AIHA

[Guest guest]

, (Pardon the bad grammar and bad spelling etc.)

You can also take Anti-D (winrow), which is a similar med to IVIG except there

is an important difference in the mechanism between the two. Also, IVIG is

safer if thats possible as it is given quite regularly to Pregnant women who's

babies blood is producing such antibodies and is threatening to kill them and

the baby both.

So, Anti-D is not a medicine that has been gathering dust on the shelf. It is

used constantly and it has been perfected to a high science of safety, as you

can imagine with pregnant mothers. There is one other major benefit to Anti-D,

which is that it can be given by a simple injection rather than the dreaded and

time consuming IV infusion. It also has a better statistical opportunity to be

successful for longer periods of time to the patient. Sometimes up to 3 or 4

months or more.

In other words it's not a good long time fix like Rituxan but it is a much

better fix than IVIG for all of the above listed reasons.

The whole thing even gets a bit deeper. Rituxan is the best fix at the moment

as a majority of the antibodies that are produced also have CD20 cell markings

so it makes another malady that can be fixed by Rituxan, a nice accident of luck

or fate for those of us who have other forms of blood disease. However it is

all a blood disease and AIHA is not that unlike CLL or any other form of

Leukemia, it is a very serious blood disease which in fact the medical

profession at one time referred to as Leukemia when they ahd no other logical

explanation. Leukemia at one time years ago took the blame for most blood

diseases that made you weak and killed you.

The main reason that Rituxan is not considered the automatic standard treatment

for AIHA or most Thrombocytopenias (ITP) is because the jury is still out on

whether or not Rituxan causes " Delayed Onset Neutropenia " . Meaning that we

might be in fact giving ourselves the same problem of Anemia that we are trying

to cure by taking Rituxan, even worse we might be giving ourselves a later dose

of crashing WBC and Neuts. Something akin to what happened to you with

Fludurabine. You doubt it was Fludurabine......I find that to be wishful

thinking, the tests that are coming out now are very disheartening concerning

the evidence that shows that Fludurabine almost certainly will cause Delayed

Onset Neutropenia down the line after you take it. AIHA again is a very close

relative of Neutropenia at least one phase of it and as with all these blood

diesease, they are different but they are all similar in that they can make your

life miserable and kill you also.

So, to make things more difficult in the decision making process of what to use

to treat it with, Rituxan has recently been referred to by many researchers and

Doctors as not being able to produce Neutropenia at any time, now or later,

which was explained to me emphatically by the recently acclaimed Researcher and

Leukemia expert Dr.Tuscano of UC in Sacramento. He is testing a new

monoclonal antibody that attacks the CD-22 marked cells and which he is hoping

will provide another new part of the management of CLL puzzle, which he is soon

going into phase II studies for. Then to confuse the issue more, there is

further evidence now even more recent that Rituxan does indeed cause Delayed

Onset Neutropenia, offering proof etc. etc. However, it is determined that the

opportunity of a patient developing Delayed Onset Neutropenia later from

Rituxamab is very low, like 2% or something. I have yet to discuss this further

with Dr. Tuscano, but will in the near future.

So, at the moment we are between a rock and a hard place because as you all know

the thing that really kills us and the think that is really hard to live with is

Anemia and Neutropenia, not CLL. i.e. which in this case was not the chicken but

the egg, nonetheless, we don't want to be doing anything to enhance the

possibility of either of those deadly conditions occuring in our bodies for any

reason, again because those are the two diseases that are going to kill each and

every one of us most likely.

So, here we have Rituxan which is a miracle and yet potentially a deadly

damaging treatment also in a small set of patients. Not a nice thought.

However, the main answer off the top of my head is that Rituxan is still much

the less dangerous medicine, far less damaging than Fludurabine or any of the

other Chemo's or CLL or blood treatments and here is an important point, even

if you do develop Neutropenia and/or Anemia from Rituxan however unlikely, the

marrow will eventually heal as the damage from Rituxan shows that it is a

temporary marrow damage. Whereas the Fludurabien damage is questionable if it

ever heals or returns to normal. All damaging and frightening thoughts.

Also a new and quite appropriate opportunity comes to mind now because of this

questionable puzzle for Rituxan at the moment, meaning that it would naturally

be the best thing to take automatically for ITP or AIHA if it had no possibility

for causing neutropenia but since it does it puts the brakes on for all of us

with such diseases and we look around for a temporary fix that will buy us time

or like everyone admits, allows us a chance to " manage " the problem as we are

trying desperately to do with CLL. So, this is where Anti-D comes into the

picture. It is not a harmful or damaging treatment. It can be given by

injection (a simple shot) and is used safely by pregnant mothers the world over.

It also lasts longer than IVIG and it lasts longer in it's fix than anything

else other than Rituxan.

So here with Anti-D we have a treatment that will manage AIHA and ITP and other

blood disorders without damage to the body, in fact it will temporarily boost

the immune system without side effects which is also another great benefit.

So, you can see that I am now thinking of the use of this for myself if needed

or for or others of you out there and most definitely for my Dad who is

suffering from severe ITP.

The interesting thing, if this wasn't enough all ready by itself) I have

learned that once my Dads Hgb was brought to low normal ranges by the use of

Aranesp and his other blood counts were all brought back to good safe ranges,

like the overproduction of Uric Acid which damages the kidneys (corrected by

Allopurinol which can be taken forever without any side effecfts (unless you are

allergic to it), and by bringing his Potassium levels up to par and bringing his

Creatinine down to normal and other counts too numberous to mention here, his

ITP problem has slowly gotten better on it's own. His platelets which were at

10 or less have come up to about 50 or more and are holding there.

The point I am making here is that this shows that the CBCs that we get every

now and then probably should be given weekly without fail. Simply so that we

can all stay on top of " ALL " our blood counts! BECAUSE, when the body is not

running in normal areas, when it is missing on many cylinders and not running

properly in many areas it does have an amazing negative effect on all other

areas of the body because the body runs on a system of balance. So simply

put, when we are out of balance we suffer in the areas that may be critical to

all of us with CLL. So, there is a lot to think about here as you can see.

This CLL and body balance system is a very complicatedmess and most doctors will

not keep an adequate eye on the blood counts, hell they hardly order one that

requires indepth Chem-panels except ever 2 or 3 months or longer at times. that

is not a good idea for a CLL patient, especially if we are ailing in one area of

another.

I guess thats enough for now, we can discuss this more later. Any help in

solving any of this or adding new info that will help the understanding of all

this is always welcome. Hope everyone is doing well out there. Cheers, Kurt

AIHA

I thought some of you might be interested in the topic of AIHA (autoimmune

hemolytic anemia).

This is a nasty little complication that affects 15-20% of us.

You first notice that you're tired, and then your blood test reveals crashing

red counts, but the other numbers don't look bad. So it's an anemia, which is

not caused by an excess of white cells blocking the normal production of red

cells. Rather, it is an autoimmune thing, a cytopenia, where the body turns on

itself.

Further positive identification is made with a so-called Coombs test, and a

reticulocyte count. A high reticulocyte count indicates that the marrow is

overproducing young red cells, to try to make up for the killing going on.

As in so many other things in this lousy disease, nobody knows what causes

AIHA.

First line TX is Prednisone and sometimes also Rituxan.

If you're lucky it goes away, but probably lurks somewhere and you may or may

not get another " attack " .

In my case, I have concluded that the AIHA presents a larger potential

problem than the underlying CLL, which appears to be in a nice remission since

2000.

There are opinions that the Fludarabine taken earlier might have been a

potential cause for the AIHA, but that was four years ago in my case, so I

suspect

not.

If it recurs, one can try Pred and Rit again, but repeated high doses

Prednisone are not a good thing. Other TX includes IVIG (gammaglobulin), and,

much to

my distress, a spleenectomy. It seems that much of this cell murder takes

place in the spleen. People can live perfectly well without a spleen, with a

larger risk of infection, as the spleen also acts as a gigantic infection

filter

and battleground. My concern with a spleenectomy is, " what do you do after

that " ?

Am happy to discuss further if any issues.

[Guest guest]

AIHA, or Auto Immune Hemolytic Anemia, is a disease where the body's own immune system fails to recognize red blood cells as "self" and begins destroying ...

Maureen,

I used to hate acronyms when I was young and remember feeling myself totally lost at gatherings where people were talking about work and I had no idea what they were talking about, then after I was diagnosed with CLL I found myself almost in identical situations as 30 years previously. I still have to look up some acronyms very often as time goes by there is always something I read that I do not know.

regards

Chonette

[Guest guest]

Hello ,

Thanks four your mail

Sorry couldnt reply before were just settling in at New York where we arrived day before.

Prof Catovsky started my wife off on prednisolone 60 mg for 1 week then asked us to reduce it by 5 gms daily on alternate days to 50 mg. , get a blood test done and then reduce to 40 mg and stay at that till we get back to London on the 18th .

Regarding the transplant, we have more or less decided on getting her treated at the Royal Free in London .

Prof Mackinnon at the Royal Free seems very competent and the advantages of having Prof Catovsky as an additional advisor who has known her case for the last 8 years outweighs a US option.

When we arrived in New York, Dr. Brown at Dana Faber sent a mail that she hadnt received my wifes detailed case history which I had mailed her before we left Delhi so sent it again

Maybe get a second opinion from her.

Havent got any reply from Seattle so dont know whether its worth sending them the details again.

My be can try calling them and seeing what happens.

Thank you for your support.

In a few days will mail you the protocol decided for her for your response.

Best wishes

from Delhi

Wife diagnosed with CLL in 1997 at age 44,Fish del 13q, unmutated, Zap 70 positive2001 : Chlorambucil partial remmission2002 :RF 6 cycle Tests showed CR after that.Feb 2008 - Oct 2008 RFCcycle 1,2 FC only, cycle 4to 6 RFC cycle 7 Rituximab , cycle 8 Rituximabfinished October 2008Now relapsed since March 2009 - lymph nodes in abdomen, axilla and neck .Diagnosed now as Non Hodgekins Lymphoma - CLL / Small Lymphocytic Lymphoma

Recently diagnosed with AIHA .

Advised BMT/SCT from sister

[Guest guest]

AIHA occurs in 11% of advanced stage CLL patients. Prednisone is the first

treatment of choice, with 90% responses and 65% complete responses. More than

60% of patients relapse when treatment is stopped. Intravenous immunoglobulin,

the next line of treatment, causes responses in 40% of patients.

Nearly all cases of autoimmune hemolytic anemia are associated with a Coombs

test called positive direct antiglobulin test (DAT). In some cases of AIHA,

including hepatitis B, the Coombs test may be negative.

Autoimmune hemolytic anemia may be classified as cold or warm depending on

whether the antibodies are cold IgM antibodies, which react at room temperature

or warm IgG antibodies, which react at 37 degrees. Some patients may have mixed

AIHA. which means that they have both cold and warm reacting antibodies.

Many CLL patients are treated with Rituxan now for warm AIHA. Often a

splenectomy is a consideration for non-responders to glucocorticoids and may

offer a success rate of up to 70% in patients with idiopathic warm AIHA.

Some links

http://www.ncbi.nlm.nih.gov/pubmed/20736453

http://www.ncbi.nlm.nih.gov/pubmed/20656187

~chris

CLL CANADA

[Guest guest]

11% is just one figure from one trial. Older literature reports up to 35%

in heavily pretreated patients. My own estimate is about 15% overall, mainly

in patients who have unmutated IGVH genes and mainly in more advanced

disease. It is much more common in patients who have been treated and

fludarabine is the worst trigger.

In a message dated 26/10/2010 14:57:36 GMT Daylight Time, rhudy@...

writes:

11% is not a lot. So I assume it's pretty rare. Does it

occur more often in those who've already had tx?

Thanks,

Ellen

cllcanada wrote:

> AIHA occurs in 11% of advanced stage CLL patients.

[Guest guest]

11% is not a lot. So I assume it's pretty rare. Does it

occur more often in those who've already had tx?

Thanks,

Ellen

cllcanada wrote:

> AIHA occurs in 11% of advanced stage CLL patients.

[Guest guest]

Somewhere around 33% of case of AIHA occurs without treatment.

Around 20% of patients will have a positive Coombs test , but not all will

develop AIHA, so Dr. Hamblin's figure of 15% overall is pretty good...

~chris