1 / 28

Type 2 diabetes in youth and young adults

Diagnosis of type 2diabetes in youth

30947
Download Presentation

Type 2 diabetes in youth and young adults

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. SUBTYPE OF TYPE 2DIABETES IN CHILDREN AND ADOLESCENCE Professor / Mohammed Ahmed Bamashmos Professor of internal medicine and endocrinology

  2. 1- TYPE 2 DIABETES IN YOUTH Definition and prevalence: Type 2 diabetes in children that diagnosed at the age between 12- 18 years Type 2 diabetes occurs more commonly in adults. In fact, it used to be called adult-onset diabetes. But type 2 diabetes in children is on the rise, fueled by the obesity epidemic. Prevalence ; 12 %

  3. RISK FACTORS 1- overweight and obesity ; The following terminology is used to describe states of excess weight in childhood and adolescence Overweight – BMI ≥85th and <95th percentile. Obesity – BMI ≥95th percentile. 2- genetic susceptibility 3- age and gender ; About 40 percent of pediatric cases present between 10 and 14 years of age, and the remaining 60 percent between 15 and 19 years. Girls are 1.3 to 1.7 times more likely than boys to develop T2DM during adolescence .Although the reason for this increased risk in girls is not clear, it may be related to an increased risk of insulin resistance, as seen in adolescent girls with polycystic ovary syndrome (PCOS). Many patients with pediatric T2DM present at the onset of puberty (mean age of 13.5 years) ,a stage of development when there is increased insulin resistance. During puberty, insulin sensitivity decreases by approximately 30 percent ,related to the increased activity of growth hormone and insulin-like growth factor-1

  4. 4- Prenatal exposures — One hypothesis suggests that prenatal exposure to maternal under nutrition or gestational diabetes causes metabolic and hormonal changes that promote obesity and insulin resistance and increase T2DM risk in adult offspring. This phenomenon has been termed “metabolic programming”. 5- -Low birth weight for gestational age resulting from intrauterine undernutrition is associated with insulin resistance. The combination of low birth weight and weight gain in adult middle age increases insulin resistance and the risk for T2DM. 6- Polycystic ovary syndrome  Insulin resistance is a component of PCOS and may play a role in its pathogenesis. Patients with PCOS are at increased risk for developing T2DM. 7- Gestational diabetes – The abnormal intrauterine metabolic environment of a diabetic pregnancy appears to increase the risk of T2DM. Intrauterine exposure to hyperglycemia and hyperinsulinemia may affect the development of adipose tissue and pancreatic beta cells, leading to future obesity and altered glucose metabolism.

  5. PATHOGENESIS

  6. CLINICAL PRESENTATION • 1- classical diabetes symptoms (57-70%) • 2- asymptomatic (40%) , in the absence of symptoms the diagnoses of diabetes should not be based on single plasma glucose • 3- acute complication ; DKA (5-13%) , or HHS its rare but serious

  7. DIAGNOSIS 1- investigation to diagnose diabetes 2- investigation to differentiate type 2 diabetes of youth from type 1 diabetes • A- Assessment of B –cell function • - serum insulin • - C- peptide • - urine creatinine to C- peptide ratio • B- Assessment of IR • - by HOMA –IR

  8. SCREENING OF TYPE 2 DIABETES OF YOUTH Indication ; in 2015 the American diabetic Association recommended screening for T2DM in children with over weight ( BMI ≥ 85th percentile for age and sex , weight for height ≥ 85 th percentile , oe weight ≥ 120% of ideal for height ) with two additional risk factors for T2DM ; - family history of T2DM in first or second degree relatives - race / ethnicity - sign of IR - maternal history of diabetes or GDM during the child gestation The age of screening initiation for type 2 diabetes in children is 10 years or at the onset of puberty

  9. DIFFERENTIAL DIAGNOSIS • 1- differentiate type 1 from type 2 clinical -Body habitus – Patients with T2DM are usually obese, (body mass index (BMI) ≥95th percentile for age and gender). In contrast, children with type 1 diabetes (T1DM) are often not overweight and usually have a recent history of weight loss, although up to 25 percent are overweight or obese (BMI ≥85th). - Age ; Youth with T2DM generally present after the onset of puberty, at a mean age of 13.5 years, and almost all present after 10 years of age .By contrast, about 50 percent of youth with T1DM present prior to 10 years of age.   -Insulin resistance – Patients with T2DM usually have clinical features associated with insulin resistance such as acanthosis nigricans, hypertension, dyslipidemia, and polycystic ovary syndrome (PCOS), which are not commonly seen in children with T1DM.

  10. -Family history – 75 to 90 percent of those with type 2 diabetes have an affected close relative, whereas up to 10 percent of patients with type 1 diabetes have an affected close relative. - Ethnicity – In the United States, most pediatric patients with T2DM belong to minority racial and ethnic groups including non-Hispanic Black, Hispanic, Native American, Asian American, and Pacific Islanders. - Insidious onset of diseases - Ketoacidosis ,Patients with T1DM are somewhat more likely to present with ketoacidosis, due to severe insulin deficiency, but this presentation occurs in 5 to 10 percent of adolescents with T2DM • Laboratory

  11. COMPLICATION Table 1Screening for diabetes complications and comorbidities in children with type 2 diabetes Complication/Comorbid condition Indications and intervals for screening Screening test Neuropathy Yearly screening commencing at diagnosis of diabetes Questioned and examined for: • Symptoms of numbness, pain, cramps and paresthesia•Vibration sense•Light touch and ankle reflexes Retinopathy Yearly screening commencing at diagnosis of diabetes •7 -standard field, stereoscopic-colour fundus photography with interpretation by Nephropathy Yearly screening commencing at diagnosis of diabetes •First morning (preferred) or random ACR•Abnormal ACR requires confirmation at least 1 month later with either a first morning ACR or timed overnight urine collection for ACR•Repeated sampling should be done every 3 to 4 months over a 6- to 12-month period to demonstrate persistence Dyslipidemi Screening should commence at diagnosis of diabetes and yearly thereafter Fasting TC, HDL-C, TG, calculated LDL-C Hypertension At diagnosis of diabetes and every diabetes-related clinical encounter thereafter (at least twice annually) BP measurement using appropriately sized cuff NAFLD Yearly screening commencing at diagnosis of diabetes ALT and/or fatty liver on ultrasound PCOS Yearly clinical screening commencing at diagnosis of diabetes in pubertal females Clinical assessment on history and physical exam for oligo/amenorrhea, acne and/or hirsutism OSA At baseline, and yearly clinical screening Symptoms suggestive of obstructive sleep apnea include: snoring, apneas, morning headaches, fatigue, daytime sleepiness, nocturia and enuresis Depression Screening at diagnosis and yearly thereafter Clinical assessment on history of symptoms of depression, including fatigue, depressed or irritable mood, loss of interest or pleasure, feelings of worthlessness or guilt Binge Eating Screening at diagnosis and yearly thereafter Clinical assessment on history: frequency of having lost control while eating, eating unusually large amounts ACR, albumin-to-creatinine ratio; ALT, alanine aminotransferase; BP, blood pressure; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; NAFLD, non-alcoholic fatty liver disease; OSA; obstructive sleep apnea; PCOS, polycystic ovary syndrome; TC, total cholesterol; TG, triglycerides.

  12. TREATMENT Treatment goal ; 1- weight loss 7% 2- increase in exercise capacity 3- normalization of glycaemia 4- control of comorbidity Treatment target ; HbA1C 6.5 – 7 % Types ; 1- life style ; • - Education ; - healthy eating habit - carbohydrate counting

  13. - reading food label - glucose monitoring • - ketone testing • - psychological support • - diet ; aim to decrease body weight by 7-10% • - Exercise ; • Pharmacological therapy ; • types and indication ;

  14. 1- metformin ; • - in asymptomatic metabolically patients with HbA1C less than 8.5 • 2- basal insulin ; • - in symptomatic patients with marked hyperglycemia ( BG more than 250mg , HbA1C more than 8.5 % and no acidosis • - if metformin is contraindicated or not tolerated • 3- basal insulin and metformin • 4- basal bolus insulin

  15. 2- KETOSIS PRONE TYPE 2 DIABETES • Its group of the patients who are present at first time with DKA and not fit the typical characteristic of autoimmune type 1 diabetes • term used ; • - atypical diabetes • - flatbush diabetes • - diabetic type 1B • - ketosis prone type 2 diabetes

  16. CHARACTERISTICS 1- DKA cases without predicting causes 2- present acutely as DKA but eventually improve after short period of insulin therapy 3- prolonged remission is often possible , with eventual cessation of insulin treatment and maintenance of glycemic control with diet or oral antihyperglycemic agents 4- fasting C- peptide level ≥ 1 ng /dl and stimulated C- peptide level ≥1.5 ng/dl are productive of long term normoglycemic remission in patients with history oh DKA

  17. CLASSIFICATION • They proposed a new Aβ classification scheme based on the presence or absence of β-cell autoantibodies and the β-cell function to predict whether patients with DKA will have preserved β-cell function and long-term insulin independence. The proposed Aβ classification scheme divided patients with DKA into four groups. Patients with autoimmune disease with absent (A+β−) or preserved (A+β+) β-cell function and those without autoimmune diabetes with absent (A−β−) or preserved (A−β+) β-cell function. This classification was found to have a sensitivity of 99.4%, specificity of 95.9%, positive predictive value of 97.1%, and negative predictive value of 99.2% in predicting whether patients with DKA will have preserved β-cell function and long-term insulin independencehe • T high predictive value was driven mainly by the presence of β-cell function following the resolution of DKA rather than the presence of autoimmune markers. • -Patients with negative β-cell function, with or without autoimmune markers ( A+ B- or A-, B- ), have clinical and biochemical characteristics of type 1 diabetes, i.e., they require exogenous insulin to preserve life (12). Less than 1% of the subjects classified initially as β− showed improvement in β-cell function during followup

  18. 1- A-. B+ its most common type 54% and it has clinical and laboratory similar to type 2 diabetes 2- A+ , B+ ; 8% • 3- A+, B- 18% • 4 - A-. B- 20% they resemble type 1 DM and require insulin therapy

  19. The group of major interest includes those patients without autoimmunity but preserved β-cell function (A−β+). They represent 74% of adult patients with newly diagnosed diabetes presenting with DKA. Despite the presentation with severe metabolic decompensation, most patients showed clinical and biochemical characteristics of type 2 diabetes. Most A−β+ subjects had new-onset diabetes and were obese, middle-aged males with a strong family history of type 2 diabetes. In these patients, β-cell function is substantial when measured within 1–2 weeks of the index DKA and improves further when measured after 6–12 months (12). Several observational and prospective studies have reported that ∼70% of such patients achieve near-normoglycemia remission within 10 weeks of follow-up (7,8,10) and that 40% of patients remained free of insulin injections 10 years after their first presentation

  20. PATHOGENESIS -β-cell autoimmunity and HLA associations are uncommon. -Impaired insulin sensitivity at presentation that significantly improves at time of follow-up. -Impaired pancreatic β-cell reserve at presentation that significantly improves with follow-up. -Short-term glucotoxicity and lipotoxicity are not primary pathophysiologic factors in the development of β-cell decompensation.

  21. CLINICAL FEATURES • Most patients with new-onset KPDM present with <4 weeks of polyuria, polydipsia and weight loss (Table 2). In addition, patients can complain of nausea, vomiting and abdominal pain and are found to have severe hyperglycemia accompanied with urinary ketonuria or frank DKA. The majority of patients are overweight or obese and the unintentional weight loss reported at time of diagnosis varies between 4 and 12 kg [7,8,25]. The age of onset is usually in the fourth or fifth decade of life; however, KPDM has been increasingly reported in the pediatric population [29,30].

  22. DIAGNOSIS • 1- clinical diagnosis ； • A-from type 1 diabetes • 2- laboratory • - to diagnose DM • - to diagnose DKA • - to know which subgroup of ketosis prone • - serological diagnosis • - assessment of B- cell function • - serum C-peptide • - glucagon stimulation test ； 1 mg glucagon stimulated C- peptide test at 0, 3 and 6 min

  23. Treatment ; Steps of treatment ; 1- treatment of DKA ; 2- Following discharge from the hospital ▪ Monitor patients every 2 weeks for the first 2 months to adjust insulin therapy, then every 2 or 3 months depending on glycemic control. Mean insulin requirement to achieve target BG is usually 1–1.2 units/kg of bodyweight ▪ Start tapering insulin once fasting BG levels reach <130 mg/dl for 2 weeks or if patient experiences hypoglycemia. Decrease total insulin dose by 25% at each visit 3- order for following investigation ;

  24. - assessment of B-cell function - serological test 4- Insulin tapering can begin once fasting BG (FBG) levels are ≤ 130 mg/dl for 2 weeks or if the patient experiences hypoglycemia as defined as a BG <70 mg/dl. Over the course of 12 weeks, most patients can completely discontinue insulin by decreasing the total insulin dose by 25% at each follow-up visit. Balasubramanyam et al. suggested any attempt to withdraw insulin treatment should be based on a precise autoimmunity and β-cell function (Aβ) classification that has 99% sensitivity and 97% positive predictive value

  25. Over the course of 10–12 weeks, most patients can completely discontinue insulin. - 5-After discontinuation of insulin therapy ▪ Subjects with negative GAD and with fasting or stimulated C-peptide levels >1.5 ng/dl and >2.25 ng/dl, respectively, start low-dose sulfonylurea (glyburide 1.25–2.5 mg/day), pioglitazone 30 mg/day or metformin (500 mg b.i.d.) therapy ▪ Patients with positive GAD or with inadequate insulin secretion are more likely to relapse and may be kept on insulin therapy, and/or should be carefully monitored for recurrence of hyperglycemia or ketosis

More Related