Ask Our Doctors – Archive
Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.
My wife and I are at a loss at this point…first miscarriage was at 7 weeks, low fetal heartbeat…second miscarriage was a chemical pregnancy…most recent was at 6 weeks when everything looked fine and happened spontaneously…all were PGD tested…most recent cycle included lovenox and 5mg prednisone….we are being told not really much else could be done…are we at the end of the road..?
Hello Doctor Sher
I am now 7w pregnant/
From last night i have severe virulent cough with congestion. I was told that sudafed can be taken .I am worried about its safety during but the cough is severe too. Please advice. Thanks so much.
Should not do any harm, in my opinion!
Good luck!
Geoff Sher
TTC 4 years, 1 MC in 2014 @ 8 wks.
Underactive thyroid: TSH 63.2 mU/L, FT4 `19.7 pmoS/L, TPO 269.4
– Diagnosed with profound autoimmune hypothyroidism
– Now on Eltroxin (150 mg/day)
– TSH 0.07 mU/L, FT4 26 (July 2017)
Egg collection in summer 2017 caused mild OHSS but only 9 eggs viable and 7 embryo blasts frozen.
Also revealed tubes leaking into uterus.
Tubes removed (Sept 2017) + plan for FET in Nov 2017
Protocol includes Prednisolene but Dr. won’t test for NK cells or any other AI factors
Could IL be required – if no time to test could they be included anyway?
Indeed, in my opinion, you could well have an immunologic implantation dysfunction linked to NK cell activation.
Between 2% and 5% of women of the childbearing age have reduced thyroid hormone activity (hypothyroidism). Women with hypothyroidism often manifest with reproductive failure i.e. infertility, unexplained (often repeated) IVF failure, or recurrent pregnancy loss (RPL). The condition is 5-10 times more common in women than in men. In most cases hypothyroidism is caused by damage to the thyroid gland resulting from of thyroid autoimmunity (Hashimoto’s disease) caused by damage done to the thyroid gland by antithyroglobulin and antimicrosomal auto-antibodies.
The increased prevalence of hypothyroidism and thyroid autoimmunity (TAI) in women is likely the result of a combination of genetic factors, estrogen-related effects and chromosome X abnormalities. This having been said, there is significantly increased incidence of thyroid antibodies in non-pregnant women with a history of infertility and recurrent pregnancy loss and thyroid antibodies can be present asymptomatically in women without them manifesting with overt clinical or endocrinologic evidence of thyroid disease. In addition, these antibodies may persist in women who have suffered from hyper- or hypothyroidism even after normalization of their thyroid function by appropriate pharmacological treatment. The manifestations of reproductive dysfunction thus seem to be linked more to the presence of thyroid autoimmunity (TAI) than to clinical existence of hypothyroidism and treatment of the latter does not routinely result in a subsequent improvement in reproductive performance.
It follows, that if antithyroid autoantibodies are associated with reproductive dysfunction they may serve as useful markers for predicting poor outcome in patients undergoing assisted reproductive technologies.
Some years back, I reported on the fact that 47% of women who harbor thyroid autoantibodies, regardless of the absence or presence of clinical hypothyroidism, have activated uterine natural killer cells (NKa) cells and cytotoxic lymphocytes (CTL) and that such women often present with reproductive dysfunction. We demonstrated that appropriate immunotherapy with IVIG or intralipid (IL) and steroids, subsequently often results in a significant improvement in reproductive performance in such cases.
The fact that almost 50% of women who harbor antithyroid antibodies do not have activated CTL/NK cells suggests that it is NOT the antithyroid antibodies themselves that cause reproductive dysfunction. The activation of CTL and NK cells that occurs in half of the cases with TAI is probably an epiphenomenon with the associated reproductive dysfunction being due to CTL/NK cell activation that damages the early “root system” (trophoblast) of the implanting embryo. We have shown that treatment of those women who have thyroid antibodies + NKa/CTL using IL/steroids, improves subsequent reproductive performance while women with thyroid antibodies who do not harbor NKa/CTL do not require or benefit from such treatment.
Good luck!
Geoff Sher
Hello Dr. She’d,
I did blood work 7 days after FET of hatching blastocyst. I am so happy to see that B-hCG is 91.9.
But progesterone P4 is only 4.91. Is this a reason for concern? (I am taking progesterone vaginally 3x 300mg).
Thank you,
Aga
The P4 level is often low with FET’s. This is because the ovaries are not producing the hormone. Just talk to your RE about bolstering your supplemental progesterone.
Geoff Sher
Hi Dr Geoffrey
A little bit of background, I am 37 of age and on July 2015 I was diagnosed with hydrosalpinx, on Feb 2016 I had a laparoscopy to remove left Fallopian tube and re open the right one. Since then I went through 3x short protocols of unsuccessful IVF cycles (London, 2 at Chelsea and Westminster & 1 at St Guy’s Thomas hospitals) My response for the simulation was great, egg collected 14, 21 & 9 fertilised and grown to blastocyst stage 2, 4 & 3. Transferred 2, 2, & 2. No problem with lining, also had an endometrial scratch and glue. However the embrios for some reason have not implanted. What could be the reason for this, what can I do to have successful implantation. I am willing to attend one more cycle before I decide to stop the treatments as whole process is emotionally exhausting, and I don’t have much more strength to go through it. Please any advice will help. Thanks J