CURRENT ISSUES IN PEDIATRICS
From the 31st Semi-Annual Family Practice Review, presented March 25-30, 2007, by Temple University School of
Medicine and Lancaster General Hospital
| ATTENTION-DEFICIT/HYPERACTIVITY DISORDER —David W. Goodman, MD, Assistant Professor, Department of
Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD
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| Attention-deficit/hyperactivity disorder (ADHD) in children: prevalence in United States—8%; persistence into
adulthood, 50%; most common neuropsychiatric disorder in children; lack of training contributes to difficulty in evaluating
adults and adolescents (considered childhood condition)
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| Factors for persistence into adulthood: genetics—heritability, 75%; 30% to 40% likelihood that child with ADHD has
parent with ADHD; 50% likelihood that adult with ADHD has child with ADHD; psychosocial adversity—symptoms
more likely to persist in more chaotic and disruptive households; psychiatric comorbidity—eg, oppositional defiant disorder
(ODD), conduct disorder (CD), depression, anxiety; construct treatment plan with longitudinal course
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| When ADHD untreated: failure to complete high school and failure to enter or complete college (identifying and managing
patients can affect their financial and occupational futures); tobacco smoking—4-yr prospective study saw 2-fold
higher risk in children with ADHD, compared to controls (statistically significant); important to identify ADHD in children
5 to 10 yr of age; substance abuse—compared to control group, individuals with ADHD had small increase at early
ages, and large increase in adolescence (2-fold higher in untreated individuals); stimulant medications used for ADHD do
not increase substance abuse and may reduce substance abuse 2-fold (discuss risks and benefits with parents and patients);
sexual behavior—sexual intercourse occurs sooner in individuals with ADHD; number of sexual partners
greater; pregnancy rate 10 times higher; higher rate of sexually transmitted diseases; higher risk for HIV; negative driving
outcomes—driving before obtaining license, traffic citations, speeding tickets, license suspension, and accidents
more prevalent in adolescents and young adults with ADHD; presence of ADHD contributes significantly to motor vehicle
accidents in teenagers; discuss treatment and relative risk with parents (speaker encourages “no meds, no keys”)
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| Diagnosis: symptoms—inattention; hyperactivity; impulsivity; age criteria (<7 yr of age) currently in debate; if child 5 to
13 yr of age has symptoms and fulfills criteria for chronic pervasive symptoms documented by outside informant, consider
ADHD; “the older they get, the brighter they are” (less likely to have been diagnosed before age 7 yr and more
likely to be inattentive type [eg, sits in back of classroom, earns adequate grades, not disruptive]); associated problems
develop by age 17 yr; criteria—symptoms chronic, pervasive, and unchanging for 6 mo; impairments; criteria set by
field studies in children 6 to 12 yr of age (difficult to translate to adolescents and adults)
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 | Identification of ADHD in younger vs older patients: younger children—child who presents with inattention symptoms
without documented ADHD before age 7 yr may have ADHD; symptoms present in childhood; children with ADHD
typically identified by behavioral problems (eg, hyperactivity, disruptive behavior) rather than inattention problems;
ratio of boys to girls, 3:1 (girls with inattentive-type ADHD identified later); adolescents and young adults—patients
15 to 25 yr of age with ADHD complain about impairments due to mounting adult responsibilities (idiosyncratic mechanisms
to compensate, eg, intelligence, structured environment, involvement of supervisory parents, now insufficient);
symptoms present in childhood, but patients able to compensate; inattentive and disorganized patients generally referred
when older; girls with more severe impairment identified in childhood (girls 5-10 yr of age identified with
ADHD have significant disorder); intelligence quotient (IQ) vs age of diagnosis—brighter children with inattention-
type ADHD identified later in life; patients with combined-type ADHD identified at age 5 to 15 yr, regardless of IQ
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| ADHD as clinical diagnosis: diagnosis not made by neuropsychologic testing (although testing helpful and complementary);
based on presentation, longitudinal and chronic course, family psychiatric history, and outside observer documentation
of symptoms and impairments (in contrast to intelligence, learning disabilities, and executive function);
executive function—involves organization, strategizing, and prioritizing; ADHD can be present without executive
dysfunction; ≈35% of patients with ADHD have executive dysfunction; misinterpreting disorganization as outgrowth
of ADHD and presuming medication dose should be increased, can lead to overshooting of optimal dose; prefrontal
cortex activity (involves response inhibition, memory, set shifting [moving from one task to another], and interference
or impulse control); maturation of brain occurs at age 22 to 23 yr (bimodal cerebral growth development; accounts in
part for why 30-yr-olds less impulsive than 15-yr-olds)
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| Psychiatric comorbidity: lifetime comorbidity rate in children ≈50%, ≈70% in adults; ADHD tends to be principal focus
in children, while primary depression, bipolar disorder, and anxiety disorders main focus in adults
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| Pharmacotherapy: mechanisms of action—methylphenidate, amphetamine-based agents, atomoxetine, bupropion, and desipramine
block transporter that takes up neurotransmitter; amphetamines diffuse into presynaptic neuron and decrease vesiculation
of neurotransmitters, increasing cytoplasmic concentration; excess cytoplasmic transporter diffuses through
reuptake transporter; categories—1) methylphenidate; many preparations; initially classified as C3 controlled substance,
later classified as C2 (to avoid abuse potential); immediate- and extended-release formulations; preparations based on wax
matrix, beaded preparation, OROS osmotic technology, and transdermal patch; 2) amphetamine-based products; immediate-
release and beaded preparations (pH-dependent polymer; delayed release in small bowel); 3) atomoxetine; new products—
extended-release guanfacine; prodrug amphetamine; triple-beaded amphetamine
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| DIABETES IN CHILDREN —Iraj Rezvani, MD, Clinical Professor of Pediatrics, Temple University School of Medicine,
Philadelphia, PA
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| Diagnostic criteria: serum glucose >200 mg/dL with symptoms; fasting blood glucose (FBG) >126 mg/dL or two 2-hr
postprandial oral glucose tolerance tests >200 mg/dL; sticks and monitors calibrated to plasma rather than whole blood
glucose more accurate
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| Classification: type 1—destruction of β-cells; usually autoimmune; type 2—insulin resistance with relative insulin deficiency;
other types—eg, diabetes after glucocorticoid use, acromegaly, cystic fibrosis; pathogenesis and treatment varied;
most cases of gestational diabetes behave similarly to type 2 diabetes; ≈50% of women (usually obese) with
gestational diabetes develop type 2 diabetes
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| Body weight: adults—adults at normal weight more likely to have type 1 diabetes or, eg, maturity-onset diabetes of
young (MODY); obese adults more likely to have type 2 diabetes or other types; children—if normal weight, more
likely to have type 1 diabetes or MODY; obese children can have type 2, type 1, or other types (difficult to differentiate;
affects prognosis and treatment)
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| Markers: insulin resistance marker of type 2 diabetes, but specific studies (eg, hyperinsulinemic euglycemic clamp)
needed; use markers to rule out type 1 diabetes; autoimmune type 1 diabetes—90% of type 1 diabetes; markers include
HLA genes (indicate risk but not diagnostic); islet cell antibodies (test not commercially available; fresh sample
of pancreas needed; use remains at research level); antibody against other proteins produced by β-cells (eg, glutamic
acid decarboxylase [GAD; abundant in β-cell; negative results do not rule out type 1 diabetes])
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| Maturity-onset diabetes of young: MODY caused by genetic defect in β-cell; usually occurs in young adults; course
usually milder than with type 1 diabetes; may respond to oral hypoglycemic agents; genetic defect gradually results in β-
cell failure, resulting in diabetes; 6 genes (mostly autosomal dominant) identified; patients usually have positive family
history, not obese, and respond to oral hypoglycemic agents; homozygous genotype causes diabetes of newborn
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| Type 2 diabetes in adults: associated with insulin resistance and obesity; onset insidious; mild-to-moderate hyperglycemia;
ketosis-resistant (patients do not become ketotic as easily as patients with type 1 diabetes); may be associated with
hypertension, dyslipidemia, polycystic ovary syndrome, and metabolic syndrome
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| Type 2 diabetes in children: associated with obesity; occurs mostly in teenagers; patients often undiagnosed and present
to emergency department (ED) with mild-to-moderate diabetic ketoacidosis; honeymoon period—≈2 wk after diagnosis,
diabetes improves and resolves temporarily; may be prolonged; factors for diagnosis—obesity; positive family history;
absence of marker for type 1 diabetes
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| Pathogenesis of type 2 diabetes: 1) insulin resistance; 2) β-cell failure (more critical factor); normal β-cell function prevents
hyperglycemia; may be due to MODY
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| Treatment: weight loss; few pharmacologic agents available for use in children; metformin (off-label use; few side effects);
insulin—regular; ultra; fast-acting; isophane (NPH); insulin glargine (Lantus); combination of regular and NPH;
insulin detemir (Levemir); Lantus cannot be mixed and patient must take 4 injections; delivery systems include vial and
syringe, pen, and insulin pump; inhaled insulin—data not optimistic; dose response not linear; only 10% of insulin absorbed;
dosing in milligrams rather than units; may affect pulmonary function over time; child in ED with serum glucose
500 mg/dL—recommended dose of insulin, 0.2 U/kg per injection (1.0 U/kg/day); not used in children—insulin-secreting
agents; thiazolidinediones (TZDs) cause weight gain (except metformin); incretins—peptides that increase insulin
secretion after glucose exposure, eg, glucagon-like peptide 1 (GLP-1) or exenatide (Byetta); slows gastric emptying (effective
for weight loss)
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| HYPERTENSION IN CHILDREN —Bonita Falkner, MD, Professor of Pediatrics and Nephrology, Jefferson Medical College,
Philadelphia
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| Definitions: based on 95th percentile of normal distribution of blood pressure (BP) in childhood; normal distribution dependent
on sex, age, and height (look for child who deviates from normal range); hypertension defined as systolic or diastolic
BP ≥95th percentile for age, sex, and height, and reproducible on ≥3 separate occasions; prehypertension—
average systolic or diastolic BP ≥90th percentile, but <95th percentile; in adolescents, 90th percentile often higher than
what is considered prehypertension in adults (for patients ≥12 yr of age, use 120/80 mm Hg as absolute number for prehypertension);
white coat hypertension—BP measured in office >95th percentile, but BP normal outside of physician’s
office; diagnosis usually requires ambulatory or home BP measurements
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| Boy 12 yr of age and average height: BP normally increases with height; cutoff for hypertension (95th percentile), BP
consistently >123/80 mm Hg
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| Classification: normal—BP <90th percentile; prehyperten-sion—90th to 95th percentile; for adolescents, 120/80 mm Hg,
up to 95th percentile; hypertension—determine whether child has mild or severe hypertension; 1) stage I; BP between
95th percentile and up to 5 mm Hg above 99th percentile (range of ≈12 mm Hg); eg, systolic BP 123 to 135 mm Hg in
medium-height boy 12 yr of age; 2) stage II; BP 5 mm Hg beyond 99th percentile; eg, systolic BP >135 mm Hg in medium-height
boy 12 yr of age
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| Recommendations: normal BP—check at next scheduled physical examination; prehypertension—recheck at ≈6 mo;
stage I hypertension—repeat measurement in 1 to 2 wk (sooner in symptomatic patients); further evaluation and intervention
required if BP persistently elevated; stage II hypertension—immediate care required
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| Management: therapeutic lifestyle modification; normal BP—encourage diet, exercise, and physical activity;
prehypertension—prevent progressive increases in BP; lifestyle interventions and counseling for weight management
(ie, physical activity and diet management); stage I hypertension—lifestyle counseling; further evaluation and intervention;
stage II hypertension—introduce dietary restrictions (eg, restrict salt intake); may require more than lifestyle
changes; pharmacologic therapy—generally not used in prehypertension unless child has underlying condition; recommended
in children with prehypertension who have high-risk condition, eg, chronic kidney disease, diabetes, left ventricular
hypertrophy (LVH); children with stage II hypertension generally require antihypertensive medication
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| Evaluation: 1) look for underlying causes (eg, kidney disease); patient history and physical examination; ≈70% renal
causes, eg, chronic glomerulonephritis, chronic interstitial nephritis, pyelonephritis, recurrent urinary tract infections,
congenital anomalies with reflux nephropathy, cystic lesions; include standard chemistry panel, serum urea nitrogen
(BUN), creatinine, urinalysis, urine culture, complete blood cell count, and renal ultrasonography; 2) evaluate for comorbidities,
eg, lipid abnormalities, prediabetes, metabolic syndrome; perform fasting lipid panel and FBG; if child overweight
with strong positive family history of diabetes, hypertension, or other cardiovascular disease, consider screening
for diabetes; other potential comorbidities include substance abuse (consider drug screening) and sleep disorders; 3) evaluate
for target organ damage from hypertension; use echocardiography; look for evidence of LVH (specifically ask laboratory
for LV mass value); LVH found in ≈30% of children with hypertension; retinal examination may be helpful; some
children may need ambulatory BP monitoring to rule out white coat hypertension; renin and aldosterone screening may
be appropriate in some children; renal vascular imaging, urine steroids, and catecholamines in children with stage II hypertension
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| Summary: normal BP—encourage healthy lifestyle; prehypertension—repeat BP measurement; monitor patients; if
child obese, institute lifestyle changes for weight reduction; if child has underlying condition (eg, diabetes), further evaluation
may be needed; focus on lifestyle changes and monitoring; hypertension—management depends on age and presence
of obesity; younger child with higher BP but not obese likely to have underlying cause (rigorous diagnostic work-up
required); if child overweight, institute lifestyle changes for weight reduction and evaluate and treat for target organ damage;
indications for pharmacologic treatment—treatable significant underlying cause for hypertension;
unresponsiveness to nonpharmacologic therapy; symptoms; stage II hypertension; target organ damage
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| Impact of childhood obesity on hypertension: childhood obesity increasing; prevalence >17% (higher in black and
Latino children); increased systolic BP more striking in black and Latino children than in whites, but diastolic BP significantly
increased in all ethnicities; 23% of adolescents in 90th percentile for body mass index (BMI) found to have hypertension,
34% at BMI >95th percentile (obese level); effects of obesity on BP seen in children as young as 2 to 5 yr of age
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Suggested Reading
Barkley RA et al: A review of driving risks and impairments associated with attention-deficit/hyperactivity disorder and
the effects of stimulant medication on driving performance. J Safety Res 38:113, 2007; Flynn JT: Evaluation and management
of hypertension in childhood. Prog Pediatr Cardiol 12:177, 2001; Gadow KD et al: Attention-deficit/hyperactivity
disorder in adults: beyond controversy. Arch Gen Psychiatry 58:784, 2001; Greenhill LL: Diagnosing attention-deficit/
hyperactivity disorder in children. J Clin Psychiatry 59 Suppl 7:31, 1998; Hannon TS et al: Childhood obesity and type 2
diabetes mellitus. Pediatrics 116:473, 2005; Katusic SK et al: Psychostimulant treatment and risk for substance abuse
among young adults with a history of attention-deficit/hyperactivity disorder: a population-based, birth cohort study. J
Child Adolesc Psychopharmacol 15:764, 2005; Lahey BB et al: DSM-IV field trials for attention deficit hyperactivity disorder
in children and adolescents. Am J Psychiatry 151:1673, 1994; Levitt Katz LE et al: Fasting c-peptide and insulin-
like growth factor-binding protein-1 levels help to distinguish childhood type 1 and type 2 diabetes at diagnosis. Pediatr Diabetes
8:53, 2007; Nehal US et al: Pediatric hypertension: recent literature. Curr Opin Pediatr 14:189, 2002; Olson DL
et al: Renal hypertension in children. Pediatr Clin North Am 23:795, 1976; Poulin C: From attention-deficit/hyperactivity
disorder to medical stimulant use to the diversion of prescribed stimulants to non-medical stimulant use: connecting the
dots. Addiction 102:740, 2007; Seikaly MG: Hypertension in children: an update on treatment strategies. Curr Opin Pediatr
19:170, 2007; Swinford RD et al: Measurement and treatment of elevated blood pressure in the pediatric patient with
chronic kidney disease. Adv Chronic Kidney Dis 11:143, 2004; The TODAY Study Group: Treatment options for type 2
diabetes in adolescents and youth: a study of the comparative efficacy of metformin alone or in combination with rosiglitazone
or lifestyle intervention in adolescents with type 2 diabetes. Pediatr Diabetes 8:74, 2007; Von Karla V et al: Type 2
diabetes in children and adolescents: screening, diagnosis, and management. JAAPA 20:51, 2007.
Cultural and Linguistic Resources
In compliance with California Assembly Bill 1195, Audio-Digest Foundation offers selected cultural and linguistic resources
on its website. Please visit this site: www.audiodigest.org/ CLCresources.
Educational Objectives
| The goal of this program is to improve recognition and reduce negative outcomes of common clinical disorders in children.
After hearing and assimilating this program, the participant will be better able to:
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| 1. Identify and treat attention-deficit/hyperactivity disorder (ADHD) in children.
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| 2. Counsel children, parents, and adolescents about the risks of leaving ADHD untreated.
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| 3. Use markers and clinical findings to differentiate between type 1 and type 2 diabetes in children.
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| 4. Classify severity of hypertension in children based on physical examination and evaluation.
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| 5. Implement appropriate therapy in children with hypertension based on evaluation and severity.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose relevant
financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts
were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial
interest. For this program, the following has been disclosed: Dr. Goodman has received financial support, is on the Speakers
Bureau, and/or is a consultant for: Cephalon Inc., Forest Labs, GlaxoSmithKline, Lilly and Co., McNeil Pharmaceutical,
New River Pharmaceuticals, Novartis Pharmaceuticals Corp., Shire Inc., and Wyeth.
Acknowledgements
Drs. Goodman, Rezvani, and Falkner spoke in Lancaster, PA, at the 31st Semi-Annual Family Practice Review, presented
March 25-30, 2007, by Temple University School of Medicine and Lancaster General Hospital. The Audio-Digest Foundation
thanks the speakers and sponsors for their cooperation in the production of this program.
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