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  Diabetes mellitus in adolescence 03/29/2024 10:09am (UTC)
   
 

Diabetes mellitus in adolescence                                                     Content        Next  
 

    Adolescence begins and progresses across a wide range of chronologic ages and differs between sexes. It has been divided into early, middle and late in terms of stages of pubertal development ie. pubic hair, the breast and genitalia in females and males respectively. Adolescence starts at the age of 10-14yrs in males and 10-13 years in females and ends with young adulthood at the age of 17-21 years.


    In present times, when an adolescent develops diabetes, he may be expected to live a long and fruitful life provided he is taught to take proper care of his disease.


    Diabetes in adolescent differs from that in adults in several important aspects. First, unlike the adult type, the onset of diabetes tends to be sudden, with rapid appearance of symptoms and rapid loss of weight. Second, once diagnosed and properly treated with insulin, it tends to go into a remission, during which the insulin requirement may even drop to zero. Third, adolescent diabetes is characteristically labile and blood sugar may vary widely and rapidly.
 

   Etiopathogenesis-The basic underlying defect in adolescent diabetes is diminished secretion of insulin. Several factors point to autoimmune destruction of pancreatic islets. There is a strong association of Type I DM with other autoimmune disorders. It is also known to be associated with an increased frequency with HLA B8-DR3, DR4, and BW15. When both D3 and D4 are inherited, the risk of developing diabetes is increased by 7-10 fold.
 

   A genetic type of predisposing factor B(BSF1) is found in more than 20% of Type I DM patients.


   The homozygous absence of aspartic acid at position 57 of HLA DQB Chain confers about 100 fold relative risk of developing type I DM.


   Viral infections have been proposed as triggering factors for adolescent diabetes. Epidemics of mumps, rubella and coxsackievirus infections have been associated with subsequent increase in Type I DM. Virus may directly destroy B cells, or may share antigenic determinants with B cells-molecular mimicry-or may trigger a widespread autoimmune response.


   Exposure to cow's milk or milk products in early life predisposes to autoimmune DM. The environmental trigger proposed is bovine albumin operating through the mechanism of molecular mimicry. Diabetic subjects were found to have antibodies to bovine albumin which tends with a 69 KDa protein of the surface of pancreatic B cell thus destroying them.


   Other forms of DM in young - The other types of DM encountered in young age are MRDM and MODY. Malnutrition related DM (MRDM) is common between ages 16 and 30 years in males and may account for upto 50% of young onset DM in tropical countries. Deficiency of dietary protein and malnutrition is said to play a role in pathogenesis of PDDM while contribution of food (Cassava) and environmental toxins initiates pathogenesis of FCDM.


   MODY is also a cause of juvenile DM, in which the clinical picture resembles adult onset DM with relative resistance to ketosis, unresponsiveness to oral hypoglycemics and relative resistance of insulin. Islet cell changes in pancreas are responsible for the development of MODY.


   Clinical Presentation - The classical presentation is with polyuria, polydepsia, polyphagia and weight loss. When diabetes becomes decompensated, loss of appetite, nausea and vomiting occur. Fatigue is conspicuous and deterioration in school performance may occur. The vision may become blurred. Pyogenic skin infections and in adolescent girls monilial vaginitis are present occasionally. Ketoacidosis is responsible for the initial presentation in approximately 25% of diabetic children. An insidious onset is characterized by lethargy, weakness and weight loss is also quite common. The most typical physical finding is loss of weight and dehydration.


   Natural History - The following phases are recognized in the natural course of adolescent diabetes;
     (i) Prediabetes - It is defined as the period of time in a diabetics' life before diabetes can

         be detected clinically. It lasts from conception to the first abnormal GTT in a person

         genetically predisposed to diabetes.
     (ii) Chemical Diabetes- It is the period in which diabetes can be detected by special tests

         as GTT, but during which no symptoms of the disease are present. The stage tends to

         be very short in adolescent diabetes.
     (iii) Overt Diabetes - 90% of the juvenile diabetics tend to become total diabetics between

         3-5 years after the onset of disease. Total diabetes is characterized by (a) pancreatic

         islet atrophy (b) no extractable insulin from pancreas (c) Sulfonylurea ineffectiveness.
 

(iv) Remission - Within days, weeks or several months of antidiabetic treatment, 30 - 50% of all children enter into a phase of remission termed as 'Honeymoon Remission'.
 

   Honeymoon Remission - After the initial stablization period, some 45% of newly diagnosed diabetic children require progressive reductions in the daily dose of insulin. Recurrent hypoglycemia is a manifestation prompting reduction in the insulin dose. The remission commonly lasts several weeks or months and may Last as long as 1-2 years. It is related to residual insulin secretion in this period which may be measured by C-peptide levels. Insulin treatment should be continued in this period unless the patient develops hypoglycemia.


   Complications - The acute metabolic complications of adolescent diabetes are hypoglycemia and ketoacidosis, while the major late ones are retinopathy, neuropathy, nephropathy and circulatory abnormalities. Infections are common in diabetics, the order of frequency being skin, urinary tract, lungs and bone. The frequency of retinopathy appears to vary with the age of onset as well as the duration of disease. Proliferative retionopathy appears to be more common in insulin treated patients than in those 'not treated with insulin. Older patients usually with NIDDM, develop retinopathy earlier, but proliferative retinopathy is less common.


   The metabolic or 'Snowflake' cataract is commonly encountered I in the poorly controlled juvenile diabetics and may be seen at the time of diagnosis of type I DM.


   Diabetic nephropathy is the leading cause of death and [disability. Prevalence in NIDDM varies from 15-60 percent, while 35 percent IDDM patients develop this complication. Nephropathy is influenced, like other complications, by the genetic background of the |patient. In NIDDM, other factors causing microalbuininuria like lypertension, UTI and nondiabetic glomerulopathy may contribute to nephropathy,


   Prevalence of neuropathy is determined largely'by the duration of diabetes. Peripheral neuropathy with pain and for motor weakness seen as foot drop may be the primary symptom of type I diabetes.


   Psychological Problems - The parents, on learning of the child's diagnosis may be initially stunned, and there is a feeling of guilt and of shame and anxiety. Diabetes in the child affects the life style and interpersonal relationships of the entire family. The child may be overprotected. He may be accused of committing dietary indiscretions, affecting parent-child relationships.


   Adolescent patients are often very interested and highly motivated in their care, but equally are readily discouraged. A few reject treatment, especially the administration of insulin due to fear of pin-pricks. The child may be entitled special and unrealistic considerations due to his disease and this may create in the child feelings of inadequacy and being defective or unable to cope with the daily demands of life.


   These feeling find expression in non- adherence to instructions regarding nutritional and insulin therapy and in non-compliance with self monitoring. Deliberate overdosage with insulin resulting in hypoglycemia or omission of insulin resulting in ketoacidosis may be plea for psychologic help or manipulative events to escape an environment perceived as undesirable or intolerable.


   Insistence on strict dietary adherence may do more psychologic damage than physiologic good. A weekly sweet- dish may be incorporated in the dietary program to prevent this feeling of deprivation.


   Lipodystrophy in a diabetic child may create problems with insulin therapy. Also the fat atrophy may be mistaken for muscular atrophy, creating a fear of body dissolution. Treatment consists of reassurance.


   Fear of death and decreased life span is common in the diabetic child. The knowledge of complications like amputation and vision loss also fosters anxiety. Feelings of being alone and being isolated are also quite common. However, no specific personality disorder or psychopathology is characteristic of diabetes.


   Management - A child presenting with classical symptoms and who documents hyperglycemia in the absence of clinical dehydration and ketoacidosis, is started therapy with subcutaneous injections of a rapid acting insulin, initiated in a dose of 0.1 to 0.25 U/kg every 6-8 hourly, before meals, with simultaneous monitoring of blood glucose and necessary adjustments of insulin dose accordingly.


   The aims of therapy are -
        (i) to treat any precipitating cause of ketoacidosis e.g. infection,
        (ii) to stabilize the patients metabolic status by adjusting insulin dosage,
        (iii) to institute the appropriate nutritional pattern for the child.
        (iv) to educate the patient and the parents in the principles of disease management.
 

   Insulin therapy, when given as a single daily dose, should have 2/3rd of the daily total dose as an intermediate acting insulin and the remainder as regular insulin. Usually two daily injections are recommended. In this plan 2/3rd before the breakfast and 1/3 with the evening meal are given. Adjustments have to be made for the adolescents during the pubertal growth spurt, during which the requirement increases and becomes lower when puberty is completed.


   The nutritional management involves the total recommended calorie intake to be based on the size or body surface area. The caloric mixture should consist of approximately 55% Carbohydrates, 30% fat and 15% protein. 70% of the carbohydrate should be derived from complex carbohydrates like starch. Intake of fat is adjusted so that the polyunsaturated: saturated fat ratio is 1-2:1. Total daily caloric intake may be divided to provide 20% of the requirement of breakfast, 20% at lunch and 30% at dinner, and 10% each as midmorning, midafternoon and evening snacks. Occasional allowances at special occasions are permissible in order not to foster rebellion.


   Prevention of DKA in IDDM - This involves the education of the child and parents and observing certain sick day rules.


   Education of the child and parents in the treatment of diabetes and its hazards gives them courage and hope in controlling the subtly changing course of disease. The symptoms of a hypoglycemic episode and its oral and parehteral treatment as well as the symptoms, emergency nature prevention of acidosis are taught.


   Sick day rules should be explained and observed by the child. During an illness, the basic dose of insulin may be continued and additional insulin given as indicated by urine tests or blood glucose monitoring.


   Travelling - Insulin should be stored at a cool temperature without freezing. Insulin dose may be delayed to match with meals, and if the meal is missed, a correspondingly reduced insulin dose should be taken rather than omitting insulin completely. Dietary restriction should be adhered to, as far as possible, even in travel.


   Growth problems - Even with diabetes developing in early life, a satisfactory adult stature in usually achieved. Significant growth failure occurs in less than 1% of patients.

 

   At the onset of growth spurt, failure to increase the calorie intake as necessary to fuel the spurt can result in well controlled glycemic but growth failure. Also, after the cessation of upward growth if the large energy intake necessary for growth continues, a corresponding large dose of insulin may become customary arid obesity then develops.


   Marriage, Pregnancy, Employment and Insurance - Marriage of two known diabetic persons should be discouraged. The nondiabetic partner should understand the need of life long regular medical supervision of the disease. A diabetic woman especially a teen-age girl should realize the higher chances of having a stillborn infant, and the higher chances of diabetes and congenital anamolies in a live born infant.


   During pregnancy an increased sensitivity to insulin in the first trimester occurs which may lead to severe hypoglycemia. In the subsequent two trimesters, diabetic control tends to worsen due to release of anti-insulin hormones (HCG, Prolactin) with an increased likelihood of development of ketoacidosis. Pregnancy also predisposes to aggravate the microvascular complications. Thus strict monitoring and meticulous glycemic control are desirable during pregnancy.


   The employment prospects of diabetics are better today than ever before. Diabetics can function well in high managerial positions as well as in positions requiring manual labour. A diabetic on insulin should not be assigned a job considered hazardous to himself or others example those involving driving or working at heights. He should have a regular routine so that he can regulate his insulin and diet. Good education and vocational training help in securing good jobs for diabetic patients.


   In life insurance schemes, diabetics are classified as substandard insurance risks because of reduced longevity The age at onset, duration of disease, adequacy of control and the severity of disease are taken into account in evaluating a diabetic. Juvenile diabetics are accepted by many companies but at a higher premium. In Health Insurance too, diabetics are charged a higher premium or offered more restrictions because of the chronicity of the condition.


   Life Span - Diabetes in adolescence is not a benign disease, although survival during childhood is excellent. Despite the potential for, development of complications, survival for 40 years and greater is feasible. When compared to non-diabetics, in IDDM life span is reduced on an average by 10-15 years.

 

   The course of patients with good glycemic control is encouraging. Many are able to attend college and some enter professional courses. Those who marry can successfully have children, although the associated risks are greater.


   Conclusion - Adolescence is a period marked by large daily variations in energy output, variability in the nature and timing of meals, and a generally increased inner turmoil, both emotional and hormonal. The marked anabolism of growth is a special feature of this period as are the difficulties in self-discipline in members of this age group.


   The successful therapy of adolescent diabetes is based on a proper explanation of the therapeutic regimens to the patient and the parents, a wider flexibility to allow variation from day to day to meet altered states of exercise, timing of nature of food and emotions and specialized attention to growth problems.


   With these intensifications and a healthy psychological upbringing, the improvement in care of adolescent diabetics has been marked and continued.


REFERENCES
        1. Mark A.Sperling : Diabetes Mellitus. Nelson- Textbook of Paediatrics, 15th Edition.

            W.B.Saunders Company, 1996; 1646-1666.
        2. Priscilla White : Child with Diabetes Mellitus, Treatment of Diabetes Mellitus. Joslin

           Root, White Marble, llth Edition, Chapter 13, Lea and Febiger, Philadelphia, 1971;

           339-359.
       3. Robert G. Thompson : The Management of Diabetes Mellitus in the Adolescent.

           Adolescent Medicine, MCNA 59:6, Nov. 75; 1349-58-
       4. C.Cabell Bailey : Diabetes in Adolescence. Medical Care of the Adolescent, MCNA

           49:2, March 65, 451-466.
       5. J.I.Bell and TDR Hockaday : Diabetes Mellitus, Oxford Textbook of Medicine, 3rd

           Edition, Chapter 11.11, Oxford University Press, New York 1996; 1448- 1504.
 

 
  What is Diabetes?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
  CONTENTS



1. Diabetes mellitus : a historical review


2. Insulin-some physiological considerations,


3. Epidemiology of diabetes mellitus


4. Pathogenesis of diabetes mellitus in young


5. Impaired glucose tolerance


6. Secondary diabetes mellitus.


7. Laboratory diagnosis and work up for assessment of complications & of diabetes mellitus


8. Oral glucose tolerance test.


9. Neurological involvement in diabetes mellitus


10. Glycation products in diabetes mellitus


11. Diabetes mellitus in adolescence


12. Diabetic keto acidosis


13. Case of brittle diabetes


14. Lipoprotein disorders in diabetes mellitus


15. Diabetes and cardiovascular system


16. Myocardial infarction in diabetes


17. The Syndrome of insulin resistance.


18. Gastro intestinal manifestation of diabetes mellitus


19. Pregnancy and diabetes


20. Skin manifestations of diabetes mellitus


21. Diabetic nephropathy


22. The diabetic foot


23. Sexual dysfunction m diabetes mellitus


24. Joint and Bone manifestation of diabetes mellitus


25. Alcohol and diabetes mellitus


26. Live: and. diabetes mellitus


27. Management of infections m diabetes


28. Diabetes mellitus and surgery


29. Canter arid diabetes


30. Diabetes in elderly


31. Non drug therapy of diabetes mellitus


32. Nutrional approaches in the management of diabetes mellitus


33. Insulin therapy in diabetes mellitus


34. Insulin sensitivity


35. Insulin resistance


36. Oral drugs in non insulin dependent diabetes


37. Lactic acidosis


38. Use of indigenous plant products in diabetes


39. Prevention of diabetes mellitus


40. Pancreatic transplantation in Type I DM (IDDM)


41. Hypoglycemia


42. Diabetes and eye


43. Diabetes mellitus and pulmonary tuberculosis


44. Pitfalls in diagnosis and management of diabetes mellitus


45. Mortality patterns in diabetes mellitus


46. Diabetic education


47. Diabetes mellitus and associated syndromes


48. Diabetes mellitus: socio economic considerations


49. Obesity and diabetes mellitus


50. Proinsulin


51. C-Peptide


52. Glucagon


53. Drug induced diabetes mellitus


54. Insulin anologues


55. Insulin delivery system


56. Micro nutrients in diabetes mellitus


57. Defects in glucose metabolism in neonates


58. Sulphonylurea failure


59. Diabetes control and complications


60. Diabetes mellitus & oral health


61. Common procedures for recording data in diabetes


62. Profile of a lean Type-2 diabetes mellitus


63. Management of post prandial

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