Femara side effects?
 

I have only been on Femara two weeks, but have developed pressure headaches, brain fog, hearing disturbances (as if I were at the oceanside, waves crashing).

Can those of you who are on it or have been please tell me of your experiences? I am weakly ER+ (it was not quanitified) and wonder if the good I will receive will be worth the side effects.

No one here is on Femara?

Dear Deborah,
Sorry you feel you've been ignored. I just got back on-line.
I've been on Femara for about 16 months. Since chemo/Herceptin I've had some odd side effects. Not sure who to blame for the side effects but I know that my oncologists strongly suggested taking it at bedtime to avoid side effects so unless you've tried that, try that. If you read the side effect label it just about includes everything. If you're worried about anything talk to the pharmacist, your oncologist and general practioner, you never know who'll come up with a way to deal with some of the problems. I've just accepted the side effects I have as part of the price I pay to stay alive. One of the most annoying for me - caused by the cortisone during chemo - is cataracts which I'm putting off doing anything about for all long as I can still drive safely but reading is a real bore and I'm a big reader. Also fatigue still hounds me and weight gain. Also hot flashes!!!!
I do get headaches but they pass and achy bones and skin rashes and.....but from what???? I haven't had the waves crashing yet.
I do hope you find an answer to your problems. Since more than just HER2 people take Femara - in fact more non-HER2 people probably do since HER2 is generally PR and ER negative, you might try a regular breast cancer site to see if they have any suggestions.
Sorry not to be able to be more helpful.
Good luck and keep fighting and stay strong,
try taking it at night and see if that helps.
sarah

Thanks for that suggestion, Sarah. I hadn't heard that one. Yes, the label lists a plethora of side effects, so it's like 'choose one.'

I know there are others on the board who are on Femara. Sometimes it gets really discouraging on a support site when one posts for support and after 30 views of the post no one bothers to reply.

Thank you for taking the time to help. I hope you can get the cataracts taken care of. I don't know what I would do with myself if I couldn't read! It's a major, major part of my life.

All the best to you and thanks again for your reply.

I have been on Femara for almost 3 years. No weird side effects, just the normal. I will have hot flashes if I drink coffee or have wine/beer and I need to do moderate excercise every other day to avoid joint stiffness.

Cheryl

Deborah,

I am not taking Femora - was taking Arimidex - had to stop when I started TCH chemo - and I am certain I will go back to Arimidex after I complete my chemo.
But I strongly advise what Sarah told you regarding taking the medication in the late evening. When I first started Arimidex after about three weeks I began to have extremely heavy headaches. I stopped the Arimidex for two weeks and gave my body a rest then started the Arimidex again only this time I took it at 10PM each and every night. The headaches stopped and I did much better.
Did have joint and bone aches - but I also found that exercise helped keep me
limber which helped to deal with the joint pain. Wish you luck - on Femora.

Regards,
Jean

Deborah,
Hope the time change helps. I wonder why doctors don't suggest this more often???
I never know what's an important side effect versus a not important one. while on Taxol and Herceptin, my feet and ankles swelled enormously plus a petscan showed fluid in the lungs! and all my doctors including the bigwig oncologist thought nothing about this although I was worried for my heart! I suppose since my Muga and heart sonogram were good, they just said those were normal side effects!!! so after that I decided not to worry! they only became extremely worried when I developed a tennis ball lump in my neck area!!! then I was given anti-coagulant shots to do twice a day - myself!!! and other stuff!!!
Keep up the good fight
sarah
PS I'm still reading all the time but it's harder. We'll have to exchange names of books we've loved!

kat in the delta
 

My sister had to switch because of the joint pain of femara to aromasin. Kat

Kat
 

Did the joint pain go away when the switch from Femara to Aromosin was made?

Thank you in advance

Becky

Femara side effects
 

Side effects.

http://66.102.9.104/search?q=cache:D...ient=firefox-a


It is reported above as an aromatse inhibitor. eg inhibits P450.


P450 is reported to derive from COX which is a product on the fat pathway.

Oestrogen results in the secretion of growth factors.

Fats are needed in growth to create cell membranes etc.

Does aromatase inhibition intervene in the fat elongation pathways eg production DHA and EPA in some.

You might like to read Smart Fats or the updated version M Scmidt. Spaciness tinitus etc is reported as being potentially improved by intake of omeg threes EPA DAH and balancing omega three six.

If you have time to read it you may find it thought provoking. It can be found second hand on the WEB for a few dollars.

Please discuss dietary changes with your advisors.

RB

I did a search on "fat syntesis P450" and this was on of the trials that came up.


This is a huge subject and every dooropened leads on to more. I do not pretend to understand the implications of this.

But I do not that it seems to suggest that P450 (Aromatase) may be involved in fat synthesis as well oestrogen regulation.

IF it is blocking aspects of fat synthesis it could have wider implications - see posts on omega three and six.

The impact of any potential blocking could be mitigated by ensuring that the body has an adequate intake of long chain fats particularly DAH and EPA.

Please discuss any dietary changes with your medical advisors.

RB

http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum
1: J Pharmacol Exp Ther. 2006 May;317(2):732-8. Epub 2006 Jan 18. Related Articles, Links
Click here to read
Induction of renal cytochrome P450 arachidonic acid epoxygenase activity by dietary gamma-linolenic acid.

Yu Z, Ng VY, Su P, Engler MM, Engler MB, Huang Y, Lin E, Kroetz DL.

Department of Biopharmaceutical Sciences, University of California San Francisco, San Francisco, CA 94143, USA.

Dietary gamma-linolenic acid (GLA), a omega-6 polyunsaturated fatty acid found in borage oil (BOR), lowers systolic blood pressure in spontaneously hypertensive rats (SHRs). GLA is converted into arachidonic acid (AA) by elongation and desaturation steps. Epoxyeicosatrienoic acids (EETs) and 20-hydroxyeicosatetraenoic acid (20-HETE) are cytochrome P450 (P450)-derived AA eicosanoids with important roles in regulating blood pressure. This study tested the hypothesis that the blood pressure-lowering effect of a GLA-enriched diet involves alteration of P450-catalyzed AA metabolism. Microsomes and RNA were isolated from the renal cortex of male SHRs fed a basal fat-free diet for 5 weeks to which 11% by weight of sesame oil (SES) or BOR was added. There was a 2.6- to 3.5-fold increase in P450 epoxygenase activity in renal microsomes isolated from the BOR-fed SHRs compared with the SES-fed rats. Epoxygenase activity accounted for 58% of the total AA metabolism in the BOR-treated kidney microsomes compared with 33% in the SES-treated rats. More importantly, renal 14,15- and 8,9-EET levels increased 1.6- to 2.5-fold after dietary BOR treatment. The increase in EET formation is consistent with increases in CYP2C23, CYP2C11, and CYP2J protein levels. There were no differences in the level of renal P450 epoxygenase mRNA between the SES- and BOR-treated rats. Enhanced synthesis of the vasodilatory EETs and decreased formation of the vasoconstrictive 20-HETE suggests that changes in P450-mediated AA metabolism may contribute, at least in part, to the blood pressure-lowering effect of a BOR-enriched diet.

PMID: 16421287 [PubMed - indexed for MEDLINE]

aromatase multifunctional physiological factor, estrogens, impaired bone fat carbohyd
 

****************** "Similarly, because aromatase is productive for a multifunctional physiological factor, estrogens, impaired metabolisms of bone, carbohydrate, and fat etc. result from the deficiency." *****************

I will look for links try and access full article but the above would suggest that intervention inthe aromatase pathways have the potential for a very wider range of side effects.

On the balance of probabilities we will see more long term effects with time.

I would reiterate my previous comments on fats.

RB














1: Nippon Rinsho. 2004 Feb;62(2):368-72. Related Articles, Links

[Aromatase deficiency]

[Article in Japanese]

Harada N.

Department of Biochemistry, Fujita Health University School of Medicine.

Aromatase, a key enzyme in estrogen synthesis, is tissue-specifically regulated in various tissues and plays an important role through endocrine and intracrine estrogen production in various physiological functions. Therefore, aromatase deficiency caused crucial impairments of physiological functions in the gonadal tissues as well as extra-gonadal tissues. Because aromatase is protective for androgenic exposure by catabolizing, virilization of a pregnant mother and pseudohermaphroditism of a baby girl consequently result from the deficiency. Similarly, because aromatase is productive for a multifunctional physiological factor, estrogens, impaired metabolisms of bone, carbohydrate, and fat etc. result from the deficiency. We discuss the etiology, clinical symptoms, and therapeusis by classifying it into two types of complete and incomplete aromatase deficiencies.

Publication Types:

* Review


PMID: 14968547 [PubMed - indexed for MEDLINE]

Thanks for all the replies
 

The linked articles read as if too much AI is not an ideal situation. As I am only weakly ER+ this makes me wonder if any AI will be of much benefit or could even do more harm than good.

I will definitely be discussing this with my onc next visit. I'm going to put Femara on hold until then.

Dear Deborah,

Would have replied sooner, but have had trouble accessing the site.

I have been on Femara a little over 4 years. I am only slightly ER+ (less than 10%) but a BC specialist I consulted for a second opinion at UCSF thought it would be a good thing to add to the arsenal.

I also take it at bedtime and don't know if that makes a difference, but side effects don't seem too bad(or else I have just gotten used to them!)

Anyway, I do think exercise is of huge benefit. I think it definitely helps with joint stiffness, and as you know weight bearing exercise is so important for our bones. Also, don't know if it's the exercise or the fish oil that I have recently added to my diet, but a recent Muga scan showed the best score I have had in my almost 5 years of being on Herceptin.

Off subject here, but my husband and I are planning a trip to N. Carolina next month to check out possible retirement places. I am a huge horse addict and have a friend that moved her dressage training barn to Pinehurst last year, and she says she absolutely loves it there. She said this would be a good time to come to see if we could cope with the heat! I am in Northern CA and we live in an area the neighbors call Pneumonia Gulch because we get so much wind and fog in the summer! So, it would really be a change for us, but sounds like an adventure too.

Take Care, Kim in CA

I have been on Femara for 3 months. The only side effect I've had so far is hot flashes - really bad ones. I like the idea of taking the drug at bedtime because I don't seem to have hot flashes as much during the day as during the night. Might help. Good luck in your treatment.

Femara Side Effects
 

Hi Kim,

I live in Concord, NC. Pinehurst is a lovely resort. Golfer's paradise! I think you would love the area. The summer can be very hot, but the fall and spring are very comfortable. Our winter season is usually mild, not too cold.

Susan

Femara Side Effects
 

Hi Deborah,

I have been on Femara now for over six weeks. I originally started on Arimidex in May of 2005, and had Herceptin weekly for one year starting in June 2005. I finished a year of Herceptin on June 20 and I can say I am feeling better.

I still have the joint pain on Femara but not as bad as I had on the Arimidex. Hot flashes were horrible when I first started the Femara but they have calmed down considerably. My runny nose while on chemo and Herceptin has improved greatly. I really think I am feeling better on the Femara but it has taken at least five weeks for me to feel this way.

I will see my oncologist on Friday to see if he thinks I should stay on the Femara and then will post.

Hang in there.

Susan

kat in the delta
 

Yes, my sister has no joint pain taking the aromasin. She could not take the Femara & even told her ONc. that if she cont. Femara she needed Pain pills ....But, the switch to Aromasin has been good---no pain for her. Kat in the delta

kat in the delta
 

I talked my surgeon who only has her own breast clinic--top notch female MD and she said that if it was enough to show up as even "weakly" positive that she would advice taking an aromatose inhibitor-----I was also Weakly Positive and just asked her that same "?", and I am calling my Onc today. Kat in the delta

kat in the delta
 

Becky, YES it did go away for my sister after the femara got out of her system. Kat in the delta

I'm not on A.I.'s (yet) so I found this thread quite interesting. I am also minimally ER pos (< 15%). My onc felt also that the benefits outweighed the side effects to put me on tamoxifen. So, the plan is to eventually put me on A.I.'s.
I was wondering however -of the ladies that have hot flashes, which I KNOW are unbearable, did your onc's put you on anything to counteract them? I have been taking a 1/2 dose of Effexor (37.5 mg) and I have not had a hot flash for over a year. A while back I did not get my refill on time and I missed 2 days of Effexor and I thought I was going to implode. For me it really works. I know we all hate taking this for that and that for this, but at this point, if it helps- I will take it!

I hope that in five years something else is invented that may work as well with even less side effects...

Maria

I am taking Femara, at night since June 1st, 2006 and having headaches. About 2 weeks ago I had an episode of double vision. Several times seemed to be dizzie. I am also taking Herceptin every 3 weeks since 12-15-2005.

I went to the opmarthologist and he saw pressure build up behind the eyes - no glucoma yet - after discussion decided to wait until I had another episode of double vision before doing a cat scan for behind the eye.

The brain fog - YES - but I think that is from fatigue, my rad was done 4-28-2006. The ability to concentrate and focus is so hard. Some days are fine but lately it seems to be getting worse especially if you try to skip on sleep or just relaxing. This weekend I took care of my 7 year old nephew - went swimming etc. Talking to people and starting something new is so hard. I have notes everwhere.

So you are not alone, that fatigue creeps up on you and then your brain fails.

Sheryl

Sheryl Ann
 

Did the opth say what s/he thought the pressure in your eye was from?

You're not too far from rads, so it's to be expected you still have the fatigue and brain fog. It seemed like it took several months for me to recover from the 33 rads I took in 2003 I actually fared worse with the rads than with chemo as far as the fatigue factor..

DeborahNC
 

No the eye doctor could not say what it came from, just wants to see me in 4 months.

AI's longterm
 

A while back, Dr. Susan Love's website had two commentaries (pro and con) about the value of taking AI's. It may still be there somewhere....

AI's are not a perfect answer, and as RB notes, questions about use likely are not limited to bone health long term. Since they do not yet have a really long history of use, plus they are being used now by younger women who achieve menopausal status by unnatural means, there are unknowns about them.

We each have to make our own personal guess about our own personal risk level.

As a personal side note, in trying to address the problem of weight gained during chemo, I have been gradually increasing weightbearing exercise. Over 2 decades ago I had very slight knee damage successfully repaired that has never given me any trouble over a very active life. Recently that knee started falling apart. It "might" have happened with or without the use of AI's -- but my interpretation is that the reason joints hurt so much with use of some AI's is that by reducing the estrogen we also lose not just the lubrication in places like the vagina but in the joints and many other places as well. For example, my eyes are much drier now than they were previously. I don't want to make this a long post but I just raise the question of the need to balance out the likely net effects long-term with any benefit. I happen to be highly ER/PR and that would weigh in favor of using an AI, whereas someone barely positive might not want to take on the early progressive deterioration. I happen to be Stage 1, which might be some reason NOT to take an AI.

It is also known that resistance to AI's often develops. So if someone is low risk in the first place, would it make more sense not to take an AI so as not to allow resistance to it to build?

Lots of questions about AI's, not a lot of answers....

AlaskaAngel

This is another guess/question.

In the enormous complexity of the body how does oestrogen react with the desaturase pathway that makes the long chain fats DHA and EPA.

PGE2 produced via cox one and cox two control oestrogen according to trials, which pathway is used in AIs.

But does oestrogen somehow influence or control in part DHA production.

Given the rise in DHA production reported in pregancy, and the need for oestrogen in reprodution it would seem a reasonable question.

This trial would suggest that it may be the case that oestrogen controls production of DAH and EPA at least in part.

The consequence of oestrogen blocking would be blocking DHA and EPA production.

The implication of this for AI takers would be a need to take DHA and EPA.

Fish oil which contain DHA and EPA have been associated with dry eye improvement, dry mouth improvement, impovement in arthritis, and combined with a reduction in omega shix should help with weight loss.

This is the first trial I have seen directly suggesting oestorgen as a controller of the FAS pathways. If I find more I will post.

(Why not a cyclical feed back loop - no DHA EPA = upgrades of oestrogen levels to try and make fats required for reproductive / femininty, upgrades Fattty acid synthesis = impacts on growth factors. The counter of which would be supply DHA EPA - no need to make = downgrade oestrogen downgrade FAS etc. Added to this what happens if no omega three raw material and over supply PGE2 to P450 to E2 to growth factors through excess omega six in diet and membranes etc -?????????)

RB






http://www.ncbi.nlm.nih.gov/entrez/q...ats+desaturase

1: Proc Nutr Soc. 2006 Feb;65(1):42-50. Related Articles, Links
Click here to read
Long-chain n-3 PUFA: plant v. marine sources.

Williams CM, Burdge G.

Hihj Sinclair Unit Human Nutrition, School of Food Biosciences, University of Reading, UK. c.m.williams@reading.ac.uk

Increasing recognition of the importance of the long-chain n-3 PUFA, EPA and DHA, to cardiovascular health, and in the case of DHA to normal neurological development in the fetus and the newborn, has focused greater attention on the dietary supply of these fatty acids. The reason for low intakes of EPA and DHA in most developed countries (0.1-0.5 g/d) is the low consumption of oily fish, the richest dietary source of these fatty acids. An important question is whether dietary intake of the precursor n-3 fatty acid, alpha-linolenic acid (alphaLNA), can provide sufficient amounts of tissue EPA and DHA by conversion through the n-3 PUFA elongation-desaturation pathway. alphaLNA is present in marked amounts in plant sources, including green leafy vegetables and commonly-consumed oils such as rape-seed and soyabean oils, so that increased intake of this fatty acid would be easier to achieve than via increased fish consumption. However, alphaLNA-feeding studies and stable-isotope studies using alphaLNA, which have addressed the question of bioconversion of alphaLNA to EPA and DHA, have concluded that in adult men conversion to EPA is limited (approximately 8%) and conversion to DHA is extremely low (<0.1%). In women fractional conversion to DHA appears to be greater (9%), which may partly be a result of a lower rate of utilisation of alphaLNA for beta-oxidation in women. However, up-regulation of the conversion of EPA to DHA has also been suggested, as a result of the actions of oestrogen on Delta6-desaturase, and may be of particular importance in maintaining adequate provision of DHA in pregnancy. The effect of oestrogen on DHA concentration in pregnant and lactating women awaits confirmation.

Publication Types:

* Review


PMID: 16441943 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum



1: Hum Reprod. 2006 Jun 23; [Epub ahead of print] Related Articles, Links
Click here to read
Urinary estrogen and progesterone metabolite concentrations in menstrual cycles of fertile women with non-conception, early pregnancy loss or clinical pregnancy.

Venners SA, Liu X, Perry MJ, Korrick SA, Li Z, Yang F, Yang J, Lasley BL, Xu X, Wang X.

Division of Epidemiology and Biostatistics, University of Illinois at Chicago, School of Public Health, Chicago, IL.

BACKGROUND: Knowledge is limited of how estrogen and progesterone variability in fertile women are associated with achieving pregnancy. METHODS: From 1996 to 1998, we enrolled 347 textile workers without hormone treatment in Anhui, China, who provided daily urine and data upon stopping contraception for up to 1 year until clinical pregnancy. Urinary hCG was assayed to detect conception and early pregnancy losses. We compared urinary concentrations of estrone conjugates (E1C) and pregnanediol-3-glucuronide (PdG) in 266 clinical pregnancies, 63 early pregnancy losses and 272 non-conception cycles from 347 women and also in 94 clinical pregnancy and 94 non-conception cycles from the same women. RESULTS: Using generalized estimating equations and relative to 266 clinical pregnancy cycles, log(E1C) was lower in 272 non-conception cycles [beta = -0.3 ng/mg creatinine (Cr); SE = 0.1; P < 0.0001]. On average, daily E1C was 18 ng/mg Cr lower in non-conception cycles than in clinical pregnancy cycles. Relative to 94 clinical pregnancy cycles, log(E1C) was lower in 94 non-conception cycles (beta = -0.4 ng/mg Cr; SE = 0.1; P < 0.0001) from the same women (average difference in daily E1C was 20 ng/mg Cr). The odds of E1C less than the 10th percentile (<30 ng/mg Cr) were higher in early pregnancy loss cycles [odds ratio (OR) = 4.8; P = 0.0027] than in clinical pregnancy cycles in the early luteal phase. Compared with clinical pregnancy cycles, log(PdG) concentrations were lower in non-conception cycles during the follicular phase, but this analysis lacked power for multiple testing. CONCLUSIONS: Estrogen concentrations varied from cycle to cycle, and higher estrogen was associated with achieving clinical pregnancy.

PMID: 16798842 [PubMed - as supplied by publisher]