The aetiological classification of diabetes was described by the WHO [1] and also approved by the ADA [2]. The classification of type 2 diabetes is largely characterized by exclusion. The most recent WHO classification published in 2019 is shown in Table 2.3 [3].

As new causes are discovered they are included as ‘other specific types’, such as maturity- onset diabetes of the young (MODY). The WHO has revisited the classification several times with no major modifications. IGT was removed from the formal classification of type 2 diabetes, but was retained as a risk state. A new cate gory of risk status, IFG, was introduced.

Type 1 diabetes

 In most cases, type 1 diabetes occurs as a result of cellular- mediated autoimmune destruction of pancreatic β cells, causing an absolute deficiency of endogenous insulin. People with type 1 diabetes are dependent on exogenous insulin for survival and are ketosis prone. Markers of the immune destruction of the β cell include islet cell autoantibodies, autoantibodies to insulin, glutamic acid decarboxylase (GAD), and autoantibodies to the tyrosine phosphatases IA- 2 and IA- 2β. One or more of these autoantibodies are present in 85–90% of individuals when fasting hyperglycaemia is initially detected. The disease also has strong HLA associations, with linkage to the DQA and DQB genes, and is influenced by the DRB genes.

The rate of destruction of β cells is usually rapid in infants, young children, and adolescents and they often have ketoacidosis at the time of first presentation. Some people with type 1 diabetes, mostly adults, have a slower deterioration of β- cell function and show detectable levels of plasma C- peptide for many years. Type 1 diabetes is associated with other autoimmune disorders such as Graves’ disease, Hashimoto’s thyroiditis, Addison’s disease, vitiligo, coeliac- sprue, autoimmune hepatitis, myasthenia gravis, and pernicious anaemia.

About 2–12% of people diagnosed with type 1 diabetes show phenotypic characteristics of type 2 diabetes at diagnosis and initially have glucose levels within target on oral anti- diabetes agents, before rapidly progressing to requiring insulin. They also show the presence of autoimmune markers of β- cell destruction, such as GAD autoantibodies. This subgroup was termed latent autoimmune diabetes of adults (LADA), but in the recent WHO classification the term LADA was removed because there was considerable controversy as to whether this was a separate condition to type 1 diabetes. It now comes under hybrid forms of diabetes with slowly evolving immune- mediated diabetes of adults [3].

A few people with type 1 diabetes may have no evidence of auto immunity, but are prone to episodic ketoacidosis and may exhibit varying degrees of insulin deficiency and insulin dependency during those periods. This form, termed idiopathic diabetes, is commonly seen in people of African and Asian ethnicity and is strongly familial [4].

Type 2 diabetes

 Type 2 diabetes constitutes more than 95% of the total population with diabetes. Its prevalence is increasing globally, but the most striking changes are now seen in low- and middle- income countries. Type 2 diabetes may remain asymptomatic for many years and is undetected in nearly 50% of people affected by the disease [4, 1]. It is commonly diagnosed incidentally when a medical check- up is done for other reasons. Type 2 diabetes is characterized by a relative insulin deficiency; although there is insulin secretion, this is insufficient to overcome insulin resistance. Though many people with type 2 diabetes manage their diabetes with lifestyle changes alone, with time oral anti- diabetes agents are needed to maintain normoglycaemia, with many people eventually requiring insulin. Chronic exhaustion of β- cell function is a major cause of this.

Although research studies have focused on the molecular mechanisms underlying type 2 diabetes, only modest success has been achieved in unravelling the genetic abnormalities. In the past two decades, type 2 diabetes in children and adolescents has become common in Asian populations and could be partly attributed to the rising rates of obesity and changing lifestyle patterns [5]. A minority of people with type 2 diabetes are prone to episodes of ketosis. They have insulin deficiency but no immune markers. This hybrid form is termed ketosis- prone type 2 diabetes [3].

There has been a proposal to modify the classification of type 2 diabetes to identify people at increased risk of complications and support precision treatment by tailoring the type of therapy with greatest benefit for the individual with diabetes. Recently, a sub- stratification in 8980 individuals with newly diagnosed diabetes was undertaken in Sweden using clusters based on six variables: GAD antibodies, age at diagnosis, body mass index (BMI), HbA1c, and estimates of β- cell function and insulin resistance. The analysis was based on prospective data from medical prescriptions and development of complications from electronic records of the examined individuals [6]. Five clusters of phenotypes with dis tinct characteristics were identified. Individuals in cluster 1 (severe autoimmune diabetes) had early- onset disease, low BMI, relatively higher HbA1c, insulin deficiency, and presence of GAD antibodies. Cluster 2 (severe insulin- deficient diabetes) was GAD antibody negative, with low age at onset, low BMI, low insulin secretion, and relatively higher HbA1c. Cluster 3 (severe insulin- resistant diabetes) had high insulin resistance and high BMI, while cluster 4 (mild obesity- related diabetes) had obesity but not insulin resistance. Cluster 5 (mild age- related diabetes) was older but was similar to cluster 4 with modest metabolic derangements. Among these the highest percentage (39.1%) was cluster 5 and the lowest cluster 1 (6.4%).

The clusters had varied dispositions to specific complications of diabetes such as kidney disease, coronary events, and stroke. Clusters 1 and 2 had a higher HbA1c at diagnosis than the other clusters and a higher frequency of ketoacidosis. Cluster 2 had the highest risk of retinopathy, and cluster 3 had the highest prevalence of non- alcoholic fatty liver disease and chronic kidney disease. Cluster 4 had an increased risk of diabetes kidney disease and cluster 5 appeared to have a lower risk of renal disease.

The authors suggested that further improvement in the stratification may be possible through the inclusion of additional variables such as biomarkers, genotypes, or genetic risk scores. Therefore, the study suggested the superiority of identifying the new clusters during classification, which will possibly provide better guidance for appropriate treatment regimens. However, the tests required for identifying the clusters are costly and are available only in a limited number of advanced research institutions and hospitals. More detailed clinical trials are required to confirm the utility of this classification.

Other specific types

These forms of diabetes are relatively less common. The underlying defects of the disease processes can be identified in these forms, such as those listed in Table 1. Some of these defects are remediable and the diabetes can be cured [4, 1].

Table1. Classification of diabetes.

Gestational diabetes

For many years, gestational diabetes was defined a state of carbohydrate intolerance resulting in hyperglycaemia of variable severity, with onset or first recognition during pregnancy. It does not exclude the possibility that the glucose intolerance may antedate pregnancy but has previously gone unrecognized. The definition applies irrespective of whether or not insulin is used for treatment or whether the condition persists after pregnancy [2, 3]. According to this definition, gestational diabetes may develop at any stage of pregnancy, but many now consider diabetes detected during the first trimester of pregnancy to be previously undiagnosed pre- existing diabetes. The term gestational diabetes is then reserved for diagnoses made in the second or third trimester of pregnancy. Women who have diabetes and subsequently become pregnant are termed as having diabetes mellitus and pregnancy and should be treated accordingly during and after the pregnancy. This is discussed in greater detail in Chapter 71. The International Association of Diabetes and Pregnancy Study Groups’ (IADPSG) criteria for diagnosis of gestational diabetes are shown in Table 2 [7]. These criteria have been adopted by main national guidelines, including those of the ADA, but not by all countries [2]. Establishing a uniform approach to diagnosis will have extensive benefits for women, caregivers, and policy makers.

Women with any of the following risk factors should be screened with an appropriate blood test as shown in Table 2, during the first prenatal visit; if the result is found to be normal, they should be tested again between 24 and 28 weeks of pregnancy [2, 3]. The risk factors for gestational diabetes include older age, obesity (BMI >30 kg/m2), history of elevated blood glucose levels or gestational diabetes during previous pregnancy, women who have large- for- gestational age babies, a strong family history of diabetes, and women from high- risk ethnic groups such as Asians [8].

Hyperglycaemia may resolve after the delivery, but 5–10% of women may continue to have diabetes, most often type 2 diabetes. These women require treatment with lifestyle changes and appropriate anti- diabetes agents. Women with gestational diabetes should be screened for diabetes immediately postpartum and again at 6–12 weeks postpartum using non- pregnant OGTT criteria [9]. HbA1c cannot be used in the immediate postpartum period, but is an effective alternative way of screening for persistent glucose abnormalities from 12 weeks postpartum where the facilities for accurate measurement are available. Women with gestational diabetes are at risk of future diabetes outside pregnancy and should be offered screening on an annual basis. Women who show impaired glucose regulation at this stage should be treated with lifestyle interventions and in some circumstances metformin.

Table2. Screening for and diagnosis of gestational diabetes.

References

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1. World Health Organization (WHO) (1999). Definition, Diagnosis and Classification of Diabetes Mellitus and Its Complications: Report of a WHO Consultation. Part 1: Diagnosis and Classification of Diabetes Mellitus. WHO/NCD/ NCS/99.2. Geneva: WHO.

2. American Diabetes Association (2021). Diab. Care 44 (Suppl. 1): S15–S33.

3. World Health Organization (2019). Classification of Diabetes Mellitus. Geneva: WHO.

4. American Diabetes Association (2014). Diab. Care 37: S81.

5. International Diabetes Federation (2019). IDF Diabetes Atlas, 9e. Brussels: www.diabete satlas.org.

6. Ahlqvist, E., Storm, P., Käräjämäki, A. et al. (2018). Lancet Diab. Endocrinol. 6: 361–369.

7. International Association of Diabetes and Pregnancy Study Groups Recommendations on the Diagnosis and Classification of Hyperglycemia in Pregnancy. International Association of Diabetes and Pregnancy Study Groups Consensus Panel (2010). Diab. Care 33 (3): 676–682.

8. Ramachandran, A., Snehalatha, C., Shetty, A.S., and Nanditha, A. (2012). World J. Diab. 15 (3): 110–117.

 9. Committee on Practice Bulletins- Obstetrics (2018). Obstet. Gynecol. 131: e49–e64.

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