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Old 03-21-2008, 10:30 AM   #1
Donna
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Location: Shingle Springs, CA - near Sacramento
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Another Question

Hi Amazing Group,

What I am wondering is this: I was already post menopausal and had none of these side effects. Is there something else in these medications doing the damage to the joints? I don't hear menopausal women complaining of trigger finger. This seems to uniformly hit our tendons, thumb first - should we as a group go to the manufacturers and demand answers?

I am thinking of visiting a remarkable hand specialist I know to see if he can shed some light on this.

Hoping we figure this out! Happy Easter to all!

Donna
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Donna in the Sierra Foothills of California

Diagnosed 6/7/06 invasive ductal carcinoma/ductal carcinoma in situ
Lumpectomy 6/21/06
Pathology: Er 99% Pr 10% Her2/neu 3+
DNA Index 1.0
S-Phase 3/High
Primary Tumor 2.4 cm Sentinel Node Tumor 2.1cm
A/C/T+ Herceptin + rads + Arimidex
stopped Herceptin after 7 mos. due to low MUGA
Surgery for thickened uterine tissue May 2008 - conclusion: side effect of Arimidex
Switched from Arimidex to Femara - joint/tendon problems significantly better!
2 year mark Pet scan and Echo shows all clear!
5 year mammogram with ultrasound shows no sign of cancer - yay!
11 years, 11 months new breast cancer - found lump
Mastectomy 4/30/2018
Pathology: Er99%, PR 28%, Her2 negative! (new type)
Faslodex
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Old 03-21-2008, 11:33 AM   #2
Becky
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Menopausal women still have some estrogen. The adrenal glands make it and fat cells make it. It is made using androgens that get converted via a (bio)chemical reaction to estrogen. The reaction needs an enzyme to make it go and that enzyme is aromotase. An aromatase inhibitor binds to aromatase and makes it unable to function as an enzyme in this reaction. Therefore you make less or in many cases no estrogen. Women with functioning ovaries (premenopausal) cannot take an AI because the ovaries produce estrogen in a different way so an AI would still block the way it is made from the adrenal and fat but that is such a small amount versus the ovarian mechanism - and a premenopausal woman would have no benefit as there would be tons of estrogen around.

Therefore, there can be a big difference in a menopausal woman versus a menopausal woman on an AI especially a menopausal woman who is also overweight (as they would be producing more estrogen).

No or very little estrogen is what is causing the symptoms - not necessarily the AI itself.
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Becky

Found lump via BSE
Diagnosed 8/04 at age 45
1.9cm tumor, ER+PR-, Her2 3+(rt side)
2 micromets to sentinel node
Stage 2A
left 3mm DCIS - low grade ER+PR+Her2 neg
lumpectomies 9/7/04
4DD AC followed by 4 DD taxol
Used Leukine instead of Neulasta
35 rads on right side only
4/05 started Tamoxifen
Started Herceptin 4 months after last Taxol due to
trial results and 2005 ASCO meeting & recommendations
Oophorectomy 8/05
Started Arimidex 9/05
Finished Herceptin (16 months) 9/06
Arimidex Only
Prolia every 6 months for osteopenia

NED 18 years!

Said Christopher Robin to Pooh: "You must remember this: You're braver than you believe and stronger than you seem and smarter than you think"
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Old 03-21-2008, 01:55 PM   #3
Hopeful
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Becky,

Question for you. I have read a few places that the "next generation" of AI's will be ones that target only aromatase in breast tissue. My question is, when bc develops, even if some of the cells move out of the breast and into the body, they are still breast cells, right? So that an AI that targeted breast tissue would be able to exert its effect on all ER+ bc cells, wherever they may roam?

Hopeful
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