An etiologically (causally) based classification according to the recommendations of the American Diabetes Association (ADA) and WHO is shown in the table below.
Classification of diabetes mellitus
I. Type 1 diabetes mellitus – absolute insulin deficiency due to destruction (destruction) of ß-cells (site of insulin production):
- Type 1a: immunologically mediated form Special form: LADA (latent autoimmune diabetes (with onset) in adults) – type 1 diabetes with manifestation in adulthood (> 25 years); insulin deficiency develops relatively slowly. No insulin requirement in the first 6 months, detection of GAD-Ak (glutamic acid decarboxylase; English : glutamic-acid-decarboxylase = GAD; a ß-cell-specific enzyme).
- Type 1b: idiopathic form/disease that develops without a tangible cause (rare in Europe).
II Type 2 diabetes mellitus – 4 factors in varying degrees of severity underlie this:
- Insulin resistance (reduced or abolished effect of the hormone insulin).
- Secretory (“concerning secretion”) defect of the ß-cells.
- Secretory defect of the A cells (hyperglucagonism/increased secretion of glucagon → blood glucose level ↑)
- Progressive apoptosis (programmed cell death) of ß cells.
III. other specific forms of diabetes with a known cause
- A. Genetic defects of β-cell function (autosomal dominant inheritance) – “Maturity-onset diabetes of the young” (MODY) without auto-Ak detection and obesity. Manifestation before the age of 25. Approximately 1% of all diabetics. There are currently 11 known forms, of which the following four most common forms account for approximately 90% of all MODY cases (all other forms of MODY diabetes occur ≤ 1% and are therefore not listed here):
MODY form Gene Abbreviation Chromosome PPh Notes MODY 1 (approx. 3 %) Hepatocyte nuclear factor 4 alpha HNF-4alpha 20q Reduced insulin secretion, decreased glycogen synthesis. Low triglycerides (blood lipids). MODY 2 (approx. 15 %) Glucokinase GK 7p Reduced insulin secretion Mild course, usually without late complications MODY 3 (approx. 70%) Hepatocyte nuclear factor 1 alpha HNF-1alpha 12q Reduced insulin secretion Renal (“kidney-related”) glucosuria (excretion of glucose in the urine) MODY 5 (about 3%) Hepatocyte nuclear factor 1 beta HNF-1beta 17q Reduced insulin secretion Renal cysts, malformations of the genitals (malformations of the sex)
- B. Genetic defects of insulin action.
- C. Diseases of the exocrine pancreas/disease of the pancreas associated with insufficient production of digestive enzymes (chronic pancreatitis/chronic pancreatitis): diabetes mellitus secondary to a pancreatic tumor is also called type 3c diabetes
- D. Endocrinopathies/diseases caused by impaired function of endocrine glands or the defective action of hormones (acromegaly, aldosteronom, Cushing’s syndrome, glucagonom, hyperthyroidism, pheochromocytoma, somatostatinoma).
- E. Drug-induced (e.g., glucocorticoids, thyroid hormones, betaadrenergics, thiazides, hormonal contraceptives); see also under “Diabetogenic effects due to drugs”
- F. Infections (e.g., congenital rubella infection, CMV infection).
- G. Rare immunologically determined forms (e.g., anti-insulin receptor antibodies).
- H. Genetic syndromes that are occasionally associated with diabetes (e.g., Down syndrome, Klinefelter syndrome, Turner syndrome)
IV.Gestational diabetes (GDM)
Proposal for a new diabetes type 2 classification
The authors, led by Professor Leif Groop of Lund University Diabetes Center in Sweden, propose a new diabetes type 2 classification based on:
Diagnosis age, BMI (body mass index), HbA1c, beta cell function (HOMA 2B: assessment of beta cell function based on C-peptide concentration), insulin resistance (HOMA2-IR: assessment of insulin sensitivity), and autoantibodies (glutamic acid decarboxylase antibodies (GAD antibodies; identification of patients with autoimmune diabetes), they propose a division into five forms in adults:
| Cluster | Description | Clinical symptoms/laboratory | Age group | Beta cell function | Frequency | Therapy |
| 1 | Severe autoimmune diabetes (SAID); essentially LADA diabetes: latent insulin-dependent diabetes mellitus in adulthood). |
|
Manifestation in younger adulthood | Destroyed beta cells (= no insulin production) | 6-15 %22 % | Patients need insulin therapy early in the course |
| 2 | Severe insulin-deficient diabetes (SIDD): similar to cluster 1. |
|
Affected people are usually young and slim | Clear insulin deficiency | 9-20 %3 % | Patients often require insulin relatively early |
| 3 | Severe insulin-resistant diabetes (SIRD) |
|
Significant insulin resistance at the time of diagnosis | 11-17 %11 % | ||
| 4 | Mild obesity-related diabetes (MOD) |
|
Metabolism is less disturbed than in patients in cluster 3 | 18-23 %29 % | ||
| 5 | Mild age-related diabetes (MARD) in elderly patients |
|
Older patients | 39-47 %35 % |
According to the researchers, all five forms were genetically distinct, so they were different types rather than stages of disease. Furthermore, the authors pointed out that many cluster 1+2 patients were not receiving insulin at manifestation.