I finished my last 3 month cycle of high T BAT in late April. Stayed on Lupron of course and reintroduced Bicalutimide. Psa levels during the last three months were (month1 2.2 -> 7.9, Month2 7.9-> 7.5, Month3 7.5 -> 11.86) . PSA level since. (month1 3.02, month2 2.2, Month3 1.78 month4 2.16*, month5 1.4, today 1.29)
*Month4 was an anomaly, in that I had 5 spinal injections for stenosis which have been very beneficial thus far.
At start of BAT PSA was .28 and had tripled in last 7 months. This was after 11 years on ADT3 with recurring returns to .02.
My MO prescribed Xtandi but I advised I would like to see how first line treatment of original ADT would fare after BAT. I still have first 30 day pills.
Here us what I am taking from this, 1. PSA is still going down after 20 months and was doubling every 1.5 months prior to starting BAT. 2. I am still chemo and other treatments naive after almost 14 years. 3. When PSA decides to rise again I will try BAT before moving to second line treatments.
I don't know if others can be helped so get good advice from Med pros before trying this.
Bigdon
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That is just great! Just to clarify... you didn't "reintroduce bicalutamide" while you were taking testosterone, right? Xtandi, being a stronger version of bicalutamide, might result in a longer time in which BAT remains effective. Also, BAT may make Xtandi be effective longer.
Correct, I had stopped Casodex prior to starting BAT. I started it late in the first month of of the last off cycle. That is when I got the drop of 11 to 3 of PSA. My decision to continue it was to try to determine the true effectiveness of BAT with respect to retarding MCRPC. I was also concerned with Xtandi SE's.
where it was caused by a Drug Nilutamide (Anandron)
which was replacing Bicalutamide, given to me for the PC treatment as a side-effect.
I was overloaded with unnecessary antibiotics and other drugs,was 2 months on oxygen and almost dyed.
The only treatment should have been to remove the drug
and be treated with antiinflamatory Corticosteroids.
this CHEMICAL PHEUMONITIS IS REVERSABLE,
but many doctors do not know about this.
I had to diagnosed myself and later my DX was confirmed by 3 specialists
Please see this from Mayo clinic:
Patient Care & Health Information
Diseases & Conditions
Pneumonitis
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Pneumonitis
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Overview
Pneumonitis (noo-moe-NIE-tis) is a general term that refers to inflammation of lung tissue. Technically, pneumonia is a type of pneumonitis because the infection causes inflammation. Pneumonitis, however, is usually used by doctors to refer to noninfectious causes of lung inflammation.
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Common causes of pneumonitis include airborne irritants at your job or from your hobbies. In addition, some types of cancer treatments and dozens of drugs can cause pneumonitis.
Difficulty breathing — often accompanied by a dry (nonproductive) cough — is the most common symptom of pneumonitis. Specialized tests are necessary to make a diagnosis. Treatment focuses on avoiding irritants and reducing inflammation.
Symptoms
The most common symptom of pneumonitis is shortness of breath, which may be accompanied by a dry cough. If pneumonitis is undetected or left untreated, you may gradually develop chronic pneumonitis, which can result in scarring (fibrosis) in the lungs.
Signs and symptoms of chronic pneumonitis include:
Shortness of breath
Cough
Fatigue
Loss of appetite
Unintentional weight loss
When to call a doctor
Call your doctor anytime you have difficulty breathing, no matter what might be the cause.
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Causes
Bronchioles and alveoli in the lungs
Bronchioles and alveoli in the lungs
Pneumonitis occurs when an irritating substance causes the tiny air sacs (alveoli) in your lungs to become inflamed. This inflammation makes it difficult for oxygen to pass through the alveoli into the bloodstream.
Many irritants, ranging from airborne molds to chemotherapy drugs, have been linked to pneumonitis. But for most people, the specific substance causing the inflammation is never identified.
Pneumonitis causes may include:
Drugs. A variety of drugs can cause pneumonitis, including some antibiotics, several types of chemotherapy drugs and medications that keep your heartbeat regular. An overdose of aspirin can cause pneumonitis.
Molds and bacteria. Repeated exposure to some molds and bacteria can cause the lungs to become inflamed. Specific varieties of mold-related pneumonitis have received nicknames, such as "farmer's lung" or "hot tub lung."
Birds. Exposure to feathers or bird excrement is a common cause of pneumonitis.
Radiation treatments. Some people who undergo radiation therapy to the chest, such as for breast or lung cancer, may develop pneumonitis. Pneumonitis also can occur after whole-body radiation therapy, which is needed to prepare a person for a bone marrow transplant.
Risk factors
Occupations or hobbies
Some occupations and hobbies carry higher risks of pneumonitis, including:
Farming. Many types of farming operations expose workers to aerosolized mists and pesticides. Inhaling airborne particles from moldy hay is one of the most common causes of occupational pneumonitis. Mold particles also can be inhaled during harvests of grain and hay.
Bird handling. Poultry workers and people who breed or keep pigeons are often exposed to droppings, feathers and other materials that can cause pneumonitis.
Hot tubs and humidifiers. Moldy conditions in hot tubs can trigger pneumonitis because the bubbling action makes a mist that can be inhaled. Home humidifiers are another common reservoir for mold.
Cancer treatment
Some chemotherapy drugs can cause pneumonitis, as can radiation therapy to the lungs. The combination of the two increases the risk of irreversible lung disease.
Complications
Pneumonitis that goes unnoticed or untreated can cause irreversible lung damage.
In normal lungs, the air sacs stretch and relax with each breath. Chronic inflammation of the thin tissue lining each air sac causes scarring and makes the sacs less flexible. They become stiff like a dried sponge. This is called pulmonary fibrosis. In severe cases, pulmonary fibrosis can cause right heart failure, respiratory failure and death.
Great info, thanks for the update. So the BAT period re-sensitized PCa to ADT it seems. So you dipped your toes in castrate-resistance and went back. Nice.
I'm not familiar with details of JH BAT protocol yet. Help me understand please: do you stay on Lupron through the T injection cycle? That's what I think logically makes sense: rather than letting your body to restore and make T, you control the amount and timing so if required to terminate the T would drop fast.
Hi bigdon, thanks for your report. I am 16 years after diagnosis. I recently did something similar. When primary ADT(1) failed my oncologist put me on bicalutamide which failed after a year or so. Then I stopped the bicalutamide, waited a month to let it wash through then went on BAT (see my description at DIY BAT). Then I did a shot of testosterone cypionate (400 mg) each month while staying on primary ADT1. Then I stopped when PSA started to rise again (after about 8 months), then rechallenged with bicalutamide. PSA halved in first month, which is where I am at now. Its interesting that for us BAT seems to reverse resistance to bicalutamide which has not really been yet tested in trials. Most trials so far deal with enzalutamide resistance. Enzalutamide is a more powerful androgen blocker but is still under patent - very costly. And some side effects. Bicalutamide is old and cheap and better tolerated - the longer you can stay on it the better, I think. Like you I am inclined to try it all again once the bicalutamide fails this second time. While we are one-offs, anecdotal cases, I think it shows that for us at least that BAT may be a useful management tool to extend the effectiveness of the secondary androgen blockers like bicalutamide (and enzalutamide too I think)
Pardon my ignorance but with the recent flurry of interest in off label use, it is reported that drugs like Niclosamide could be used to ressensetize PCa cells to bicalutamide when resistance has set in due to ARV7 etc mutations. In the light of such findings can some of our members who are well informed enlighten us if those who have stopped Bicalutamide due to resistance could now go back to it with Niclosamide. Am also wondering as to what would be the difference in sensitization and knock down of resistance between Niclosamide use and BAT as they both seem to have the same end point ie keep Bicalutamide working as long as possible.
UCDavis is enthusiastic and is pursuing expanded trials. However, a group of investigators at University of Washington Seattle found that they could not get plasma levels high enough to be effective without incurring dose-limiting toxicity:
I have no opinion - these were both very small studies. But, considering the potential toxicity, I'd recommend that if this is something you wish to pursue, you do it as part of the UC Davis clinical trial.
On second thought I remember Gus did post about taking Indomethacin 50mg while on Enzalutamide, which according to him was about the only thing that dropped his PSA. Since Enzo and Bicalutamide are similar and work the same way do you reckon we could use Ino to knock down Bicalutamide or even Zytiga resistance? Has anyone looked at this?
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6 months after MRI Guided SBRT at MSK
Castration resistant after 20 months on ADT
E2 skyrockets on BAT therapy
Now Undetectable PSA on BAT Regimen
