Testosterone after Brachytherapy.

[pjoshea13]

New Japanese study below [1].

When I was diagnosed in 2004, it was already old news that PCa somehow reduces testosterone [T] production. In 1998, Patrick Walsh had published a Johns Hopkins study [2] of 63 men who had undergone prostatectomies. 12 months after surgery "there was a statistically significant increase in serum testosterone, free testosterone ...". The study was repeated by two other institutions, with similar results.

This certainly influenced my view of T as the presumed dangerous "fuel" for PCa.

There were also a few studies back then associating lower T with a poorer prognosis. One could look at those studies as an indication of hypogonadism being a risk factor for PCa, but the Walsh study turns that around. PCa becomes more aggressive when it somehow inhibits T production.

So one might expect T to ultimately increase after brachytherapy.

"Median pre-implantation {T was 418 ng/dL.}"

"{T} decreased significantly to a median nadir of 89.4% of baseline {372 ng/dL} occurring at 6 months, and then recovered to baseline at 18 months after {brachytherapy}."

i.e. brachytherapy itself lowers T. And, even at 18 months, recovery was only to baseline - not to the higher levels seen following prostatectomy. "Patients were followed for 24-60 months", but increases over baseline were not reported, at least in the Abstract.

The paper defines the cutoff for hypogonadism as 300 ng/dL, although 350 ng/dL is more common these days IMO.

"The group of patients whose {Ts} fell below {300 ng/dL} (biochemical hypogonadism) after {brachytherapy} started with lower baseline {Ts (median: 354 ng/dL)} than patients whose {Ts} did not fall below {300 ng/dL (median: 490 ng/dL)}."

-Patrick

[1] ncbi.nlm.nih.gov/pubmed/967...

[2] ncbi.nlm.nih.gov/pubmed/307...

Urology. 2019 Feb 1. pii: S0090-4295(19)30089-5. doi: 10.1016/j.urology.2019.01.022. [Epub ahead of print]

Testosterone Profiles after Brachytherapy for Localized Prostate Cancer.

Taniguchi H1, Kawakita S2, Kinoshita H2, Murota T2, Matsuda T2.

Author information

1

Department of Urology and Andrology, Kansai Medical University, Hirakata, Osaka, Japan. Electronic address: [e-mail].

2

Department of Urology and Andrology, Kansai Medical University, Hirakata, Osaka, Japan.

Abstract

OBJECTIVE:

To evaluate patients' serum total testosterone levels (STLs) after brachytherapy (BT) for prostate cancer.

METHODS:

We enrolled 102 men who underwent permanent interstitial BT using I125 without androgen deprivation therapy for localized prostate cancer. Seed BT radiation dose was 145 Gy. Patients were followed for 24-60 months after BT. The primary outcome was STL kinetics after BT. Predictors of testosterone decrease were also analyzed.

RESULTS:

Median pre-implantation STL was 4.18 ng/mL. STL decreased significantly to a median nadir of 89.4% of baseline (3.72 ng/mL) occurring at 6 months, and then recovered to baseline at 18 months after BT. The group of patients whose STLs fell below 3.00 ng/mL (biochemical hypogonadism) after BT started with lower baseline STLs (median: 3.54 ng/mL) than patients whose STLs did not fall below 3.00 ng/mL (median: 4.90 ng/mL). The group of patients whose STLs decreased by more than 1.00 ng/mL over the study period had significantly higher median baseline STLs (median: 5.05 ng/mL) than the group whose STLs decreased by less than 1.00 ng/mL (median: 3.64 ng/mL).

CONCLUSIONS:

Although STL decreased significantly after I125-based BT, STL decline after treatment for localized prostate cancer was not large and recovered over time.

Copyright © 2019. Published by Elsevier Inc.

KEYWORDS:

Brachytherapy; Hypogonadism; Prostate cancer; Radiotherapy; Testosterone

PMID: 30716344 DOI: 10.1016/j.urology.2019.01.022

[Adam10]

Hi pjoshea13

Thanks for posting this info.

I was diagnosed with hypogonadism in 2014 and received hormone replacement treatment (HRT) since then via 1000 mcg Nebido injections every 3 months.

My urologist stopped the HRT in May 2018 when I was diagnosed with PCa. My PSA test was 6.9, Gleeson was 3+4 and NAID 4.

I had the tumor ablated (I hope) or ‘zapped’ in December 2018 by high intensity frequency ultrasound. Am waiting to see if tumor was destroyed. I saw slivers of tissue passed in my water for 4-6 weeks afterwards. Have stopped passing blood.

My next PSA test is in Match 2019.

My total testosterone serum in January 2019 was 11.7 nmol/L (range 6.68-25.7). In September 2018 my testosterone total was 12.51 nmol/L (9.9-27.8).

Could the Nebido have caused my PCa?

Would it be safe to restart HRT again in the future as I believe I still suffer from hypogonadism.

I will consult urologist innMarch 2019 but what like your and others’ thoughts. Comments gratefully received.

[pjoshea13 in reply to Adam10]

Hi Adam,

There was a study of men with hypogonadism a while back. The group of men who were treated with T later developed less PCa than the untreated group.

The only time that hypogonadism is protective - IMO - is when T levels are so low, that the man is effectively on ADT.

The literature on T replacement invariably finds no added PCa risk. I don't think your Nebido "caused" your PCa or accelerated its development.

But there will be many who will say you would be crazy to restart HRT. And many doctors tend to play it safe too. Which does nothing to improve the QoL in hypogonal patients.

You were diagnosed with hypogonadism in 2014 & treated until May 2018. Do you have T numbers at diagnosis & following treatment?

In September 2018, T was 12.51 nmol/L (360 ng/dL).

In January 2019, T was 11.7 nmol/L (337 ng/dL).

Hypogonadism is often defined as T <350 ng/dL.

According to Morgentaler's saturation model, androgen receptors [AR] have all the T they can use at the 250 ng/dL level, or less.

According to Dr. Myers, men coming off ADT can see their PSA rising (as T passes up to the saturation point), but once T goes higher than 350 ng/dL, there is no added effect on PSA.

You haven't had ADT - which can alter the AR - so I doubt that increasing T by a couple hundred points would cause a problem. But I'm not your doctor (or even a doctor).

-Patrick

[George71 in reply to pjoshea13]

Hi Patrick,

In your post above you said:

"According to Morgentaler's saturation model, androgen receptors [AR] have all the T they can use at the 250 ng/dL level, or less.

According to Dr. Myers, men coming off ADT can see their PSA rising (as T passes up to the saturation point), but once T goes higher than 350 ng/dL, there is no added effect on PSA."

I would seem that anyone with t over 350 -- or certainly 450 would not fueling their PCa by adding T to increase their overall levels -- and everything I've read says that super high T is therapeutic and slows prostate cancer progression. Is that your take on it also?

[pjoshea13 in reply to George71]

George,

My belief is that T can continue to have a regulatory role in the early stages. However, this may not be true after ADT has induced AR alterations.

And restoring a normal E2:T ratio will reverse some of the metabolic syndrome issues that arise with hypogonadism.

-Patrick