Wells' Syndrome.... it's a flare up via 4 yrs!!!

Itching, itching, and mild swelling... annoying deep skin pain!!

Definition

Wells syndrome is a rare condition of unknown cause. It is also called ‘eosinophilic cellulitis’. What does Wells syndrome look like? Typically the rash is preceded by itching or burning skin and consists of markedly swollen nodules and plaques (lumps) with prominent borders. The patches are usually bright red at first, frequently looking like cellulitis, then fade over four to eight weeks, leaving green, grey or brown patches. They can blister. The rash most commonly occurs on the limbs, but may also affect the trunk. The patient often feels very tired and has a fever in approximately 25% of cases. Recurrent cellulitis followed by an eruption of skin lesions that are usually brawny, filled with fluid, and heavily infiltrated by eosinophils and histiocytes. Also called eosinophilic cellulitis. A blood count may reveal increased numbers of white blood cells called eosinophils – these are often associated with allergy or insect bites. The diagnosis of Wells syndrome can be established by a skin biopsy finding of typical histopathological features with many eosinophils and characteristic ‘flame figures’. However, flame figures are not diagnostic of Wells syndrome and can be seen in other conditions that have increased numbers of eosinophils. An important part of the management of patients with Wells syndrome is to exclude underlying causes such as parasitic disoders (e.g. a worm infestation) or an allergic contact dermatitis with the help of the appropriate tests. Treatment Oral corticosteroid treatment with prednisone can lead to a dramatic improvement within days and the course is typically tapered over one month. Other treatments include minocycline, dapsone, griseofulvin, ciclosporin and oral antihistamines. Mild cases may respond to topical steroid therapy alone.

Approach Considerations

There are numerous treatment options for Wells Syndrome (eosinophilic cellulitis), including the use of topical corticosteroids, calcineurin inhibitors, griseofulvin, H1 antihistamines, cyclosporine, dapsone, and systemic corticosteroids.^[38]
Systemic corticosteroids are the most effective treatment, but they may lead to corticosteroid dependence.

I'm a Rare Disease Person....in addition to diabetes huh?

Wells Syndrome:  Background

In 1971, George Wells first described this syndrome as a recurrent granulomatous dermatitis with eosinophilia.^[1] Wells and Smith renamed it eosinophilic cellulitis in 1979.^[2]
Wells syndrome (eosinophilic cellulitis) is an uncommon condition of unknown etiology. The presentation usually involves a mildly pruritic or tender cellulitis-like eruption with typical histologic features characterized by edema, flame figures, and a marked infiltrate of eosinophils in the dermis.^[3] Papular and nodular eruptions at the clinical presentation have also been reported.^{[4, 5]} The condition can recur and may be preceded by a pruritic papular eruption. Although Wells syndrome is usually sporadic, some familial cases have been reported.
One study showed the successive occurrence of vasculitis, Wells syndrome, and Sweet syndrome in a patient. This finding suggests that there is an overlap between these diseases.^[6] Another report describes a dominant syndrome consisting of eosinophilic cellulitis, mental retardation, and abnormal body habitus in one family.^[7]

Next Section: Etiology

Pathophysiology

At least some cases of Wells syndrome (eosinophilic cellulitis) may represent hypersensitivity to an arthropod bite or sting. An impressive response of peripheral lymphocytes to mosquito salivary gland extracts has been documented in some patients with Wells syndrome.^[8] A dermal infiltrate of histiocytes, eosinophils, and eosinophilic granules occurs between collagen bundles, which forms the classic flame figures. The eosinophilic infiltrate is almost always restricted to the epidermis and the dermis, but it has also been found in the subcutaneous tissue and the underlying muscle. The location of the infiltrate is correlated with the different clinical features.
In one study, immunophenotyping of peripheral T cells revealed an increased proportion of CD3⁺ and CD4⁺ T cells.^[9] These lymphocytes spontaneously release significant amounts of interleukin 5 (IL-5); this finding suggests that activated T cells may be involved in the pathogenesis of blood and tissue eosinophilia. The eosinophils then degranulate in the dermis, causing edema and inflammation.^[10]
With immunofluorescent stains, eosinophil major basic protein is identified in the granules of the flame figures. On electron microscopy, the collagen fibers are intact; this finding suggests that an initial degeneration of collagen is not a factor in initiating the formation of flame figures.

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Next Section: Etiology

Etiology

The etiology of Wells syndrome (eosinophilic cellulitis) is unknown. Wells syndrome may be due to drugs, various infections, and, possibly, nonhematologic malignancies as trigger events.^{[11, 12]}
Wells syndrome is usually sporadic, but some familial cases have been described. Suggested precipitating factors include the following:

• Arthropod bites and stings, including those of the honeybee^[13]
• Cutaneous viral infections; there is a possible link between parvoviral infection and Wells syndrome^[14]
• Cutaneous parasitic infestations, including toxocariasis,^{[15, 16]} ascariasis,^[17] and onchocerciasis^[18]
• Leukemia
• Myeloproliferative disorders
• Atopic dermatitis
• Fungal infections
• Hypersensitivity reactions to medications or metals, including metallic alloy implants^[19]
• Churg-Strauss syndrome: This syndrome has been associated in a few patients^[20] ; these reports are noteworthy for the presence of bullae and of antineutrophil cytoplasmic antibodies^[21] ; only a few other autoimmune diseases have been associated, including a case report of systemic lupus erythematosus^[22] ; sometimes, differentiating between these disorders can be challenging^[23]

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Next Section: Etiology

Epidemiology

Wells syndrome (eosinophilic cellulitis) is rare. Only about 80 cases have been reported worldwide.
Wells syndrome usually affects adults, but it has been known to occur in children.^{[24, 25, 26, 27]} In one case series of 19 patients, the classic plaque-type presentation was the most common variant found in children, whereas the annular granuloma–like variant was the most common variant in adults.^[28]

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Next Section: Etiology

Prognosis

The prognosis for patients with Wells syndrome (eosinophilic cellulitis) is excellent. It tends to resolve in weeks or months, usually without scarring. It occasionally recurs. In these recurrent cases, it can take years to ultimately resolve.

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 Contributor Information and Disclosures

Author  Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School 

Additional Contributors   David F Butler, MD Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Rosalie Elenitsas, MD Herman Beerman Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System
Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology
Disclosure: Lippincott Williams Wilkins Royalty Textbook editor; DLA Piper Consulting fee Consulting
Takeji Nishikawa, MD Emeritus Professor, Department of Dermatology, Keio University School of Medicine; Director, Samoncho Dermatology Clinic; Managing Director, The Waksman Foundation of Japan Inc
Disclosure: Nothing to disclose.

References

1. Wells GC. Recurrent granulomatous dermatitis with eosinophilia. Trans St Johns Hosp Dermatol Soc. 1971;57(1):46-56. [Medline].
2. Wells GC, Smith NP. Eosinophilic cellulitis. Br J Dermatol. Jan 1979;100(1):101-9. [Medline].
3. Brehmer-Andersson E, Kaaman T, Skog E, Frithz A. The histopathogenesis of the flame figure in Wells' syndrome based on five cases. Acta Derm Venereol. 1986;66(3):213-9. [Medline].
4. Ghislain PD, Van Eeckhout P. Eosinophilic cellulitis of papulonodular presentation (Wells' syndrome). J Eur Acad Dermatol Venereol. Mar 2005;19(2):226-7. [Medline].
5. Holme SA, McHenry P. Nodular presentation of eosinophilic cellulitis (Wells' syndrome). Clin Exp Dermatol. Nov 2001;26(8):677-9. [Medline].
6. Consigny S, Courville P, Young P, et al. [Histological and clinical forms of the eosinophilic cellulitis]. Ann Dermatol Venereol. Mar 2001;128(3 Pt 1):213-6. [Medline].
7. Davis MD, Brown AC, Blackston RD, et al. Familial eosinophilic cellulitis, dysmorphic habitus, and mental retardation. J Am Acad Dermatol. Jun 1998;38(6 Pt 1):919-28. [Medline].
8. Koga C, Sugita K, Kabashima K, Matsuoka H, Nakamura M, Tokura Y. High responses of peripheral lymphocytes to mosquito salivary gland extracts in patients with Wells syndrome. J Am Acad Dermatol. Jul 2010;63(1):160-1. [Medline].
9. Plotz SG, Abeck D, Behrendt H, Simon HU, Ring J. [Eosinophilic cellulitis (Wells syndrome)]. Hautarzt. Mar 2000;51(3):182-6. [Medline].
10. Espana A, Sanz ML, Sola J, Gil P. Wells' syndrome (eosinophilic cellulitis): correlation between clinical activity, eosinophil levels, eosinophil cation protein and interleukin-5. Br J Dermatol. Jan 1999;140(1):127-30. [Medline].
11. Kaufmann D, Pichler W, Beer JH. Severe episode of high fever with rash, lymphadenopathy, neutropenia, and eosinophilia after minocycline therapy for acne. Arch Intern Med. Sep 12 1994;154(17):1983-4. [Medline].
12. Hirsch K, Ludwig RJ, Wolter M, et al. Eosinophilic cellulitis (Wells' syndrome) associated with colon carcinoma. J Dtsch Dermatol Ges. Jul 2005;3(7):530-1. [Medline].
13. Lin HL, Lin JN, Chen CW, Kuo LC, Lee WC. Eosinophilic cellulitis after honeybee sting. J Formos Med Assoc. Dec 2009;108(12):964-6. [Medline].
14. Cherng E, McClung AA, Rosenthal HM, Hicks J, Levy ML. Wells' Syndrome Associated with Parvovirus in a 5-Year Old Boy. Pediatr Dermatol. Dec 9 2011;[Medline].
15. Hurni MA, Gerbig AW, Braathen LR, Hunziker T. Toxocariasis and Wells' syndrome: a causal relationship?. Dermatology. 1997;195(4):325-8. [Medline].
16. Bassukas ID, Gaitanis G, Zioga A, Boboyianni C, Stergiopoulou C. Febrile "migrating" eosinophilic cellulitis with hepatosplenomegaly: adult toxocariasis - a case report. Cases J. Nov 28 2008;1(1):356. [Medline].
17. Tsuda S, Tanaka K, Miyasato M, Nakama T, Sasai Y. Eosinophilic cellulitis (Wells' syndrome) associated with ascariasis. Acta Derm Venereol. Jul 1994;74(4):292-4. [Medline].
18. van den Hoogenband HM. Eosinophilic cellulitis as a result of onchocerciasis. Clin Exp Dermatol. Jul 1983;8(4):405-8. [Medline].
19. Zhu L, Hu D, Wang Q, Hou J, Li M. Diffuse polymorphic eosinophilic cellulitis in a patient with metallic alloy implants: a possible association?. Int J Dermatol. Dec 2011;50(12):1535-7. [Medline].
20. Lee SH, Roh MR, Jee H, Chung KY, Jung JY. Wells' syndrome associated with churg-strauss syndrome. Ann Dermatol. Nov 2011;23(4):497-500. [Medline]. [Full Text].
21. Fujimoto N, Wakabayashi M, Kato T, Nishio C, Tanaka T. Wells syndrome associated with Churg–Strauss syndrome. Clin Exp Dermatol. Jan 2011;36(1):46-8. [Medline].
22. Yin G, Xie Q. Systemic lupus erythematosus associated with Wells' syndrome. Rheumatol Int. Feb 22 2011;[Medline].
23. Omiya W, Fujita Y, Baba K, Shibaki A, Odani T, Shimizu H. Unusual cutaneous manifestations of Churg-Strauss syndrome mimicking Wells' syndrome. Eur J Dermatol. Jun 15 2012;[Medline].
24. Anderson CR, Jenkins D, Tron V, Prendiville JS. Wells' syndrome in childhood: case report and review of the literature. J Am Acad Dermatol. Nov 1995;33(5 Pt 2):857-64. [Medline].
25. Nielsen T, Schmidt H, Sogaard H. Eosinophilic cellulitis. (Well's syndrome) in a child. Arch Dermatol. Jul 1981;117(7):427-9. [Medline].
26. Shams M, Hudgens J, Lesher JL Jr, Florentino F. Wells' syndrome presenting as a noninfectious bullous cellulitis in a child. Pediatr Dermatol. Mar 2012;29(2):224-6. [Medline].
27. Powell JG, Ramsdell A, Rothman IL. Eosinophilic cellulitis (Wells syndrome) in a pediatric patient: a case report and review of the literature. Cutis. Apr 2012;89(4):191-4. [Medline].
28. Caputo R, Marzano AV, Vezzoli P, Lunardon L. Wells syndrome in adults and children: a report of 19 cases. Arch Dermatol. Sep 2006;142(9):1157-61. [Medline].
29. Spinelli M, Frigerio E, Cozzi A, Garutti C, Garavaglia MC, Altomare G. Bullous Wells' syndrome associated with non-Hodgkin's lymphocytic lymphoma. Acta Derm Venereol. 2008;88(5):530-1. [Medline].
30. Odia SG, Purschel W, Worret WI, Rakoski J. Hypereosinophilic cellulitis(Wells' syndrome) resembling urticaria. Acta Derm Venerol (Ljubljana). 1994;6:193-195.
31. Mutasim DF, Cooper CH. A case of Wells' syndrome in a patient with lymphocytic lymphoma. Geriatr Dermatol. 1996;4(1):11-14.
32. Falagas ME, Vergidis PI. Narrative review: diseases that masquerade as infectious cellulitis. Ann Intern Med. Jan 4 2005;142(1):47-55. [Medline].
33. Leiferman KM, Peters MS. Reflections on eosinophils and flame figures: where there's smoke there's not necessarily Wells syndrome. Arch Dermatol. Sep 2006;142(9):1215-8. [Medline].
34. Moossavi M, Mehregan DR. Wells' syndrome: a clinical and histopathologic review of seven cases. Int J Dermatol. Jan 2003;42(1):62-7. [Medline].
35. Stern JB, Sobel HJ, Rotchford JP. Wells' syndrome: is there collagen damage in the flame figures?. J Cutan Pathol. Dec 1984;11(6):501-5. [Medline].
36. Peters MS, Schroeter AL, Gleich GJ. Immunofluorescence identification of eosinophil granule major basic protein in the flame figures of Wells' syndrome. Br J Dermatol. Aug 1983;109(2):141-8. [Medline].
37. Aberer W, Konrad K, Wolff K. Wells' syndrome is a distinctive disease entity and not a histologic diagnosis. J Am Acad Dermatol. Jan 1988;18(1 Pt 1):105-14. [Medline].
38. Herr H, Koh JK. Eosinophilic cellulitis (Wells' syndrome) successfully treated with low-dose cyclosporine. J Korean Med Sci. Oct 2001;16(5):664-8. [Medline].
39. Church MK, Maurer M, Simons FE, et al. Risk of first-generation H(1)-antihistamines: a GA(2)LEN position paper. Allergy. Apr 2010;65(4):459-66. [Medline].
40. Brown J, Schwartz RA. Wells' syndrome (eosinophilic cellulitis). Cesko-Slovenska Dermatol. 2002;77:261-263.

 

 

 

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Happy Wednesday !

Rejoicing over Diabetes....

Hurray.... for a being a GOOD DIABETIC  !! live long, live well!

Black Folk eating good ol' Greens (aka Kale)

Yippee! My Vitamin D ~ Guide sheet

The Aretha Franklin Snicker Commercial

Habits form when you associate pleasure to an action, whether that action is going to serve you in reaching your goals or not is another story. However, you can use this information to your advantage and practice creating new, positive associations to habits you want to form - like eating a salad instead of having fries, or drinking a glass of water before anything in the morning....


CRAP vs. FOOD   Wellness Blogger/site

I've found a blog friend named Annie's Ruby Slipperz

Annie's Ruby Slipperz

Luvin my Healthy Life Choices

. . . .you probably already knew about all the bad things

 that can happen to you if you are in a

 "STRESS MESS" 

Thought processes go awry, not thinking clearly, inability to remember.
 Stress affects emotions, (feeling extra sad, frustrated, irritable)

It's dangerous to the heart, (high blood pressure, blood clots, strokes)
Stress can reek havoc on stomach and intestines (ulcers, acid reflux
irritable bowls, vomiting, and diarrhea).  And, skin suffers too,
(eczema, acne, cold sores and fever blisters), and...
with stress the immune system is in a weakened state.   

Some things that can help...

1)

Music...Playing calm music has a positive effect on

the brain and body, can lower blood pressure, and reduce cortisol,

 a hormone linked to stress.

2) 

Call a Friend...when stress hits, take a minute and

call a friend to discuss your problems.  A kind, reassuring voice,

even for a minute can bring things into perspective.

3)

 Eat right (and take vitamins)...stress levels and diet are closely related

When we are stressed we tend to want sugar and fatty foods.

These can make stress worse.  Fruits and Vegetables are

And, fish with high levels of omega-3 fatty acids,

which have been shown to reduce the symptoms of stress.

A tuna sandwich really is brain food.

4) 

 Laughter is good medicine...yep, it's true!  It releases

endorphins that improve mood and decrease levels of the

stress-causing hormones cortisol and adrenaline.

 5)

 Exercise (Even For a Minute)...you don't have to power lift

or train for a marathon.  Even a short walk around the office

or taking a short break to stand and stretch can relieve stress.

Getting your blood moving releases endorphins and can improve

mood almost immediately.  I need to go for a walk instead
of walking to the pantry!

 6)

 Sleep...stress causes many to lose sleep. And, lack of

sleep causes stress...Yikes! a vicious circle.  Make every effort

to get enough sleep (at least 7-8hrs).  It may be the best stress buster

HEALTH wisdom

Today's Lunch hour was serene

and  beautiful..... The OU Medical center outside eating area was so calming.  After I've have blood work done to check my Vit D levels...

 Above picture of an ORANGE SHERBERT (color and tasty) cupcake was not to be resisted.   It's OK... since I truly turn down breakfast donuts and other sugary foods..... THIS was my heavenly moment to indulge!

A little nostalgia.... I'm planning my 5960 Birthday party for the 1st Saturday in January 2013!!!  I'm remembering that my favorite color really is this peachy - orange sherbert!...   I was married in this color.... with a light blue coordinate... and I think I'll find me a casket and clothing to match warm-hearted peachy color!!!  

Wednesday Words for T2D (type2diabetes)

".......Unwilling to let the debilitating disease take his life, he began micro-managing every move he made and took control, one bite of food, one insulin injection, and one step at a time.
Mandell learned to live differently and, in doing so, realized that the restorative journey he'd embarked upon was one that could help others live better as well. "If everybody lived as if they were diabetic, you'd see all kinds of diseases going out the window," he said.

online magazine reading....  Type 2 Trudges Across America to Defeat Diabetes  Andy Mandell

Aug 17, 2012 

Diabetes and Muscle Cramps last night....

Potassium (K), 

A problem with muscle cramps can sometimes be a problem with the muscle not being able to function properly due to a lack of proper electrolite balance. Potassium (K),

Calcium (Ca), 

and Magnesium (Mg) are absolutely essential for a muscle to be able to properly fire....and to properly relax. 

If there is a lack of these minerals in the body, the muscle can temporarily lose the ability to relax and, therefore, cramps. 

Try taking K, Ca, and Mg suppliments regularly and see if that doesn't make a huge difference.

This could also be the effect of insulin resistance. I'm not sure of your weight or sugar intake, but if you have too much sugar or processed crap in your diet for a prolonged period of time, the body goes into what is called insulin resistance. Insulin is an anabolic hormone that also serves to store calcium and magnesium. Insulin resistance, by these means, can be a cause of not only muscle cramps

Read more: http://wiki.answers.com/Q/Why_do_you_get_leg_cramps_at_night#ixzz24koTLFQw

Water for T-2 Diabetics

It has been a theory . . . . .that a rapid drop in blood sugars can cause muscle cramping. I would suggest testing your blood glucose to see if this is the case with you.

Also dehydration sometimes causes muscle cramps, and patients with diabetes can potentially dehydrate faster. Make sure you drink enough water during the day.

What's a 'nonreactive' pot

NONREACTIVE  aka Lemon Meringue Pie

When a recipe calls  a 'nonreactive' pot for using or pan to cook something in, it is calling for a pan made of a material that will not react with acids or brines (tomatoes, pickles, etc). Glass, stainless steel and enameled are the most common nonreactive pans.  Undamaged nonstick pans may also be used, but be sure there are no scratches or other damage to the non-stick coating. Acid foods may react by discoloring food, forming toxic substances, and may effect both flavor and texture.  Salty mixtures may also pit aluminum pans if they are left standing in the pan.

Reasons to Eat Fruit !!

Living well,,, Total Wellness.... Loving Life....!!!

Eating Calcium Rich Foods!

hmnnnn....

I Love the Greens.... and Okra....!!!

God is answering the Lonesome Question...

Dear Hubby is taking the time to listen to my diabetes numbers . . . .

The Dawn Phenomenon

I learned how my body reacts to the Dawn Phenomenon, that early morning rise in glucose levels that occurs when the liver dumps glucose into the bloodstream to prepare the body to awaken.  I found that my body begins this process as early as 4:00 AM, 

...sharing what a fellow blogger said....... think about my blood sugar readings as information from my body. She was just about as cynical as I usually would be....and said, “Easier said than done.” The therapist went on to tell her . . . . . .to let go of the “bad” and “good” labels and to think of the numbers more scientifically. For example, 250 was telling me I needed more insulin (for whatever reason, miscalculation of carbs, over treating a low etc.), just like 50 was telling me I needed less insulin and more glucose.

Still a skeptic.... thinking, it’s easy for her to say don’t get emotional about the numbers, but her words stuck !  She related how... over the next few days when she got a 200+ reading, she took a deep breath and thought, okay, what do I need to do here? Slowly, it began to work.

Slowly, the black hole began to dissipate like a rain puddle after the clouds part. She began to chant the phrase in my head “It’s just a number.” And it worked.

My Drawing of What is Diabetes

Type 2 diabetes (link = Tudiabetes.com)is a chronic (lifelong) disease marked by high levels of sugar (glucose) in the blood. Type 2 diabetes is the most common form of diabetes... When you have type 2 diabetes, the body does not respond correctly to insulin. This is called insulin resistance.

Insulin resistance means that fat, liver, and muscle cells do not respond normally to insulin. As a result blood sugar does not get into cells to be stored for energy.

High Blood Sugar: Damage is cumulative

Glucose is the body's primary energy source. After a meal, carbohydrates usually are broken down into glucose and other simple sugars. This causes blood glucose levels to rise and stimulates the pancreas to release insulin into the bloodstream. Insulin is a hormone produced by the beta cells in the pancreas. It regulates the transport of glucose into most of the body's cells and works with glucagon, another pancreatic hormone, to maintain blood glucose levels within a narrow range. If someone is unable to produce enough insulin, or if the body's cells are resistant to its effects (insulin resistance), then less glucose is transported from the blood into cells. Blood glucose levels remain high and the body's cells "starve." This can cause both acute and chronic problems depending on the severity of the insulin deficiency.

Acute hyperglycemia can be a medical emergency. The body tries to rid the blood of excess glucose by flushing it out of the system with increased urination. This process can cause dehydration and upset the body’s electrolyte balance as sodium and potassium are lost in the urine. With severe insulin deficiency, glucose is not available to the cells and the body may attempt to provide an alternate energy source by metabolizing fatty acids. This less efficient process leads to a buildup of ketones and upsets the body's acid-base balance, producing a state known as ketoacidosis. Left unchecked, acute hyperglycemia can lead to severe dehydration, loss of consciousness, and even death.

Glucose levels that rise over time and become chronically elevated may not be initially noticed. The body tries to control the amount of glucose in the blood by increasing insulin production and by eliminating glucose in the urine. Symptoms usually begin to arise when the body is no longer able to compensate for the higher levels of blood glucose. Chronic hyperglycemia can cause long-term damage to blood vessels, nerves, and organs throughout the body and can lead to other conditions such as kidney failure, loss of vision, strokes, cardiovascular disease and circulatory problems in the legs. Damage from hyperglycemia is cumulative and may begin before a person is aware that he or she has diabetes. (link: labtests online)  The sooner that the condition is detected and treated, the better the chances of minimizing complications.

What's Normal and Abnormal ????

The human body wants blood glucose (blood sugar) maintained in a very narrow range. 

Our bodies desire blood glucose to be maintained between 70 mg/dl and 110 mg/dl (mg/dl means milligrams of glucose in 100 milliliters of blood). Below 70 is termed "hypoglycemia." Above 110 can be normal if you have eaten within 2 to 3 hours.  That is why your doctor wants to measure your blood glucose while you are fasting...it should be between 70 and 110.  Even after you have eaten, however, your glucose should be below 180. Above 180 is termed "hyperglycemia" (which translates to mean "too much glucose in the blood"). If your 2 two blood sugar measurements above 200 after drinking a sugar-water drink (glucose tolerance test), then you are diagnosed with diabetes.

Insulin and glucagon are the hormones which make this happen. Both insulin and glucagon are secreted from the pancreas, and thus are referred to as pancreatic endocrine hormones. The picture (below) shows the intimate relationship both insulin and glucagon have to each other. Note that the pancreas serves as the central player in this scheme.  It is the production of insulin and glucagon by the pancreas which ultimately determines if a patient has diabetes, hypoglycemia, or some other sugar problem.

Insulin and glucagon are hormones secreted by islet cells within the pancreas. (link)  They are both secreted in response to blood sugar levels, but in opposite fashion!



Insulin is normally secreted by the beta cells (a type of islet cell) of the pancreas. The stimulus for insulin secretion is a HIGH blood glucose...it's as simple as that!  Although there is always a low level of insulin secreted by the pancreas, the amount secreted into the blood increases as the blood glucose rises. Similarly, as blood glucose falls, the amount of insulin secreted by the pancreatic islets goes down.

As can be seen in the picture, insulin has an effect on a number of cells, including muscle, red blood cells, and fat cells. 

Glucagon is secreted by the alpha cells of the pancreatic islets in much the same manner as insulin...except in the opposite direction. If blood glucose is high, then no glucagon is secreted.
When blood glucose goes LOW, however, (such as between meals, and during exercise) more and more glucagon is secreted. Like insulin, glucagon has an effect on many cells of the body, but most notably the liver.

The HUNGER GAMES. . . . via Diabetes

What is diabetes?

• a disorder of metabolism—the way the body uses or converts food for energy and growth

PWD T2 Days Remaining 147

I gotta have my morning coffee.....

that is..... KENYA darkest roast (3/4 of a 16 oz cup) adding steamed milk and English Toffee flavorings.   It foams richly at the top....  I bring along a glass coffee cup to pour about a third of it into.... it's hot and smooth.   I keep refilling cup till its gone on the remaining 20 minute drive to work...

Oh... but first I take my meter numbers.   I remember today that I forgot LAST NIGHT to inject my Lantus.... man -- I was tired at 10:22 pm.      So it goes.  UP DOWN AND ALL AROUND!  This mornings number is 114 mg/dl    Now... back to the coffee.... I take my medicine along with it and then I chill (I caffeine UP!) for about an hour!

There are certain other little perks to my morning coffee break! 

Now for more bad news.....Diabetic ketoacidosis is an emergency condition

With such a high amount of glucose outside the cells,
and a decreasing amount inside the cells (since it's been used for energy),
.................the water in the cells is forced out of the cells in an attempt to even out the amounts of glucose.

This causes rapid dehydration and the body tissues begin to collapse as they lose water. Then the kidneys go to work filtering out all of the excess water, which is what causes the frequent urination. In the process, many essential compounds, such as sodium ions, are flushed out in the urine. The loss of sodium causes many cells to have difficulty functioning properly and eventually cells begin to die. 

Now the Liver works in the Dark!!!!

When glucose isn't able to enter the body's cells, the body is unable to produce energy. When your body has no other energy sources, it will turn to digesting proteins (muscles) and fats for energy. Muscles will break down their own proteins, releasing amino acids, the building blocks of protein, into the blood stream. When the amino acids reach the liver they are converted to glucose.


For a person whose pancreas functions like it's supposed to, the glucose produced by the liver would trigger the pancreas to release insulin and let the glucose into the body's cells to produce energy. This would be a temporary... good thing for the body...


But for someone whose pancreas doesn't work right, all the liver is doing is dumping more sugar that's not needed in the bloodstream.
Unfortunately, the liver doesn't realize that there is already too much glucose in the blood because it doesn't test glucose levels like the pancreas does. The liver tests for insulin.

When insulin is not being produced, the liver is tricked into thinking the body is starving and needs more sugar. The liver will create more and more glucose as muscle is broken down. This has catastrophic effects.

A Key.... and a Rusty Locked Cell

Normal Pancreatic Function

After you eat, nutrients such as carbohydrates, fats, and proteins are broken down by the digestive system. Through this process, nutrients become smaller and simpler molecules that can be absorbed into the blood stream. One of these nutrients is glucose. As the concentration of glucose in the bloodstream rises, the pancreas receives a signal to release insulin.
The insulin attaches to a place on the cell much the same way a key would fit into a lock. This opens the door for glucose to enter the cell. In a muscle cell, this means that the insulin will open up the muscle cells to allow glucose to enter and eventually create the energy needed for the muscle to contract.

Insulin Resistance

The cause of abnormal pancreas function in diabetics is insulin resistance. Insulin resistance is when the cells stop responding to insulin, meaning the door which allows glucose to enter won't open. Because the cells aren't allowing glucose to enter, the amount of glucose in the blood gets higher and higher. As long as there is too much glucose in the blood, and too little glucose in the cell, the pancreas will continue to produce insulin until the glucose level goes down. However, if the cells in the body have become insulin resistant, the amount of glucose in blood will never go down. The pancreas will continue to try to lower glucose levels by producing more and more insulin, but eventually it will wear out.

 ........with insulin failing to open cells so glucose can leave the bloodstream, glucose begin to build up in tissues such as the kidneys, eyes, heart, and around nerve endings. This build-up has very serious short and long-term complications.

Diabetes and the My Body

 Pancreatic Function

The pancreas is a small organ located just behind the stomach. Its main function is to produce insulin in just the right amount to maintain constant glucose levels in the body.

What the Body Needs

The body's cells are designed so that they function best when there is a certain amount of glucose, or sugar, in the fluid that surrounds them. Too much glucose in the body will turn the fluid that surrounds the body's cells into a bath of sugar that hinders many normal functions of these cells.

Why we need glucose

Although glucose is not of much use to the body in the bloodstream, or in the fluid that surrounds the body's cells, it is still something that we need. In fact, it is glucose that is the body's main source of energy, but glucose must get inside cells to create the energy that the cells need to function. The problem is that cells have a membrane or covering around the outside that won't let glucose in. This is where insulin becomes important, because it is insulin that opens up cells to glucose.
Maintaining a constant level of glucose is a delicate process that is controlled by the pancreas and the insulin it produces. Under normal conditions, this process is almost like a dance. Glucose levels in the blood lead the pancreas to release just the right amount of insulin to keep the amount of glucose in the blood stream and surrounding the cells at an even level.

A Broken Pancreas

The pancreas produces two hormones your body needs: insulin and glucagon. These are produced in a cluster of cells called the islets of Langerhans. Glucagon is produced by the alpha cells in the islets of Langerhans and Insulin is produced by the beta cells. In my case, the beta cells no longer produce insulin.

Among other things, insulin is used for regulating the level of glucose in your blood. It does this by stimulating your body cells to use the glucose in your blood. Glucose is essentially the gasoline which fuels your body. Insulin is the key to unlocking the gas tank. Here is a diagram:
The process should work something like this:

1. you eat something,
2. the carbohydrates in the food are changed into glucose molecules
3. the glucose molecules go into your bloodstream to be transported throughout the body (which raises your blood sugar level)
4. when the glucose gets to a cell that needs energy, insulin allows the cell to take the glucose (which lowers your blood sugar level)
5. your body gets the energy it needs

Problems arise at step #4.

This is where my body's pancreas makes insulin but for some reason the cells are resistant to it (much as rust in a key hole can make opening a door difficult), your body can't use the glucose. I am a type 2 diabetic or an insulin-resistant diabetic.

My body will continue to pump out insulin to try and get the glucose it needs. Enough of the insulin will usually "work" so that the body won't shut down.   But because glucose is not getting into my cells - - - -I live in a state of hyperglycemia (too much sugar).

This does a number of things, primarily slowing or stopping circulation in the smaller blood vessels of the body. This is why diabetes is the primary cause of blindness, amputations, strokes, etc.

On the bright side, type 2 diabetics don't have to worry about their body eating itself. This is because another function of insulin is to store fat. So all that extra insulin that was being made is put to good use by storing the glucose in the fat cells of the body. They get bigger, the person gets fatter. If left uncontrolled, the person will eventually die of heart failure or a stroke--morbidly obese, likely lacking a leg or two and probably blind.