Type 1 diabetes mellitus
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Contents |
Summary
Type 1 diabetes in which pancreatic β-cell destruction almost always leads to absolute insulin deficiency has an increasing incidence worldwide and accounts for about 5–10% of cases of diabetes mellitus.[1] It has a strong genetic component, and while it can be triggered by viral illness many of the factors that triggers remain unknown. More details can be found in articles linked from category:diabetes.
- Seen in younger individuals - usually under 40 years of age
- North european predominance
- Human lymphocyte antigen DR3/DR4 very common
- Destruction of the islets of Langerhans - insulitis
- Possibly viral triggered autoimmune disease
- May be other autoimmune diseases - thyroid failure, ovarian failure, Addison's disease
- Antibodies found
- Seems to present more when viral illnesses more prevalent
- Suggested viruses are coxsackie B
- Prone to ketoacidosis
- Presentation is polyuria, polydipsia, weight loss, balanitis and sometimes with diabetic ketoacidosis
- All patients will require Insulin as well as dietary measures
Subtypes
- Type 1A results from a cell-mediated autoimmune attack on β cells and is associated with HLA haplotype on chromosome 6.
- Type 1B is rare, usually in those of Asian or African descent and has varying degrees of insulin deficiency between sporadic episodes of ketoacidosis.Monogenetic diabetes needs to be excluded[2] and there is an association with +49 A/G polymorphism of CTLA-4 gene [3][4]
Genetic Risk Type 1A
See genetics of diabetes. The HLA locus (6p21-31) confers about 50% of the genetic susceptibility with roughly 15% from insulin-VNTR (IDDM2 at 11p15.5), 15% from CTLA-4 (IDDM12 at 2q33) and the remainder from a number of genes, not all well characterised.
High risk HLA haplotypes
- DR3/4
- DQA1*0301-DQB1*0302
- DQA1*0501-DQB1*0201
Protective genes
- DQA1*0102-DQB1*0602 (diabetes resistance)
- DRB1*1401
Associations
There is no association with childhood vaccination[5]
Triggers
- Viruses (eg, enteroviruses, coxsackie, congenital rubella)
- Environmental toxins
- N-nitroso-compounds[6])
- Early exposure to cow's milk proteins, cereals, or gluten
- Congenital rubella
Autoimmune disease
- Hashimoto's thyroiditis
- Graves' disease
- Addison's disease
- Coeliac disease
- Myasthenia gravis
- Vitiligo
Management
- Appropriate insulin delivery
- Compensation for non-basal conditions such as physical activity, intercurrent illness, stress
- Appropriate self-monitoring of blood glucose
- Nutritional planning with flexible programmes, including carbohydrate counting
- Treatment (and recognition training) of severe hypoglycaemia and diabetic ketoacidosis
- Monitor for and treat associated conditions
- Thyroid(? yearly measurement of thyroid function)
- Coeliac disease
- Monitoring for and treatment of complications.
- Microvascular
- Retinopathy (eg, fundus photography)
- Nephropathy (microalbuminuria)
- Neuropathy (vibration sense, pin prick postural hypotension)
- Macrovascular
- Microvascular
- Psychological and psychosocial wellbeing monitoring and interventions
Cure
In principle this should be a curable disease. Transplants have been done, for instance adding the pancreas to a renal transplant, but this is late and large. Cell culture and implantation either of generic beta cells, or of autologous stem cells [7] seem appropriate directions of endeavour.
References
- ↑ Daneman D. Type 1 diabetes. Lancet. 2006;367:847-58. (Direct link – subscription may be required.)
- ↑ Zhang D, Zhou Z, Li L, Weng J, Huang G, Jing P, et al. Islet autoimmunity and genetic mutations in Chinese subjects initially thought to have Type 1B diabetes. Diabetic medicine : a journal of the British Diabetic Association. 2006;23:67-71. (Direct link – subscription may be required.)
- ↑ Liang H, Yagi K, Asano A, Kobayashi J, Mabuchi H. Association between CTLA-4 +49 A/G polymorphism and type 1B diabetes in Japanese population. Endocrine. 2004;25:105-9.
- ↑ Abiru N, Kawasaki E, Eguch K. Current knowledge of Japanese type 1 diabetic syndrome. Diabetes Metab Res Rev. 2002;18(5):357-66.
- ↑ Hviid A, Stellfeld M, Wohlfahrt J, Melbye M. Childhood vaccination and type 1 diabetes. The New England journal of medicine. 2004;350:1398-404. (Direct link – subscription may be required.)
- ↑ Helgason T, Jonasson MR. Evidence for a food additive as a cause of ketosis-prone diabetes. Lancet. 1981;2:716-20.
- ↑ Couri, C. E. B. et al. C-Peptide Levels and Insulin Independence Following Autologous Nonmyeloablative Hematopoietic Stem Cell Transplantation in Newly Diagnosed Type 1 Diabetes Mellitus. The Journal of the American Medical Association, Vol. 301, April 15, 2009, pp. 1573-79. "In conclusion, autologous nonmyeloablative haematopoietic stem cell transplantation was able to induce prolonged and significant increases of C-peptide levels associated with absence of or reduction of daily insulin doses in a small group of patients with type 1 diabetes mellitus" http://jama.ama-assn.org/cgi/content/short/301/15/1573
