Type 1 Diabetes Mellitus



          Type 1 diabetes mellitus (Type 1 diabetes, insulin dependent diabetes mellitus, juvenile diabetes) is a form of diabetes mellitus. Type 1 diabetes mellitus is an autoimmune disease that results in destruction of insulin-producing beta cells of the pancreas. Lack of insulin causes an increase in fasting blood glucose level (around 70-120 mg/dL in nondiabetic people) that begins to appear in the urine above the renal threshold (about 190-200 mg/dl in most people) which results in the classical symptoms are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss.


          Type 1 diabetes mellitus (formerly known as "childhood" diabetes mellitus) is not exclusively a childhood problem; the adult incidence of type 1 diabetes mellitus is noteworthy—in fact, many adults who contract type 1 diabetes mellitus are misdiagnosed with type 2 diabetes mellitus due to confusion at this point.


          Incidence of diabetes mellitus varies from eight to 17 per 100,000 in Northern Europe and the U.S., with a high of about 35 per 100,000 in Scandinavia, to a low of one per 100,000 in Japan and China.


          Type 1 diabetes mellitus is fatal unless treated with insulin.Insulin replace the missing hormone formerly produced by the now non-functional beta cells in the pancreas. In recent years, pancreas transplants have also been used to treat type 1 diabetes mellitus. Islet cell transplant is also being investigated and has been achieved in  mice, and in experimental trials in humans as well. Use of stem cells to produce a new population of functioning beta cells seems to be a future possibility.


symptoms of Type 1 Diabetes Mellitus

The classical symptoms of type 1 diabetes mellitus includes
  • polyuria (frequent urination)
  • polydipsia (increased thirst)
  • polyphagia (increased hunger)
  • fatigue and 
  • weight loss.


Insulin-dependent diabetes mellitus characterized by dramatic and recurrent swings in blood glucose levels, often occurring for no apparent reason, is sometimes known as brittle diabetes mellitus, unstable diabetes mellitus or labile diabetes mellitus. The results of such swings can be irregular and unpredictable hyperglycemias, frequently involving ketosis, and sometimes serious hypoglycemias. Brittle diabetes mellitus occurs no more frequently than in 1% to 2% of diabetics


Other Symptoms that may arise are



  • nausea
  • vomiting
  • abdominal pain
  • fatigue
  • absence of menstruation


Diagnosis of  diabetes mellitus





  • Urinalysis shows glucose and ketone bodies in the urine, but a blood test is required for diagnosis
  • Fasting blood glucose is 126 mg/dL or higher
  • Random (nonfasting) blood glucose exceeds 200 mg/dL (this must be confimed with a fasting test)
  • Insulin test (low or undetectable level of insulin)
  • C-peptide test (low or undetectable level of the protein C-peptide, a by-product of insulin production)


Type 1 Diabetes Mellitus Pathophysiology



          The cause of type 1 diabetes mellitus is still not fully understood. Some theories suggest that type 1 diabetes mellitus is generally a virally triggered autoimmune response in which the immune system attack on virus infected cells is also directed against the insulin producing beta cells in the pancreas. The autoimmune attack may be triggered by reaction to an infection, for example by one of the viruses of the Coxsackie virus family or German measles, although the evidence is inconclusive. In type 1 diabetes mellitus, pancreatic beta cells in the Islets of Langerhans are destroyed or damaged sufficiently to effectively abolish endogenous insulin production. This etiology distinguishes type 1 diabetes mellitus origin from type 2 diabetes mellitus. It should also be noted that the use of insulin in treating a patient does not mean that patient has type 1 diabetes mellitus; the type of diabetes mellitus a patient has is determined only by the cause—fundamentally by whether the patient is insulin resistant (type 2 diabetes mellitus) or insulin deficient without insulin resistance (type 1 diabetes mellitus).


          This vulnerability is not shared by everyone, for not everyone infected by the suspected organisms develops type 1 diabetes mellitus. This has suggested presence of a genetic vulnerability and there is indeed an observed inherited tendency to develop type 1 diabetes mellitus. It has been traced to particular HLA genotypes, though the connection between them and the triggering of an auto-immune reaction is still poorly understood.


          Some researchers believe that the autoimmune response is influenced by antibodies against cow's milk proteins. A large retrospective controlled study published in 2006 strongly suggests that infants who were never breastfed had a risk for developing type 1 diabetes mellitus twice that of infants who were breastfed for at least three months. The mechanism is not fully understood. No connection has been established between autoantibodies, antibodies to cow's milk proteins, and type 1 diabetes mellitus. A sub type of type 1 diabetes mellitus (identifiable by the presence of antibodies against beta cells) typically develops slowly and so is often confused with type 2 diabetes mellitus. In addition, a small proportion of type 2 diabetes mellitus cases manifest a genetic form of the disease called maturity onset diabetes of the young (MODY).


          Vitamin D in doses of 2000 IU per day given during the first year of a child's life has been connected in one study in Northern Finland (where intrinsic production of Vitamin D is low due to low natural light levels) with an 80% reduction in the risk of getting type 1 diabetes mellitus later in life. The causal connection, if any, is obscure.


          Type 1 diabetes mellitus was previously known as juvenile diabetes mellitus because it is one of the most frequent chronic diseases mellitus in children; however, the majority of new-onset type 1 diabetes mellitus is seen in adults. Scientific studies that use antibody testing ( islet cell antibodies (ICA), glutamic acid decarboxylase antibodies (GADA) and insulinoma-associated (IA-2) autoantibodies) to distinguish between type 1 and type 2 diabetes mellitus demonstrate that most new-onset type 1 diabetes mellitus is seen in adults.


          Some suggest that deficiency of Vitamin D3 (one of several related chemicals with Vitamin D activity) may be an important pathogenic factor in type 1 diabetes mellitus independent of geographical latitude, and so of available sun intensity.


          Some chemicals and drugs preferentially destroy pancreatic cells. Pyrinuron (Vacor, N-3-pyridylmethyl-N'-p-nitrophenyl urea), a rodenticide introduced in the United States in 1976, selectively destroys pancreatic beta cells, resulting in type 1 diabetes mellitus after accidental or intentional ingestion. Vacor was withdrawn from the U.S. market in 1979, but is still used in some countries. Zanosar is the trade name for streptozotocin, an antibiotic and antineoplastic agent used in chemotherapy for pancreatic cancer; it also kills beta cells, resulting in loss of insulin production. Other pancreatic problems, including trauma, pancreatitis or tumors (either malignant or benign), can also lead to loss of insulin production leading to type 1 diabetes mellitus


Complications of Type 1 Diabetes Mellitus

Emergency Complications


Diabetic ketoacidosis

          In a person with type 1 diabetes mellitus, the body will use fat as a fuel if insulin is not present. The by-products of fat metabolism are ketones. Ketones build up in the blood and "spill" over into the urine. A condition called ketoacidosis develops when the blood is made acidic by the ketones.



Hypoglycemia

          Hypoglycemia (low blood glucose) occurs when the balance between insulin, food intake, and exercise is disturbed. Symptoms of mild hypoglycemia include hunger, nervousness, and fast heart rate. More serious hypoglycemia can lead to confusion and even loss of consciousness. Loss of consciousness due to low blood sugar is called hypoglycemic coma.


Long term complications

People who have had Type 1 diabetes mellitus for several years are likely to develop long-term complications, which can be minimized but not entirely eliminated by proper diabetic management:


Vascular disease

          By age 55, about 35% of men and women with type 1 diabetes mellitus have died from a heart attack compared to 8% of nondiabetic men and 4% of nondiabetic women.
          People with type 1 diabetes mellitus are also at higher risk to develop blockages in the major arteries of the legs than non diabetics. Lower the risk of vascular disease by aggressively treating cholesterol and blood pressure, exercising regularly, and avoiding or quitting tobacco products.


Microvascular Disease

          Microvascular (small vessel) changes occur in capillaries of every organ of the body. There is a thickening of the wall of the small blood vessels. These changes are responsible for many of the diabetes mellitus complications.


Eye Complications

          Changes in the small blood vessels of the retina (also known as diabetic retinopathy) predispose the diabetic to several eye disorders. After 15 years of diabetes mellitus, 80% of diabetics will have some diabetic retinopathy.
          If bleeding and scarring has developed, a retinal detachment may occur, causing blindness. Vascular changes in the iris may cause obstruction of the flow of ocular fluid and cause glaucoma. Diabetics are also more likely than non diabetics to develop cataracts.


Diabetic Nephropathy (kidney disease)

          Kidney abnormalities may be noted early in diabetes mellitus disease. Poorly controlled diabetes mellitus may accelerate the development of kidney failure. Urinary tract infections in diabetics tend to be more severe and may result in kidney damage.
Diabetics are more vulnerable to kidney damage from high blood pressure than non diabetics.


Diabetic Neuropathy (nerve damage)

          People with diabetes mellitus may develop temporary or permanent damage to nerve tissue. Diabetic neuropathy is more likely to develop if blood glucose is poorly controlled. Some diabetics will not develop neuropathy, while others may develop this condition relatively early.
          On average, symptoms such as numbness and tingling occur 10 to 20 years after diabetes mellitus has been diagnosed.


Diabetic Foot Problems

          The feet of people with diabetes mellitus are very susceptible to infection and injury. Many diabetes mellitus-related hospital admissions are for foot problems, and a significant number of non-accident-related leg amputations are performed on diabetics.
          Several foot problems are common in people with diabetes mellitus, including skin changes (loss of hair; loss of ability to sweat; and dry, cracked skin), arterial insufficiency (impaired blood supply to feet), neuropathy, and specific foot deformities (hallux valgus, bunion, hammertoe, and calluses).


Skin and mucous membrane problems

          People with diabetes mellitus are more likely than non diabetics to develop infections. Hyperglycemia (high blood sugar) predisposes diabetics to fungal infections of the skin, nails, and female genital tract and to urinary tract infection.


Management of Type 1 Diabetes Mellitus

          These goals are accomplished through education, insulin use, meal planning and weight control, exercise, foot care, and careful self-testing of blood glucose levels.


Insulin therapy

Type 1 diabetes mellitus is treated with insulin replacement therapy—either via subcutaneous injection or insulin pump, along with attention to dietary management, typically including carbohydrate tracking, and careful monitoring of blood glucose levels using glucose meters. Today, the most common insulins are biosynthetic products produced using genetic recombination techniques; formerly, cattle or pig insulins were used, and even sometimes insulin from fish.[31] Major global suppliers include Eli Lilly and Company, Novo Nordisk, and Sanofi-Aventis. A more recent trend, from several suppliers, is insulin analogs which are slightly modified insulins with different onset or duration of action times.


          Untreated type 1 diabetes mellitus commonly leads to coma, often from diabetic ketoacidosis, which is fatal if untreated. Continuous glucose monitors have been developed and marketed which can alert patients to the presence of dangerously high or low blood sugar levels, but technical limitations have limited the impact these devices have had on clinical practice so far.


          Treatment of diabetes mellitus focuses on lowering blood sugar or glucose (BG) to the near normal range, approximately 80–140 mg/dl (4.4–7.8 mmol/L).[32] The ultimate goal of normalizing BG is to avoid long-term complications that affect the nervous system (e.g. peripheral neuropathy leading to pain and/or loss of feeling in the extremities), and the cardiovascular system (e.g. heart attacks, vision loss). People with type 1 diabetes mellitus always need to use insulin, but treatment can lead to low BG (hypoglycemia), i.e. BG less than 70 mg/dl (3.9 mmol/l). Hypoglycemia is a very common occurrence in people with diabetes mellitus, usually the result of a mismatch in the balance among insulin, food and physical activity, although the nonphysiological method of delivery also plays a role.


Diabetes mellitus Diet management

          The patient should be instructed on an ADA diet, with caloric intake of 25-35 kcal/kg body weight, but no greater than 2400 kcal or less than 1800 kcal. Actual weight gain with confirmation of actual caloric intake will further aid in adjusting the patient's caloric needs to allow appropriate weight gain. Women who are under their ideal weight have additional weight to gain in addition to the recommended 11-kg weight gain (a minimum of 7 kg for obese patients). The diet should be 40-50% carbohydrate, 30% fat, and 20-30% protein. Women with renal disease should have protein limited to 90 g of protein to minimize the impact of pregnancy on their disease. The calories are divided into 3 meals and 3 snacks, with the evening snack recommended to be a half-sandwich. The protein in meat provides calories in the early morning hours, when intermediate insulin is peaking and fetal glucose utilization is maximized due to increased movements during sleep.


          The snack for hypoglycemia should be milk or peanut butter with crackers. Orange juice should be discouraged unless it is the only food available, because it causes an abrupt rise in glucose that is not sustained. Glucagon emergency kits should be given to all type 1 diabetes mellitus patients and their spouses taught how to use it if the patient is found unresponsive.


          Soluble fiber assists in satiating hunger, but more importantly, it helps reduce glycemic swings. The patient should note exactly what she ate, the amount, and the mode of preparation when she has a postprandial glucose level over 130 mg/dL. Attention should be directed to the bedtime snack when there is elevation or lowering of the fasting glucose.


          The dietitian is a crucial team member in the care of a type 1 diabetic pregnant patient. Visits should occur as often as needed to obtain proper compliance. The dietitian should make a concerted effort to individualize the diet, respecting different lifestyles and ethnicity. A minimum of two visits is always necessary, and family involvement is encouraged to improve compliance.


Physical Activity

Regular exercise is especially important for the person with diabetes mellitus, as it helps control the amount of sugar in the blood and helps burn excess calories and fat to achieve optimal weight.


          Before people with diabetes mellitus begin any exercise program, they should obtain medical approval. Type 1 diabetics must take special precautions before, during and after participation in intense physical activity or exercise.


Self-Testing

          Blood glucose monitoring is done by checking the glucose content of a small drop of blood. The testing is done on a regular basis and will inform the person with diabetes mellitus how well diet, medication, and exercise are working together to control diabetes mellitus.


          The results can be used to adjust meals, activity, or medications to keep blood-sugar levels within an appropriate range. It will provide valuable information for the health care provider to suggest changes to improve care and treatment. Testing will identify high and low blood-sugar levels before serious problems develop.


Foot Care

          People with diabetes mellitus are prone to foot problems because of complications related to the illness. Diabetes mellitus causes damage to the blood vessels and nerves, which can result in a decreased ability to sense trauma or pressure on the foot. A foot injury could go unnoticed until severe infection develops.


          Additionally, diabetes mellitus alters the bodies immune system, decreasing the body's ability to fight infection. Small infections can rapidly progress to death of the skin and other tissues, necessitating amputation of the affected limb.
To prevent injury to the feet, diabetics should adopt a daily foot care routine.


Treating Low Blood Sugar

          Low blood sugar, known as hypoglycemia, can occur in diabetics when they use too much insulin, exercise too much, or have not eaten enough food. Hypoglycemia can develop quickly in people with diabetes mellitus. Symptoms of low blood sugar typically appear when the sugar level falls below 70. Watch for weakness, shaking, sweating, headache, nervousness, and hunger.


          If these symptoms occur and you have a blood sugar test kit available, do a blood sugar check. If the level is low, the person with diabetes mellitus should eat something with sugar: fruit juice, several teaspoons of sugar, a cup of skim milk, or regular soda. If you don't have a test kit handy, sugar should be eaten anyway - it can't hurt. Symptoms should subside within 15 minutes. If the symptoms don't subside, more sugar should be eaten and the sugar level tested again.


          After the symptoms subside, more substantial food can be eaten. Eat simple sugar First to get the situation under control. Even if you or your child is hungry, "real" food should not be eaten until the sugar level comes up - real food won't produce enough sugar and takes too long to digest.


          If you are a parent, relative, or friend of someone experiencing these symptoms, monitor the person closely. If symptoms become worse -- confusion, seizures, or unconsciousness -- give the person a shot of glucagon. You should have some glucagon stored for emergencies. Make sure everyone in your home, as well as babysitters and caregivers, knows how to use it. Periodically remind everyone how to use it, and check the expiration date. Don't panic. Glucagon works very fast -- usually within 15 minutes. While you are waiting for the person to revive, keep him on his side to prevent choking.


Treating High Ketones

          When there is not enough insulin to move glucose into cells, glucose can build up in the blood. The body then looks for other forms of energy and uses fat as a fuel source. As fats are broken down, acids called ketones build up in the blood and urine. In high levels, ketones are poisonous to body tissue. This condition is known as ketoacidosis.


          You can check for ketones using a simple urine test available at pharmacies. This test should be performed every 4-6 hours anytime a person with diabetes mellitus is registering blood sugar above 240; sick; unusually thirsty or has a dry mouth; urinating frequently; or vomited


          The warning signs that ketoacidosis is getting serious might include flushed face, dry skin and mouth, nausea or vomiting, stomach pain, deep, rapid breathing, or fruity breath odor. If these symptoms occur, call the doctor or go to the emergency room right away. If left untreated, this condition will lead to coma and even death.


Monitoring

          Visit your physician and/or diabetes mellitus educator at least 4 times a year.
Have your glycosylated hemoglobin (HbA1c) measured 2-4 times a year to evaluate your overall glucose control. (Ask your doctor how often you should be tested.)
Have your cholesterol and triglyceride levels and kidney function evaluated yearly.
Visit your ophthalmologist (preferably one that specializes in diabetic retinopathy) at least once a year, more frequently if signs of diabetic retinopathy develop. Every 6 months have a thorough dental cleaning and examination. Inform your dentist and hygienist that you have diabetes mellitus. Monitor your feet every day for early signs of injury or infection. Make sure your health care provider inspects your feet at each visit.
Stay up-to-date with all of your vaccinations (including pneumococcal), and get a flu shot every year in the fall.


Education

          You are the most important person in managing your diabetes mellitus. Diabetes mellitus education is a crucial part of the treatment plan. Diabetes mellitus education basically involves learning how to live with your diabetes mellitus.


          Knowledge of disease management is imperative to avoid developing short-term complications such as hypoglycemia and hyperglycemia and to delay or slow the onset of long-term complications of the disease such as diabetic retinopathy (eye disease) or diabetic nephropathy (kidney disease).


Type 1 Diabetes mellitus Treatment

          Type 1 diabetes mellitus is treated with insulin replacement therapy—usually by insulin injection or insulin pump, along with attention to dietary management, typically including carbohydrate tracking, and careful monitoring of blood glucose levels using glucose meters. Today the most common insulins are biosynthetic products produced using genetic recombination techniques; formerly, cattle or pig insulins were used, and even sometimes insulin from fish. Major global suppliers include Eli Lilly and Company, Novo Nordisk, and Sanofi-Aventis. A more recent trend, from several suppliers, is insulin analogs which are slightly modified insulins which have different onset of action times or duration of action times.


          Untreated type 1 diabetes mellitus commonly leads to coma, often from diabetic ketoacidosis, which is fatal if untreated. Continuous glucose monitors have been developed and marketed which can alert patients to the presence of dangerously high or low blood sugar levels, but technical limitations have limited the impact these devices have had on clinical practice so far.


          In more extreme cases, a pancreas transplant can restore proper glucose regulation. However, the surgery and accompanying immunosuppression required is considered by many physicians to be more dangerous than continued insulin replacement therapy, and is therefore often used only as a last resort (such as when a kidney must also be transplanted, or in cases where the patient's blood glucose levels are extremely volatile). Experimental replacement of beta cells (by transplant or from stem cells) is being investigated in several research programs. Thus far, beta cell replacement has only been performed on patients over age 18, and with tantalizing successes amidst nearly universal failure.


Pancreas transplantation

          In more extreme cases, a pancreas transplant can restore proper glucose regulation. However, the surgery and accompanying immunosuppression required is considered by many physicians to be more dangerous than continued insulin replacement therapy, so is generally only used with or some time after a kidney transplant. One reason for this is that introducing a new kidney requires taking immunosuppressive drugs such as cyclosporine. Nevertheless this allows the introduction of a new, functioning pancreas to a patient with diabetes mellitus without any additional immunosuppressive therapy. However, pancreas transplants alone can be wise in patients with extremely labile type 1 diabetes mellitus.


Islet cell transplantation

          Experimental replacement of beta cells (by transplant or from stem cells) is being investigated in several research programs. Islet cell transplantation is less invasive than a pancreas transplant, which is currently the most commonly used approach in humans.
In one variant of this procedure, islet cells are injected into the patient's liver, where they take up residence and begin to produce insulin. The liver is expected to be the most reasonable choice because it is more accessible than the pancreas, and islet cells seem to produce insulin well in that environment. The patient's body, however, will treat the new cells just as it would any other introduction of foreign tissue, unless a method is developed to produce them from the patient's own stem cells or an identical twin is available who can donate stem cells. The immune system will attack the cells as it would a bacterial infection or a skin graft. Thus, patients now also need to undergo treatment involving immunosuppressants, which reduce immune system activity.
Recent studies have shown islet cell transplants have progressed to the point where 58% of the patients in one study were insulin-independent one year after transplantation. Scientists in New Zealand with Living Cell Technologies are currently in human trials with Diabecell, placing pig islets within a protective capsule derived of seaweed which enables insulin to flow out and nutrients to flow in, while protecting the islets from immune system attack via white blood cells.


Diabetes Mellitus Type 1 Inheritance

          Type 1 diabetes mellitus is a polygenic disease, meaning many different genes contribute to its expression. Depending on locus or combination of loci, it can be dominant, recessive, or somewhere in between. The strongest gene, IDDM1, is located in the MHC Class II region on chromosome 6, at staining region 6p21. This is believed to be responsible for the histocompatibility disorder characteristic of type 1 diabetes mellitus: Insulin-producing pancreas cells (beta cells) display improper antigens to T cells. This eventually leads to the production of antibodies that attack these beta cells. Weaker genes are also located on chromosomes 11 and 18.


Prognosis

          Prognosis is primarily dependent on the level of glucose control. Good control requires a motivated patient, an active management approach (education, diet, insulin, and exercise) with trained health care providers, and frequent patient-provider interactions. Another factor influencing prognosis is the amount of degenerative changes. With diligent antenatal care, the patient can anticipate a normal labor and delivery experience. Severe hypoglycemia and diabetic ketoacidosis can result in maternal compromise and even death. The fetus, if spared from congenital malformation or death in utero, may suffer significant impairment in the hostile uterine environment, with poor glucose control affecting brain development as well as that of other organs.

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