Managing Prostate Cancer Admissions: Educational Series by Houssein Safa

Houssein Safa, Heme/Onc fellow at BCM Houston, shared a post on X:

“Oncology for The Non-Oncologist

(A practical educational series for internal medicine trainees and physicians).

Episode 10: Prostate cancer is very common.. here’s what to do if they get admitted?

Disclaimer: This thread is for educational purposes only and is not medical advice. Always consult hematology and medical oncology or appropriate specialists for patient-specific decisions.

Let’s start with a case

72M with metastatic prostate cancer, dx 1y ago, on leuprolide+abiraterone+prednisone w/ regular follow-ups in clinic. In the ED for pneumonia, missed all his home meds. You admit him to medicine and he’s now stable, labs normal.

What’s your next move?

• Stop Abiraterone/pred
• Send PSA Asap
• Give leuprolide inpatient
• Resume Abi/pred

Prostate cancer is one of the most common cancer in men. Odds are, you’ll admit a patient with it maybe for the cancer itself, maybe for something totally unrelated. Either way, you’ll need a game plan. Let’s talk about what to do on the wards.

Prostate Cancer 101

So what is prostate cancer, and why is it so different?

Is this an inherited disease?

•  Most cases are sporadic (pop up without a clear inherited mutation). But family history does raise risk, and mutations like BRCA2 or DNA repair genes can tip the balance toward developing disease.

What kind of cancer are we talking about?

•  Almost always it’s an adenocarcinoma, cancer starting in the gland cells of the prostate (the ones that make seminal fluid).
•  Very rarely, prostate cancer can transform into small cell carcinoma, an aggressive form that’s treated totally differently.

So what’s the story with testosterone and prostate cancer?

• Prostate cells are wired to listen to testosterone. Normally, testosterone tells them when to grow. Cancer hijacks that system, testosterone becomes jet fuel for the tumor.
• That’s why cutting off or blocking testosterone (androgen deprivation therapy) is a cornerstone of treatment.

So why do people say prostate cancer ‘isn’t that serious’?

•  Because compared to many cancers, prostate cancer often grows slowly. Many men live for years to decades with it, and modern treatments can keep it under control.
•  But ‘slow-growing’ ≠ harmless. Aggressive subtypes can still be lethal, which is why recognizing and treating it matters.

Put simply: prostate cancer usually starts in the gland, feeds on testosterone, is often slow-growing, but when it turns aggressive, it can be just as deadly as any other cancer.

What’s the deal with PSA? Why do we talk about it so much?

• PSA = Prostate-Specific Antigen. It’s a protein made by prostate cells (both normal and cancerous) that leaks into the blood.
• In healthy men, PSA is low. In prostate cancer, it often climbs; so a high PSA can be a red flag that something’s wrong.

Why is it such a big deal?

•  Because it’s the main blood test we use to detect, monitor, and follow prostate cancer.
• Think of PSA as a ‘smoke alarm’, not perfect, but it tells you when you might need to check the house.

However, PSA is not specific for cancer.

•  It can rise with benign prostate enlargement (BPH), infections (prostatitis), or even after a bike ride or recent ejaculation.
•  That’s why PSA can lead to false alarms → unnecessary biopsies, anxiety, and overtreatment.

So what about PSA screening?

•  This is where things get controversial.
•  Pro: Screening can catch prostate cancer early when it’s curable.
•  Con: It can also over-diagnose indolent cancers that never would’ve caused harm.
•  Guidelines now say: use shared decision-making. But what does that mean? Basically, there are nuances in who should and shouldn’t be screened. It’s still a gray area, your primary care or urologist can guide you based on age, family history, race, prior biopsy results, and overall health.

Once prostate cancer is diagnosed though, PSA becomes very reliable.

• In clinic, PSA is our compass. If it’s going down on treatment, we know the disease is responding.
•  That’s why most men on therapy don’t need routine short-term imaging if PSA is steadily declining; the lab is enough to follow the cancer.

How does prostate cancer actually show up in real life?

Three common scenarios:

1.  Completely silent.
   Many men feel totally fine. A routine screening PSA test comes back high → triggers more workup (MRI of the prostate → biopsy) → and that’s how the cancer is caught.
2.  Subtle clinic symptoms.
   Some may develop urinary issues (slower stream, getting up at night to pee, urgency, hesitancy). Others notice blood in urine or semen. These aren’t unique to cancer (BPH and infections do this too), but they can be a clue.
3.  Hospital presentation: metastatic disease.
   Sometimes the first time prostate cancer is found is when it’s already spread We call this (De novo metastatic).

Common ways this shows up:

• Severe back pain from bone mets or pathologic fractures
• Spinal cord compression with weakness/numbness
• Weight loss, fatigue, or anemia from advanced disease
• Widespread bone lesions seen ‘incidentally’ on imaging

Bottom line: prostate cancer can creep in silently, show up with vague urinary complaints, or crash the party with dramatic metastatic complications. That’s why context (age, PSA, imaging) is key.

One last “boring” post before we move into the practical side of internal medicine…

People often ask:

If MRIs are so good at spotting tumors, why do we still stick needles into the prostate for a 12-core biopsy? And why don’t we do this in other cancers?

Here’s why: prostate cancer is patchy. It doesn’t usually grow as one big, obvious lump you can always see on MRI. Instead, it can pop up in scattered little areas. That’s why we divide the prostate into 12 zones and sample each one, like cutting a pizza into slices to make sure nothing is missed. And 12 is just the minimum; in practice, pathologists often ask for even more cores if the gland looks suspicious.

If you’ve ever looked at a prostate biopsy report, you’ll see something called the Gleason score. So what is that?
When the pathologist reviews the biopsy, they’re grading how ‘organized’ the cells look compared to normal prostate tissue. And they use this scoring scale:

•  1 = almost normal
•  2–3 = still somewhat organized
•  4 = disorganized, abnormal
•  5 = totally chaotic, aggressive

They look at the most common pattern (say, grade 3) and the second most common pattern on the same slide (say, grade 4), then add them together. That’s your Gleason score: 3 + 4 = 7. They do this for every one of the 12 cores.

•  The higher the score, the more aggressive the disease.
•  That number is one of the main guides for deciding between active surveillance and aggressive treatment.

Alright, enough theory; let’s move to real life on the wards.

This thread will zoom in on two scenarios you’re guaranteed to see on the inpatient side:

1.  A patient presenting with newly diagnosed metastatic prostate cancer.
2.  A patient with known prostate cancer, already on treatment, who’s admitted for something else (UTI, pneumonia, diabetes, etc.).

We’ll focus on the cancer side of management in these situations: what to continue, what to hold, and what to keep in mind while medicine takes care of the acute admission.

Scenario 1: De novo metastatic prostate cancer

When prostate cancer first shows up in the hospital, it’s usually not because someone ‘felt a lump’.

It’s the complications that bring them in:

• Spinal cord compression → severe back pain, weakness, numbness, sometimes incontinence. A true red flag.
• Obstructive uropathy / hydronephrosis → rising creatinine, decreased urine output, flank pain.
• Bone pain or fractures → skeleton is the favorite landing spot for prostate mets, so patients may show up with new hip, spine, or rib pain.
• Constitutional symptoms → weight loss, fatigue, loss of appetite.
• Bone marrow involvement → cytopenias (low counts), sometimes pancytopenia with fatigue, infections, or bleeding.
• Lymph node disease → pelvic/retroperitoneal nodes causing leg swelling or pelvic discomfort.
• Hematuria (less common) → blood in urine, especially when the primary tumor itself grows locally.

Bottom line: these patients often don’t walk in saying ‘I think I have prostate cancer’. They walk in with the fallout of advanced disease.

So what happens next when someone shows up with these presentations?

The workup usually starts as follows:

• CBC (blood counts)
• CMP (metabolic panel) + LFTs (part of CMP)
• Coags (clotting studies)

But the real star here is imaging.

A CT chest/abdomen/pelvis +\- spine imaging if cord compression is a concern. What you might see: enlarged prostate, pelvic lymph nodes, hydronephrosis from obstruction, or classic sclerotic bone lesions that scream prostate cancer.

If imaging raises suspicion → add on a PSA (prostate-specific antigen) to your labs. Elevated PSA in this context can really point you toward the diagnosis.

Ultimately, diagnosis requires a biopsy. That’s what seals the deal.

Don’t forget: not every lytic or sclerotic lesion = prostate cancer. Always keep a broad differential. Depending on the case, you may need other tumor markers (like SPEP/UPEP for myeloma, or AFP/β-HCG for germ cell tumors) – refer to my prior thread in the link below.

By this point, heme/onc will usually be looped in and steer the ship. But here, we’re focusing on how to think about it when prostate cancer is on the table.

Where do you actually biopsy when you suspect metastatic prostate cancer?

General oncology rule: go for the easiest, safest, distant and most informative site.

• Soft tissue (like lymph nodes, liver, lung lesions) is ideal → better yield l, will prove metastasis AND you can send tissue for next-generation sequencing (NGS) or molecular testing. DO NOT BIOPSY THE PROSTATE IF YOU HAVE ACCESIBLE METASTATIC SITES.
• Bone lesions are classic in prostate cancer but not the best for molecular testing. They can still give you a diagnosis, but the tissue is harder to process and often less informative.
• If bone is the only site of mets → try biopsying the prostate, if the latter is not possible get bone, it’s still better than nothing.

What about PSA?

• A sky-high PSA (think 80, 200, even 1000+) makes prostate cancer extremely likely.
•  But PSA alone is never enough for a final diagnosis. You always need tissue confirmation before moving forward with long-term treatment decisions.

So bottom line: PSA + imaging raises your suspicion, but biopsy is what locks in the diagnosis and sets the stage for treatment planning.

The biopsy comes back: adenocarcinoma of the prostate (the classic histology). b is sky-high. Now it’s official: prostate cancer.

So what do we actually do for treatment?

The backbone of therapy in metastatic prostate cancer is cutting off testosterone: the fuel that drives the disease. This is called androgen deprivation therapy (ADT).

But here’s the thing: ADT alone is no longer enough in most cases. Over the last decade, the standard has shifted. We now combine ADT with other agents (like abiraterone, enzalutamide, apalutamide) or even chemo in selected patients to get deeper, faster responses.

Let’s dissect this treatment strategy even more:

Step 1: Androgen Deprivation Therapy (ADT)

Androgen Deprivation Therapy (ADT)
This is the backbone of treatment for metastatic prostate cancer. The idea is simple: starve the cancer of testosterone.

• Normally, the hypothalamus releases GnRH → tells the pituitary to release LH/FSH → testes make testosterone.
• ADT drugs (like leuprolide, goserelin, degarelix, relugolix) either shut down the GnRH signal (antagonists) or flood the receptor until it shuts off (agonists).
• End result: the testes stop making testosterone, dropping levels to “castrate” range (<50 ng/dL, often much lower).
• Think of it as “turning off the factory” where most testosterone is made.

Step 2: Abiraterone (+ prednisone)

• Even after ADT, testosterone is still made in other “side factories” (such as adrenal glands, even the tumor itself).
• Abiraterone blocks CYP17A1, a key enzyme in that pathway → cutting off testosterone production everywhere.

What about the prednisone then? 

CYP17A1 has two main activities in the adrenals:

•  17α-hydroxylase → makes cortisol precursors
•  17,20-lyase → makes androgen precursors

What abiraterone does.
It blocks both of those activities, but the clinical effect is much more noticeable on the androgen side (testosterone/DHT) that’s why we use it.

But cortisol isn’t spared.
Cortisol synthesis also gets reduced → the pituitary senses “low cortisol” and ramps up ACTH → that ACTH drive then pushes more precursors into the mineralocorticoid pathway → the side effects we talked about (HTN, hypokalemia, edema).

That’s why prednisone is paired with abiraterone:

• It replaces the small cortisol drop
• It quiets down ACTH stimulation
• It indirectly reduces the mineralocorticoid “overflow.”

So to answer directly:

Abiraterone does hit the cortisol pathway: but the main therapeutic target is androgen suppression, and the steroid replacement with prednisone smooths out the cortisol/mineralocorticoid imbalance to mitigate the side effects

Step 3: Androgen Receptor Blocker (the ‘-lutamides’)

•  Even tiny bits of testosterone can still signal growth through the androgen receptor on the cancer cell.
•  Enzalutamide, apalutamide, darolutamide → lock the androgen receptor so testosterone can’t ‘dock’ and give its growth signal.
• No prednisone needed.

Put together:

• ADT (injection)= shut down the main factory.
• Abiraterone + prednisone (both oral)= block the side factories and prevent hormone imbalances.
• Lutamides (oral)= jam the lock on the receptor itself.

This layered approach is why modern regimens often combine ADT + abiraterone OR a lutamide, to choke off androgen signaling at multiple points.

So you will hear oncology often say patient is on ADT/Abi/Pred, or ADT with a blocker

‘So wait… what’s the deal with bicalutamide? I’ve seen it used in these patients with a new diagnosis’

Here’s the story:

• Bicalutamide (Casodex) is one of the earliest androgen receptor blockers.
•  Think of it as a ‘plug’ that sits on the androgen receptor so testosterone can’t turn it on.

Why isn’t it the go-to anymore?

• It’s not as strong as the newer drugs (enzalutamide, apalutamide, darolutamide).
•  By itself, it doesn’t control disease nearly as well.
•  That’s why we rarely use it as chronic therapy today.

So why do you still see it?

• When a patient starts on a GnRH agonist (like leuprolide/Lupron), the pituitary initially surges LH → testosterone shoots UP before crashing down.
• This ‘testosterone flare’ lasts a week or two.
• In a patient with bone mets, that surge can make pain worse, or in bad cases, trigger cord compression or urinary obstruction.

Bicalutamide is given as a safety net: started a few days before the Lupron shot and continued for ~2 weeks. It blocks the receptor on the cancer cell during the flare until testosterone levels drop.

After that? It’s usually stopped, and replaced with abiraterone or the modern ‘-lutamides’ (enzalutamide, apalutamide, darolutamide) are the real long-term players.

Quick note: The only time you don’t need bicalutamide is if the patient is getting a GnRH antagonist (like degarelix or relugolix).

Why? Because antagonists block the GnRH receptor directly → no testosterone surge, so no need for the ‘flare protection’ that bicalutamide provides.

‘So what does this all mean in real life when a patient rolls into the hospital with new metastatic prostate cancer?’

Here’s the workflow you’ll usually see:

• Inpatient: oncology often starts bicalutamide (Casodex) right away. This blocks the receptor and protects against the testosterone ‘flare’.
• Outpatient: the patient will get scheduled for an ADT injection (like leuprolide/Lupron) in clinic, usually 2–3 weeks after starting bicalutamide.
• About a month later: bucalutamide is replaced with abiraterone + prednisone or one of the modern ‘-lutamides’ (enzalutamide, apalutamide, darolutamide).

What about chemo?

• Chemo (like docetaxel) can be layered in for very high-volume or aggressive disease.
• But this almost never happens while the patient is admitted. It’s typically planned weeks later in the outpatient setting once hormonal therapy is underway.

Other caveats:

Patients with severely symptomatic disease (e.g., spinal cord compression, painful bone mets, bladder obstruction) may need urgent palliative radiation or surgery long before chemo is even considered.

Refer to my thread on cord compression for a detailed walkthrough on management, link.

There’s one rare but critical scenario you need to know.

A patient with prostate cancer on treatment gets admitted. Suddenly there’s concern for progression either new symptoms (bone pain, weight loss, neuro changes) or clear progression on imaging. Naturally, you send a PSA.

But here’s the curveball: the PSA comes back stable or very low.

That’s when you should always think about small cell transformation. What does that mean? Essentially, the prostate cancer has transformed into a totally different cancer type small cell carcinoma. Unlike the usual adenocarcinoma, small cell tumors behave like small cell lung cancer: aggressive, fast-growing, and they don’t secrete PSA.

What to do:
This is an oncologic emergency. Hormone therapy won’t work. These patients need urgent chemotherapy (platinum-based, e.g. cisplatin/etoposide), guided by oncology.

Bottom line: PSA flat + clear progression = suspect small cell transformation. Don’t miss it.

HOWEVER: not every patient who progresses on hormonal therapy has transformed into small cell. Most will still have adenocarcinoma that’s just outsmarted the drugs.

Those patients are managed with other treatment options (second-line ARPIs, chemotherapy, radioligand therapy, clinical trials, etc.) all important, but beyond the scope of this thread. I’ll save that for another day.

Done with scenario 1.

Let’s talk Scenario 2: Patients with known stable prostate cancer gets admitted for something unrelated (e.g. Pneumonia, UTI, CHF…)

‘What do I do with abiraterone + prednisone when they get admitted?’

So what do you do with a patient on abiraterone + prednisone (or another ARPI) when they land on your medicine service?

General rule:

•  Don’t auto-stop. Most of the time these meds are safe to continue.
•  But keep an eye on the big 3: liver, kidney, heart.
•  And remember: prednisone is usually given at low doses (5 mg once or twice daily). Even though the dose is small, you can’t stop it cold because abiraterone shuts down cortisol production.

Liver dysfunction:

• Abiraterone can cause hepatotoxicity.
• If CMP shows LFT elevation that is anticipated to worsen → hold.
• Otherwise, you can usually restart at lower dose once labs normalize.

Renal dysfunction:

• Not directly nephrotoxic.
• But hypokalemia + fluid retention can drive AKI.
• If severe AKI + electrolytes out of whack → hold until corrected.

Cardiac dysfunction:

• Watch out in decompensated CHF, uncontrolled HTN, or arrhythmias.
• Hold during acute instability.

Critical illness / NPO / septic shock:

• Abiraterone can be held, but prednisone (or equivalent) must be continued.
• If NPO → switch to IV hydrocortisone.
• If critically ill → give stress-dose hydrocortisone (50–100 mg IV q6–8h).

Diabetes:

• Abiraterone can worsen hypokalemia + fluid retention.
• Prednisone, even at low doses, can worsen hyperglycemia.
• If patient comes in with DKA or uncontrolled sugars → continue steroid coverage, but loop in endocrine/oncology to adjust regimen.
• Sometimes you’ll hold abiraterone until sugars are controlled, but you never cut the steroid without a replacement plan.

Drug interactions:

• Abiraterone: CYP3A4/2D6/2C8 substrate.
• Always review med list.

Bottom line:

• Continue unless there’s a clear contraindication.
• If you hold abiraterone → Continue steroids.
• Watch the liver, kidneys, heart, and sugars.
• Always run the plan by oncology.

What to do with enzalutamide, apalutamide, or darolutamide when your patient gets admitted?

These are the -lutamides, androgen receptor pathway inhibitors (ARPIs).

General rule:

•  If the patient is stable and can take pills → keep going.
•  If they’re critically ill, NPO, or you’re worried about safety → it’s okay to hold and restart later.

When you might hold:

• Liver failure: all are metabolized in the liver. If LFTs are crashing, press pause.
• Cardiac trouble: uncontrolled HTN, acute CHF, arrhythmia → ARPIs can make things worse.
• Neurologic issues: enzalutamide and apalutamide lower seizure threshold. If a patient has new seizures, acute delirium, or is falling left and right → stop until stable.
• Drug interactions: enzalutamide and apalutamide are CYP inducers. They mess with warfarin, DOACs, anticonvulsants, psych meds. If a critical drug is involved, better to hold.
• Darolutamide is the ‘kinder cousin’: fewer CNS effects, fewer drug interactions.

Hospital basics:

• No steroid coverage needed (unlike abiraterone).
• If the patient’s NPO → just hold. Restart when oral meds are back.
• Always loop in oncology before making the call.

Bottom line:

• If stable → continue.
• If unstable (liver, heart, brain, drug interactions) → hold.
• Restart once things settle.

‘So what if my patient is on outpatient ADT? Should I worry about that while they’re admitted?’

Not really. ADT (GnRH agonists like leuprolide or antagonists like degarelix/relugolix) are depot injections usually given every 1, 3, or 6 months.

• If they’re not due during admission → nothing to do.
• If they are due, and the drug is available + covered → give it inpatient.
• If not available → it’s fine to delay a few days or weeks and let oncology give it outpatient.

You don’t need to scramble. Just check when the last shot was given, document it, and loop in oncology so the schedule stays on track.

‘Should I send a PSA while the patient is admitted?’

It depends.

• If your patient with know prostate cancer has been lost to follow-up and hasn’t had a PSA checked in >6 months in clinic, and you’re worried about progression as the cause of admission(new bone pain, weight loss, otherwise unexplained anemia), then yes, a PSA can help frame the picture.
• But remember: not all PSA bumps = cancer progression. UTIs, prostatitis, recent catheterization… all can falsely elevate PSA. Always check the clinical context before overinterpreting the number.
• If there’s no concern for progression and the patient is plugged in with oncology, there’s no rush. The inpatient setting is not the place to trend PSA just for the sake of it.
• Most importantly, if the patient has been out of follow-up, make sure oncology is looped in during the admission so they can help re-establish continuity in clinic.

‘What if my patient had prostate cancer years ago, got definitive treatment (surgery or radiation), and has been in remission, should I check a PSA while he’s admitted for something unrelated?’

Usually no.

•  If they’re actively followed in clinic and up to date with PSA, you don’t need to re-check it in the hospital.
•  PSA in remission is a long-term surveillance tool, not an acute inpatient test.

When might you consider it?

• If they’ve been lost to follow-up for years and you have new red flags (bone pain, weight loss, anemia, hematuria) → a PSA could be reasonable as part of a workup for recurrence.
• Even then, the more important step is to loop in oncology/urology for outpatient surveillance or re-staging.

Bottom line:

In the inpatient setting, PSA is almost never urgent. For patients in remission, the hospital is not the place to restart surveillance unless there are new, unexplained concerning symptoms and no recent oncology follow-up.

I’m pretty sure you’ve heard oncologists throw around the terms castrate-sensitive and castrate-resistant prostate cancer.

Let’s demystify this and cut through the confusion.

Remember when we said testosterone fuels prostate cancer? When we use the word castrate, we mean driving testosterone levels below 50 ng/dL.

In clinic, we track two values:

• Testosterone (to confirm the fuel is gone)
• PSA (to check how the cancer is reacting)

1. Castrate-sensitive (CSPC):

• Testosterone <50
• PSA is falling
• The cancer is still obeying the “fuel rules” you cut testosterone, the cancer slows down

2. Castrate-resistant (CRPC):

Remember, cancer is a smart disease. With time it always finds a way to become resistant.

• Sometimes the androgen receptor mutates, so it ignores the blockade.
• Sometimes it gets overexpressed, making the cell hypersensitive to even tiny hormone levels.
• Some tumors even make their own testosterone inside the cell.
• Others activate completely different pathways to survive.

In these cancers:

Despite Testosterone <50, PSA is rising or scans show progressio

To wrap this up:

Prostate cancer is, for the most part, a slow-growing disease. That’s why on the wards you’ll meet so many patients with a history of prostate cancer who were treated years even decades ago and are still doing well. I’ve seen patients treated back in the 1990s who remain in remission today.

In the modern era, with hormonal therapy, newer agents, and close follow-up, many patients live long, good-quality lives. You’ll admit them for pneumonia, UTI, or diabetes and prostate cancer is just a line in their PMH.

But not every case is indolent. Some patients, especially with advanced or transformed disease, can present with aggressive complications. That’s where your vigilance matters.

So bottom line:

• Most prostate cancer patients live long and well.
• Some need you to be sharp for aggressive presentations.
• And that balance is what makes understanding this disease so important on the wards.

And that’s a wrap, folks! That’s it for today.

If you’ve been following along, I’m hoping to grow this series into a go-to resource for hospital-based docs navigating hematology oncology cases.

Open to suggestions or feedback.

If you like this format, like, repost, and share the love.”

More posts featuring Houssein Safa on OncoDaily.