ITP info

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ITP, idiopathic thrombocytopenic purpura, also known as immune

thrombocytopenic purpura, is classified as an autoimmune disease. In

an autoimmune disease the body mounts an attack toward one or more

seemingly normal organ systems. In ITP, platelets are the target.

They are marked as foreign by the immune system and eliminated in the

spleen and sometimes, the liver.

Researchers have identified more than eighty autoimmune diseases.

More than 50 million people in the US suffer from a chronic condition

related to an autoimmune disease. Approximately 200,000 people in the

US have ITP. In adults, about three times more women have the disease

than men. In children, the ratio is about even. It affects all age

groups.

The percentage rate of ITP cases is increasing. Each year there are

approximately 20,000 new cases or about 10 to 125 per million people.

The estimates vary.

ITP is characterized more by its description than the specific

properties of the disease. It is the diagnosis when platelets are

abnormally low and other diseases that could cause low platelets have

been ruled out. Usually there is the presence of antiplatelet

antibodies indicating that the body has decided to consider the

platelets foreign. It attacks them with an antibody as it would

bacteria. The body then does what it is programmed to do with

bacteria: eliminate them. This is done in the spleen or liver.

ITP can present itself with small purple spots called petechiae in

the mouth and legs, nose bleeds, and bleeding gums during normal

dental care. Some people develop bruises on their arms and legs with

no provocation. It is often accompanied by fatigue and sometimes

depression.

There are many types of ITP. ITP in children is not the same as adult

ITP. Children have a much greater chance of recovering with little or

no intervention. Adolescent ITP has more of the characteristics of

adult ITP.

While most cases of ITP are controlled, it can be fatal in a small

percentage of ITP patients.

Extensive information about the nature of ITP is currently available

on the web. Our aim in this section is to summarize or enhance rather

than duplicate what others have defined . Below are other sites with

general ITP information.

Warnings

Below are a list of drugs and other substances that may reduce blood

platelet counts in some individuals. Reactions vary.

According to an article by Dr. , " Quinidine, quinine,

sulfonamides, nonsteroidal anti-inflammatory drugs, and gold

compounds were among the most frequently reported drugs... " (that

cause thrombocytopenia).See http://moon.ouhsc.edu/jgeorge for more

information.

Another list of adverse side effects is maintained by the FDA.

Drugs that can significantly reduce platelet counts

Major Sources:

[A]Drug Induced Thrombocytopenia

http://moon.ouhsc.edu/jgeorge/DITP.html

[E] The Essential Guide to Prescription Drugs, 1997, J.

Rybacki, Pharm.D. and W. Long, M.D.

Anxiety/Depression

diazepam [A,E] - antianxiety, tranquilizer (Valium, among others)

chlorpromazine [A] - antipsychotic, tranquilizer (Chlorpromanyl,

Largactil, Thorazine)

imipramine [E] - antidepressant (Antipress, Apo-imipramine, Impril,

Janimine, Tipramine)

thiothixene [A] (Navane)

Arthritis

penicillamine [E] - antiarthritic, heavy metal poisoning, (Cuprimine,

Depen)

Attention Deficit Disorder

methylphenidate hydrochloride (Ritalin) thrombocytopenia purpura is

listed as a side-effect

Cancer

levamisole [A,E] (Ergamisol)

interferon alpha [A] (Roferon A, Intron A)

tamoxifen [A] (Nolvadex)

Cholesterol

atorvastatin calcium (lipitor) - binds to plasma proteins See:

Atorvastatin-induced severe thrombocytopenia. (Research Letters)

Author/s: a -Ponte Issue: Oct 17, 1998 - Lancet

Diabetes

chlorpropamide [A,E] - antidiabetic, (Apo-Chlorpropamide, Chloronase,

Diabinese, Glucamide)

Fungus Infection

amphotericin B [A] (Amphocin, Fungizone)

Gout

allopurinol [E] - Used to control gout (Alloprin, Lopurin, Novopurol,

Purinol, Zurinol, Zyloprim)

Hair Loss

minoxidil [A,E] - antihypertensive, hair growth stimulant (Minodyl,

Minoximen, Rogaine)

Heartburn

cimetidine [A,E] - Heartburn Tagamet, also Zantac, Pepcid in same

class of Histamine H-2 blocking drugs

ranitidine [A,E] - H-2 Receptor blocker (Zantac)

Heart Conditions

acetazolamide [E]- Used for glaucoma, seizures, retention of fluid in

congestive heart failure, mountain sickness

amiodarone [A,E] (Cordarone)

amrinone [A] (Inocor)

diltiazem [E] - antianginal, antihypertensive, calcium channel

blocker (Apo-Diltiaz, Cardizem)

digoxin[A,E] - digitalis preparations, congestive heart stimulant and

treatment of heart rhythms. (Lanoxicaps, Lanoxin, Novodigoxin.)

procainamide [A,E] - antiarrhythmic (Apo-Procainamide, Procamide,

Procanbid, Promine, Rhythmin)

quinidine [A,E] - antiarrhythmic (Apo-Quinidine, Cardioquin,

Duraquin, Quinora)

High Blood Pressure / water retention

chlorothiazide [A,E] - diuretic, antihypertensive (Aldoclor,

Diachlor, Diupres, Didudrigen, Diuril, Supres

chlorthalidone [E] - antihypertensive, diuretic (Apo-Chlorthalidone,

Combipres, Hygroton-Reserpine, Thalitone, Uridon)

furosemide [E] - antihypertensive, diuretic (Lasix, Lo-Aqua, Luramide)

quinapril hydrochloride (Accupril)

Infections

ampicillin [A,E] - antibiotic used to treat infections (Amcill,

Ampicin, Ampilean, Omnipen, Polycillin, Penbritin, Principen)

cephalosporins[E] - anti-infectives

cefaclor (Ceclor), cefadroxil (Duricef, Ultracef), cefamandole

(Mandol) cefazolin (Ancef, Kefzol, Zolicef) cefixime (Suprax)

cefmetazole (Zefazone), cefonicid (Monocid) cefoperazone (Cefobid)

ceforanide (Percef) cefotaxime (Claforan), cefotetan (Cefotan)

cefoxitin (Mefoxin) cefprozil (Cefzil) ceftazidime (Fortaz, Tazidime,

Tazicef) ceftizoxime (Cefizox), ceftriaxone (Rocephin) cefuroxime

(Ceftin, Kefurox, Zinacef) cephalexin (Keflex, Keftab) cephalothin

(Keflin) cephapirin (Cefadyl) cephradine (Anspor, Velosef) moxalactam

(Moxam) Omnicef

nalidixic acid [A]- (Negram)

penicillin V [E] - antibiotic causes abnormal bleeding or bruising

pentamidine isethionate - (Pentam, NebuPent, Pentacarinate)

rifampin [A,E] - antibiotic (Rifadin, Rifamate, Rofact)

sulfamethoxazole [A]- anti-infective (Apo-Sulfatrim, Bactrim,

Comoxol, Septra, etc.)

trimethoprim/sulfamethoxazole [A,E] - anti-infective (Apo-sulfatrim,

Bactrim, Coptin, Septra)

vancomycin [A,E] - anti-infective (Vancocin, Vancoled, Vancor)

Inflammation/Pain

acetaminophen [A] (Tylenol, Panadol, others) - considered safe by

many, however, some incidences of platelet reduction were found in

journal articles.

aspirin [E] (acetylsalicylic acid, ASA) relief of mild to moderate

pain and inflammation. Causes decreased number of white blood cells

and platelets.

ibuprofen [A] - NSAID

diclofenac [A,E] - analgesic NSAID, (Apo-Diclo, Arthrotec, Cataflam,

Novo-difenac,Voltaren)

meclofenamate sodium [A] - NSAID (Meclomen)

morphine [E] - analgesic, opioids

naproxen - NSAID, (Naprosyn)

piroxicam [E] - NSAID, analgesic, (Apo-Piroxicam, Feldene,

Novopirocam, Nu-Pirox)

sulfasalazine [A,E] - bowel anti-inflammatory (Azaline, Azulfidine,

Salazopyrin)

Malaria

chloroquine [E] - used to treat malaria and amebic infection , causes

bone marrow depression (Aralen, Kronofed-A-JR)

hydroxychloroquine (Plaquenil) - antimalarial, immunosuppressant,

used in lupus, rheumatoid arthritis, causes bone marrow suppression

Premenstrual Distress

Sarafem

Seizure Disorders

acetazolamide [E] - anticonvulsant (Ak-Zol, Dazamide, Diamox,

Storzolamide)

carbamazepine [A,E]- anticonvulsant , reduced formation of all blood

cells (Apo-carbamazepine, Epitol, Mazepine, Tegretol).

phenytoin [A,E] - anticonvulsant (Dilantin, Ekko JR, Mebroin,

Phelantin)

topiramate - anticonvulsant (Topamax)

valproic acid - anticonvulsant (Depakote, Epival)

zonisamide - (Zonegran) also used for migraine and weight loss

Tuberculosis

isoniazid [A,E] - antituberculosis (Isotamine, Laniazid, Vitamin B-6)

ethambutol [A]- (Myambutol)

Others substances that can reduce the number of platelets

alcohol

alfalfa sprouts (may harbor salmonella)

allicin (contained in Kwai, Kyolic and other garlic supplements)

chlorine

dong quai (angelica sinensis) According to Dr. Hoang, it should be

avoided in ITP and autoimmune diseases because it has an estrogenic

effect and will make autoimmune conditions worse. He said there is a

rule: herbs which stimulate female hormones are contraindicated for

autoimmune diseases and those which enhance male hormones and

vitality are indicated for autoimmune disease

gold and gold salts

Metabalife contains Ma Huang and other substances that interfere with

blood clotting (see list below). One of our readers reported a

decreased platelet count while using.

pesticides

phenylpropanolamine (found in decongestants and weight loss products -

linked to hemorrhagic strokes) Click for list of products

quinine (found in tonic water)

medications that contain salicylates (ex. Pepto-Bismol, Alka Seltzer)

aminoglutethimide (Cytraden), aminosalicylic acid (Paser),

chenodeoxycholic acid, chlorpheniramine, desferrioxamine, diazoxide,

diatrizoate meglumine, gentamicin, hydrochlorothiazide, levamisole,

lopanoic acid (Telepaque), meprobamate, methyldopa, mianserin,

naphazoline (Privine, Vasocon-A), nitrofurantoin, oxprenolol,

oxyphenbutazone, phenylbutazone, sodium aminosalicylate,

sulfonamidesthioguanine, valproate

Substances that reduce the ability to clot

aspirin

aspartame

beer

blueberries

heparin (can also cause thrombocytopenia)

vitamin E

garlic/onions

gingko biloba (can also reduce the number of platelets)

ginger

ginseng

goldenseal

guarana

red/purple grape products (grape juice, red wine, raisins)

pycnogenol

Omega 3 fatty acids

SSRI's (Prozac, etc.)

Quercetin, rutin, and related bioflavonoids

ticlopidine (ticlid) used to prevent blood clots

tomatoes

dipyridamole (Persantine)

sulfinpyrazozne (Anturane)

About Platelets

This is what platelets look like. For some of us , it is the closest

we are going to get to seeing them. Study their shape. Meditate on

their line. Perhaps it will help.

All blood cells originate and mature in the bone marrow. They begin

in 'stem' cells, then differentiate into the red cells, white cells,

and platelets. The white blood cells include three varieties,

granlocytes, monocytes (macrophages) and lymphocytes.

Normal platelet counts range from 150,000 to 400,000 per cu/ml. Those

with ITP have a lower platelet count. It can range from severe cases

that hover close to zero to more mild cases where the counts stay in

closer to 100,000. 30,000 is often considered a `safe' count', one

that is high enough to protect against cerebral hemorrhage.

In people with ITP the platelets are often enlarged. They stay in the

blood stream from a few hours to close to the normal eight to ten

days depending on the severity of the disease.

Platelets play a crucial part in the blood clotting process by

forming a platelet plug. This is a two step process. First, single

platelets bind to the site of the wound (adhesion). Next, the

platelets bind to each other (activation). Activation can be

stimulated by components released when the blood vessel is damaged

and by thrombin, released during the blood clotting process. When

platelets become activated they change. They release agents which

recruit and activate the surrounding platelets. The result of these

two processes is the formation of fibrin which stabilizes the

platelet plug, stops bleeding and allows injuries to heal.

In your body, 2% of the serotonin, a mood elevating neurotransmitter,

is stored in platelets. In addition to serotonin, your platelets also

carry its 'parent' or precursory chemical L-tryptophan. While

serotonin can't pass through the blood brain barrier, L-tryptophan

can. These substances are involved in such processes as sleep/wake

cycles, biological rhythms, appetite, mood regulation, etc.

Causes of Autoimmune Diseases

No one really knows what causes ITP. Here are some general theories

on the causes of autoimmune diseases. Although these are presented as

three theories, they can be viewed as pieces of a larger puzzle.

Microbial Trigger Theory

Scientists have discovered that we have immune cells which, when

activated, can target the body's own molecules. Researchers at the

National Institute of Allergy and Infectious Diseases, Yale

University, and Duke Medical Center, among others, have found these

cells can be activated by bacteria, at least in mice.

When it is fighting a reaction, the body produces a compound called

interleukin-12 during it's normal immune response. Interleukin-12

then creates many other immune compounds specific to a particular

microbe. Researchers think this flurry of activity may activate any

dormant self-reactive cells that may be near the infection. (If the

self-reactive cell is for platelets, you get ITP) This also suggests

that interleukin-12 inhibitors may aid people with auto-immune

disorders.

(Summarized from " Microbial Trigger for Autoimmunity? " Science News,

6/21/97)

Molecular Mimicry Theory

This theory suggests that autoimmune diseases are caused when a

person's immune response gets confused between it's own cells and

invading virus and bacteria if the invaders are similar to the host

cells.

When a virus invades our body, special cells chop it up into

thousands of fragments and put some of them in a type of pocket for

the immune system to disable. A person's genes determine which of the

invader fragments go in the pocket. T cells latch on to the fragments

in the pocket and send signals to destroy all of the tissues that

have that type of fragment.

The problem comes when some part of the body has the same amino acid

sequence on its surface as the invader fragment. When this happens T

cells attack the `good' cells with the twin fragments as well as

those with the pocketed viral fragment. Another study suggests that

the good cells might not need the same amino acids sequence. Perhaps

just having another similar property, such as a negative charge, can

create the same confusion. This means that a larger number of

proteins with different amino acid sequences can stimulate the same T-

cell, setting off an auto-immune disease.

The thymus contains a master list of the body's most abundant

proteins. When T cells are born, they are compared to the master

list. Those that recognize self-proteins are killed off. There are,

however, some proteins that are not on the master list. So T cells

that recognize these proteins are not destroyed. Other immune factors

suppress these self-reactive T cells. When that control is lost, an

auto-immune disease can begin.

According to the research scientists, the disease process involves

many more steps. The bad luck may unfold over several years and

require multiple infections and a genetic predisposition to activate.

(Summarized from " Virus's Similarity to Body's Proteins May Explain

Autoimmune Diseases " 12/31/96, New York Times)

Free Radical Damage

In this theory, the DNA in our cells can be altered or destroyed by

reactive substances in our bodies. When the destroyed DNA is a part

of the immune control function, it can result in a specific

autoimmune disease.

Oxygen outside our bodies can cause iron to rust and is necessary for

paper to burn. On the inside, it can be equally destructive. Free

radicals are particles that have an unstable molecular structure.

They act as scavengers in the body and rob electrons from other

molecules to increase their stability. The particles that are robbed

don't function as they should and can be toxic. There are several

types of free radicals. Some of the most common have an oxygen base.

For people with ITP, imagine that our platelets are cooked by it.

Free radicals build over time. They are a natural byproduct of our

metabolism and immune system functions. They are a natural component

of aging. Their production is hastened by stress, pollution,

fertilizers, pesticides, prescription drugs, alcohol, electromagnetic

radiation, etc.

Our bodies have built in controls for free radicals and ways of

changing them into neutral substances. These detoxification

mechanisms require specific enzymes to make them function well. If

our bodies do not have the vitamins and minerals to make up the

enzymes, or if the detoxification mechanism is damaged, perhaps by

free radicals, the result is a surplus of free radicals and other

toxic substances. This can also happen if our life style and

environment results in our having too many toxins for even a good

working system to neutralize.

The excess free radicals and other noxious byproducts of a failed

detox process roam our bodies and attack our weakest links. These

weak links may be due to genetics. They may be other parts of our

immune system that happen to be nearby. Depending on the DNA

attacked, the electron grabbing can cause an auto-immune disease.

Theoretically, if a surplus of free radicals is the cause of the

disease, reducing the amount of things that promote their production

(ex. stress) , ingesting substances that reduce the number of free

radicals (ex. Vitamin C) and making sure our detoxification

mechanisms have sufficient nutrients (eating well) may be part of the

cure.

(Summarized from Sharma, Hari, M.D. Freedom from Disease, Toronto,

Ontario:Veda Publishing, 1993, , Sherry A, M.D., Tired or

Toxic? A Blueprint for Health. Syracuse, NY: Prestige Publishing,

1990, and a conversation with a research scientist at Rutgers

University)