1 / 51

UPDATE ON CHILDHOOD DIABETES MELLITUS

UPDATE ON CHILDHOOD DIABETES MELLITUS. Abdelaziz Elamin MD, PhD, FRCPCH Professor of Child Health Sultan Qaboos University. DEFINITION. The term diabetes mellitus describes a metabolic disorder of multiple etiologies characterized by chronic

Olivia
Download Presentation

UPDATE ON CHILDHOOD DIABETES MELLITUS

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. UPDATE ON CHILDHOOD DIABETES MELLITUS Abdelaziz Elamin MD, PhD, FRCPCH Professor of Child Health Sultan Qaboos University

  2. DEFINITION • The term diabetes mellitus describes a metabolic disorder of multiple etiologies characterized by chronic hyperglycemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects of insulin secretion, insulin action or both.

  3. DIABETES EPIDEMIOLOGY • Diabetes is the most common endocrine problem & is a major health hazard worldwide. • Incidence of diabetes is alarmingly increasing all over the globe. • Incidence of childhood diabetes range between 3-50/100,000 worldwide; in Oman it is estimated as 4/100000 per year.

  4. OLD CLASSIFICATION (1985) • Type 1, Insulin-dependent (IDDM) • Type 2, Non Insulin-dependent (NIDDM) • obese • non-obese • MODY • IGT • Gestational Diabetes

  5. WHO CLASSIFICATION 2000 • Is based on etiology not on type of treatment or age of the patient. • Type 1 Diabetes (idiopathic or autoimmune b-cell destruction) • Type 2 Diabetes (defects in insulin secretion or action) • Other specific types

  6. WHO CLASSIFICATION/2 • Both type 1 & type 2 can be further subdivided into: • Not insulin requiring • Insulin requiring for control • Insulin requiring for survival • Gestational diabetes is a separate entity • Impaired Glucose Tolerance (IGT) indicates blood glucose levels between normal & diabetic cut off points during glucose tolerance test.

  7. Fasting blood glucose level Diabetic Plasma >7.0 mmol Capillary >6.0 mmol IGT Plasma 6.0-6.9 mmol Capillary 5.6-6.0 mmol 2 hours after glucose load (Plasma or capillary BS) IGT 7.8-11.0 Diabetic level > 11.1 (200 mg) DIAGNOSTIC CRITERIA

  8. Types of Diabetes in Children • Type 1 diabetes mellitus accounts for >90% of cases. • Type 2 diabetes is increasingly recognized in children with presentation like in adults. • Permanent neonatal diabetes • Transient neonatal diabetes • Maturity-onset diabetes of the young • Secondary diabetes e.g. in cystic fibrosis or Cushing syndrome.

  9. MODY • Usually affects older children & adolescents • Not rare as previously considered • 5 subclasses are identified, one subclass has specific mode of inheritance (AD) • Not associated with immunologic or genetic markers • Insulin resistance is present

  10. TRANSIENT NEONATAL DIABETES • Observed in both term & preterm babies, but more common in preterm • Caused by immaturity of islet b-cells • Polyuria & dehydration are prominent, but baby looks well & suck vigorously • Highly sensitive to insulin • Disappears in 4-6 weeks

  11. PERMANENT NEONATAL DIABETES • A familial form of diabetes that appear shortly after birth & continue for life • The usual genetic & immunologic markers of Type 1 diabetes are absent • Insulin requiring, but ketosis resistant • Is often associated with other congenital anomalies & syndromes e.g. Wolcott-Rallison syndrome.

  12. TYPE 1 DIABETES: ETIOLOGY • Type 1 diabetes mellitus is an autoimmune disease. • It is triggered by environmental factors in genetically susceptible individuals. • Both humoral & cell-mediated immunity are stimulated.

  13. GENETIC FACTORS • Evidence of genetics is shown in • Ethnic differences • Familial clustering • High concordance rate in twins • Specific genetic markers • Higher incidence with genetic syndromes or chromosomal defects

  14. AUTOIMMUNITY • Circulating antibodies against b-cells and insulin. • Immunofluorescent antibodies & lymphocyte infiltration around pancreatic islet cells. • Evidence of immune system activation. Circulating immune complexes with high IgA & low interferon levels. • Association with other autoimmune diseases.

  15. ENVIRONMENTAL INFLUENCE • Seasonal & geographical variation. • Migrants take on risk of new home. • Evidence for rapid temporal changes. • Suspicion of environmental agents causing disease which is confirmed by case-control experimental animal studies.

  16. ENVIRONMENTAL SUSPECTS • Viruses • Coxaschie B • Mumps • Rubella • Reoviruses • Nutrition & dietary factors • Cow’s milk protein • Contaminated sea food

  17. OTHER MODIFYING FACTORS • The counter-regulatory hormones: • glucagon • cortisol, • catecholamines • thyroxin, • GH & somatostatin • sex hormones • Emotional stress

  18. ETIOLOGIC MODEL • The etiologic model of type 1 diabetes resembles that of Rheumatic fever. • Rheumatic fever was prevented by elimination of the triggering environ. factor (b-streptococci). • Similarly type 1 diabetes may be prevented by controlling the triggering factors in high risk persons.

  19. CLINICAL PRESENTATIONS • Classical symptom triad: • polyuria, polydipsia and weight loss • DKA • Accidental diagnosis • Anorexia nervosa like illness

  20. DIAGNOSIS • In symptomatic children a random plasma glucose >11 mmol (200 mg) is diagnostic. • A modified OGTT (fasting & 2h) may be needed in asymptomatic children with hyperglycemia if the cause is not obvious. • Remember: acute infections in young non-diabetic children can cause hyperglycemia without ketoacidosis.

  21. NATURAL HISTORY • Diagnosis & initiation of insulin • Period of metabolic recovery • Honeymoon phase • State of total insulin dependency

  22. METABOLIC RECOVERY During metabolic recovery the patient may Develop one or more of the following: • Hepatomegaly • Peripheral edema • Loss of hair • Problem with visual acuity These are caused by deposition of glycogen & metabolic re-balance.

  23. HONEYMOON PERIOD • Due to b-cell reserve optimal function & initiation of insulin therapy. • Leads to normal blood glucose level without exogenous insulin. • Observed in 50-60% of newly diagnosed patients & it can last up to one year but it always ends. • Can confuse patients & parents if not educated about it early.

  24. COMPLICATIONS OF DIABETES • Acute: • DKA • Hypoglycemia • Late-onset: • Retinopathy • Neuropathy • Nephropathy • Ischemic heart disease & stroke

  25. TREATMENT GOALS • Prevent death & alleviate symptoms • Achieve biochemical control • Maintain growth & development • Prevent acute complications • Prevent or delay late-onset complications

  26. TREATMENT ELEMENTS • Education • Insulin therapy • Diet and meal planning • Monitoring • HbA1c every 2-months • Home regular BG monitoring • Home urine ketones tests when indicated

  27. EDUCATION • Educate child & care givers about: • Diabetes • Insulin • Life-saving skills • Recognition of Hypo & DKA • Meal plan • Sick-day management

  28. INSULIN • A polypeptide made of 2 b-chains. • Discovered by Bants & Best in 1921. • Animal types (porcine & bovine) were used before the introduction of human-like insulin (DNA-recombinant types). • Recently more potent insulin analogs are produced by changing aminoacid sequence.

  29. FUNCTION OF INSULIN • Insulin being an anabolic hormone stimulates protein & fatty acids synthesis. • Insulin decreases blood sugar • By inhibiting hepatic glycogenolysis and gluconeogenesis. • By stimulating glucose uptake, utilization & storage by the liver, muscles & adipose tissue.

  30. TYPES OF INSULIN • Short acting (neutral, soluble, regular) • Peak 2-3 hours & duration up to 8 hours • Intermediate acting • Isophane (peak 6-8 h & duration 16-24 h) • Biphasic (peak 4-6 h & duration 12-20 h) • Semilente (peak 5-7 h & duration 12-18 h) • Long acting (lente, ultralente & PZI) • Peak 8-14 h & duration 20-36 h

  31. INSULIN CONCENTRATIONS • Insulin is available in different concentrations 40, 80 & 100 Unit/ml. • WHO now recommends U 100 to be the only used insulin to prevent confusion. • Special preparation for infusion pumps is soluble insulin 500 U/ml.

  32. INSULIN REGIMENS • Twice daily: either NPH alone or NPH+SI. • Thrice daily: SI before each meal and NPH only before dinner. • Intensive 4 times/day: SI before meals + NPH or Glargine at bed time. • Continuous s/c infusion using pumps loaded with SI.

  33. INSULIN ANALOGS • Ultra short acting • Insulin Lispro • Insulin Aspart • Long acting without peak action to simulate normal basal insulin • Glargine

  34. NEW INSULIN PREPARATIONS • Inhaled insulin proved to be effective & will be available within 2 years. • Nasal insulin was not successful because of variable nasal absorption. • Oral insulin preparations are under trials.

  35. ADVERSE EFFECTS OF INSULIN • Hypoglycemia • Lipoatrophy • Lipohypertrophy • Obesity • Insulin allergy • Insulin antibodies • Insulin induced edema

  36. PRACTICAL PROBLEMS • Non-availability of insulin in poor countries • injection sites & technique • Insulin storage & transfer • Mixing insulin preparations • Insulin & school hours • Adjusting insulin dose at home • Sick-day management • Recognition & Rx of hypo at home

  37. DIET REGULATION • Regular meal plans with calorie exchange options are encouraged. • 50-60% of required energy to be obtained from complex carbohydrates. • Distribute carbohydrate load evenly during the day preferably 3 meals & 2 snacks with avoidance of simple sugars. • Encouraged low salt, low saturated fats and high fiber diet.

  38. EXERCISE • Decreases insulin requirement in diabetic subjects by increasing both sensitivity of muscle cells to insulin & glucose utilization. • It can precipitate hypoglycemia in the unprepared diabetic patient. • It may worsen pre-existing diabetic retinopathy.

  39. MONITORING • Compliance (check records) • HBG tests • HbA1 every 2 months • Insulin & meal plan • Growth & development • Well being & life style • School & hobbies

  40. ADVANCES IN MONITORING • Smaller & accurate meters for intermittent BG monitoring • Glucowatch continuous monitoring using reverse iontophoresis to measure interstitial fluid glucose every 20 minutes • Glucosensor that measures s/c capillary BG every 5 minutes • Implantable sensor with high & low BG alarm

  41. ADVANCES IN MANAGEMENT • Better understanding of diabetes allows more rational approach to therapy. • Primary prevention could be possible if the triggering factors are identified. • The DCCT studies proves beyond doubt that chronic diabetic complication can be controlled or prevented by strict glycemic control.

  42. TREATMENT MADE EASY • Insulin pens & new delivery products • Handy insulin pumps • fine micro needles • Simple accurate glucometers • Free educational material • computer programs for comprehensive management & monitoring

  43. TELECARE SYSTEMS • IT has improved diabetes care • Internet sites for education & support • Web-based systems for telecare are now available. The patient feeds his HBGM data and get the physician, nurse & dietician advice on the required modification to diet & insulin treatment.

  44. PITFALLS OF MANAGEMENT • Delayed diagnosis of IDDM • The honey-moon period • Detection & treatment of NIDDY • Problems with diagnosis & treatment of DKA & hypoglycemia • Somogi’s effect (dawn phenomenon) may go unrecognized.

  45. FUTURE PROMISES • The cure for IDDM is successful islet cell transplantation, which will be available in the near future. • Primary prevention by a vaccine or drug will be offered to at risk subjects identified by genetic studies. • Gene modulation therapy for susceptible subjects is a promising preventive measure.

  46. Pancreas & Islet Cell Transplantation • Pancreas transplants are usually given to diabetics with end stage renal disease. • Islet cell transplants, the ultimate treatment of type 1 diabetes is under trial in many centers in the US & Europe with encouraging results but graft rejection & recurrence of autoimmunity are serious limitations.

  47. IMMUNE MODULATION • Immunosuppressive therapy for • Newly diagnosed • Prolonged the honey moon • For high risk children • Immune modulating drugs • Nicotinamide • mycophenolate

  48. GENE THERAPY • Blocks the immunologic attack against islet-cells by DNA-plasmids encoding self antigen. • Gene encode cytokine inhibitors. • Modifying gene expressed islet-cell antigens like GAD.

  49. PREDICTION OF DIABETES • Sensitive & specific immunologic markers • GAD Antibodies • GLIMA antibodies • IA-2 antibodies • Sensitive genetic markers • HLA haplotypes • DQ molecular markers

  50. PREVENTION OF DIABETES • Primary prevention • Identification of diabetes gene • Tampering with the immune system • Elimination of environmental factor • Secondary prevention • Immunosuppressive therapy • Tertiary prevention • Tight metabolic control & good monitoring

More Related