Hey Betts,

Has anyone said anything about Anti-Phospholipid Antibody Syndrome?  It
would explain your miscarriages and difficult births, and possibly the
passing on of the "proteins" to your daughter.  I have this and know a
lady who has it and has had the exact thing happen to her.  Two
miscarriages, and almost lost all 3 of her kids, and her youngest
daughter is sick too.

I was sick all the time as a kid too, and had the tongue thing all my
life.

Do you have any history of Agent Orange exposure in you or your
parents?

I understand there's a huge clinic in Dallas, TX that has been
researching these diseases and has done alot of good work.  They call
it "Environmental Medicine".  I know they have a website but I don't
have it.  Try to look it up and I'll try to get it and post it for you.
They've been trying to get me to go down there but I don't have anyone
to drive me to Dallas and flying is as bad and then Dallas is a mess to
navigate.

I'm 30 and seem to be in the same place you were at that time in your
life.  Almost exactly.  The sun turns me bright red and swells me up
for 2 days.  

I hope some of this helps!

(((HUGS)))

Krista

Hi Betts,
I was thinking that maybe the reverse would happen if they diagnose your
daughter.
If not, maybe they could give you a lead on who to see or if you should see an
allergist/immunologist...

I did some searching and was reading thsse websites
http://www.emedicine.com/MED/topic1119.htm (too long to post, - I just read
some sections there)
# C4 is encoded as 2 tandem, highly polymorphic genes, C4A and C4B, located in
the major histocompatibility complex on chromosome 6. Two copies of each gene
determine the phenotype. Null alleles are called C4a*Q0 and C4b*Q0. Deletion of
the C4A gene is the most common mechanism. A single null allele reduces the C4
level by 35-40%. Four null alleles encode a complete deficiency of C4. It is
transmitted as an autosomal recessive trait.

# Partial C4 deficiency predisposes to SLE. Deficiency of C4A or C4B has been
associated with the development of scleroderma, immunoglobulin A nephropathy,
Henoch-Schönlein purpura, diabetes mellitus, chronic hepatitis and membranous
nephropathy. Complete C4 deficiency is rare. Characteristics of SLE with
complete C4 deficiency include early onset, mild renal disease, skin
manifestations, anti-SSA antibody, and an absence of anti-dsDNA antibody.
Complete C4 deficiency also may manifest with infection or may not be
associated with any symptoms.

# Defective expression or function also may lead to SLE, as occurs with
medications such as hydralazine, penicillamine, and procainamide, which react
with the thioester bond of C4a and block its function.

My mouse is acting up. I'll post this then come back and read it again.
J

http://www.mtio.com/lupus/lfalt1.htm#no3 Lab Tests Common for Lupus
C4 is a component of the classic complement pathway. Depressed levels usually
indicate classic pathway activation.
Increased in: Various malignancies: not clinically useful.

Decreased by: Decreased synthesis, increased catabolism (SLE, rheumatoid
arthritis, proliferative glomerulonephritis, hereditary angioedema), and
increased loss (burns, protein-losing enteropathies). Congenital deficiency.

Additional: Low C4 accompanies acute attacks of hereditary angioedema, and C4
is used as a first-line test for the disease. C1 esterase inhibitor levels are
not indicated for the evaluation of hereditary angioedema unless C4 is low.
Congenital C4 deficiency occurs with an SLE-like syndrome. Test as usually
performed is an immunoassay and not a functional assay.

http://www.ghg.net/schwerpt/ASLFAQ/diag.htm
#8  Immune complexes or complements (C3, C4, CH50) which tend to be low when
lupus is very active, and can also be an important gauge of disease severity.

http://www.jcaai.org/Param/Immune/Comp.HTM
Clinical Evaluation of Complement Component Deficiency
Deficiencies of the early components of complement (C1q,r,s C4, C2) are
associated with systemic lupus erythematosus-like symptoms, glomerulonephritis
and, less frequently, with pyogenic infections.

# Normal C3 and C4 levels in the face of undetectable CH50 is strong evidence
of congenital complement component deficiency, whereas a decrease in C4 and/or
C3 with undetectable CH50 suggest complement consumption.
# The evaluation of specific component deficiency requires tests not available
in the majority of clinical laboratories.
Management of Complement Deficiencies

It should be recognized that:

   * There is no specific treatment for the congenital deficiency of
complement components.
   * In C1 inhibitor deficiency, the administration of semi-synthetic
androgens such as danazol and stanozolol is associated with a decrease in
angioedema attacks and increased levels of C1 inhibitor. Because of possible
androgenic effects, these drugs must be used with caution in children.
   * If there is knowledge that a patient has a complement component
deficiency, it is very important to alert the physician to the risk of severe
infections that require more aggressive evaluations.
   * Patients with deficiency of early complement components may develop
autoimmune diseases particularly SLE or glomerulonephritis.
   * Patients may be immunized with vaccines for pneumococci, H. influenzae,
and Neisseria meningitidis.

III. Special Considerations

It should be recognized that:

   * Obtaining a family history of complement component deficiency is
extremely important in arriving at a proper diagnosis.
   * Complement components lose activity very rapidly at room temperature and
for this reason serum for functional assays requires special handling.
   * A common cause of very low or absent complement activity (CH50) is
inappropriate handling of specimens; confirmation of results is indicated
before more elaborate studies are performed.
   * A purified C1 inhibitor preparation for treatment of hereditary
angioedema attacks may be available in specialized medical centers.
   * Gene therapy of complement component deficiency is a possible type of
therapy under development.

IV. The Immunologist as Consultant

It should be recognized that:
   * All patients with recurrent infections should be considered for referral
to an allergist/immunologist for evaluation of complement component deficiency.

   * Patients with recurrent bouts of angioedema should be considered for
referral to an allergist/immunologist for evaluation of congenital or acquired
C1 inhibitor deficiency.
   * The allergist/immunologist has special expertise in evaluating,
diagnosing and managing patients with complement deficiencies.

Hello All,

I been reading some of the replies to the post, and before I read any
of them my first thought was:  Did she grow up near any contaminated
land.  Here in Buffalo, it would have been Love Canal.  Then I got to
reading the post and thought, I was too far off.  It would be
something worth checking into.    Help with you and your daughter.

Hopes this helps.  Good Luck

Marie