- why we still get hives

[Guest guest]

>>>...if we hive because too many histamines are being released

into our bodies, and we take an over-abundance of ANTI-histamines to

counteract that, why do we still get HIVES!<<<<

,

Hopefully someone more in the know (like Myra) will see your question and

jump in here to answer. I think it has something to do with all the

biomechanics of mast cell degranulation. It's not just that we have too much

histamine, but too much mast cell activity. When mast cells degranulate,

they fire off histamine, as well as a bunch of other stuff. Even though we

take antihistamines to counter the histamine, we still have mast cells doing

their thing, plus all the other chemicals released by them.

Here's an explanation (by Myra) from an earlier posting:

" Mast cells are part of our body's immune system. They are one of

only two cells in the body which release histamine. Without

histamine release there can be no hiving. Mast cells are activiated

by antigens (in allergy cases, classically antigens) or directly by

certain substances or conditions. Mast cells are beleived to start

at as " stem cells " which are produced in the blood marrow and migrate

outside the blood vessel walls into surrounding tissue in the " open "

vunerable areas of the body; the skin, the gastro-intestinal tract

and the mouth and respiratory system. Mast cells contain granules which

they use like little grenades to " bomb " incoming antigens or in response to

sytemic conditons within the body. These granules have many compotents,

such as histamine, heparin, chondrotin sulfates, neutral proteases, acid

hydrolases and a few other enzemes. On the surface of these mast cells are

little receptors (molecules) of IgE (immunoglobulin E antibody) as well as

other types of receptors. Think " velcro " . When an antigen comes into the

body it " sticks " to the " velcro " and the mast cell starts firing its

grenades. In medical terms this firing is called " mast cell degranulation " .

This degranulation causes hives, if the degranulation is very fast it

produces anaphylaxis. The release of inflamatory materials into the

surrounding tissues cause other inflamatory cells to " turn on " . Since mast

cells position themselves close to capillaries, blood vessels, and nerves,

the skin, gastrointestinal and respiratory tracts these areas become

" targets " for their grenades. The " bombing " causes fluid to leak from the

capillaries, white blood cells, which include T cells, neutrophils, and

eosinophils which leach into the skin and cause swelling, which produces

hives. (Joint swelling can be caused by mast

cell " bombing " .) So, medicines that control mast cells or their

grenades is the principle approach. Granted this is treating the

symptom and not the cause. But until a cause is determined, I think

it is in your best interest to try to gain some kind of control over

the symptoms that are driving you crazy. In most cases this means

using a H1 blocker (Zyrtec, has been found to be in medical studies

superior for the wheal and flare of hives ), a H2 blocker (Zantac).

When I say Zantac, most people say, HUH? I thought that Zantac was an

anti-acid. No, Zantac is anti-histamine which controls stomach

histamine which is the cause of excessive stomach acid. And since

skin mast cells have on them receptors for both H1 and H2 histamine

the use of both tends to control most hivers better.

Here's the deal......... when mast cells or basophils degranulate

they trigger many things to happen. Here is one of the things that

happens which causes swelling and angioedema.

Mast cells contain a chemical called arachidonic acid, which is

stored lipids (liquid fats) within the cell. (Arachidonic Acid can

also be found in macrophages, monocytes, eosinophils and basophils.)

When mast cells degranulate they start a very complicated chain of

events. One thing that happens is that arachonic acid is released

from cell membrane or cell " skin " . After it's release, arachidonic

acid undergoes a change (in medical terms it metabolizes) through

two pathways. The first and most common pathway is called

cyclooxygenase pathway, producing prostaglandins (PGD2) and

thromboxanes, and the second pathway is the 5-lipoxygenase pathway,

producing leukotrienes, (LTC4). It is believed that skin mast cells

tend to produce far more PGD2 and intestinal mast cells tend to

produce far more leukotrine C4. Just for reference,

prostaglandins D2 (PGD2) constrict smooth muscles (particularly in

the lungs), attract neutrophils (a type of white blood cell) and

inhibits the aggregation of platelets, which is the first step to

blood clotting. (PAF) It helps the blood vessels to dialate and

become " leaky " . Remember the second pathway involves

leukostrienes. Leukotrienes also cause the constriction of the

smooth muscle fibers in the lungs and blood vessels, and increased

secretion of mucus. Leukotrienes attract eosinophiles, another type

of white blood cells.

It should be remembered that mast cells produce many more things

through this cascade, including various types of proinflammatory and

growth factor cytokines, including tumor necrosisfactor (TNF),

interleukin-3 (IL-3), IL-4, and IL-16. Some of this I have a bit of

an understanding of, other things I haven't been able to wrap my

mind around as yet.....what can I say, it's a work in progress.

Anyway, PGD2 is largely responsible for swelling which ALL people

with angioedema experience, which may include " localized " swelling in

joints. PGD2 can be controlled with the use of pred, NSAID's,

aspirin, omega 3 fish oil or flax seed oil. "

Hope this helps.

Air hugs,

Jackie

Life is tough, but I'm tougher.

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