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Issues In Peri-Conception Care
Peri-conception care is rapidly becoming a
specialized area in obstetrics. It has got many new developments
and thanks to a high failure rate of nidation and sustenance of
pregnancy in ART, this subject has become all the more
important.
A blastocyst is a friendly being. It loves
to make friends with many a mucosa. As soon as it arrives into
existence, it knows it has to nidate – it has to make a home. It
simultaneously starts talking with different mucosae. All
mucosae of the genital tract are by and large sensitive to its
talks. This friendliness can cause ectopic pregnancies. It has
got a great enticing capacity. Usually all mucosae other than
uterine pay limited heed to its signals. But sometimes they too
respond and respond quickly. If such a response occurs from
fallopian tube – tubal ectopic pregnancy results.
It lures the mucosa to allow it not only to
stick to the mucosa but also burrow through. It is not an
encroacher however. It is a nice being that knows its
limitations and stops burrowing at a particular point. If it
does not stop: an adherent placenta is the result. Also, all
this has to be finely tuned and coordinated.
HCG has a vital role in this! As the conductor of the orchestra, HCG
generates a series of immunologicaly active substances that act
like messengers and ambassadors of the blastocyst going to the
endometrium (now the decidua) queering the pitch for a
successful and lasting nidation. Clinical result is a successful
pregnancy outcome. This could be one of the bases of the use of
HCG in clinical practice for cases of pregnancy loss.
This HCG is released by the blastocyst in
very early days of its development. So, not only should the
blastocyst release HCG in high amounts, but also at a great
speed. Thus in a very short time it has to respond very quickly.
If it fails, there will be a deficient or an uncoordinated cross
talk and the conceptus doesn’t nidate well. If this occurs it
results in: Menstrual Abortions and Spontaneous Early First
Trimester Abortion.
Thus this cross talk opens up new vistas in explaining:-
bEctopic pregnancies
bMorbid adhesions of placenta
bPlacenta previa
bInfertility and abortions in endometriosis
bDifference in fertilization: conception rates with ovulogens
bIncreasing uterine receptivity
bInterception in contraception.
HCG in periconception care: There is
another aspect of HCG as well. In late 1996 there were reports
that indicated that HCG helps in preventing pregnancy loss
because it is contaminated by growth factors. It is now well
known that HCG has a strong immunological face. Infact late 1997
and early 1998 strongly hinted at a similarity in structure
between GF and HCG. Only within six months of this research it
was proved that HCG itself is the growth factor. It is therefore
understandable why HCG administration is much more successful
than progesterone in recurrent pregnancy loss and even
prevention of immunological growth retardation.
This is a clinical break through. So when
one administers HCG in recurrent pregnancy loss you are not
administering a hormone but an immunological substance.
This is not a case for indiscriminate use
of HCG in maintaining pregnancies. That will not help. In
carefully selected cases where there are reasons to believe that
an immunological cause is working –HCG helps. It was again too
simplistic to practice periconception care by assessing
circulating levels of HCG. If HCG levels were low supplement it
with HCG and maintain. This is not rational at all. There is no
arithmetic additions in maintaining pregnancy.
Threatened abortion: On its way out! With
every bleeding in periconception period now being explainable,
in the realms of periconception care the term “threatened
abortion” is fast becoming obsolete.
Immunology of Recurrent Pregnancy Loss: 40%
of losses in RSA could be due to immunology. There are two basic
causes : allo-immune and auto-immune.
Allo-immune: - A conceptus of 3000grms is tolerated, protected
and nourished by the mother for 280 days. After birth even 30
grams of say renal tissue of that conceptus is not tolerated and
immune rejection occurs why? Husbands renal tissue transplanted
in the mother during pregnancy is not accepted: How his
conceptus is accepted: How come?
At feto-maternal interface when the mature immune system senses
that a different immune system has arrived it mounts a
protective response
This is through the syncitio-trophoblasts. Functioning of the
trophoblasts is such that it will sense only on immunologicaly
distinct entity. Infact if it is immunologicaly similar, the
syncitiotrophoblast will not sense and the mother’s immune
system will destroy it. This can occur repeatedly and results in
RSA.
This can be applied in renal transplants or any other
transplants. If transplant scientists can create an artificial
trophoblast like shield around the donated organ, once again the
recipient will protect it and there will be no rejection. Infact,
then after tissue typing HLA testing and all will become
obsolete because you will require the donor and the recipient to
be different and not similar as in the case of the conceptus. If
they are similar then there will be a problem of total rejection
now.
For alloimmune causes treatment modalities like paternal
leukocyte transfusion and alike or so-called immune potentiation,
have been found to be irrational, unethical and even dangerous.
In current literature they have no validity and be therefore
discontinued.
If at all anything helps: 1) HCG: immunological face and
2) Immunoglobulins (empirically)
Auto immune: many syndrome antibodies are
implicated. But most influential and consistent have been
antiphospholipid antibodies. These
generate a vasculopathy by preventing the second wave of
migration of trophoblasts. Sludging of platelets in these vacant
spaces and covering of trophoblasts by fibrin and like material
serving as a barrier
Diagnosis
Negative ® <10 GPL units
Low positive ®10-20 GPL units
Mod. Positive ® 20-100 GPL units
Strong positive ® > 100 GPL units
Once the diagnosis is well established,
treatment plans are instituted.
Nearly 18 different protocols have been
tried over the period of years for the treatment of APA
syndrome. But the main stay is Heparin, Low dose Aspirin and
corticosteroids.
We use the following protocol:
In interval period :
® For low and moderate positive: Aspirin in a dose of 1.2
mg/kg./day till conception – Allow a conception – Restart
aspirin in the same dose from 12 to 36 weeks.
®For High positive: Prednisolone in a dose of 10 mgms./day till
conception in the interval period. Allow conception- start
aspirin from 12 weeks upto 36 weeks.
In Pregnancy:
® For these cases we give only the post-conception protocol of
aspirin as specified
This is where aspirin helps. Recent literature has also shown an
upcoming role of nitric oxide donors with aspirin. This will
treat the cause as well as the effects.
Carry home messages:
Peri conception care is a separate speciality
Blastocyst talks with the endometrium to achieve a successful
outcome. If this fails a bizarre array of clinical effects can
result
HCG is not only an endocrinal molecule. It has a more important
immunological face
Supplementing HCG has a rationale in pregnancy loss at
blastocyst endometrium cross talk level and at the level of
immune supplementation.
Threatened abortion is on its way out
APA has an important role in R.S.A.
Aspirin corticosteroids and heparin are used successfully to
treat these cases
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