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Editorial

Indian Pediatrics 1999; 36:445-448 

Diabetes in Immigrant Asian Children



Insulin dependent diabetes mellitus (IDDM) is a chronic disorder with high morbidity. There is a high demand on resources and adequate planning is necessary to be able to assist such patients and their families for a long time. The cause of IDDM is not well understood; genetic predisposition and environmental factors have been implicated. The incidence of IDDM varies from country to country, being higher in the temperate climates of the northern hemisphere. However, even in these countries, the highest incidence is observed further north in Finland (25.6/100,000/year) as compared to Scotland (23.9/100,000/year)(1) and England (18.6/100,000/year). In comparison, South India has a lower incidence of 10.5/100,000/year(2) and Pakistan has reported an even lower incidence of 1.021 100,000/year(3).

There are indications that the incidence of IDDM in children might be rising. Burden et al.(4) reported a threefold increase in the incidence of IDDM from 3.84/100,000/year to 10.6/100,000/year over a 30 year period between 1951 and 1980, in Leicestershire (middle of England). Further evidence of an increase in incidence of IDDM was also shown by Metcalf(5) with a twofold increase over a period of 15 years. In this study, one quarter of the children with IDDM were under 5 years of age. It is not clear, whether a similar trend is taking place in Asia. However, it is interesting to note that the incidence of IDDM has increased in Asian immigrants to England from 3.1/I00,000/year to 11.7/100,000/year over a period of just 10 years on and is now approaching that of indigenous population(6). This work concentrated on an area of England with a high concentration of immigrant population from the Asian subcontinent. It is important to know that most of these people have lived in this same locality and data was collected using several sources, all of which had been established for a long time and not just specifically to monitor Asian children. It appears that full ascertainment was achieved in this study and a threefold increase noted over just 10 years was a reliable data. There is further evidence for this observation from Leicestershire, an area of high Indian immigrant population, where no difference in the incidence of IDDM between Asian children and their caucasian counterparts was ob. served(7). A few years later, an epidemic of IDDM was reported in Leicestershire in the same population which prompted another study to look into the possible causal link between their lifestyle and onset of diabetes(8). A comparison was made between children with IDDM and their non-diabetic peers whose forefathers or themselves came from the Indian sub-continent. Cultural adoption was investigated in some detail and it was found that diabetic children had adapted to the English culture much better than their non- diabetic peers. Based on this observation, it seems that children of Asian origin may have the genetic predisposition to develop IDDM if exposed to the same environment as their peers in Europe. It is important to recognize these developments as there may be implications in terms of research into the causes of IDDM.

An Italian study(9) looked at the incidence of IDDM among Sardinian heritage children born in Lazio. Lazio population has a lower incidence of diabetes than Sardinia. In this study, details of children with IDDM born to both Sardinian parents or one Sardinian parent, were compared to Lazio born parents. They found that children with one Sardinian parent had a rate half that of Sardinia and double that of the indigenous population. This study emphasizes the role of genetic predisposition since there was no significant need for cultural adaptation. Their conclusion was that genetic susceptibility determines the frequency of IDDM in response to the environment. This same phenomenon is observed in the Asian children but there are no studies on intermarriages (with Europeans) since these are still uncommon. Similarly, a higher risk of IDDM in African-American and Hispanic children in Chicago has been documented in comparison to reports from the indigenous populations(10). Research regarding the role of environmental influence on the development of IDDM is ongoing(11). Bodansky(6) showed circumstantial evidence but did not identify the offending factors. Parslow et al. (ll) found that the development of IDDM was associated with nitrate in drinking water. This study was conducted in the same area where Bodansky did his original work on the immigrant population. This study there- fore covers the same population and is informative on the changes over a prolonged period. This was an interesting finding linking IDDM to ecological or nutritional factors but could not explain the rapidly rising incidence in the selective population of immigrants.

Infection has been implicated(l2) but the study population has been very small. This study linked reduced exposure to infection with subsequent development of diabetes. It is important to pursue this line of research as well in view of the high incidence of infections in the developing world. The link of developing IDDM to viral infections has not been fully elucidated.

Over the past 10 years there has been a rapid rise in the prevalence of IDDM specially in children aged 5 years or less. In the Scottish study the rate for 0-4 year was 24.4 and this incidence was reported to be 17.5 in the Oxford (England) study done over an 11 year period(13). The time trend analysis in the Scottish study with 97.5% ascertainment showed an overall annual increase of 4%. In comparison the figure for the age range 0-4 years in Oxford (England) was 11 %. These figures are similar to those observed elsewhere in the country. For example, in Middlesbrough (North England) where I practice the incidence for this age group has increased from 10.6 to 26.6/100,000/yr over a 10 year period in the Caucasian children.

This increasing incidence in the under five children has major clinical implications in patient management. Most of them present with diabetic ketoacidosis (DKA). There may be delay in diagnosis for the unsuspecting clinician thus increasing the morbidity and mortality associated with management of DKA.

In a separate study in Birmingham- England, looking at clinical presentation, children of Asian origin were more likely to present in DKA and were of a younger age (S. Alvi, Personal communication). Thus the belief that IDDM ,is rare in this population may be a danger to some patients and we need to raise the awareness both in the general public and medical fraternity.

The role of genetic component in the etiology of IDDM has been investigated in south India, Korea, China and Japan(l4-l7) but more extensively in Europe. Glutamic acid decarboxylase antibodies (GAD65Ab) and insulin Cytoplasmic antibodies (ICA) found in these diabetic populations showed a similar pattern to that observed in other countries. Mohan et al.(14) found that GAD antibodies were lower in those patients with fibrocalculus pancreatic diabetes as compared to those with IDDM (type 1). Thus autoimmunity was indirectly implicated in their conclusion. Lee et al.(15) investigated the predictive value of GAD in a Korean population. They found a relationship with HLA_DR, DQA1 and DQB 1 genes. Other studies have showed a significantly lower percentage positivity of GAD in Koreans and Thai when compared to Australians of European descent( 16). A high prevalence was found in the Japanese and Chinese population(17, 18).

The genetic susceptibility has not been studied in great detail for the Indian, Pakistan or Bangladesh population. This needs to be done, although there is no reason to believe that the findings would be different from the observations already made in immigrants in Europe. Comparative data, however, may elucidate those individuals susceptible to environmental factors.

In conclusion, the incidence of IDDM is increasing in Asian immigrants to United Kingdom. The prevalence is approaching that of the indigenous population. The changing life styles in Asia may have implications for the children in Asia with regard to developing IDDM in those who are genetically susceptible. Further monitoring and ascertainment is required to determine the true incidence of IDDM and the trend in Asia. If there is an in- creasing trend similar to that in Europe, then there are important implications for research and health provision.
 


M.S. Kibirige,
Consultant Pediatrician,
South Cleveland Hospital,
Middlesbrough, UK.
E-mail: [email protected]
 

References

1. Rangasami JJ, Greenwood DC, McSporran B, Smail PJ, Patterson CC, Waugh NR on behalf of the Scottish Study Group for the Care of Young Diabetics. Rising incidence of type 1diabetes in Scottish children, 1984-93. Arch Dis Child 1997; 77: 210-213.

2. Ramachandran A, Snehalatha C, Krishnaswamy CV. The incidence of lODM in children in urban population in southern India. Madras lODM Registry Group Madras, South India. Diabetes Res Clin Pract 1996; 34: 79-82.

3. Staines A, Hanif S, Ahmed S, McKinney P A, Shera S, Bodansky HJ. Incidence of insulin dependent diabetes mellitus in Karachi, Pakistan. Arch Dis Child 1997; 76: 121-123.

4. Burden AC, Hearnshaw JR, Swift PGF. Childhood diabetes: An increasing incidence. Diabetic Med 1989; 6: 334-336.

5. Metcalfe MA, Baum JD. Incidence of insulin- dependent diabetes in children aged under 15 years in the British Isles during 1988. BMJ 1991; 302: 443-447.

6. Bodansky HJ, Staines A, Stephenson C, Haigh D, Cartwright R. Evidence for an environmental effect in the etiology of insulin dependent diabetes in a transmigratory population. BMJ 1992;304: 1020-1022.

7. Samanta A, Burden AC, Jones GR, Woollands, Clarke M, Swift PGF, et al. Prevalence of insulin dependent diabetes mellitus in Asian children. Diabetic Medicine 1987; 4: 65-67.

8. Bodington MJ, Burden AC. The epidemic of Indian childhood diabetes in Leicester. Social and cultural differences between cases and control population. Practical Diabetes 1993; 10: 32-34.

9. Muntoni S, Fonte MT, Studuto S, Marrietti G, Bizzarri C, Crino A, et al. Incidence of insulin dependent diabetes mellitus among Sardinian- heritage children born in Lazio region, Italy. Lancet. 1997; 349: 160-162.

10. Lipton RB, Fivecoate JA. High risk of lODM in African-American and Hispanic children in Chicago, 1985-1990. Diabetes Care 1995; 18: 476-482.

11. Parslow RC, Mckinney PA, Law GR, Staines A, Williams R, Bodansky HJ. Incidence of childhood diabetes mellitus in Yorkshire, northern England, is associated with nitrate in drinking water:. An ecological analysis. Diabetologica 1997; 40: 550-556.

12. Gibbon C, Smith T, Egger P, Betts P, Phillips D. Early infection and subsequent insulin de- pendent diabetes. Arch Dis Child 1997; 77: 384-385.

13. Gardner SG, Bingley PJ, Sawtell PA, Weeks S, Gale EA. Rising incidence of insulin dependent diabetes in children aged under 5 years in Oxford region: Time trend analysis. BMJ 1997;315:713-717.

14. Mohan V, Deepa R, Bhatia E, Singh AK, Hitman GA, Zimmet PZ, et al. Antibodies to pancreatic islet cell antigens in diabetes seen in southern India with particular reference to tibrocalculous pancreatic diabetes. Diabetic Med 1998; 15: 156-159.

15. Lee HC, Cha BS, Nam MS, Song YD, Lim SK, Kim DH, et al. Relationship among 64k au- toantibodies, pancreatic beta-cell function, HLA-DR antigens and HLA-DQ genes in patients with insulin dependent diabetes mellitus in Korea. Korean J Int Med 1995; 10: 1-9.

16. Tuomi T, Zimmet P, Rowley MJ, Min HK, Vichayanrat A, Lee H K, et al. Differing frequency of autoantibodies to glutamic acid decarboxylase among Koreans, Thais and Australians with diabetes mellitus. Clinical Immunol Immunopathol 1995; 74: 202-206.

17. Sugihara S, Konda S, Wataki K, Kobayashi Y, Murata A, Miyamoto S, et al. Clinical significance and time course of antibodies of glutamic acid decarboxylase in Japanese children with type 1 (insulin-dependent) diabetes mellitus. Acta Paediatric a 1996; 85: 558-563.

18. Huang FY, Lee YJ, Lo FS, Wang CH, Lin SP, Hsu CH, et al. DQA1* Arg52, DQB1*non Asp, and DRB 1*04 genotypes in Chinese children with insulin dependent diabetes mellitus. Exp Clin Immunogen 1998; 15: 33-45.
 

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