Practice Essentials

Type 1 diabetes is a chronic illness characterized by the bodys

inability to produce insulin due to the autoimmune destruction of the
beta cells in the pancreas. Onset most often occurs in childhood, but
the disease can also develop in adults in their late 30s and early 40s.

See Clinical Findings in Diabetes Mellitus , a Critical Images slideshow, to

help identify various cutaneous, ophthalmologic, vascular, and
neurologic manifestations of DM.

Essential Update: New Abridged Recommendations for Primary Care

Providers

The American Diabetes Association has released condensed recommendations

for Standards of Medical Care in Diabetes: Abridged for Primary Care Providers ,
highlighting recommendations most relevant to primary care. The abridged
version focusses particularly on the following aspects:

Prediabetes

Self-management education

Nutrition

Physical activity

Smoking cessation

Psychosocial care

Immunizations

Glycemic treatment

Therapeutic targets

Diagnosis and treatment of vascular complications

Intensification of insulin therapy in type 2 diabetes

The recommendations can be accessed at American Diabetes Association

DiabetesPro Professional Resources Online, Clinical Practice Recommendations
2015 .[1]

Signs and symptoms

The classic symptoms of type 1 diabetes are as follows:

Polyuria

Polydipsia

Polyphagia

Unexplained weight loss

Other symptoms may include fatigue, nausea, and blurred vision.

The onset of symptomatic disease may be sudden. It is not unusual for

patients with type 1 diabetes to present with diabetic ketoacidosis
(DKA).

See Clinical Presentation for more detail.

Diagnosis

Diagnostic criteria by the American Diabetes Association (ADA) include

the following[2]:

A fasting plasma glucose (FPG) level 126 mg/dL (7.0 mmol/L), or

A 2-hour plasma glucose level 200 mg/dL (11.1 mmol/L) during a 75-g
oral glucose tolerance test (OGTT), or

A random plasma glucose 200 mg/dL (11.1 mmol/L) in a patient with

classic symptoms of hyperglycemia or hyperglycemic crisis

Lab studies

A fingerstick glucose test is appropriate for virtually all patients

with diabetes. All fingerstick capillary glucose levels must be
confirmed in serum or plasma to make the diagnosis. All other laboratory
studies should be selected or omitted on the basis of the individual
clinical situation.

An international expert committee appointed by the ADA, the European

Association for the Study of Diabetes, and the International Diabetes
Association recommended the HbA1c assay for diagnosing type 1 diabetes
only when the condition is suspected but the classic symptoms are
absent.[3]

Screening

Screening for type 1 diabetes in asymptomatic low-risk individuals is

not recommended.[2]However, in patients at high risk (eg, those who have
first-degree relatives with type 1 diabetes), it may be appropriate to
perform annual screening for anti-islet antibodies before the age of 10
years, along with 1 additional screening during adolescence.[4]

See Workup for more detail.

Management

Glycemic control

The ADA recommends using patient age as one consideration in the

establishment of glycemic goals, with different targets for preprandial,
bedtime/overnight, and hemoglobin A1c (HbA1c) levels in patients aged 0-
6, 6-12, and 13-19 years.[5]Benefits of tight glycemic control include
not only continued reductions in the rates of microvascular
complications but also significant differences in cardiovascular events
and overall mortality.

Self-monitoring

Optimal diabetic control requires frequent self-monitoring of blood

glucose levels, which allows rational adjustments in insulin doses. All
patients with type 1 diabetes should learn how to self-monitor and
record their blood glucose levels with home analyzers and adjust their
insulin doses accordingly.

Real-time continuous monitoring of glucoseusing continuous glucose

monitors (CGMs)can help patients improve glycemic control.[6, 7]CGMs
contain subcutaneous sensors that measure interstitial glucose levels
every 1-5 minutes, providing alarms when glucose levels are too high or
too low or are rapidly rising or falling.

Insulin therapy

Patients with type 1 diabetes require lifelong insulin therapy. Most

require 2 or more injections of insulin daily, with doses adjusted on
the basis of self-monitoring of blood glucose levels. Insulin
replacement is accomplished by giving a basal insulin and a preprandial
(premeal) insulin. The basal insulin is either long-acting (glargine or
detemir) or intermediate-acting (NPH). The preprandial insulin is either
rapid-acting (lispro, aspart, insulin inhaled, or glulisine) or short-
acting (regular).

Common insulin regimens include the following:

Split or mixed: NPH with rapid-acting (eg, lispro, aspart, or glulisine)

or regular insulin before breakfast and supper

Split or mixed variant: NPH with rapid-acting or regular insulin before

breakfast, rapid-acting or regular insulin before supper, and NPH before
bedtime (the idea is to reduce fasting hypoglycemia by giving the NPH
later in the evening)

Multiple daily injections (MDI): A long-acting insulin (eg, glargine or

detemir) once a day in the morning or evening (or twice a day in about
20% of patients) and a rapid-acting insulin before meals or snacks (with
the dose adjusted according to the carbohydrate intake and the blood
glucose level)

Continuous subcutaneous insulin infusion (CSII): Rapid-acting insulin

infused continuously 24 hours a day through an insulin pump at 1 or more
basal rates, with additional boluses given before each meal and
correction doses administered if blood glucose levels exceed target
levels

Diet and activity

All patients on insulin should have a comprehensive diet plan, created

with the help of a professional dietitian, that includes the following:

A daily caloric intake prescription

Recommendations for amounts of dietary carbohydrate, fat, and protein

Instructions on how to divide calories between meals and snacks

Exercise is also an important aspect of diabetes management. Patients

should be encouraged to exercise regularly.

See Treatment and Medication for more detail.

Background
Type 1 diabetes mellitus (DM) is a multisystem disease with both
biochemical and anatomic/structural consequences. It is a chronic
disease of carbohydrate, fat, and protein metabolism caused by the lack
of insulin, which results from the marked and progressive inability of
the pancreas to secrete insulin because of autoimmune destruction of the
beta cells. (See Pathophysiology.) (See also Glucose Intolerance .)

Type 1 DM can occur at any age. It is most common in juveniles but can
also develop in adults, especially in those in their late 30s and early
40s. (See Epidemiology.)

Unlike people with type 2 DM , those with type 1 DM usually are not
obese and usually present initially with diabetic ketoacidosis (DKA).
The distinguishing characteristic of a patient with type 1 DM is that if
his or her insulin is withdrawn, ketosis and eventually ketoacidosis
develop. Therefore, these patients are dependent on exogenous insulin.
(See Presentation.)

Treatment of type 1 DM requires lifelong insulin therapy. A

multidisciplinary approach by the physician, nurse, and dietitian, with
regular specialist consultation, is needed to control glycemia, as well
as to limit the development of its devastating complications and manage
such complications when they do occur. (See Treatmentand Medication.)

Despite the differences between type 1 and type 2 DM, the costs of the 2
conditions are often combined. In a study that focused on type 1 alone,
Tao et al estimated that in the United States, type 1 DM is responsible
for $14.4 billion in medical costs and lost income each year.[8]

Pathophysiology
Type 1 DM is the culmination of lymphocytic infiltration and destruction
of insulin-secreting beta cells of the islets of Langerhans in the
pancreas. As beta-cell mass declines, insulin secretion decreases until
the available insulin no longer is adequate to maintain normal blood
glucose levels. After 80-90% of the beta cells are destroyed,
hyperglycemia develops and diabetes may be diagnosed. Patients need
exogenous insulin to reverse this catabolic condition, prevent ketosis,
decrease hyperglucagonemia, and normalize lipid and protein metabolism.

Currently, autoimmunity is considered the major factor in the

pathophysiology of type 1 DM. In a genetically susceptible individual,
viral infection may stimulate the production of antibodies against a
viral protein that trigger an autoimmune response against antigenically
similar beta cell molecules.

Approximately 85% of type 1 DM patients have circulating islet cell

antibodies, and the majority also have detectable anti-insulin
antibodies before receiving insulin therapy. The most commonly found
islet cell antibodies are those directed against glutamic acid
decarboxylase (GAD), an enzyme found within pancreatic beta cells.

The prevalence of type 1 DM is increased in patients with other

autoimmune diseases, such as Graves disease, Hashimoto thyroiditis, and
Addison disease. Pilia et al found a higher prevalence of islet cell
antibodies (IA2) and anti-GAD antibodies in patients with autoimmune
thyroiditis.[9]

A study by Philippe et al used computed tomography (CT) scans, glucagon

stimulation test results, and fecal elastase-1 measurements to confirm
reduced pancreatic volume in individuals with DM.[10]This finding, which
was equally present in both type 1 and type 2 DM, may also explain the
associated exocrine dysfunction that occurs in DM.
Polymorphisms of the class II human leukocyte antigen (HLA) genes that
encode DR and DQ are the major genetic determinants of type 1 DM.
Approximately 95% of patients with type 1 DM have either HLA-DR3 or HLA-
DR4. Heterozygotes for those haplotypes are at significantly greater
risk for DM than homozygotes. HLA-DQs are also considered specific
markers of type 1 DM susceptibility. In contrast, some haplotypes (eg,
HLA-DR2) confer strong protection against type 1 DM.[11]

Sensory and autonomic neuropathy

Sensory and autonomic neuropathy in people with diabetes are caused by

axonal degeneration and segmental demyelination. Many factors are
involved, including the accumulation of sorbitol in peripheral sensory
nerves from sustained hyperglycemia. Motor neuropathy and cranial
mononeuropathy result from vascular disease in blood vessels supplying
nerves.

Angiopathy

Using nailfold video capillaroscopy, Barchetta et al detected a high

prevalence of capillary changes in patients with diabetes, particularly
those with retinal damage. This reflects a generalized microvessel
involvement in both type 1 and type 2 DM.[12]

Microvascular disease causes multiple pathologic complications in people

with diabetes. Hyaline arteriosclerosis, a characteristic pattern of
wall thickening of small arterioles and capillaries, is widespread and
is responsible for ischemic changes in the kidney, retina, brain, and
peripheral nerves.

Atherosclerosis of the main renal arteries and their intrarenal branches

causes chronic nephron ischemia. It is a significant component of
multiple renal lesions in diabetes.

Vitamin D deficiency is an important independent predictor of

development of coronary artery calcification in individuals with type 1
DM.[13]Joergensen et al determined that vitamin D deficiency in type 1
diabetes may predict all causes of mortality but not development of
microvascular complications.[14]

Nephropathy

In the kidneys, the characteristic wall thickening of small arterioles

and capillaries leads to diabetic nephropathy, which is characterized by
proteinuria, glomerular hyalinization (Kimmelstiel-Wilson), and chronic
renal failure. Exacerbated expression of cytokines such as tumor growth
factor beta 1 is part of the pathophysiology of glomerulosclerosis,
which begins early in the course of diabetic nephropathy.
Genetic factors influence the development of diabetic nephropathy.
Single-nucleotide polymorphisms affecting the factors involved in its
pathogenesis appear to influence the risk for diabetic nephropathy in
different people with type 1 DM.[15]

Double diabetes

In areas where rates of type 2 DM and obesity are high, individuals with
type 1 DM may share genetic and environmental factors that lead to their
exhibiting type 2 features such as reduced insulin sensitivity. This
condition is termed double diabetes.

In a study that included 207 patients with type 1 DM, Epstein et al used
the estimated glucose disposal rate (eGDR) to assess insulin resistance
and found that mean eGDR was significantly lower (and, thus, insulin
resistance was higher) in black patients (5.66 mg/kg/min) than in either
Hispanic patients (6.70 mg/kg/min) or white patients (7.20 mg/kg/min).
In addition, low eGDR was associated with an increased risk of vascular
complications of diabetes (eg, cardiovascular disease, diabetic
retinopathy, or severe chronic kidney disease).[16, 17]

Etiology
Type 1A DM results from autoimmune destruction of the beta cells of the
pancreas and involves both genetic predisposition and an environmental
component.

Genetic factors

Although the genetic aspect of type 1 DM is complex, with multiple genes

involved, there is a high sibling relative risk.[18]Whereas dizygotic
twins have a 5-6% concordance rate for type 1 DM,[19]monozygotic twins
will share the diagnosis more than 50% of the time by the age of 40
years.[20]

For the child of a parent with type 1 DM, the risk varies according to
whether the mother or the father has diabetes. Children whose mother has
type 1 DM have a 2-3% risk of developing the disease, whereas those
whose father has the disease have a 5-6% risk. When both parents are
diabetic, the risk rises to almost 30%. In addition, the risk for
children of parents with type 1 DM is slightly higher if onset of the
disease occurred before age 11 years and slightly lower if the onset
occurred after the parents 11th birthday.

The genetic contribution to type 1 DM is also reflected in the

significant variance in the frequency of the disease among different
ethnic populations. Type 1 DM is most prevalent in European populations,
with people from northern Europe more often affected than those from
Mediterranean regions.[21]The disease is least prevalent in East Asians.
[22]

Genome-wide association studies have identified several loci that are

associated with type 1 DM, but few causal relations have been
established. The genomic region most strongly associated with other
autoimmune diseases, the major histocompatibility complex (MHC), is the
location of several susceptibility loci for type 1 DMin particular,
class II HLA DR and DQ haplotypes.[23, 24, 25]

A hierarchy of DR-DQ haplotypes associated with increased risk for type

1 DM has been established. The most susceptible haplotypes are as
follows[26]:

DRB1*0301 - DQA1*0501 - DQB1*0201 (odds ratio [OR] 3.64)

DRB1*0405 - DQA1*0301 - DQB1*0302 (OR 11.37)

DRB1*0401 - DQA1*0301 - DQB*0302 (OR 8.39)

DRB1*0402 - DQA1*0301 - DQB1*0302 (OR 3.63)

DRB1*0404 - DQA1*0301 - DQB1*0302 (OR 1.59)

DRB1*0801 - DQB1*0401 - DQB1*0402 (OR 1.25)

Other haplotypes appear to offer protection against type 1 DM. These

include the following[26]:

DRB1*1501 - DQA1*0102 - DQB1*0602 (OR 0.03)

DRB1*1401 - DQA1*0101 - DQB1*0503 (OR 0.02)

DRB1*0701 - DQA1*0201 - DQB1*0303 (OR 0.02)

From 90% to 95% of young children with type 1 DM carry HLA-DR3

DQB1*0201, HLA-DR4 DQB1*0302, or both. Carriage of both haplotypes (ie,
DR3/4 heterozygotes) confers the highest susceptibility.

These high-risk haplotypes are found primarily in people of European

descent; other ethnic groups are less well studied. In African
Americans, the DRB1*07:01 - DQA1*03:01 -DQB1*02:01g haplotype is
associated with increased risk (OR 3.96), whereas the DRB1*07:01-
DQA1*02:01 - DQB1*02:01g haplotype appears to be protective (OR 0.34).
[27]

The insulin gene (INS), which encodes for the pre-proinsulin peptide, is
adjacent to a variable number of tandem repeats (VNTR) polymorphism at
chromosome 11p15.5.[28]Different VNTR alleles may promote either
resistance or susceptibility to type 1 DM through their effect on INS
transcription in the thymus; for example, protective VNTRs are
associated with higher INS expression, which may promote deletion of
insulin-specific T cells.[29]

Other genes that have been reported to be involved in the mechanism of

type 1 DM include CTLA4 (important in T-cell activation), PTPN22
(produces LYP, a negative regulator of T-cell kinase signaling), and
IL2RA (encodes for CD25 which is involved with regulating T-cell
function). UBASH3A (also known as STS2), may be involved in the
increased risk not only of type 1 DM but also of other autoimmune
disease and Down syndrome; it is located on locus chromosome 21q22.3.
[30]

In addition, genome-wide association studies have implicated numerous

other genes, including the following[31]:

SH2B3

ERBB3

CLEC16A

IL18RAP

PTPN2

CCR5

Environmental factors

Extragenetic factors also may contribute. Potential triggers for

immunologically mediated destruction of the beta cells include viruses
(eg, enterovirus,[32]mumps, rubella, and coxsackievirus B4), toxic
chemicals, exposure to cows milk in infancy,[33]and cytotoxins.

Combinations of factors may be involved. Lempainen et al found that

signs of an enterovirus infection by 12 months of age were associated
with the appearance of type 1 DMrelated autoimmunity among children
who were exposed to cow's milk before 3 months of age. These results
suggest an interaction between the 2 factors and provide a possible
explanation for the contradictory findings obtained in studies that
examined these factors in isolation.[34]

One meta-analysis found a weak but significant linear increase in the

risk of childhood type 1 DM with increasing maternal age.[35]However,
little evidence supports any substantial increase in childhood type 1 DM
risk after pregnancy complicated by preeclampsia.[36]

A study by Simpson et al found that neither vitamin D intake nor 25-

hydroxyvitamin D levels throughout childhood were associated with islet
autoimmunity or progression to type 1 DM.[37]This study was based in
Denver, Colorado, and has been following children at increased risk of
diabetes since 1993.

Early upper respiratory infection may also be a risk factor for type 1
diabetes. In an analysis of data on 148 children considered genetically
at risk for diabetes, upper respiratory infections in the first year of
life were associated with an increased risk for type 1 diabetes .[38,
39]All children in the study who developed islet autoimmunity had at
least 2 upper respiratory infections in the first year of life and at
least 1 infection within 6 months before islet autoantibody
seroconversion.

Children with respiratory infections in the first 6 months of life had

the greatest increased hazard ratio (HR) for islet autoantibody
seroconversion (HR = 2.27), and the risk was also increased in those
with respiratory infections at ages 6 to almost 12 months (HR = 1.32).
[38, 39]The rate of islet autoantibody seroconversion was highest among
children with more than 5 respiratory infections in the first year of
year of life. Respiratory infections in the second year of life were not
related to increased risk.[38, 39]

Epidemiology
United States statistics

A 2011 report from the US Centers for Disease Control and Prevention
(CDC) estimated that approximately 1 million Americans have type 1 DM.
[40]The CDC estimated that each year from 2002 to 2005, type 1 DM was
newly diagnosed in 15,600 young people. Among children younger than 10
years, the annual rate of new cases was 19.7 per 100,000 population;
among those 10 years or older, the rate was 18.6 per 100,000 population.
[40]

Type 1 DM is the most common metabolic disease of childhood. About 1 in

every 400-600 children and adolescents has type 1 DM. In adults, type 1
DM constitutes approximately 5% of all diagnosed cases of diabetes.[40]

International statistics

Internationally, rates of type 1 DM are increasing. In Europe, the

Middle East, and Australia, rates of type 1 DM are increasing by 2-5%
per year.[41]The prevalence of type 1 DM is highest in Scandinavia (ie,
approximately 20% of the total number of people with DM) and lowest in
China and Japan (ie, fewer than 1% of all people with diabetes). Some of
these differences may relate to definitional issues and the completeness
of reporting.
Age-related demographics

Previously referred to as juvenile-onset diabetes, type 1 DM is

typically diagnosed in childhood, adolescence, or early adulthood.
Although the onset of type 1 DM often occurs early in life, 50% of
patients with new-onset type 1 DM are older than 20 years of age.

Type 1 DM usually starts in children aged 4 years or older, appearing

fairly abruptly, with the peak incidence of onset at age 11-13 years
(ie, in early adolescence and puberty). There is also a relatively high
incidence in people in their late 30s and early 40s, in whom the disease
tends to present less aggressively (ie, with early hyperglycemia without
ketoacidosis and gradual onset of ketosis). This slower-onset adult form
of type 1 DM is referred to as latent autoimmune diabetes of the adult
(LADA).[40]

The risk of development of antibodies (anti-islet) in relatives of

patients with type 1 DM decreases with increasing age. This finding
supports annual screening for antibodies in relatives younger than 10
years and 1 additional screening during adolescence.[4]

Sex- and race-related demographics

Type 1 DM is more common in males than in females. In populations of

European origin, the male-to-female ratio is greater than 1.5:1.

Type 1 DM is most common among non-Hispanic whites, followed by African

Americans and Hispanic Americans. It is comparatively uncommon among
Asians.

Prognosis
Type 1 DM is associated with a high morbidity and premature mortality.
More than 60% of patients with type 1 DM do not develop serious
complications over the long term, but many of the rest experience
blindness, end-stage renal disease (ESRD), and, in some cases, early
death. The risk of ESRD and proliferative retinopathy is twice as high
in men as in women when the onset of diabetes occurred before age 15
years.[42]

Patients with type 1 DM who survive the period 10-20 years after disease
onset without fulminant complications have a high probability of
maintaining reasonably good health. Other factors affecting long-term
outcomes are the patients education, awareness, motivation, and
intelligence level. The 2012 American Diabetes Association (ADA)
standard of care emphasizes the importance of long-term, coordinated
care management for improved outcomes and suggests structural changes to
existing systems of long-term care delivery.[5]
The morbidity and mortality associated with diabetes are related to the
short- and long-term complications. Such complications include the
following:

Hypoglycemia from management errors

Increased risk of infections

Microvascular complications (eg, retinopathy and nephropathy)

Neuropathic complications

Macrovascular disease

These complications result in increased risk for ischemic heart disease,

cerebral vascular disease, peripheral vascular disease with gangrene of
lower limbs, chronic renal disease, reduced visual acuity and blindness,
and autonomic and peripheral neuropathy. Diabetes is the major cause of
blindness in adults aged 20-74 years, as well as the leading cause of
nontraumatic lower-extremity amputation and ESRD.

In both diabetic and non-diabetic patients, coronary vasodilator

dysfunction is a strong independent predictor of cardiac mortality. In
diabetic patients without coronary artery disease, those with impaired
coronary flow reserve have event rates similar to those with prior
coronary artery disease, while patients with preserved coronary flow
reserve have event rates similar to non-diabetic patients.[43]

Type 1 diabetic patients also have a high prevalence of small-fiber

neuropathy.[44, 45]In a prospective study of 27 patients who had type 1
diabetes with a mean disease duration of 40 years, almost 60% of the
subjects showed signs or symptoms of neuropathy, including sensory
neuropathy symptoms (9 patients), pain (3 patients), and carpal-tunnel
symptoms (5 patients).[44, 45]Of the 27 patients, 22 were diagnosed with
small-fiber dysfunction by means of quantitative sensory testing.

Abnormal results on intraepidermal nerve-fiber density measurement

(IENFD) were seen in 19 patients.[45]IENFD was negatively correlated
with HbA1c, but this relation was no longer significant after adjustment
for age, body mass index, and height. N--(carboxymethyl) lysine (CML),
which is linked to painful diabetic neuropathy, remained independently
associated with IENFD even after adjustment for these variables. Large-
fiber neuropathy was also common, being found in 16 patients.

Although ESRD is one of the most severe complications of type 1 DM, its
incidence is relatively low: 2.2% at 20 years after diagnosis and 7.8%
at 30 years after diagnosis.[46]A greater risk is that mild diabetic
nephropathy in type 1 diabetic persons appears to be associated with an
increased likelihood of cardiovascular disease.[47]Moreover, the long-
term risk of an impaired glomerular filtration rate (GFR) is lower in
persons treated with intense insulin therapy early in the course of
disease than in those given conventional therapy.[48]

Although mortality from early-onset type 1 DM (onset age, 0-14 y) has

declined, the same may not be true for late-onset type 1 DM (onset age,
15-29 y). One study suggest that women tend to fare worse in both
cohorts and that alcohol and drug use account for more than one third of
deaths.[49]

Control of blood glucose, hemoglobin A1c (HbA1c), lipids, blood pressure,

and weight significantly affects prognosis. Excess weight gain with
intensified diabetes treatment is associated with hypertension, insulin
resistance, dyslipidemia and extetnsive atherosclerotic cardiovascular
disease.[50]

Patients with diabetes face a lifelong challenge to achieve and maintain

blood glucose levels as close to the normal range as possible. With
appropriate glycemic control, the risk of both microvascular and
neuropathic complications is decreased markedly. In addition, aggressive
treatment of hypertension and hyperlipidemia decreases the risk of
macrovascular complications.

The benefits of glycemic control and control of comorbidities must be

weighed against the risk of hypoglycemia and the short-term costs of
providing high-quality preventive care. However, studies have shown cost
savings due to a reduction in acute diabetes-related complications
within 1-3 years of starting effective preventive care.

Patient Education
Education is a vital aspect of diabetes management. Patients with new-
onset type 1 DM require extensive education if they are to manage their
disease safely and effectively and to minimize long-term complications.
Such education is best coordinated by the patients long-term care
providers.

At every encounter, the clinician should educate the patientand, in

the case of children, the parentsabout the disease process,
management, goals, and long-term complications. In particular,
clinicians should do the following:

Make patients aware of the signs and symptoms of hypoglycemia and

knowledgeable about ways to manage it

Help patients understand and acknowledge the course of diabetes (eg, by

teaching patients that they have a chronic condition that requires
lifestyle modification and that they are likely to have chronic
complications if they do not take control of their disease)
Reassure patients about the prognosis in properly managed type 1 DM

ADA guidelines urge that attention be paid to older adolescent patients

who may be leaving their home and their current health care providers.
At the transition between pediatric and adult health care, older teens
can become detached from the health care system, putting their medical
care and their glycemic control at risk.[5]The guidelines identify the
National Diabetes Education Program (NDEP) as a source of materials that
can help smooth the transition to adult health care.

Education about an appropriate treatment plan and encouragement to

follow the plan are especially important in patients with diabetes.
Physicians must ensure that the care for each patient with diabetes
includes all necessary laboratory tests, examinations (eg, foot and
neurologic examinations), and referrals to specialists (eg, an
ophthalmologist or podiatrist).

A dietitian should provide specific diet control education to the

patient and family. A nurse should educate the patient about self
insulin injection and performing fingerstick tests for blood glucose
level monitoring.

For patient education information, see the Diabetes Center , as well as

Diabetes .