Download diagnosis

Diabetes Mellitus
• Diabetes mellitus is characterized by
hyperglycemia and glycosuria and is an
endpoint of a few disease processes
• The most common type occurring in
childhood is DM1, which is caused by autoimmune destruction of the insulin-producing
beta cells (islets) of the pancreas. Patients
with DM1 have permanent insulin deficiency
and require insulin. Type 2 diabetes mellitus
(DM2) is less common in children and results
from insulin resistance and relative insulin
deficiency, usually with obesity.
• A diagnosis of diabetes mellitus is made if a
fasting serum glucose concentration is greater
than 126 mg/dL or a 2-hour postprandial serum
glucose concentration is greater than 200 mg/dL
on two separate occasions. A patient is
considered glucose intolerant if fasting serum
glucose concentrations are greater than 110
mg/dL but less than 126 mg/dL and if 2-hour
post-prandial values are greater than 140 mg/dL
but less than 200 mg/dL
• Sporadic hyperglycemia occurs in children,
usually in the setting of an intercurrent illness.
When the hyperglycemic episode is clearly
related to an illness or other physiologic
stress, the probability of incipient diabetes is
small (<5%). Sporadic hyperglycemia occurring
without a clear precipitating physiologic stress
is of more concern because diabetes develops
in at least 30%
•INSULIN-DEPENDENT
(TYPE 1) DIABETES
MELLITUS
• DM1 results from the autoimmune destruction of
the insulin-producing beta cells (islets) of the
pancreas. In addition to the presence of diabetes
susceptibility genes, an unknown environmental
insult presumably occurs to trigger the
autoimmune destruction. A variety of crosssectional, retrospective, and prospective studies
have produced conflicting data regarding a host
of environmental factors and their etiologic role
in DM1. These include cow's milk feeding before
age 2 years and viral infectious agents (coxsackie
B virus, cytomegalovirus, mumps, and rubella).
•NON-INSULINDEPENDENT (TYPE 2)
DIABETES MELLITUS
• DM2 can occur as the result of various
pathophysiologic processes; however, the
most common form results from peripheral
insulin resistance with failure of the pancreas
to maintain compensatory hyperinsu-linemia
• of DM2 also can occur in children. Maturityonset diabetes of youth (MODY) comprises a
group of dominantly inherited forms of
relatively mild diabetes. Insulin resistance
does not occur in these patients; instead the
primary abnormality is an insufficient insulin
secretory response to glycemic stimulation
• DM2 was thought to be uncommon in
childhood; the prevalence of this disorder in
children is increasing in parallel with the
increased prevalence of childhood obesity.
The prevalence is highest in children of ethnic
groups with a high prevalence of DM2 in
adults, including Native Americans, Hispanic
Americans, and African Americans. Obesity,
the metabolic syndrome, and a family history
of DM2 are risk factors.
• The diagnosis of DM2 may be suspected on the
basis of polyuria and polydipsia and in a
background of the metabolic syndrome.
Differentiating DM2 from DM1 in children
sometimes can be challenging. The possibility of
DM2 should be considered in patients who are
obese, have a strong family history of DM2, have
other characteristics of the metabolic syndrome
and acanthosis nigricans on physical examination,
or have absence of antibodies to beta cell
antigens at the time of diagnosis of diabetes.
• Acanthosis nigricans is a dermatologic
manifestation of hyperinsulinism that presents as
hyperkeratotic pigmentation in the nape of the
neck and in flexural areas. Although ketoacidosis
occurs far more commonly in DM1, it also can
occur in patients with DM2 under conditions of
physiologic stress and cannot be used as an
absolute differentiating factor. The diagnosis of
DM2 can be confirmed by evaluation of insulin or
C-peptide responses to stimulation with oral
carbohydrate.
• DM2 is the result of a combination of insulin
resistance and insulin hyposecretion.
Asymptomatic patients with mildly elevated
glucose values (slightly >126 mg/dL for fasting
or slightly >200 mg/dL for random glucose)
may be managed initially with lifestyle
modifications, including nutrition therapy
(dietary adjustments) and increased exercise.
Exercise has been shown to decrease insulin
resistance
• The most common treatment is either
metformin or one of the thiazolidinediones. A
rare side effect of metformin is lactic acidosis,
which occurs mainly in patients with
compromised renal function. The most common
side effect is gastrointestinal upset. If ketonuria
or ketoacidosis occurs, insulin treatment is
necessary at first, but may be switched within
weeks to oral medications. Insulin can be used in
children with DM2, but may lead to continued
weight gain. Oral drugs may be used as
combinations
• As in adults, significant lifestyle modifications,
such as improved eating habits and increased
exercise, have a role in preventing or
decreasing the morbidity of DM2.