PSA increase after zytiga and steroid switch

[Peterd110]

Exactly 2 months ago, PSA was 2.26 switched from prednisone to dexamethasone. Today’s results are 2.68. In May psa was 0.1. Go to see oncologist next week. Not sure what to do next.

[Hidden]

In general you wouldn't change treatments based on PSA rise alone. I'd have imaging done, but probably when the PSA rises a bit more. Looks like the doubling time is around 5-6 months. Until you have radiographic progression, I'd continue with Zytiga.

Have you had any molecular testing done for potentially treatable mutations? You could do a liquid biospy that looks at circulating tumor cells or have a tissue sample analyzed from an active met after imaging if that's possible.

These are things you can discuss with your doctor.

[Peterd110 in reply to Hidden]

I sure will! Thanks Gregg!

I feel fine. No pain. I hate to give up too soon.

[Hidden in reply to Peterd110]

Your PSA is not rising that fast so you have some time. Of course you want to keep an eye on it. You may find that it levels off somewhere or even goes slightly up and down for a while. Technically your treatment is still working so I'd want to get the most out of it.

After Zytiga becomes ineffective you could go to Docetaxel chemotherapy or another second line AR treatment such as Enzalutamide.

I'm currently on Zytiga myself with a PSA of .01. When it stops working, my plan is to go to chemotherapy next, then try another AR-based treatment after that. I've already had chemo and it was tolerable so nothing to be afraid of there.

Wishing the best for you. Let us know what your MO says.

[Tall_Allen]

pcnrv.blogspot.com/2019/12/...

[Pleroma in reply to Tall_Allen]

Thanks, Tall_Allen, I had not seen that article.

[JLS1 in reply to Tall_Allen]

I wonder where Xofigo fits into that optimal sequencing.

[Tall_Allen in reply to JLS1]

Xofigo is given as 6 injections, 4 weeks apart, so one can complete it and move onto the next therapy after 20 weeks. You might consider it before undertaking a longer therapy like abiraterone. It's probably OK with abiraterone as long as one uses a bone-preserving agent at the same time, but for now, there is a warning against that.

[Grumpyswife in reply to Tall_Allen]

Geez my husband is way out of whack with that optimal sequencing.

[j-o-h-n]

"okay doc.... now what the fcuk do we do?"

Plain and simple...........

Good Luck, Good Health and Good Humor.

j-o-h-n Sunday 12/15/2019 6:46 PM EST

[Patrick-Turner]

I had been on ADT for 6 years after 2010, then Psa began to rise like yours, so in mid 2016 I had added Cosadex which worked for 6 months, then Psa went up to about 6 after nadir of 0.4, then I began taking Zytiga ( plus prednisone to replace what adrenal glands produce ) and then Psa went up to about 12 after 8 months, after nadir of 2.2, so then I began chemo. I am continuing with monthly shots of ADT.

But just before Cosadex in mid 2016, I had PsMa-Ga68 scan to see what real Pca status was. 2 upper lymph nodes were found with tiny mets. I had IMRT plus also to PG, which had too much Pca surrounding it to have been removed in 2010,

after diagnosis in late 2009 with Gleason 9 and Psa 6 at age 62.

I figured if there were 2 mets that could be detected by PsMa Ga68 scan in 2016, there were probably countless other mets which were too small to see in the scan, so in 2016, I expected many other mets would show up in following PsMa Ga68 scans, even if the Psa showed a reduction due to Psa suppression with Cosadex or Zytiga.

I was right.

So after Zytiga failed, many mets showed up including many in bones.

The normal protocol here was to give chemo with Docetaxel. It was notorious for not working if Pca was in bones, and so I asked for Lu177 and doc said that when I failed with chemo he'd refer me to doc giving Lu177 from Theranostics Australia.

After 4 x chemo shots, another PsMa scan showed bone mets increasing and Psa was 50, 4 times higher than the 12 before chemo, so 13 months ago I had my first Lu177 shot, and had my 4th Lu177 in May this year.

2 months later the follow-up Psma scan showed bone mets healing and all soft tissue mets gone. They found my Pca was all of one type, so the Lu177 had worked on all my Pca which was not considered to have mutated to different varieties.

But I after quitting Chemo in October 2018, Psa went from 50 to 25, and docs could not say why, so chemo did do something, but nobody knew what it was.

Psa hardly moved after 2nd Lu177 shot, but after 3rd shot Psa began to go down and then I began Xtandi, said to help thr action of Lu177, and by 4th Lu177, Psa was going down fast.

Last November Psa was 0.32, and I had no Pca symptoms at all. Docs said I have had a very good response to Lu177 therapy.

Side effects are dry mouth sometimes, but not all the time.

Effects from 5 shots of chemo have affected me much more; its terrible stuff.

But I have learnt to get back into cycling 200km+ a week and I have been doing since 2007 to stay fit and healthy as I could during and through all treatments.

If I were you, I would have PsMa Ga68 PET/CT scan immediately to see what your Pca status is. The radiologist can see whether your Pca may respond well to Lu177, or only partially to Lu177, because if your Pca has mutated into different types, Lu177 might kill 70% of the total, and not have any effect on a remaining 30%, which left untreated will kill you.

Killing 70% with Lu177 is a benefit because it can't later mutate to something that can kill you, and hopefully a fix for the already mutated Pca might be found, typically by having DNA analysis to see if you have Brca2 gene, and maybe they would use PARP inhibitors. But the chances of PARPs working well are low, but worth trying. All this fancy-smancy therapy is very expensive and not covered by Medicare in Australia and may be difficult to get in USA, so usually US ppl go to Germany for Lu177, and I don't know where they go for PARP.

I am now 72, have survived 10 years after Dx. But 3 weeks ago part of my small intestine became adhered to scar tissue formed where docs opened me to attempt an RP in 2010. They could not remove PG because Pca was wrapped around capsule but it had not invaded any other organ, and has not since.

But the adhesions which were likely had me spend the worst 11 days in hospital but after severing the adhesions in a small op I am recovering slowly, and hope to get back to cycling 200km a week as I was doing before these adhesions cause the blockage.

Its 2 weeks since I was discharged from hospital, I lost 8Kg, But I cycled 22km yesterday and 22km today, and food is going through me OK, but I have been temporarily been weakened by this experience which I plan to work through.

My gut bacteria was all killed during hospital stay, and will take time to re-grow and allow me my former strength and endurance.

My local GP doc said I have a 12% risk of cadio-vascular failure so there's nothing in the way of getting better, before I get worse, caused by what is not now known. I may indeed have Pca that has mutated to something un-treatable but I'll cross that bridge when I get there......

Patrick Turner.

[sandy4510 in reply to Patrick-Turner]

Hi Patrick just wondering how the radiologist can tell if you will respond well to LU treatments!

[Patrick-Turner in reply to sandy4510]

Good question, and I am not fully qualified to answer it, I am just a bloke, skilled at building work and electronics and not able to know more than a few simple things about PsMa Ga PET/CT scans that are required to be used to determine suitability for Lu177 treatment. The scans can later to see what progress has been made during PsMa treatment with another 2 months+ after the 4th Lu177 final infusion of Lu177.

Basically, the scans show where Ga68 has gathered at Pca sites. The Ga68 is a radioactive form of Galium, a normally harmless metal not used anywhere in the body, but when made radioactive in a nuclear reactor, it can be made to have a short half life of days, and the radiation is harmless, but needed to be able to make an image of where Pca is if the Pca is able to attract Ga68 plus what is called a ligand chemical, which clings to Pca sites that have PsMa expression and then tie the Ga68 alongside or within the Pca sites.

The scans are diagnostic, and when Lu177 is used, it is also brought to gather where there is PsMa expression at Pca cells and Lu177 is also a metal that has no place in the body, and is made radioactive in a reactor, and given a short half life, but a long enough life to emit radioactive particles to damage Pca cells so badly that they die fast, or die when they try to grow later.

So Lu177 is therapeutic, and the method used to give Ga68 for a scan or Lu177 for therapy is the same, so someone called this targeted theranostic nuclear radiation. The Radiologist can see the Pca mets that are larger than 2mm dia if they attract Ga68 in scans, and they can determine what is called SUV, or specific uptake value, ie, the amount of Ga68 uptake, for a given amount of injected Ga68, and from that they get an SUV number for where many sites of Pca exist. From this they can tell an oncologist or nuclear specialist doctor whether or not its worth giving a man Lu177.

Sometimes there is Pca present that does not attract Ga68, so Lu177 will not be effective at killing those Pca cells. Research is continuing at Peter Mac in Melbourne to better understand what can be done where Lu177 suitability looks ok according to scans, but the man does not get a benefit because there is Pca present that has not got PsMa expression. 30% do not get a benefit from Lu177. I know 70% do get a benefit. The research is trying to help the 30% and I suggest you read about research by a Dr Hoffman at Peter Mac to know a lot more. There is quite a lot that any person of average intelligence can understand about theranostic treatments. I have been following its development since it was first mentioned online, maybe 5 years ago. Huge interest was given to Lu177 and also to Ac225.

So how do these radioactive metals become able to be injected? After being bombarded in a nuclear reactor, ( maybe by protons, but I am not sure ) the metals are combined with chlorine, so you have something like sodium chloride, or what is known as plain old salt. The salt made with Lu177 is soluble in water, and thus easily injected, and it circulates around the blood stream path of veins and arteries and tends to lodge and gather where Pca exists. But while moving around the body it does negligible damage to healthy cells because the dosage just is never strong enough. But there are places where LU177 does gather, even though there is no Pca present. and these are a saliva glands, so they are a bit damaged by a course of Lu177 infusions. In my case if I sleep on my back I get a dry mouth, but when I wake the saliva runs to mouth again and I am OK. On the bike when working hard the same thing can happen, but a sip of water fixed things. So damage I got to saliva glands has been minimal. I know men who had IMRT to cancer sites in their neck, and they have had almost complete dry mouth, so they chew special gum, drink more water, and yet they cope OK.

There is a lot more online about theranostic treatment. It is a new thing, and still remains to be understood, to reduce the fear about it, and to understand why authorities are slow to approve it.

I am enjoying a very good QOL following Lu177, and would now be in palliative care if Lu177 had not been available.

Patrick Turner.