is higher that in the general population but less prevalent than in type 2 diabetic patients.
Conclusions:
Although the presence of LADA in the diabetic populations is high (at least 10%), the diagnosis of this affection is not normally done, despite having only 3 requirements to be made to achieve this goal: Adult onset diagnosis of diabetes, the presence of diabetes-associated autoantibodies and not treated with insulin within the first 6 months after diagnosis to manage hyperglycemia.
Prospective follow-up of these patients shows that complete ß-cell failure occurs in almost all of these patients, but it may take up to 12 years until it develops depending on concentration and quantity of this antibodies. Although not insulin requiring at diagnosis, patients who are positive with islet cell antibodies have impaired ß-cell function. Hence, insulin is the treatment of choice and indicated since the time of diagnosis.
As seen in our example, not all patient with diabetes can be made to fit only the typical diagnosis of type 1 insulin requiring and type 2 not insulin requiring diabetes, with the increase in incidence of diabetes in our population due to the obesity epidemic, probably the greatest area of confusion will involve the distinction of LADA from other types of diabetes occurring in individuals over the age of 30–35 years.
