Clinical Performance of a Fully Implanted Long Term Glucose Sensor (LTGS)

DMDIDka

Basic Science LectureMa. Giselle G. Genovata, MD3rd Year Pedia ResidentMedical Center ParanaqueDiabetes InsipidusDiabetes MellitusDiabetic Ketoacidosisa. the passage of large volumes (>4ml/kg/hr) of dilute urine (< 300 mOsm/kg).c. A common chronic metabolic syndrome characterized as hyperglycemia as a cardinal biochemical featureb. A combination of hyperglycemia, acidosis and ketonesGist Definitions

DMDIDka

Diabetes InsipidusDiabetes Insipidus (DI) a heterogeneous clinical syndrome of disturbance in water balance, characterized by polyuria (urine output > 4 ml/kg/hr), polydypsia (water intake > 2 L/m2/d) and failure to thrive.

CENTRAL DIABETES INSIPIDUSVassopresin deficiencyNEPHROGENIC DIABETES INSIPIDUSVassopresin insensitivity at the level of the kidney

both central and nephrogenic DI can be hereditary, or secondary to variety of causesSource: Nelsons Textbook of Pediatrics 19th Ed.DI presents clinically with plyuria and polydipsia and may result from either vasopressin deficiency (central DI) or vasopressin insensitivity at the level of the kidney (nephrogenic DI). They can both rise from inherited defects with congenital or neonatal onset or secondary to variety of causesNelson's Textbook of Pediatrics 19th Edition

Regulation of VP secretion and Serum Osmolality

This table represents the regulation of vasopressin secretion and serum osmolality. *Hyperosmolality, hypovolemia and hypotension are sensed by *osmosensors, volume sensors and barosensors. These stimulate vasopressin secretion and thirst. Vasopressin acts on the kidney to increase water reabsorption (antidiuresis). Thirst causes increased water ingestion. The results of this negative feedback loop causes reduction in hyperosmolaloty or hypotension/hypovolemia. Additiional stimuli for vp secretion includes nausea, hypoglycemia and pain. Nelson's Textbook of Pediatrics 19th EditionCauses of Diabetes Insipidus

Central diabetes insipidus can result from multiple etiologies, including genetic mutations in the vasopressin gene; trauma (accidental or surgical) to vasopressin neurons; congenital malformations of the hypothalamus or pituitary; neoplasms; infiltrative, autoimmune, and infectious diseases affecting vasopressin neurons or fiber tracts; and increased metabolism of vasopressin. In approximately 10% of children with central DI, the etiology is idiopathic. Other pituitary hormone deficiencies may be present Nephrogenic (vasopressin-insensitive) DI (NDI) can result from genetic or acquired causes. Genetic causes are less common but more severe than acquired forms of NDI. The polyuria and polydipsia associated with genetic NDI usually presents within the first several weeks of life, but may only become apparent after weaning or with longer periods of nighttime sleep. Many infants initially present with fever, vomiting, and dehydration. Failure to thrive may be secondary to the ingestion of large amounts of water resulting in calorie malnutrition. Long-standing ingestion and excretion of large volumes of water may lead to nonobstructive hydronephrosis, hydroureter, and megabladder.Acquired nephrogenic DI may result from hypercalcemia or hypokalemia and is associated with the following drugs: lithium, demeclocycline, foscarnet, clozapine, amphotericin, methicillin, and rifampin. Impaired renal concentrating ability can also be seen with ureteral obstruction, chronic renal failure, polycystic kidney disease, medullary cystic disease, Sjgren syndrome, and sickle cell disease. Decreased protein or sodium intake or excessive water intake, as in primary polydipsia, can lead to diminished tonicity of the renal medullary interstitium and nephrogenic DINelson's Textbook of Pediatrics 19th Edition Clinical Presentation of DI

Establishment of pathologic polyuria or polydipsia (exceeding 2L/m2/24hr)Careful history must be obtainedNon specific features Poor suck, failure to thrive, irritabilityEarliest signs include vigorous suck w/ vomiting, fever w/o apparent cause, constipation, excessively wet diapersIn older infants and children, they can be irritableNocturiaSigns of dehydration on PE

The cause of pathologic polyuria or polydipsia (exceeding 2 L/ m2/24 hr) may be difficult to establish in children.Carefully quantify the intake and urine output of patient (ask for nocturia, secondary enuresis)Diagnosis of diabetes insipidus (DI) may be difficult in infants and children because of nonspecific presenting features (eg, poor feeding, failure to thrive, irritability). Accordingly, a high index of suspicion is necessary.The earliest signs of DI include a vigorous suck with vomiting, fever without apparent cause, constipation, and excessively wet diapers from urination. In older infants and young children, irritability is generally due to a borderline state of dehydration coupled with hypernatremia and, sometimes, fever. Nocturia is common and expected because of increased urine production. Central DI tends to develop suddenly

The typical examination reveals an irritable infant with a dripping wet diaper, along with detectable signs of dehydration (eg, dry mucous membranes, diminished skin turgor, decreased tearing, tachycardia). Often, skin turgor is not diminished in individuals with hypernatremic dehydration despite significant dehydration. In severely dehydrated patients, the pulse may be thready and rapid. Hypotension may be present because of hypovolemic shock. Mobile fecaliths may be palpable in the abdomenNelson's Textbook of Pediatrics 19th Edition Complications of DIGrowth failureNocturia and enuresisHypernatremic dehydrationSeizuresMental retardation

Dehydrationresults from an inability to reabsorb free water at a site distal to electrolyte reabsorption. Any patient unable to continuously replace water loss is vulnerable to dehydration, especially in warm weather when insensible water loss through perspiration and respiration substantially increases risk.Electrolyte abnormalities are caused by the loss of urinary free water, which produces hyperosmolar dehydration, leading to hypernatremia, hyperchloremia, and prerenal azotemia. Diminished blood volume increases blood viscosity and the risk of sludging and thrombosis.Failure to thriveoccurs because of the patients constant thirst conferring a sense of fullness that offsets the sense of hunger. The affected individual eats less than necessary for normal growth.Seizures are a consequence of the electrolyte abnormalities introduced in the central nervous system (CNS) by severe hypernatremia and hyperosmolar dehydration. Mental retardation results from the damage to the CNS caused by severe hyperosmolarity, seizures, and potential hypoxia, all of which are thought to account for the frequent occurrence of mental retardation. Death can occur from a hypovolemic shock or a hypernatremic seizure.

Nelson's Textbook of Pediatrics 19th Edition Approach to Patient with Suspected DIThe diagnosis of DI is established if:the serum osmolality is greater than 300 mOsm/kg (if 600, it is unlikely)

If pathologic polyuria or polydipsia is present, the following should be obtained: serum for osmolality, sodium, potassium, blood urea nitrogen, creatinine, glucose, and calcium; urine for osmolality, specific gravity, and glucose determination. The diagnosis of DI is established if the serum osmolality is greater than 300 mOsm/kg and the urine osmolality is less than 300 mOsm/kg. DI is unlikely if the serum osmolality is less than 270 mOsm/kg or the urine osmolality is greater than 600 mOsm/kg. If the patient's serum osmolality is less than 300 mOsm/kg (but greater than 270 mOsm/kg) and pathologic polyuria and polydipsia are present, a water deprivation test is indicated to establish the diagnosis of DI and to differentiate central from nephrogenic causes. Nelson's Textbook of Pediatrics 19th Edition Water Deprivation Test: How it is done? (Step 1)Should be done in the morning under observation8 hours fasting enough for childrenWeigh the child hourly and measure plasma and urine osmolality q2 hoursWATER DEPRIVATION TEST IS NEEDED FOR PATIENTS WITH PARTIAL AVP DEFICIENCY & ALSO TO DIFFERENTIATE DI FROM PRIMARY POLYDIPSIA WHICH IS VERY RARE IN CHILDRENSHOULD BE DONE IN THE MORNING UNDER OBSERVATION8 HOURS FAST IS ENOUGH FOR CHILDRENWEIGH THE CHILD HOURLY AND MEASURE PLASMA & URINE OSMOLALITY EVERY 2 HOURSIN NORMAL SUBJECTS PLASMA OSMOLALITY HARDLY RISES (< 300) BUT THE URINE OUTPUT IS REDUCED & ITS OSMOLALITY RISES (800-1200)

Nelson's Textbook of Pediatrics 19th Edition Water Deprivation Test: Initial Interpretation(Step 2)WATER DEPRIVATION TEST IS NEEDED FOR PATIENTS WITH PARTIAL AVP DEFICIENCY & ALSO TO DIFFERENTIATE DI FROM PRIMARY POLYDIPSIA WHICH IS VERY RARE IN CHILDRENSHOULD BE DONE IN THE MORNING UNDER OBSERVATION8 HOURS FAST IS ENOUGH FOR CHILDRENWEIGH THE CHILD HOURLY AND MEASURE PLASMA & URINE OSMOLALITY EVERY 2 HOURSIN NORMAL SUBJECTS PLASMA OSMOLALITY HARDLY RISES (< 300) BUT THE URINE OUTPUT IS REDUCED & ITS OSMOLALITY RISES (800-1200)

Nelson's Textbook of Pediatrics 19th Edition Water Deprivation Test: The VP challenge test (Step 3)At the end of the test, ADH is given (20mg DDAVP intranasally or 2mg IM) then fluid intake was allowedConcentration of dilute urine confirms central DI and failure suggest nephrogenic causesWATER DEPRIVATION TEST IS NEEDED FOR PATIENTS WITH PARTIAL AVP DEFICIENCY & ALSO TO DIFFERENTIATE DI FROM PRIMARY POLYDIPSIA WHICH IS VERY RARE IN CHILDRENSHOULD BE DONE IN THE MORNING UNDER OBSERVATION8 HOURS FAST IS ENOUGH FOR CHILDRENWEIGH THE CHILD HOURLY AND MEASURE PLASMA & URINE OSMOLALITY EVERY 2 HOURSIN NORMAL SUBJECTS PLASMA OSMOLALITY HARDLY RISES (< 300) BUT THE URINE OUTPUT IS REDUCED & ITS OSMOLALITY RISES (800-1200)

Nelson's Textbook of Pediatrics 19th Edition Treatment of Central DIFluid TherapyVasopressin AnalogsDesmopressinIn tablet and intranasal spray formsDose is determined based on the desired length of antidiuresisVasopressin Aqueous

Treatment of central DI in older children is best accomplished with the use of the long-acting vasopressin analog dDAVP (desmopressin). dDAVP is available in an intranasal preparation (onset 5-10 min) and as tablets (onset 15-30 min). The intranasal preparation of dDAVP (10 g/0.1 mL) can be administered by rhinal tube (allowing dose titration) or by nasal spray. The appropriate dose is determined empirically based on the desired length of antidiuresis. The nasal spray delivers 10 g (0.1 mL) per spray and is the standard preparation used for treatment of primary enuresis in older children. Use of dDAVP in the treatment of enuresis is a temporizing measure, because it does not affect the underlying condition and should be used with caution. To prevent water intoxication, patients should have at least 1 hr of urinary breakthrough between doses each day. dDAVP tablets are available, but require at least a 10-fold increase in the dose compared with the intranasal preparation. Oral doses of 25-300 g every 8-12 hr are safe and effective in children.

Desmopressin (minirin) usually used for central DI. For nasal dosage form (nasal spray):For treatment of diabetes insipidus:Adults and teenagers0.1 to 0.4 milliliter (mL) given as a single dose or divided into 2 or 3 doses per day. The dose is given in one nostril or divided and given in both nostrils. Your doctor may adjust the dose as needed.Children 3 months to 12 years of age0.05 to 0.3 mL given as a single dose or divided into 2 doses per day. The dose is given in one nostril or divided and given in both nostrils. Your doctor may adjust the dose as needed.Children younger than 3 months of ageUse and dose must be determined by your doctor. It also increases factor VII and VWFactorAquaeous VP: Central DI of acute onset following neurosurgery is best managed with continuous administration of synthetic aqueous vasopressin (pitressin). Under most circumstances, total fluid intake must be limited to 1 L/m2/24 hr during antidiuresis. A typical dose for intravenous vasopressin therapy is 1.5 mU/kg/h, which results in a blood vasopressin concentration of approximately 10 pg/mL. On occasion, following hypothalamic (but not transsphenoidal) surgery, higher initial concentrations of vasopressin may be required to treat acute DI, which has been attributed to the release of a vasopressin inhibitory substance. Vasopressin concentrations greater than 1,000 pg/mL should be avoided because they may cause cutaneous necrosis, rhabdomyolysis, and cardiac rhythm disturbances. Postneurosurgical patients treated with vasopressin infusion should be switched from intravenous to oral fluids as soon as possible to allow thirst sensation, if intact, to help regulate osmolality.

DESMOPRESSIN (DDAVP) A SYNTHETIC ANALOG IS SUPERIOR TO NATIVE AVP BECAUSE:IT HAS LONGER DURATION OF ACTION (8-10 h vs 2-3 h)MORE POTENT ITS ANTIDIURETIC ACTIVITY IS 3000 TIMES GREATER THAN ITS PRESSOR ACTIVITYUSUALLY GIVEN INTRANASALLY BUT CAN BE GIVEN ORALLY OR I.M. FOR COMATOSE PATIENTS OR DURING SURGERY.

DDAVP CAN ALSO BE USED IN MILD HAEMOPHILIA OR VON WILLEBRAND DISEASE AND AS TREATMENT FOR NOCTURNAL ENURESIS IN CHILDREN

Nelson's Textbook of Pediatrics 19th Edition Treatment of Nephrogenic DIProvision of adequate fluids and calorieLow Sodium DietHigh dose of DDAVPCorrection of underlying causeDrugs (thiazides, indomethacin carbamazepine)Main treatment of NDI focuses on elimination of underlying disorderCongenital NDI is difficult to treat

The treatment of acquired NDI focuses on elimination, if possible, of the underlying disorder, such as offending drugs, hypercalcemia, hypokalemia, or ureteral obstruction. Congenital nephrogenic diabetes insipidus is often difficult to treat. The main goals are to ensure the intake of adequate calories for growth and to avoid severe dehydration. Foods with the highest ratio of caloric content to osmotic load (Na < 1 mmol/kg/24 hr) should be ingested to maximize growth and to minimize the urine volume required to excrete the solute load. Even with the early institution of therapy, however, growth failure and mental retardation are common. Pharmacologic approaches to the treatment of NDI include the use of thiazide diuretics and are intended to decrease the overall urine output. Thiazides appear to induce a state of mild volume depletion by enhancing sodium excretion at the expense of water and by causing a decrease in the glomerular filtration rate, which results in proximal tubular sodium and water reabsorption. Indomethacin and amiloride may be used in combination with thiazides to further reduce polyuria. High-dose dDAVP therapy, in combination with indomethacin, has been used in some subjects with NDI. This treatment may prove useful in patients with genetic defects in the V2 receptor associated with a reduced binding affinity for vasopressin

hiazide diuretics inhibit the NaCl co-transporter (NCC/TSC) in the renal distal convoluted tubule (DCT) (8). The DCT is water impermeable and considered to be part of the diluting segment (8). Therefore, the water-preserving effect of thiazides is unlikely related to a direct effect on the DCT. In fact, the most widely accepted hypothesis suggests that the antidiuretic action of thiazides is secondary to increased renal sodium excretion (1,2,6). The renal sodium loss causes extracellular volume contraction leading to lowered GFR and increased proximal tubular sodium and water reabsorption. Hence, less water and solutes are delivered to the distal tubule and collecting duct and are lost as urine (1,2,6

Indomethacin is used with thiazide because in congenital NDI urinary prostaglandin E2 excretion is also increasid. They are used with thazides. Prostaglandin e2 decreases water absorption by decreasing the vasopressininduced water permeability in the IMCD thus increases h2o reabsorption and decrease urine volume. Side effects include gi upset

Carbamazepine. Carba was able to stimulate the V2 vasopressin receptor-Protein G complex increasing the (Pf) and water absorption. In vivo studies showed that in rats with lithium-induced DI, Carba decreased the urinary volume and increased the urinary osmolality. AQP2 expression was increased both in normal IMCD incubated with Carba and in IMCD from lithium-induced DI after Carba addition to the diet, when compared with the control.

Nelson's Textbook of Pediatrics 19th EditionCase 1: HistoryA 6-month old boy is referred because of failure-to-thrive and vomitingNo other significant past or family history, born at 37 weeks gestation, normal pregnancy1515Case 1: examinationUnremarkable examination: weight: 5.54 kg (0.4th), OCF: 42.5 cm (90% newly diagnosed +Abs; 3.54% of unaffected first-degree relatives 4050% of genetic predisposition on short arm of chromosome 6, Class II HLA region of the major histocompatibility complex (MHC) Whites HLA-DR3 or HLA-DR4, Blacks HLA-DR7, Japanese HLA-DR9~11 other loci, insulin gene chromosome 11 (INS-VNTR), T-cell activation and regulation genes (CTLA-4), protein tyrosine phosphatase N22 (PTPN22), genes in interleukin pathway (IL-2R) HLA, CTLA-4, and PTPN22 are associated with other autoimmune diseases

Specific causes and findings of type 1 DM4 antibodies are being checked: GADA, IA2, etc. 90% have at least 1 positive antibodyThis is also mentioned in NelsonsThe 40-50% of gases has genetic predisposition, here are the metioned genes..Nelson's Textbook of Pediatrics 19th Edition Symptoms of Type 1 Diabetes Mellitus

ISPAD CPG 2014 CompendiumHere are the list of simptoms of T1 DM according to ISPAD 2014 Compendium. Typical presentation includes noticeable uncontrolled urination, candidasis, more of weight loss, irritabikuity and decreasing school performance, and recurrent skin infectionsAt the ER, usually presents with DKA or HHS. Nelson's Textbook of Pediatrics 19th Edition Type 2 DMFormerly known as adult onset DM, Non insulin dependent DM (NIDDM) or Maturity onset Diabetes of the Young (MODY)Usually Obese ( dont look at me again :P )Mostly not insulin dependentInfrequently develops DKAMost prevalent form of DM among adultsPresentation is more insidiousUncommon history of polyuria and polydipsiaMost common cause of consult is excessive weight gain. . . . . . . . . .

Nelsons Textbook of Pediatrics 19th EditionThe children and adolescents with this type of diabetes are usually obese but are not insulin-dependent and infrequently develop ketosis. Some may develop ketosis during severe infections or other stresses and may then need insulin for correction of symptomatic hyperglycemia. This category includes the most prevalent form of diabetes in adults, which is characterized by insulin resistance and often a progressive defect in insulin secretion. This type of diabetes was formerly known as adult-onset diabetes mellitus, non-insulin-dependent diabetes mellitus (NIDDM), or maturity-onset diabetes of the young (MODY).Nelson's Textbook of Pediatrics 19th Edition Type 2 DM: nature, presentationsMean age of presentation: 13.8 years (10-18 years old)Autoimmune markers may be positive in 30% of DM type 2 casesAcanthosis nigricans may reflect insuliin resistancePCOS , premature adrenarche and hirsutism in some females

Nelsons Textbook of Pediatrics 19th EditionNelson's Textbook of Pediatrics 19th Edition

Dabalea D, Hanson RL, Bennett PH, et al. Increasing prevalence of Type II diabetes in American Indian children. Diabetologia. 1998;41(8):904910

Diabetes in pregnancy can lead to a cycle of diabetes affecting future generations.Causes T2: Gestational Diabetes as a Driver of T2

GDM gives high risk to fetus to develop DM. If the baby is the girll, it is higher probabilty fto develop obesity and DM and pass It when that daughter grows up and develop DMNelson's Textbook of Pediatrics 19th EditionCauses T2: Progression from Pre-diabetes to Diabetes Pre-diabetes A1C 5.8100 mg/dL25% IGT in obese,2h OGTT PG >140 mg/dLDiabetesA1C >6.4%FPG >126 mg/dL, RPG >200 mg/dL3,700/ year (TIDM 16,000)6% W, 67% AI1/3 AA, HA, APIMetabolic Syndrome Risk Factors31.3% BMI>85th percentile16.9% obeseInsulin sensitivity 75%Impaired glucose toleranceBeta-cell 50%Insulin sensitivity 50%DiabetesBeta-cell 75%Gunger N, Bacha F, Saad R, et al. Youth type 2 diabetes: insulin resistance, beta-cell failure, or both? Diabetes Care. 2005;28(3):638644; Arslanian SA, Lewy VD, Danadian K. Glucose intolerance in obese adolescents with polycystic ovary syndrome: roles of insulin resistance and beta-cell dysfunction and risk of cardiovascular disease. J Clin Endocrinol Metab. 2001;86(1):6671; and Bacha F, Saad R, Gungor N, et al. Adiponectin in youth: relationship to visceral adiposity, insulin sensitivity, and beta-cell function. Diabetes Care. 2004;27(2):547552 Family History Environmental Factors Genetic SusceptibilityBeginning in UteroMaternal ObesityBreast Feeding

Obesity Insulin sensitivity 75% Normal glucose tolerance Beta-cell function 2Xs Here is a path of a child with risk factors who are likely to develop DMObesity as the starting point. Then check . If these risk factors were not controlled, it will lead to diabetesNelson's Textbook of Pediatrics 19th Edition Different cases of an 11 8month year old female patientsChief complaint: Urinates 2 to 3 times at night times 2 monthsA1C 8.2% at outside clinicWeight 78 kg, BMI >95th percentile for age/gender Reported 30 lb weight gain last year, recent lossBP 128/83Menses at age 10 years irregularPrenatal excessive maternal weight gain, ? diabetes, Family historyMother from Arizona, AI/HA, + for obesity Father is non-Hispanic White, hypertensionChief complaint: Urinates 2 to 3 times at night times 2 weeksA1C 8.2% at outside clinicWeight 63 kg, body mass index (BMI) >85th percentile for age/genderReported 15 lb weight gain last year, recent loss Blood pressure (BP) 92/65Menses at 10 years irregularPrenatal excessive maternal weight gain, no diabetesFamily historyMother from Arizona, HA, + for obesityFather non-Hispanic White, hypertensionType 1 DMType 2 DMGoing back to our 2 different cases, here is the history of them.. Usually type 2 dm is overweigt/obese almost all of them, presents with itractable weight gainUsually bp in type 2 are more likely elevated. Irregular menses can be associated with PCOS. In fmhx, typ2 dm has history of maternal weight gain Nelson's Textbook of Pediatrics 19th EditionPresentationT1 rapid onset, severe hyperglycemia, acidosis, diabetic ketoacidosis (DKA)Results of TrialNet show T1 can be indolentT2 indolent, mild hyperglycemia, rare acidosis, no DKAAA high rate of mild DKA, higher glucose/A1C, symptomatic at presentationDiagnostic criteria is the same for T1 and T2Symptoms of diabetes plus casual glucose 200 mg/dL Fasting plasma glucose 126 mg/dL 2-hour postload glucose 200 mg/dL during oral glucose tolerance test (OGTT) ?A1C >6.5%Used in adults but not established in children

Presentation, Diagnostic Criteria, Screening

It is forever discussed that type 1 has rapid onset. Type 1 can be indolent that can proceed over months then years then aggravates. Type 2 is indolent, mild, rare acidosis. Usual complaints is polyuria polydipsia (same with type 1, weight gain, and slow healing of wounds,Other symptoms is tired, blurring of vision, dizziness (signs of hyperglycemia)Dx criteria are the same. Usual above 200 rbs 2hr ogtt . And it is repeated daw at one point in time. A1c in 6.5%

Nelson's Textbook of Pediatrics 19th EditionPresentation, Diagnostic Criteria, Screening

ISPAD CPG 2014 CompendiumNelson's Textbook of Pediatrics 19th EditionPresentation, Diagnostic Criteria, Screening Evidence of insulin resistance, hypertension, dyslipidemia, NASHPresentation during or after pubertyT2 in first-degree relativeAcanthosis nigricans, sleep apnea, polycystic ovary syndrome (PCOS), candidiasisEvidence of insulin deficiency hyperglycemia and acidosis, DKA mistaken for fluHardest diagnosis in infants/toddlersNo other family memberOther autoimmune diseasesZeitler P. Approach to the obese adolescent with new-onset diabetes. J Clin Endocrinol Metab. 2010;95(12):51635170

Type 1 DMType 2 DMFurther discussion again on more characteristics. DKA often mistaken for flu, my child is not getting better, always throwing up.. Ask what happen on the llast couple of days? Does your child urinates more often? boom boom question80% of pxs in t1 had no fmhx of dm

In type 2, evidence of insulin resistance. Like PCOS, HPNExclusively during or after puberty. It is rare in prepubertal childMany family members who have DMThe last bullet are signs of insulin resistenceNelson's Textbook of Pediatrics 19th EditionScreening for T1In the context of research trialsTrialNet, Immune Tolerance Network,TEDDY, etc.Screen with antibodies,? genesReasonPrevention studiesOral insulin, omegas, vitamin D, anti-CD3Natural history study

Immune Tolerance NetworkThe reason to screen and intervene early in T1D:

Common, serious in terms of morbidity and mortality Latency period without symptomsScreening test with sensitivity and specificityIntervention early is more effective, preservesC-peptide

Type 1 DM screening is available (ewan ko sa pinas) in the US here are the research centersScreening test particularly antibodies is highly specific and sensitive, genes, Screen also relatives who suspected to have type 1 dmIf diagnosed early, beta cells can be preserved leading to better outcome..Prevention studies stilll ongoingNelson's Textbook of Pediatrics 19th EditionAmerican Diabetic Association. Type 2 diabetes in children and adolescents. Diabetes Care. 2000;23(3):381389 Criteria*: Overweight (BMI 85th percentile for age and sex, weight for height 85th percentile, or weight 120% of ideal for height)

PLUS: any 2 of the following risk factors:Family history of diabetes mellitus (DM) 2 in first- or second-degree relativeRace/ethnicity Signs of insulin resistance

Age of Initiation: Age 10 or at onset of pubertyFrequency: Every 2 years in the context of health visitTest: Fasting plasma glucose preferred

* Clinical judgment should be used. Further Screening for T2American Diabetes Association (ADA) / American Academy of Pediatrics (AAP) Consensus Statement, 2000

I got a better and simpler description of the criteria of type 2 DM so it is easier to remember seen also on nelsonsThis is still the presence consensus statement. Signs of insulin resistance includes hypertension, dyslipidemia, PCOSNelson's Textbook of Pediatrics 19th Edition11 8/12-Year-Old Female Patients: going backObtain the following work up: Random plasma glucose 247 mg/dL, repeat A1C 8.5%CO2 20 meq/L, venous pH 7.38, LDL 178 mg/dL, triglycerides 215 mg/dL ANTIBODIES ALL NEGATIVETreatment: In- or out-patient?Do you start insulin?Metformin alone is first-line therapy when glucose level is