4 cases of aspartame-induced thrombocytopenia (very low platelets in blood)

4 cases of aspartame-induced thrombocytopenia [ very low platelets in
blood ], HJ Roberts MD, Letter in Southern Medical Journal 2007 May:
100(5); 543: Murray 2007.08.25
http://groups. yahoo.com/ group/aspartameN M/message/ 1467

This cogent clinical warning adds to the other 13 mainstream studies
in the last 24 months that justify prudent concerns
about aspartame toxicity.

Aspartame-induced thrombocytopenia
Letter to the Editor:
Southern Medical Journal 2007 May; 100(5): 543.
H.J. Roberts, MD, FACP, FCCP
Palm Beach Institute for Medical Research
West Palm Beach, FL

To the Editor:

The cause of thrombocytopenia is often not found.
Owing to my interest in reactions to aspartame products 1,
I have encountered four cases of thrombocytopenia which
may be attributed to products containing aspartame,
especially based on its recurrence on two or more occasions
after rechallenge, and the absence of any other definable factor.

Patient 1:
A 10-year-old girl developed a decline of her platelet count to 1,000
cu/mm, coupled with striking enlargement of the liver and spleen,
and a marked increase in histiocytes in the bone marrow.
There was dramatic clinical and hematological normalization
when additives were eliminated from her diet,
enabling the cessation of prednisone.
Similar recurrences occurred twice after ingesting aspartame --
first in a cereal, and later with aspartame gum --
with remissions when abstaining from aspartame products.

Patient 2:
An 11-year-old girl was hospitalized for thrombocytopenia.
She had been chewing various sugar-free gums.
There was a remission after avoiding aspartame.
Severe thrombocytopenia recurred after visiting a relative
who indulged her with aspartame sweets.

Patient 3:
A 61-year-old man developed a decline of his platelets to
54,000 cu/mm after drinking diet colas for two years,
coupled with headaches, dizziness, two convulsions, and
a nonspecific rash.
Extensive studies failed to uncover an underlying problem.
He improved after aspartame abstinence.
One retest trial resulted in an immediate exacerbation.

Patient 4:
A registered nurse began using diet colas
after her second pregnancy.
Her platelets declined to under 30,000 cu/mm,
coupled with headaches and hypertension.
The platelet count and blood pressure normalized
after avoiding aspartame products.

A reaction to aspartame products should be considered
in patients with thrombocytopenia in whom no
underlying cause can be determined.

Reference:
1. Roberts HJ.
Aspartame Disease: An Ignored Epidemic
Sunshine Sentinel Press, 2001.
West Palm Beach, FL 33416

http://www.dorway. com/tldaddic. html 5-page review
Roberts HJ Aspartame (NutraSweet) addiction.
Townsend Letter 2000 Jan; HJRobertsMD@ aol.com
http://www.sunsentp ress.com/ sunsentpress@ aol.com
Sunshine Sentinel Press P.O.Box 17799 West Palm Beach, FL 33416
800-814-9800 561-588-7628 561-547-8008 fax

http://groups. yahoo.com/ group/aspartameN M/message/ 669
1038-page medical text "Aspartame Disease: An Ignored Epidemic"
published May 30 2001 $ 60.00 postpaid data from 1200 cases
available at http://www.amazon. com
over 600 references from standard medical research

http://groups. yahoo.com/ group/aspartameN M/message/ 790
Moseley: review Roberts "Aspartame Disease: An Ignored Epidemic":
Murray 2002.02.07

Roberts, Hyman J., 1924- ,
Useful insights for diagnosis, treatment and public heath: an updated
anthology of original research, 2002, 798 pages,
aspartame disease, pages 627-685, 778-780

http://groups. yahoo.com/ group/aspartameN M/message/ 859
Roberts: the life work of a brilliant clinician: aspartame toxicity:
Murray 2002.08.02

H.J. Roberts, MD, FACP, FCCP
Protecting Mankind: One Physician's Quest 2007
Sunshine Sentinel Press, Inc.
West Palm Beach, FL 33416 223 p.
Aspartame disease 56-64
MSG 65-69

www.ncbi.nlm. nih.gov/sites/ entrez PubMed lists 43,747 items

http://en.wikipedia .org/wiki/ Thrombocytopenia

Thrombocytopenia
From Wikipedia, the free encyclopedia

Thrombocytopenia

Thrombocytopenia (or -paenia, or thrombopenia in short) is the
presence of relatively few platelets in blood.

Generally speaking a normal platelet count ranges from 150,000 and
450,000 per mm3.
These limits, however, are determined by the 2.5th lower and upper
percentile, and a deviation does not necessarily imply any form of
disease.
The number of platelets in a blood sample also decreases rather
quickly with time and a low platelet count may be caused by a delay
between sampling and analysis.

Contents

* 1 Signs and symptoms
* 2 Diagnosis
* 3 Causes
o 3.1 Decreased production
o 3.2 Increased destruction
o 3.3 Medication-induced
* 4 Treatment
o 4.1 Thrombotic thrombocytopenic purpura (TTP)
o 4.2 ITP
o 4.3 Heparin-induced thrombocytopenia and thrombosis (HITT)
o 4.4 Congenital amegakaryocytic thrombocytopenia (CAMT)
* 5 References
* 6 External links

Signs and symptoms

Often, low platelet levels do not lead to clinical problems;
rather, they are picked up on a routine full blood count.
Occasionally, there may be bruising, particularly purpura in the
forearms, nosebleeds and/or bleeding gums.

It is vital that a full medical history is elicited,
to ensure the low platelet count is not due to a secondary process.
It is also important to ensure that the other blood cell types red
blood cells, and white blood cells, are not also suppressed.

Diagnosis

Laboratory tests might include:
full blood count, liver enzymes, renal function, vitamin B12 levels,
folic acid levels, erythrocyte sedimentation rate, and peripheral
blood smear.

If the cause for the low platelet count remains unclear,
bone marrow biopsy is often undertaken,
to differentiate whether the low platelet count is due to decreased
production or peripheral destruction.

Causes

Decreased platelet counts can be due to a number of disease processes:

Decreased production

o vitamin B12 or folic acid deficiency
o leukemia or myelodysplastic syndrome
o Decreased production of thrombopoietin by the liver in
liver failure.
o Sepsis, systemic viral or bacterial infection
o Dengue fever can cause thrombocytopenia by direct
infection of bone marrow megakaryocytes as well as immunological
shortened platelet survival
o Hereditary syndromes
+ Congenital Amegakaryocytic Thromboytopenia (CAMT)
+ Thrombocytopenia absent radius syndrome
+ Fanconi anemia
+ Bernard-Soulier syndrome, associated with large
platelets
+ May-Hegglin anomaly, the combination of
thrombocytopenia, pale-blue leuckocyte inclusions, and giant platelets
+ Grey platelet syndrome
+ Alport syndrome

[edit] Increased destruction

o idiopathic thrombocytopenic purpura (ITP)
o thrombotic thrombocytopenic purpura (TTP)
o hemolytic-uremic syndrome (HUS)
o disseminated intravascular coagulation (DIC)
o paroxysmal nocturnal hemoglobinuria (PNH)
o antiphospholipid syndrome
o systemic lupus erythematosus (SLE)
o post transfusion purpura
o neonatal alloimmune thrombocytopenia (NAITP)
o Splenic sequestration of platelets due to hypersplenism
o Dengue fever has been shown to cause shortened platelet
survival and immunological platelet destruction

Medication-induced

The most comprehensive list of thrombocytopenia- inducing medications
is maintained by Dr. James George at Ohio State University at this
website, though last updated in 2004. A small subset of drug-induced
thrombocytopenia culprits:
Drug name

Heparin
Valproic acid
Quinidine
Abciximab
Sulfonamide antibiotics
Interferons
Measles-mumps- rubella vaccine
Glycoprotein IIb/IIIa inhibitors
Clopidogrel
Vancomycin [1][2]
Linezolid
Famotidine

* Direct myelosuppression
o Valproic acid
o Methotrexate
o Carboplatin
o Interferon
o Other chemotherapy drugs
* Immunological platelet destruction
o Drug binds Fab portion of an antibody. The classic example
of this mechanism is the quinidine group of drugs.
The Fc portion of the antibody molecule is not involved in the binding
process.
o Drug binds to Fc, and drug-antibody complex binds and
activates platelets.
Heparin induced thrombocytopenia (HIT) is the classic example of this
phenomenon.
In HIT, the heparin-antibody- platelet factor 4 (PF4) complex binds to
Fc receptors on the surface of the platelet.
Since Fc portion of the antibody is bound to the platelets,
they are not available to the Fc receptors of the reticulo-endothelia
l
cells,
so therefore this system cannot destroy platelets as usual.
This may explain why severe thrombocytopenia is not a common feature
of HIT.

* Heparin-induced thrombocytopenia (HIT or white clot syndrome):
this is a rare but serious condition that may occur in a hospitalized
population.
The most common clinical setting for HIT is in postoperative coronary
artery bypass graft recipients,
who may receive large quantities of heparin during surgery.
HIT typically occurs about a week after exposure to heparin.
The heparin-PF4 antibody complex will activate the platelets,
and this can often lead to thrombosis.
The term HITT, where the last T stands for thrombosis,
denotes the concept that heparin-induced thrombocytopenia often is
associated with thrombosis.

Treatment

Treatment is guided by etiology and disease severity.
The main concept in treating thrombocytopenia is to eliminate the
underlying problem, whether that means discontinuing suspected drugs
that cause thrombocytopenia,
or treating underlying sepsis.
Diagnosis and treatment of serious thrombocytopenia is usually
directed by a hematologist.

Specific treatment plans often depend on the underlying etiology of
the thrombocytopenia.

Thrombotic thrombocytopenic purpura (TTP)

Treatment of thrombotic thrombocytopenic purpura is a medical
emergency, since the hemolytic anemia and platelet activation can lead
to renal failure and changes in the level of consciousness.
Treatment of TTP was revolutionized in the 1980s with the application
of plasmapheresis.
According to the Furlan-Tsai hypothesis [3] [4] ,
this treatment theoretically works by removing antibodies directed
against the von Willebrand factor cleaving protease, ADAMTS-13.
The plasmapheresis procedure also adds active ADAMTS-13 protease
proteins to the patient,
restoring a more physiological state of von Willebrand factor
multimers. Patients with persistent antibodies against ADAMTS-13 do
not always manifest TTP, and these antibodies alone are not sufficient
to explain the how plasmapheresis treats TTP.

ITP

In many cases, ITP is self-limited, and does not require treatment.
Platelet counts less than ten thousand per mm3 usually require
treatment(less than fifty thousand requres treatment,
less than ten thousand is a potentially dangerous situation) and
patients with significant bleeding and thrombocytopenia due to ITP are
also usually treated.
The threshold for treating ITP has decreased since the 1990s, and
hematologists recognize that patients rarely bleed with platelet
counts greater than ten thousand,
though there are documented exceptions to this observation.
Treatments for ITP include:

* Prednisone and other corticosteroids
* Intravenous gamma globulin
* Splenectomy
* Danazol
* Rituximab

Thrombopoetin analogues have been tested extensively for the treatment
of ITP.
These agents had previously shown promise but had been found to
stimulate antibodies against endogenous thrombopoeitin or lead to
thrombosis.

A medication known as AMG 531 was found to be safe and effective for
the treatment of ITP in refractory patients. [5]
AMG 531 is a peptide that bears no sequence homology with endogenous
human thrombopoeitin,
so it is not as likely to lead to neutralizing antibodies as previous
peptide thrombopoeitin analogues. [6]

Heparin-induced thrombocytopenia and thrombosis (HITT)

Discontinuation of heparin is critical in a case of HITT.
Beyond that, however, care must be taken to avoid a thrombosis, and
patients started directly on warfarin after a diagnosis of HITT are at
excess risk of venous limb gangrene.
For this reason, patients are usually treated with a type of blood
thinner called a direct thrombin inhibitor such as the FDA-approved
lepirudin or argatroban.
Other blood thinners sometimes used in this setting that are not FDA-
approved for treatment of HITT include bivalirudin and fondaparinux.
Platelet transfusions are not a routine component of the treatment of
HITT,
since thrombosis, not bleeding, is the usual associated problem in
this illness.

Congenital amegakaryocytic thrombocytopenia (CAMT)

Bone Marrow/Stem Cell Transplant is the only thing that ultimately
cures this genetic disease.
Frequent platelet transfusions are required to keep the patient from
bleeding to death until transplant is done.

References

1. Howard C, Adams L, Admire J, Chu M, Alred G (1997). "Vancomycin-
induced thrombocytopenia: a challenge and rechallenge" .
Ann Pharmacother 31 (3): 315-8. PMID 9066938.

2. NEJM 2007 356:904, PMID available on 3/2/07 "Vancomycin Induced
Immune Thrombocytopenia

3. Furlan M, Lämmle B (2001). "Aetiology and pathogenesis of
thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome:
the role of von Willebrand factor-cleaving protease".
Best Pract Res Clin Haematol 14 (2): 437-54. PMID 11686108.

4. Tsai H (2003). "Advances in the pathogenesis, diagnosis, and
treatment of thrombotic thrombocytopenic purpura".
J Am Soc Nephrol 14 (4): 1072-81. PMID 12660343.

5. Bussel J, Kuter D, George J, McMillan R, Aledort L, Conklin G,
Lichtin A, Lyons R, Nieva J, Wasser J, Wiznitzer I, Kelly R, Chen C,
Nichol J (2006). "AMG 531, a thrombopoiesis- stimulating protein, for
chronic ITP".
N Engl J Med 355 (16): 1672-81. PMID 17050891.

6. Broudy V, Lin N (2004). "AMG531 stimulates megakaryopoiesis in
vitro by binding to Mpl".
Cytokine 25 (2): 52-60. PMID 14693160.

External links

* Merck Manual 11-133b
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http://groups. yahoo.com/ group/aspartameN M/message/ 1464
13 mainstream research studies in 24 months showing aspartame
toxicity, also 3 relevant studies on methanol and formaldehyde: Murray
2007.08.17

http://groups. yahoo.com/ group/aspartameN M/message/ 1457
aspartame bans, tis more an avalanche than a trend...: Rich Murray
2007.08.17

So far, USA print and broadcast media are deaf, blind, and dumb,
regarding recent major bans of aspartame and MSG in the UK and EU.

The EU Parliament voted July 12 to ban artificial sweeteners
in newly born and infant foods.

On May 15 four huge UK supermarket chains announced bans
of aspartame and MSG, food dyes, and many additives
to protect kids from ADHD --
Sainsbury, Tesco, Marks & Spencer, and ASDA, a unit of WalMart.

May 31: Coca-Cola and the much larger Cargill Inc.,
after years of secret development, with 24 patents,
will soon sell rebiana (stevia) in drinks and food
in the many nations where it is approved as a sweetener --
for decades a major sweetener in Japan, China, Korea, Taiwan,
Thailand, Malasia, Saint Kitts, Nevis,
Brazil, Peru, Paraguay, Uruguay, and Israel,
and an approved supplement in USA, Australia, and Canada,
according to Wikipedia.

http://groups. yahoo.com/ group/aspartameN M/message/ 1454
recent research and news re aspartame and stevia: Murray 2007.08.16

"Of course, everyone chooses, as a natural priority,
to actively find, quickly share, and positively act
upon the facts about healthy and safe food, drink,
and environment. "

Rich Murray, MA Room For All rmforall@comcast. net
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://groups. yahoo.com/ group/aspartameN M/messages
group with 82 members, 1,467 posts in a public,
searchable archive http://RMForAll. blogspot. com

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Aspartame Controversy, in Wikipedia democratic
encyclopedia, 72 references (including AspartameNM # 864
and 1173 by Murray, brief fair summary of much more research:
Murray 2007.01.01

http://groups. yahoo.com/ group/aspartameN M/message/ 1453
Souring on fake sugar (aspartame), Jennifer Couzin,
Science 2007.07.06: 4 page letter to FDA from 12 eminent
USA toxicologists re two Ramazzini Foundation
cancer studies 2007.06.25: Murray 2007.07.18

http://groups. yahoo.com/ group/aspartameN Mmessage/ 1451
Artificial sweeteners (aspartame, sucralose) and coloring
agents will be banned from use in newly-born and baby foods,
the European Parliament decided: Latvia ban in schools 2006:
Murray 2007.07.12

http://groups. yahoo.com/ group/aspartameN Mmessage/ 1437
stevia to be approved and cyclamates limited by
Food Standards Australia New Zealand:
JMC Geuns critiques of two recent stevia studies by Nunes:
Murray 2007.05.29

http://groups. yahoo.com/ group/aspartameN M/message/ 1427
more from The Independent, UK, Martin Hickman, re ASDA
(unit of Wal-Mart Stores) and Marks & Spencer ban of
aspartame, MSG, artificial chemical additives and dyes
to prevent ADHD in kids: urray 2007.05.16
http://news. independent. co.uk/uk/ health_medical/ article2548747.
ece

http://groups. yahoo.com/ group/aspartameN M/message/ 1426
ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer
will join Tesco and also Sainsbury to ban and limit
aspartame, MSG, artificial flavors dyes preservatives additives,
trans fats, salt "nasties" to protect kids from ADHD:
leading UK media: Murray 2007.05.15

http://groups. yahoo.com/ group/aspartameN M/message/ 1438
Coca-Cola and Cargill Inc., after years of development,
with 24 patents, will soon sell rebiana (stevia)
in drinks and foods: Murray 2007.05.31

www.ncbi.nlm. nih.gov/sites/ entrez search PubMed

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