Dead in Bed Syndrome - Part II - How to prevent?

What can be done to avoid this from happening?
1. Checking a nighttime glucose value will give you an impression of the risk of hypoglycemia.
2. If you use pen injectors, make sure the pen for your bedtime insulin looks and feels quite different from the one you use for daytime meal doses (not just another color that may be difficult to observe in the dark).
3. If you use syringes and vials, store daytime and bedtime insulin in different places. When mixing insulin, be extra careful not to take the often higher bedtime dose of the wrong type.
4.  For physically active persons, it is important to check for late hypoglycemia after the exercise, particularly in the night. Remember to decrease the bedtime dose after more strenous exercise, especially if you do not exercise regularly. If you have problems with nighttime hypoglycemia, ask your diabetes team for a continuous glucose monitoring device that may help you to detect nighttime glycemia patterns and adjust your insulin doses to avoid this.
5. HbA1c targets may need to be relaxed in persons with hypoglycemia unawareness to allow this awareness to recover. Aim for a slightly higher average blood glucose. Above all, you should avoid a blood glucose level that is lower than 65-70 mg/dl (3.5-4.0 mmol/l). Within a fortnight (two weeks), you are likely to find you can recognize symptoms of hypoglycemia more easily.
There is one pump (Medtronic Veo), so far available only on the European market, which shuts off the basal rate for two hours when the blood glucose goes below a certain threshold, thereby hopefully avoiding a further decline in blood glucose. This feature is called Low Glucose Suspend (LGS).

Courtesy: http://www.childrenwithdiabetes.com/d_0n_g00.htm

References

1. Tattersall RB, Gill GV. Unexplained death of type-1 diabetic patients. Diabetic Med 1991;8:49-58.
2. Thordarsson H, Sovik O. Dead in ded syndrome in young diabetic patients in Norway. Diabetic Med 1995;12:782-7.
3. Sartor G, Dahlquist G. Short-term mortality in childhood onset insulin-dependent diabetes mellitus: a high frequency of unexpected deaths in bed. Diabetic Med 1995;12:607-11.
4. Sovik O, Thordarson H. Dead-in-bed syndrome in young diabetic patients. Diabetes Care 1999;22 Suppl 2:B40-2.
5. Gormsen H, Lund A. The diagnostic value of postmortem blood glucose determinations in cases of diabetes mellitus. Forensic Sci Internat 1985;28:103-07.
6. Tanenberg RJ, Newton CA, Drake AJ. Confirmation of hypoglycemia in the "dead-in-bed" syndrome, as captured by a retrospective continuous glucose monitoring system. Endocr Pract 2010;16:244-8.
7. Buckingham B, Wilson DM, Lecher T, Hanas R, Kaiserman K, Cameron F. Duration of nocturnal hypoglycemia before seizures. Diabetes Care 2008;31:2110-2. Free full text available in HTML and PDF formats.
8. Weston PJ, Gill GV. Is undetected autonomic dysfunction responsible for sudden death in Type 1 diabetes mellitus? The 'dead in bed' syndrome revisited. Diabet Med 1999;16:626-31.
9. Tu E, Twigg SM, Semsarian C. Sudden death in type 1 diabetes: the mystery of the 'dead in bed' syndrome. Int J Cardiol 2010;138:91-3.
10. Cryer P. Perspectives in Diabetes. Hypoglycemia begets hypoglycemia in IDDM. Diabetes 1993;42:1691-93.
11. Ludvigsson J, Hanas R, Ter Veer A, Andreasson C, Isacson E, Johansson E. Repeated use of continuous glucose monitoring in children and adolescents improved metabolic control without increasing hypoglycemia. Diabetologia 2001;44(suppl 1):A239 (abstract).
12. Hanas R. Dead-in-bed syndrome in diabetes and hypoglycaemic unawareness. Lancet 1997;350:493-2 (letter). Reply: Lancet 1997;305:1032-33.
13. Fanelli CG, Epifano L, Rambotti AM, Pampanelli S, DiVincenzo A, Modarelli F, Lepore M, Annibale B, Ciofetta M, Bottini P, Porcellati F, Scionti L, Santeusanio F, Brunetti P, Bolli GB. Meticulous prevention of hypoglycemia (near-)normalizes the glycemic thresholds and magnitude of most neuroendocrine responses to, symptoms of and cognitive function during hypoglycemia in intensively treated patients with short-term IDDM. Diabetes 1993;42:1683-89.
14. Choudhary P, Evans M, Hammond P, Shaw J, Pickup J, Amiel S. First clinical use of automated glucose suspension during hypoglycaemia: Results of a user evaluation study. ATTD (abstract) 2010.

Ragnar Hanas, MD
January 16, 2011

Dead in Bed Syndrome - Part I

Someone with type 1 diabetes is found dead in the morning in an undisturbed bed after having been observed in apparently good health the day before. No cause of death can be established. This is the typical situation of the "dead in bed" syndrome, a very tragic outcome which leaves the family with many unanswered questions: Why, when, how, could it have been avoided?

After the first report from UK1 the observations have been confirmed from other countries.2,3 A number of young people with type 1 diabetes have been found dead in the morning without previous symptoms of illness, hyper- or hypoglycemia. The number of deaths of this kind per 10,000 patient years has been estimated to 2-6.4 For a population of 100,000 persons with diabetes, this represents 20-60 deaths per year or approximately 6% of all deaths in persons with diabetes aged less than 40 years.4 A relationship to human insulin1 or intensive insulin treatment2 has been postulated but does not seem likely.4 Autopsies have not revealed the cause of death. The diagnosis of hypoglycemia is difficult to confirm after death.5 There is however one case report where the person who died was wearing a retrospective (non-real-time) sensor, and the sensor reading demonstrated levels below 30 mg/dl (1.7 mmol/l) around the time of death (restrictions on reading glucose levels <40 mg/dl, 2.2 mmol/l, were removed by sensor manufacturer after the event), with at least 3 hours of severe hypoglycemia below <40 mg/dl, 2.2 mmol/l, before death.6 Another report using sensor tracings has shown a lag time of 2-4 hours before the onset of seizures when having severe hypoglycemia.7

In a recent review, clinical reports strongly suggest that nighttime hypoglycemia is a likely prerequisite of the event, but that the death is sudden and probably caused by cardiac arrhythmia.8 Genetic predisposition to a so called long QT syndrome can put the person with diabetes at risk of a fatal arrhythmia.9 It is postulated that early signs of nerve damage (autonomic neuropathy) can result in a disturbance of the autonomic nervous system, thereby further increasing the risk.

If it is caused by severe hypoglycemia, why doesn't the person wake up? There has been an increased concern about the phenomenon of hypoglycemic unawareness, which is defined as a hypoglycemic episode without warning symptoms of the decreasing blood glucose level. Increasing evidence has been shown that hypoglycemic episodes as such precede the development of hypoglycemic unawareness.10 Hypoglycemic unawareness will increase the risk of having a severe hypoglycemia.10

We know from recent studies with continuous glucose monitoring11 that nighttime low glucose values are much more common than previously thought. Most often, this is quite asymptomatic and the person does not wake up with hypoglycemic symptoms. Often the glucose value returns to normal or even high in the morning (so called Somogyi phenomenon) so this pattern is difficult to discover without taking nighttime tests every now and then.

Taking the wrong type of insulin before going to bed can contribute to severe nighttime hypoglycemia. We know this has accidentally happened to many young persons with diabetes.12 If a large dose of bedtime insulin (not uncommon in puberty/prepuberty) is replaced with a similar dose of regular or rapid-acting insulin, this will lower the blood glucose considerably and could presumably trigger a severe hypoglycemic reaction which in turn could be further complicated by cardiac arrythmia.

Courtesy: http://www.childrenwithdiabetes.com/d_0n_g00.htm

References

1. Tattersall RB, Gill GV. Unexplained death of type-1 diabetic patients. Diabetic Med 1991;8:49-58.
2. Thordarsson H, Sovik O. Dead in ded syndrome in young diabetic patients in Norway. Diabetic Med 1995;12:782-7.
3. Sartor G, Dahlquist G. Short-term mortality in childhood onset insulin-dependent diabetes mellitus: a high frequency of unexpected deaths in bed. Diabetic Med 1995;12:607-11.
4. Sovik O, Thordarson H. Dead-in-bed syndrome in young diabetic patients. Diabetes Care 1999;22 Suppl 2:B40-2.
5. Gormsen H, Lund A. The diagnostic value of postmortem blood glucose determinations in cases of diabetes mellitus. Forensic Sci Internat 1985;28:103-07.
6. Tanenberg RJ, Newton CA, Drake AJ. Confirmation of hypoglycemia in the "dead-in-bed" syndrome, as captured by a retrospective continuous glucose monitoring system. Endocr Pract 2010;16:244-8.
7. Buckingham B, Wilson DM, Lecher T, Hanas R, Kaiserman K, Cameron F. Duration of nocturnal hypoglycemia before seizures. Diabetes Care 2008;31:2110-2. Free full text available in HTML and PDF formats.
8. Weston PJ, Gill GV. Is undetected autonomic dysfunction responsible for sudden death in Type 1 diabetes mellitus? The 'dead in bed' syndrome revisited. Diabet Med 1999;16:626-31.
9. Tu E, Twigg SM, Semsarian C. Sudden death in type 1 diabetes: the mystery of the 'dead in bed' syndrome. Int J Cardiol 2010;138:91-3.
10. Cryer P. Perspectives in Diabetes. Hypoglycemia begets hypoglycemia in IDDM. Diabetes 1993;42:1691-93.
11. Ludvigsson J, Hanas R, Ter Veer A, Andreasson C, Isacson E, Johansson E. Repeated use of continuous glucose monitoring in children and adolescents improved metabolic control without increasing hypoglycemia. Diabetologia 2001;44(suppl 1):A239 (abstract).
12. Hanas R. Dead-in-bed syndrome in diabetes and hypoglycaemic unawareness. Lancet 1997;350:493-2 (letter). Reply: Lancet 1997;305:1032-33.
13. Fanelli CG, Epifano L, Rambotti AM, Pampanelli S, DiVincenzo A, Modarelli F, Lepore M, Annibale B, Ciofetta M, Bottini P, Porcellati F, Scionti L, Santeusanio F, Brunetti P, Bolli GB. Meticulous prevention of hypoglycemia (near-)normalizes the glycemic thresholds and magnitude of most neuroendocrine responses to, symptoms of and cognitive function during hypoglycemia in intensively treated patients with short-term IDDM. Diabetes 1993;42:1683-89.
14. Choudhary P, Evans M, Hammond P, Shaw J, Pickup J, Amiel S. First clinical use of automated glucose suspension during hypoglycaemia: Results of a user evaluation study. ATTD (abstract) 2010.

Ragnar Hanas, MD
January 16, 2011

Summer Camps - Parents get ready!

Share emergency contacts. Parents should give the camp the emergency contacts for all children, as well as the child’s physician including name, telephone numbers, fax number and the date of the last health care visit. Additionally, parents should have the emergency contact information for staff handy. If your child has a medical condition, camp staff should be notified.

• Get a physical before they get physical. Make sure your child undergoes a physical examination and that their vaccinations are up-to-date.

• Stay hydrated. Remind your child to drink plenty of water, even if they do not feel thirsty.

• Teach your child to practice sun safety. Pack lightweight clothing in light colors with a loose fit to keep the sun at bay and to keep body temperatures at a normal level. Also remind your child to use sunblock (SPF 30 or greater) regularly when outdoors for prolonged periods of time, even on hazy or cloudy days. Children should also be reminded to reapply sunblock frequently, especially after swimming.

• Teach your child to be safe in the water. Remind your child to follow all camp rules in and around pools, lakes and other bodies of water. Children should never be around water without a certified lifeguard on duty.

• Keep the bugs off. Avoid scented soaps, perfumes or hair sprays on your child. Refrain from using a product containing a combination sunscreen-DEET formulation as the directions for each are different, and the use of a combination formulation can potentially lead to DEET toxicity.

Courtesy: Stonehealth

Gastric Bypass - Road to less weight!

A shorter version and a longer version from Mayo clinic

Gastric bypass procedures (GBP) are any of a group of similar operations that first divides the stomach into a small upper pouch and a much larger lower "remnant" pouch and then re-arranges the small intestine to connect to both. Surgeons have developed several different ways to reconnect the intestine, thus leading to several different GBP names. Any GBP leads to a marked reduction in the functional volume of the stomach, accompanied by an altered physiological and physical response to food.

Courtesy: Yale medical group

The operation is prescribed to treat morbid obesity (defined as a body mass index greater than 40), type 2 diabetes, hypertension, sleep apnea, and other comorbid conditions. 

Bariatric surgery is the term encompassing all of the surgical treatments for morbid obesity, not just gastric bypasses, which make up only one class of such operations. The resulting weight loss, typically dramatic, markedly reduces comorbidities. 

Reconstructive ladder or why does plastic surgery cost so much?

Reconstructive plastic surgeons use the concept of a reconstructive ladder to manage increasingly complex wounds. This ranges from very simple techniques such as primary closure and dressings to more complex skin grafts, tissue expansion and free flaps.

The ladder

There are several small variations in the reconstructive ladder in the scientific literature, but the principles remains the same:

Rung 1: Healing by secondary intention
Rung 2: Primary closure
Rung 3: Delayed primary closure
Rung 4: Split thickness graft
Rung 5: Full thickness skin graft
Rung 6: Tissue expansion
Rung 7: Random flap
Rung 8: Axial flap
Rung 9: Free flap

What is congenital hypothyroidism?

What is congenital hypothyroidism?

Congenital hypothyroidism is a condition that affects infants from birth (congenital) and results from a partial or complete loss of thyroid function (hypothyroidism). The thyroid gland is a butterfly-shaped tissue in the lower neck. It makes iodine-containing hormones that play an important role in regulating growth, brain development, and the rate of chemical reactions in the body (metabolism).

Congenital hypothyroidism occurs when the thyroid gland fails to develop or function properly. In 80 to 85 percent of cases, the thyroid gland is absent, abnormally located, or severely reduced in size (hypoplastic). In the remaining cases, a normal-sized or enlarged thyroid gland is present, but production of thyroid hormones is decreased or absent. If untreated, congenital hypothyroidism can lead to intellectual disability and abnormal growth. In the United States and many other countries, all newborns are tested for congenital hypothyroidism. If treatment begins in the first month after birth, infants usually develop normally.

How common is congenital hypothyroidism?

Studies of populations from North America, Europe, Japan, and Australia, indicate that congenital hypothyroidism affects 1 in 3,000 to 4,000 newborns. For reasons that remain unclear, congenital hypothyroidism affects more than twice as many females as males.

What genes are related to congenital hypothyroidism?

Mutations in the DUOX2, PAX8, SLC5A5, TG, TPO, TSHB, and TSHR genes cause congenital hypothyroidism.

Gene mutations cause the loss of thyroid function in one of two ways. Mutations in the PAX8 gene and some mutations in the TSHR gene prevent or disrupt the normal development of the thyroid gland before birth. Mutations in the DUOX2, SLC5A5, TG, TPO, and TSHB genes prevent or reduce the production of thyroid hormones, even though the thyroid gland is present.

Mutations in other genes that have not been well characterized may also cause congenital hypothyroidism.

How do people inherit congenital hypothyroidism?

Most cases of congenital hypothyroidism are sporadic, which means they occur in people with no history of the disorder in their family.

An estimated 15 to 20 percent of cases are inherited. Many inherited cases are autosomal recessive, which means both copies of the gene in each cell have mutations. Most often, the parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but do not show signs and symptoms of the condition.

Some inherited cases (those with a mutation in the PAX8 gene or certain TSHR gene mutations) have an autosomal dominant pattern of inheritance, which means one copy of the altered gene in each cell is sufficient to cause the disorder.

Münchausen syndrome by proxy

Münchausen syndrome is related to Münchausen syndrome by proxy (MSbP/MSP), which refers to the abuse of another being, typically a child, in order to seek attention or sympathy for the abuser.

source: http://mkg4583.wordpress.com/2009/10/21/parental-alienation-canada-mothers-commit-vast-majority-of-parental-murders-of-children/


 Münchausen syndrome by proxy has been documented in the parent or guardian of a child. The adult ensures that his or her child will experience some medical affliction, therefore compelling the child to suffer treatment for a significant portion of their youth in hospitals. 

source: http://10sabrina.edublogs.org/files/2010/10/Munchausen-by-Proxy-Web-1ckjocx.jpg


Furthermore, a disease may actually be initiated in the child by the parent or guardian. This condition is considered distinct from Münchausen syndrome. In fact, there is growing consensus in the pediatric community that this disorder should be renamed "medical abuse" to highlight the real harm caused by the deception and to make it less likely that a perpetrator can use a psychiatric defense when real harm is done.
 Parents who perpetrate this abuse are often affected by concomitant psychiatric problems like depression, spouse abuse, psychopathy, or psychosis. In rare cases, multiple children in one family may be affected either directly as victims or as witnesses who are threatened to keep them silent.

Münchausen syndrome

Münchausen syndrome is a psychiatric factitious disorder wherein those affected feign disease, illness, or psychological trauma to draw attention or sympathy to themselves. It is also sometimes known as hospital addiction syndrome or hospital hopper syndrome. Nurses and doctors sometimes refer to them as frequent flyers, because they return to the hospital just as frequent flyers return to the airport. However, there is discussion to reclassify them as somatoform disorder in the DSM-5 as it is unclear whether or not people are conscious of drawing attention to themselves.

Courtesy: http://accessmedicine.net

Factitious syndrome These linear cuts were self-inflicted with a razor blade

In Münchausen syndrome, the affected person exaggerates or creates symptoms of illnesses in themselves to gain investigation, treatment, attention, sympathy, and comfort from medical personnel. In some extreme cases, people suffering from Münchausen's syndrome are highly knowledgeable about the practice of medicine and are able to produce symptoms that result in lengthy and costly medical analysis, prolonged hospital stay and unnecessary operations. The role of "patient" is a familiar and comforting one, and it fills a psychological need in people with Münchausen's. 

What is the difference between this and being HYPOCHONDRIAC?

It is distinct from hypochondriasis in that patients with Münchausen syndrome are aware that they are exaggerating, whereas sufferers of hypochondriasis believe they actually have a disease. Risk factors for developing Münchausen syndrome include childhood traumas and growing up with parents/caretakers who were emotionally unavailable due to illness or emotional problems. 

Arrhythmogenic Münchausen syndrome describes individuals who simulate or stimulate cardiac arrhythmias to gain medical attention

Soon  we will talk about: Münchausen syndrome is related to Münchausen syndrome by proxy (MSbP/MSP), which refers to the abuse of another being, typically a child, in order to seek attention or sympathy for the abuser.

What does Pneumonia do?

Pneumonia fills the lung's alveoli with fluid, hindering oxygenation. The alveolus on the left is normal, whereas the one on the right is full of fluid from pneumonia.

Pneumonia frequently starts as an upper respiratory tract infection that moves into the lower respiratory tract.

Viral

Viruses invade cells in order to reproduce. Typically, a virus reaches the lungs when airborne droplets are inhaled through the mouth or nose. Once in the lungs, the virus invades the cells lining the airways and alveoli. This invasion often leads to cell death, either from damage to the cell by the virus or from a protective process called apoptosis in which the infected cell destroys itself before it can be used as a conduit for virus reproduction. When the immune system responds to the viral infection, even more lung damage occurs. White blood cells, mainly lymphocytes, activate certain chemical cytokines that allow fluid to leak into the alveoli. This combination of cell destruction and fluid-filled alveoli interrupts the normal transportation of oxygen into the bloodstream.

Bacterial

Bacteria typically enter the lung when airborne droplets are inhaled, but can also reach the lung through the bloodstream when there is an infection in another part of the body. Once inside, bacteria may invade the spaces between cells and between alveoli through connecting pores. This invasion triggers the immune system to send neutrophils, a type of defensive white blood cell, to the lungs. The neutrophils engulf and kill the offending organisms, and also release cytokines, causing a general activation of the immune system. This leads to the fever, chills, and fatigue common in bacterial and fungal pneumonia. The neutrophils, bacteria, and fluid from surrounding blood vessels fill the alveoli and interrupt normal oxygen transportation.

Pneumonia - Do you know what exactly it is?

Pneumonia is a breathing (respiratory) condition in which there is an infection of the lung.

Community-acquired pneumonia is pneumonia in people who have not recently been in the hospital or another health care facility (nursing home, rehabilitation facility).

Pneumonia is an inflammatory condition of the lung—especially affecting the microscopic air sacs (alveoli)—associated with fever, chest symptoms, and a lack of air space (consolidation) on a chest X-ray. Pneumonia is typically caused by an infection but there are a number of other causes. Infectious agents include: bacteria, viruses, fungi, and parasites.

A chest X-ray showing a very prominent wedge-shaped bacterial pneumonia in the right 

Typical symptoms include cough, chest pain, fever, and difficulty breathing Diagnostic tools include x-rays and examination of the sputum. Vaccines to prevent certain types of pneumonia are available. Treatment depends on the underlying cause. Presumed bacterial pneumonia is treated with antibiotics.

Indian Home remedy for common cold!

Turmeric Milk:
Add 1 tsp of turmeric and 1 tsp of freshly ground pepper to quarter cup of milk and simmers it for 3-4 minutes. Careful - it will be spicy!
Lemon water
 Boil water along with a lemon wedge in it. Then add honey and stir in after squeezing the lemon wedge. 

Lyme disease vaccine - DO YOU KNOW?

A Lyme disease vaccine is no longer available. The vaccine manufacturer discontinued production in 2002, citing insufficient consumer demand. Protection provided by this vaccine diminishes over time. Therefore, if you received the Lyme disease vaccine before 2002, you are probably no longer protected against Lyme disease.

Reducing exposure to ticks is the best defense against Lyme disease, Rocky Mountain spotted fever, and other tickborne infections. There are several steps you and your family can take to prevent and control Lyme disease:

Avoid Direct Contact with Ticks

• Avoid wooded and bushy areas with high grass and leaf litter.
• Walk in the center of trails.

Repel Ticks with DEET or Permethrin

• Use repellents that contain 20% or more DEET (N, N-diethyl-m-toluamide) on the exposed skin for protection that lasts up to several hours. Always follow product instructions. Parents should apply this product to their children, avoiding hands, eyes, and mouth.
• Use products that contain permethrin on clothing. Treat clothing and gear, such as boots, pants, socks and tents. It remains protective through several washings. Pre-treated clothing is available and remains protective for up to 70 washings.
• Other repellents registered by the Environmental Protection Agency (EPA) may be found athttp://cfpub.epa.gov/oppref/insect/.

Find and Remove Ticks from Your Body

• Bathe or shower as soon as possible after coming indoors (preferably within two hours) to wash off and more easily find ticks that are crawling on you.
• Conduct a full-body tick check using a hand-held or full-length mirror to view all parts of your body upon return from tick-infested areas. Parents should check their children for ticks under the arms, in and around the ears, inside the belly button, behind the knees, between the legs, around the waist, and especially in their hair.
• Examine gear and pets. Ticks can ride into the home on clothing and pets, then attach to a person later, so carefully examine pets, coats, and day packs. Tumble clothes in a dryer on high heat for an hour to kill remaining ticks.

Info from CDC

Tick Removal

If you find a tick attached to your skin, there's no need to panic. There are several tick removal devices on the market, but a plain set of fine-tipped tweezers will remove a tick quite effectively.

How to remove a tick

1. Use fine-tipped tweezers to grasp the tick as close to the skin's surface as possible.
2. Pull upward with steady, even pressure. Don't twist or jerk the tick; this can cause the mouth-parts to break off and remain in the skin. If this happens, remove the mouth-parts with tweezers. If you are unable to remove the mouth easily with clean tweezers, leave it alone and let the skin heal.
3. After removing the tick, thoroughly clean the bite area and your hands with rubbing alcohol, an iodine scrub, or soap and water.

Avoid folklore remedies such as "painting" the tick with nail polish or petroleum jelly, or using heat to make the tick detach from the skin. Your goal is to remove the tick as quickly as possible--not waiting for it to detach.

Follow-up

If you develop a rash or fever within several weeks of removing a tick, see your doctor. Be sure to tell the doctor about your recent tick bite, when the bite occurred, and where you most likely acquired the tick.

A RAST test - IS this obsolete?

A RAST test (short for radioallergosorbent test) is a blood test used to determine to what substances a person is allergic. This is different from a skin allergy test, which determines allergy by the reaction of a person's skin to different substances.

Picture courtesy: http://www.allergyfreemom.com/Allergy_Testing.php

The RAST test is scored on a scale from 0 to 6:

RAST rating	IgE level (KU/L)	comment
0	< 0.35	ABSENT OR UNDETECTABLE ALLERGEN SPECIFIC IgE
1	0.35 - 0.69	LOW LEVEL OF ALLERGEN SPECIFIC IgE
2	0.70 - 3.49	MODERATE LEVEL OF ALLERGEN SPECIFIC IgE
3	3.50 - 17.49	HIGH LEVEL OF ALLERGEN SPECIFIC IgE
4	17.50 - 49.99	VERY HIGH LEVEL OF ALLERGEN SPECIFIC IgE
5	50.0 - 100.00	VERY HIGH LEVEL OF ALLERGEN SPECIFIC IgE
6	> 100.00	EXTREMELY HIGH LEVEL OF ALLERGEN SPECIFIC IgE

CAP RAST, CAP FEIA (fluorenzymeimmunoassay) is a more superior test
This new test has replaced the original RAST in approximately 80% of the world's commercial clinical laboratories, where specific IgE testing is performed. The newest version, the ImmunoCAP Specific IgE 0-100, is the only specific IgE assay to receive FDA approval to quantitatively report to its detection limit of 0.1kU/l. 

The guidelines for diagnosis and management of food allergy issues by the National Institute of Health state that:

"sIgE levels were originally measured using the radioallergosorbent test (RAST), but this test has been replaced by more sensitive fluorescence enzyme-labeled assays and the term RAST should be abandoned