Diabetes Mellitus Type 1 Disease

BASICS

DESCRIPTION

A chronic disease caused by pancreatic insufficiency (deficiency) of insulin production, resulting in hyperglycemia and end-organ complications such as accelerated atherosclerosis, neuropathy, nephropathy, and retinopathy. Features include:

Patients are insulinopenic and require insulin
Prone to ketosis
Usually of rapid onset
Nutritional status - normal or thin
Disease lability
Response to oral drugs uncommon
Seasonal: January-April are peak onset periods (children less than 6 years old have greater degree of the season)
System(s) affected: Endocrine/Metabolic
Genetics:
- Mode of genetic expression not clear
- Genes located on major histocompatibility complex on chromosome 6
- HLA DR3 and DR4 are individually associated with increased risk factor of 4; if carrying both susceptibility genes, relative risk factor increases to 12
- HLA B8 and B15 also associated with increased risk
Incidence/Prevalence in USA: Incidence of 15/100,000/ year. Racial predilection for Caucasian. African-Americans have lowest overall incidence.
Predominant age: Mean age of onset 8-12 years, peaking in adolescence; onset about 1.5 years earlier in girls than boys. Rapid decline in incidence after adolescence.
Predominant sex: Male = Female

SIGNS AND SYMPTOMS

Polyuria and polydipsia
Polyphagia is classic, but not common
Anorexia is commonly observed
Weight loss (usually from 10-30%, and often almost devoid of body fat at time of diagnosis)
Increased fatigue
Decreased energy levels and lethargy
Muscle cramps
Irritability and emotional lability
Vision changes, such as blurriness
Altered school and work performance
Headaches
Anxiety attacks
Chest pain and occasional difficult breathing
Abdominal discomfort and pain
Nausea
Diarrhea or constipation

CAUSES

The inherited defect causes an alteration in immunologic integrity, placing the beta cell at special risk for inflammatory damage. The mechanism of damage is autoimmune.
Environmental factors include:
- Viruses (such as mumps, Coxsackie, CMV, and hepatitis viruses)
- Dietary factors - breast feeding may provide a degree of protection against the disease while diets high in dairy products are associated with increased risk
- Possible risk in diets high in nitrosamines
- Environmental toxins
- Emotional and physical stress

RISK FACTORS

Certain HLA types (see above)
Presence of a specific 64K protein which may be responsible for antibody formation
Increased risk when either insulin-dependent or non-insulin dependent diabetes present in any first-degree relatives

DIAGNOSIS

LABORATORY

Blood glucose
Electrolytes
Venous pH
U/A for glucose and ketones
CBC (WBC may be elevated)
Hemoglobin A1C level
C-peptide insulin level
Islet-cell antibodies
T4 and thyroid antibodies

Drugs that may alter lab results:

The following may cause hyperglycemia (particularly in patients prone to diabetes)
- Hormones: glucagon, glucocorticoids, growth hormone, epinephrine, estrogen and progesterone (oral contraceptives), thyroid preparations
- Drugs: thiazide diuretics, furosemide, acetazolamide, diazoxide, beta-blockers, alpha-agonists, calcium channel blockers, phenytoin, phenobarbital sodium, nicotinic acid, cyclophosphamide, l-asparaginase, epinephrine-like drugs (decongestants and diet pills), nonsteroidal anti-inflammatory agents, nicotine, caffeine, sugar-containing syrups, fish oils

Disorders that may alter lab results: See Differential Diagnosis

PATHOLOGICAL FINDINGS

Inflammatory changes with lymphocytic infiltration around the Islets of Langerhans, or islet cell destruction

SPECIAL TESTS

Oral glucose tolerance test (possibly with insulin levels, if diagnosis is questionable)
Intravenous glucose test (for possible early detection of subclinical diabetes)
Consider HLA-typing

IMAGING

None indicated

DIAGNOSTIC PROCEDURES

N/A

TREATMENT

APPROPRIATE HEALTH CARE

Initial care: inpatient stabilization versus outpatient management, preferably in a diabetes unit where a team approach is used
If in diabetic ketoacidosis (DKA): initially IV fluids and IV insulin until stable, then restore electrolyte and acid-base balance, correct hyperglycemia, prevent hypoglycemia and hypokalemia, risk of cerebral edema
Remaining health care is done by the family at home. Encourage the child to do as much self-care as possible.

GENERAL MEASURES

Overall "control" of carbohydrate metabolism for the very young child:
- Normoglycemia (adjusted for age). "Tight" control with striving for blood glucose levels in range of 80-150 mg/dL (4.4-8.3 mmol/L) all the time, might be dangerous (risk of repeated hypoglycemia)
- Hemoglobin Alc level as close to the normal (nondiabetic) range as possible
Overall good health
- Asymptomatic
- Normal appearance
- Try to keep lipid profile normal
Normal growth and development
- Reach optimal height for genetic potential
- Appropriate and timely pubertal maturation
- Coping psychosocial development: Normal school or work attendance and performance. Normal future goals and career plans.
Prevent acute complications
- Hypoglycemic insulin reactions
- Ketoacidosis
Delay or prevent chronic complications

SURGICAL MEASURES

N/A

ACTIVITY

All normal activities, including full participation in sports activities
Regular, rather than periodic, aerobic exercise is preferable

DIET

Appropriate diabetes exchange (ADA) diet for age (carbohydrate-50%, protein-20%, fat-30%)

PATIENT EDUCATION

Complete initial education and ongoing education for patient and family. Team approach is ideal, if available
For a listing of sources, physicians may contact: American Academy of Family Physicians Foundation, P.O. Box 8418, Kansas City, MO 64114, (800)274-2237, ext. 4400

FOLLOW UP

PREVENTION/AVOIDANCE

None known

POSSIBLE COMPLICATIONS

Microvascular disease (retinopathy, nephropathy, neuropathy)
Hyperlipidemia
Macrovascular disease (coronary and cerebral artery disease)
Foot problems
Hypoglycemia
Diabetic ketoacidosis
Excessive weight gain
Psychologic problems related to chronic disease

EXPECTED COURSE AND PROGNOSIS

Initial remission or "honeymoon" phase with decreased insulin needs and easier overall control, usually lasts 3-6 months and rarely beyond a year
Progression to "total diabetes" when endogenous insulin is insignificant; usually is gradual, but a major stress or illness may bring it on more acutely
Current prognosis
- Increasing longevity and "quality of life" with careful blood glucose monitoring and improvement in insulin delivery regimens and systems
- At this time, probable reduced life expectancy, but this has improved dramatically over the past 20 years
- Continue to be optimistic about advances in understanding diabetes that may prevent or minimize complications

MISCELLANEOUS

ASSOCIATED CONDITIONS

Other autoimmune diseases such as hypothyroidism and Addison's Disease (screening regularly for hypothyroidism particularly important in females, who have a much higher incidence of this already)
Diabetes mellitus can also be seen as part of multiple endocrine adenomatosis

AGE-RELATED FACTORS

Pediatric: More prevalent in this age. Over the past 10 years, a larger percentage of very young children (less than 5 years of age) present with diabetes.
Geriatric: N/A
Others: N/A

PREGNANCY

At the time of embryogenesis, hyperglycemia increases the incidence of congenital malformations. Hence, tight control of blood sugar before conception is important.
Safe pregnancy possible, with vaginal delivery of a term baby.

OTHER NOTES

N/A

ABBREVIATIONS

MODY = maturity-onset diabetes of the young

Clinical Investigations

ROLE OF HOMOEOPATHY

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