Re: Hypocomplementaemia question

[Guest guest]

Hypocomplementemia is an interesting situation. There are

several etiologies that can lead to it. Hypocomplementemia

should therefore be thought of more as an " endpoint " , with

the important question being how one gets there.

Complement is a blood protein that serves to " punch holes "

in bacteria and attract immune cells to sites of infection.

Complement can be triggered, resulting it is expenditure and

the development of low levels due to many reasons. In CLL

patients it is often the result of antibodies that are

binding targets in appropriately. But it can be due to

inherited abnormalities in regulatory proteins, etc. The

complement deposition can even result in kidney failure

(called atypical HUS).

We do have an antibody that inhibits the later stages of

complement activation called eclizumab (Solaris). Its use

is very limited because of its cost, but it is quite

interesting.

It is important to determine the cause of the low complement

levels in order to best determine how to treat it.

Rick Furman

Wayne Wells wrote:

/message/15703

[Guest guest]

Rick,

Thank you for taking your time to expand our perspective

regarding this bit of CLL related complexity.

My own Angioedema event is following the course of the first

two events. Swelling has mostly disappeared as I write. I

have discontinued the prime suspect drug Lisinopril until

discussion with Docs.

The pattern that keeps popping up through my research of

similar cases to mine and some members who have responded to

my post is that these events occur in the night, are full

blown by morning and are usually gone in 24hrs. Some

patients have been put on steroids and other meds as in the

case of woman in the link supplied in my original post but

it is questionable given the characteristic NON-involvment

of impaired breathing and the focus of the transient

swelling on the facial surface as to whether the steroid

really helps.

Given my kidney issues and Severe Reaction to my first two

therapies, Hypocomplementaemia or some variant of complement

dysregulation is still a consideration with or without ACEi

allergy.

I am grateful to have an indication that my angioedema does

not, at this point, appear to jeopardize my continuing

participation in the PCI Clinical Trial given how well it is

working for me.

WWW