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Type 1 Diabetes

Introduction

Type 1 diabetes (juvenile diabetes or type I DM) occurs mostly in patients who are younger than 30 years of age.

Most of the time it happens in children or teenagers. A large number of these patients have autoimmune antibodies in the blood directed against the beta cells of the pancreas (in the Langerhans islets).

The antibodies kill these insulin producing cells until there is a severe shortage of insulin production. This can lead to a sudden crisis, particularly when the metabolism is so much out of control that the patient goes into a diabetic coma. Many research papers have shown that type 1 diabetes is due to a combination of genetic factors and environmental factors.

The genetic factors are from susceptibility genes near the HLA-D locus on chromosome 6 (thanks to www.ncbi.nlm.nih.gov for this link). The environmental factors are due to various viruses such as rubella, mumps or coxsackie B, which leads to a T lymphocyte stimulation, but can in susceptible individuals overreact causing an autoimmune reaction against the beta cells of the pancreas as shown in the link above. There might be other factors from the environment such as a cross reaction between cow’s milk protein and beta cell protein resulting in the induction of autoantibodies. But there are also possible other environmental factors as in certain European countries there is a high incidence of type 1 diabetes, but in others there is not.

Type 1 diabetes requires insulin therapy, oral diabetes medication is not helping. This makes sense in view of the fact that eventually there are no more insulin producing cells left in the pancreas and one has to replace the missing insulin with injections.

Newer research has shown that type 1 diabetes occurs more frequently in children who have overused antibiotics: https://nethealthbook.com/news/antibiotic-use-accelerates-diabetes/

Juvenile diabetes symptoms

With type 1 diabetes the symptoms may be those of symptomatic hyperglycemia (high blood sugar), in which case the symptoms described below would present over a longer period of time (weeks and months). Alternatively, the patient might present with symptoms of severe metabolic derangement ending up with mental confusion followed by a diabetic coma. With this latter presentation the symptoms would come on extremely suddenly (within hours) and lead to a coma, if untreated. This condition is called diabetic ketoacidosis (see below).

Type 1 Diabetes

Type 1 Diabetes

Symptoms from hyperglycemia

As the blood sugar is significantly elevated, the kidneys are working under the pressure of “osmotic diuresis”, which means that there is increased urine output from glucose that leaks into the urine.

Normally there should be no sugar in the urine and this is one of the first screening tests the doctor would do. With juvenile diabetes the sugar in urine test would be positive. The patient also gives a history of urinating large amounts of urine very frequently (polyuria). The patient even may have noticed that urine drops around the toilet have dried by leaving white spots of sugar behind. A lot of fluids are consumed (polydipsia) to keep up with the fluid loss through the kidneys and the doctor may notice a significant weight loss when the present weight is compared to the records (diabetes weight loss). Fatigue and nausea are common as are mouth yeast infections, vaginal yeast infections or yeast infections of the buttock creases. There are the same late complications as with type 2 diabetes and these will be dealt with there.

People with type 1 diabetes often have gastrointestinal symptoms. There is a hormone, enterostaminine that is produced in these patients and binds to the lining of gut cells. This causes symptoms of vomiting, nausea, bloating, diarrhea, and abdominal pain. It can also cause constipation and fecal incontinence. In 60 patients studied it was found that enterostaminine was five times as high as in normal controls. The researchers said that in case of prolonged hyperglycemia the liver makes more enterostaminine causing the gastrointestinal symptoms. In patients with type 1 diabetes who had kidney-pancreas transplantation enterostaminine levels came back to normal and the gastrointestinal symptoms disappeared. Research continues to see whether a drug could be developed that blocks the overproduction of enterostaminine.

Diabetic ketoacidosis

In the case of a newly diagnosed type 1 diabetic this serious metabolic derangement occurs because of the acute lack of insulin. Often, in patients who know that they have type 1 diabetes this episode is triggered by them not taking insulin. Alternatively, there might be an acute infection, acute trauma or a heart attack, which leads to a high blood sugar because there was a discrepancy between supply and demand with regard to insulin.

There is severe dehydration from a strong osmotic diuresis with loss of electrolytes (sodium and potassium loss) and water loss. The deranged liver metabolism also feeds into the forced urine output because of strong diabetes ketones, which are excreted in the urine as well. However, the kidneys can only work so hard and the blood is getting more and more acidy (acidosis diabetic), which makes the patient breathe deeper and harder in a typical pattern (Kussmaul breathing). The mentation is slow with lethargy and sleepiness, which is a sign of impending disaster. The next step could be a complete unconscious state as the ketones including acetone causing brain anaesthesia. At this point the patient goes into a diabetic coma. Often at this stage the blood pH is 7.0 or less when normal would be 7.36 to 7.44. In other words the blood is very acidy, which increases mortality.

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Unfortunately diabetes is often not apparent to the patient until suddenly a serious course such as a diabetic ketoacidosis sets in with a sudden coma.

Here is a list of symptoms that tell the patient that it is time to see a physician to be checked out

  • change of mental alertness with forgetfulness, memory and concentration problems
  • frequent urination and weight loss despite a hunger for food with sugar content (“osmotic diuresis”)
  • frequent yeast infections in mouth cavity, vagina and buttock creases
  • changes of prescriptions for people with glasses or contact lenses, but the optometrist might get different corrective lens readings on different days (the lens of the eye is very sensitive to blood sugar changes in the blood). Others will experience blurred vision for no apparent reason
  • foot ulcers or wounds that do not want to heal

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Juvenile diabetes diagnosis

Most of the diagnosis can be done by a history and by a quick examination at the bedside with testing of a urine sample with the dip stick method. This is a convenient way of checking for glucose in urine and urine ketones. However, later the physician will want to check for the three elements that make the diagnosis:

1. High glucose level in the blood

2. High levels of ketone bodies in the blood (the lab will report these as acetoacetic acid and beta-hydroxybutyric acid)

3. Metabolic acidosis (determined by blood test): this is an accumulation of acids in the blood because of the uncontrolled diabetes.

All of these elements are connected : number 1 above shows that there is uncontrolled diabetes due to a lack of insulin, number 2 shows that this has lead to a deranged liver metabolism. And number 3 shows the results of the deranged liver metabolism, which has lead to metabolic acidosis with various degrees of severity.

Associated with the metabolic acidosis are often severe electrolyte abnormalities such as hyperkalemia (high potassium count) and high blood nitrogen urea levels (indicating signs of kidney failure). High amylase levels are often present as well. An infection is not uncommon as the high glucose levels in all the tissues are an ideal breeding ground for bacteria and the physician will check for this.

Juvenile diabetes treatment

As the patient with type 1 diabetes is usually not overweight, a weight loss program is not necessary. However, the physician will likely consider a brief hospitalization for the newly diagnosed mild to moderate case.

This will allow to do all the blood tests in quick succession and carefully restore the metabolism to normal. The patient is started on insulin injections and an educational program on juvenile diabetes information is started at the same time. Depending on the response to the injections shots are needed once, twice or three times per day. It is important that reactive hypoglycemia from an inadvertent insulin overdose is avoided. On the other hand the patient needs to learn how to use the home glucometer, where initially daily blood sugars are measured fasting, and 30 minutes before meals. All of these values are recorded so that the physician can check these values at a future date. Newer data has shown that a close control of the blood sugars will prevent damage to the arterial walls, to the target organs like heart, kidneys, brain and retinas of the eyes.

Here is a brief overview regarding the complex topic of insulin injections:

  • The majority of adults patients will require around 40 IU (international units) of insulin per day. This is given divided into 3 doses, 20 IU before breakfast, 10 IU before dinner and 10 IU before bedtime. Glucometer readings of blood sugar are initially done 4 times per day and later, when things are stabilized about 2 or three times per day. Depending on the glucometer readings of the blood sugars the insulin dosages are customized to bring the sugars in line with what is normal.
  • Insulin comes in different types, the short acting insulin(or Toronto insulin), the intermediate acting insulin(also NPH insulin or lente insulin) and the long acting insulin (or ultralente insulin). On top of that there are various mixtures where a smaller percentage of intermediate acting and a larger percentage of long acting insulin is mixed into one bottle, Humulin 30/70 for instance, which is a brand name. The advantage of such fixed mixtures is that the patient does not have to mix two separate insulins and this way less mistakes are made.
  • The patient must work closely together with knowledgeable therapists such as trained nurses with experience in diabetes or doctors. It is important to go slow and check glucometer readings frequently. Somebody needs to check the technique of the patient from time to time until it is a routine.
  • The patient must know how to recognize a hypoglycemic reaction. This can occur because the patient may have mixed up insulins and inadvertently have given too high a dosage. Alternatively the patient may have exercised and used up glucose in the process of the increased metabolism thus leading to a net loss of the glucose pool with resulting hypoglycemia. Or the patient may have skipped a meal, but carried on with the same dose of insulin. The diabetics are taught in diabetes classes to always carry pieces of sugar or candies with them, just in case of a hypoglycemic reaction. For emergencies when a patient passes out, some physicians train the immediate family members how to inject glucagon, the natural body hormone to counteract insulin. The diabetic patient should carry a diabetes Medical Alert bracelet. This will clarify his condition to emergency personnel.
  • Never freeze insulin! Some, if not all of the activity would be lost. Insulin should be stored in the fridge for a longer shelf life, but most insulin preparations now are stable at room temperature for several months. Check with the pharmacist about the particular brand you are using.  It would be beyond the scope of this summary to be more detailed about insulin injections. See your family doctor or specialist for more details regarding your own situation.

Ask your physician for a repeat hemoglobin A1C blood test every 3 months to monitor how well the blood sugar is controlled.

 

References:

1. MT Kailasam et al. J Hypertens 2000 Nov 18(11): 1611-1620.

2. G Chinetti et al. Inflamm Res 2000 Oct 49(10): 497-505.

3. St. Paul’s 46th Annual Cont. Med. Educ. Course for Prim. Phys., Nov. 14-17, 2000. Dr. David Thompson, Div. of Endocr., Vancouver Hosp. and UBC.

4. B J Goldstein Int J Int Pract 2000 Jun 54(5): 333- 337.

5. M Maghnie et al. N Engl J Med 2000 Oct 5;343(14): 998-1007.

6. E Albertazzi et al. J Am Soc Nephrol 2000 Jun 11(6):1033-1043.

7. M Funk et al. American Journal of Emergency Medicine Vol.19,No.6,  Oct.2001, W. B. Saunders Company

8. Ferri: Ferri’s Clinical Advisor: Instant Diagnosis and Treatment, 2004 ed., Copyright © 2004 Mosby, Inc.

9. Rakel: Conn’s Current Therapy 2004, 56th ed., Copyright © 2004 Elsevier

Last modified: June 1, 2016

Disclaimer
This outline is only a teaching aid to patients and should stimulate you to ask the right questions when seeing your doctor. However, the responsibility of treatment stays in the hands of your doctor and you.