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Did any one get the feeling that there gyno got worse on letro...i knwo this sounds impossible...but im not sure if mine got worse...in the beginning it loooked like it was working ....Still no sensitivity or anything but deff very puffy and pointuy.....thinking about throwing in Nolva 80mg for 3 or 4 days...and then down to 10 mg for the rest of cycle along with Letro...and then 20mg ED for PCT
Letro takes some time to start working, so your gyno could have gotten worse because you didnt have anything working against it at the time. Once it kicks in it will help. Definitly add the nolva though.
nolva will inhibit the work of the letro from what people have told me.
I didn't start a thread on this because I couldn't believe it was true.
But I took letro for 3 weeks and I swear that it got worse and my chest became more sensitive.
Since stopping I'm back to roughly where I started.
It certainly has me confused and a little perplexed.
Even if I do get a handle on it, what anti-e's am I going to use if i cycle again? :scratch:
I am very prone to gyno. I started my cycle 9 days ago. I started using letro 1 week before I started the test. I started geting sensitivity in my left nipple 4 days after my first injection. The letro better sart working very soon cause I am f..cking pissed. I have some nolva, I think I am going to start taking tomorrow if I dont feel the sensitivity diminishing. I never had this problem with arimidex.
Quote:
Originally Posted by charlieuk
mudman said it can take up to 6 weeks for the letro to reach stable blood levels,not sure if this is true, but maybe someone can shed some light :unsure:
Quote:
Originally Posted by Nico
i always start anti e's at least 2-3 weeks b4 cycle. i would do that from now on just in case.
i def started my letro 2 weeks before my cycle...so i dunno....i think im going to run 80 mg for 3 or 4 days and then drop it to 10 mg ED throughout cycle with the Letro and then bump it to 20 mg ED in PCT to prevent estrogen rebound
bump
This is just one of the many studies out there on Femara/Letrozole in the treatment of breast cancer....................Quote:
Originally Posted by flabbywussy
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FEMARAź Novartis Pharmaceuticals Letrozole Nonsteroidal Aromatase Inhibitor - Inhibitor of Estrogen Biosynthesis - Antitumor Agent Action And Clinical Pharmacology: Letrozole is a potent and highly specific nonsteroidal aromatase inhibitor. It inhibits the aromatase enzyme by competitively binding to the heme of the cytochrome P450 subunit of the enzyme, resulting in a reduction of estrogen biosynthesis in all tissues.
Letrozole exerts its antitumor effect by depriving estrogen-dependent breast cancer cells of their growth stimulus. In postmenopausal women, estrogens are derived mainly from the action of the aromatase enzyme, which converts adrenal androgens - primarily androstenedione and testosterone - to estrone (E1) and estradiol (E2). The suppression of estrogen biosynthesis in peripheral tissues and the malignant tissue can be achieved by specifically inhibiting the aromatase enzyme.
In healthy postmenopausal women, single oral doses of 0.1, 0.5 and 2.5 mg letrozole suppressed serum estrone by 75 to 78% and estradiol by 78% from baseline. Maximum suppression is achieved in 48 to 78 hours.
In postmenopausal women with advanced breast cancer, daily letrozole doses of 0.1 to 5 mg suppress estradiol, estrone and estrone sulfate plasma levels by 75 to 95% from baseline in all patients treated. With 0.5 mg doses and higher, many plasma levels of estrone and estrone sulfate are below the limit of detection of the assays, indicating that higher estrogen suppression is achieved with these doses. Estrogen suppression was maintained throughout treatment in all patients.
Letrozole is highly specific in inhibiting aromatase activity. Impairment of adrenal steroidogenesis has not been observed. No clinically relevant changes in the plasma levels of cortisol, aldosterone, 11-deoxycortisol, 17-hydroxy-progesterone, ACTH (adrenocorticotropic hormone) or in plasma renin activity were found in postmenopausal patients treated with 0.1 to 5 mg letrozole daily. The ACTH stimulation test performed after 6 and 12 weeks of treatment with daily doses of 0.1 to 5 mg letrozole did not indicate any attenuation of aldosterone or cortisol production. Thus, glucocorticoid or mineralocorticoid supplementation is not required.
Letrozole had no effect on plasma androgen concentrations (androstenedione and testosterone) among healthy postmenopausal women after single doses of 0.1, 0.5 and 2.5 mg, or on plasma androstenedione concentrations among postmenopausal patients treated with daily doses of 0.1 to 5 mg. These results indicate that accumulation of androgenic precursors does not occur. Plasma levels of LH and FSH are not affected by letrozole in patients, nor is thyroid function as evaluated by TSH, T4 and T3 uptake.
In a controlled double-blind clinical trial, the overall objective tumor response rate (complete and partial response) was 23.6% in letrozole-treated patients compared to 16.4% in patients on 160 mg megestrol acetate. Treatment comparison of the response rate showed a statistically significant difference in favor of 2.5 mg letrozole (p=0.04).
Pharmacokinetics: Absorption: Letrozole is rapidly and completely absorbed from the gastrointestinal tract (absolute bioavailability=99.9%). Food slightly decreases the rate of absorption (median tmax 1 hour fasted vs 2 hours fed and mean Cmax 129±20.3 nmol/L fasted vs 98.7±18.6 nmol/L fed), but the extent of absorption (area under the curve (AUC)) remains unchanged. This minor effect on absorption rate is not considered to be of clinical relevance and therefore letrozole may be taken with or without food.
Distribution: Letrozole is rapidly and extensively distributed into tissues (Vdss=1.87±0.47 L/kg). Plasma protein binding is approximately 60%, mainly to albumin. The letrozole concentration in erythrocytes is about 80% of that in plasma. After administration of 2.5 mg 4-labeled letrozole, approximately 82% of the radioactivity in plasma was unchanged compound. Systemic exposure to metabolites is therefore low.
Biotransformation and Elimination: Metabolic clearance to a pharmacologically inactive carbinol metabolite, CGP 44645, is the major elimination pathway of letrozole (Clm=2.1 L/h), but it is relatively slow when compared to hepatic blood flow (about 90 L/h). The cytochrome P450 isoenzymes 3A4 and 2A6 were found to be capable of converting letrozole to this metabolite. Formation of minor unidentified metabolites and direct renal and fecal excretion play only a minor role in the overall elimination of letrozole. Within 2 weeks after administration of 2.5 mg 4-labeled letrozole to healthy postmenopausal volunteers, 88.2±7.6% of the radioactivity was recovered in urine and 3.8±0.9% in feces. At least 75% of the radioactivity recovered in urine up to 216 hours (84.7±7.8% of the dose) was attributed to the glucuronide of the carbinol metabolite, about 9% to 2 unidentified metabolites, and 6% to unchanged letrozole.
The apparent terminal elimination half-life in plasma is about 2 days. After daily administration of 2.5 mg steady-state levels are reached within 2 to 6 weeks. Plasma concentrations at steady-state are approximately 7 times higher than concentrations measured after a single dose of 2.5 mg, while they are 1.5 to 2 times higher than steady-state values predicted from the concentrations measured after a single dose, indicating a slight non-linearity in the pharmacokinetics of letrozole upon daily administration of 2.5 mg. Since steady-state levels are maintained over time, it can be concluded that no continuous accumulation of letrozole occurs.
can always count on mudman! thanks bro