Monitoring Stage IV

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StDrogo
Posts: 25
Joined: Thu Jun 08, 2017 7:54 pm

Monitoring Stage IV

Postby StDrogo » Tue Mar 06, 2018 9:26 pm

First off, my wife's recovery from her CRS/HIPEC in December continues to go remarkably smoothly; her fitness level is nearly back to the level it was at a couple of years ago before any of this cancer rubbish began—and her menstrual cycle has returned and is apparently regular, which she's pretty pleased about after over a year of amenorrhea and subsequently chemical menopause (from GnRH agonists). We met with her oncologist a few weeks ago, who was incredibly upbeat about her prognosis. He informed us then that he no longer saw any reason for us to see him, so my wife's continuing treatment would be referred back to the colorectal clinic. We just met with the colorectal doctor who performed my wife's colonoscopy a couple of weeks ago (which was completely normal). Said doc was similarly upbeat and has endorsed a rather unaggressive follow-up plan: quarterly CEA (the last from a couple of weeks ago was still well below 1, which is where it has been at since my wife's resection last April) and annual CT scans (the next is scheduled for May, six months after her previous unremarkable scan end of November) for the next couple of years. I surmise from this ostensibly lax monitoring plan (it seems pretty similar to the one routinely recommended for stage II/IIIa colon cancer patients) that the MDT considers my wife at a low risk for recurrence. While this is a heartening development (since last year most on the MDT considered my wife's prognosis exceptionally dismal) and we are eager to avoid as many mock executions—ahem, scans—as possible, I am having a hard time finding enough statistical or even anecdotal data of comparable cases with known outcomes to justify this approach. Besides Skifletch, has anyone on this board undergone prophylactic HIPEC (particularly after a delay of greater than six months from resection of the primary)? If so, how were you monitored for recurrence?
Wife Age 33
02/17 dx Ovarian mass, ascites, pleural effusions
03/17 Resection of 16 x 20 cm ovarian mass; CEA = 10, CA125 = 180, CA19-9 = 36
04/17 Emergency surgery, diastatic perforation, purulent peritonitis, extended right hemicolectomy, well-differentiated adenocarcinoma in splenic flexure, 1/16 lymph
11/17 CT = NED, CEA < 1
12/17 CRS (peritoneal nodules of foreign body giant cell reaction, no evidence of malignancy; liver resection—1 cm FBGCR and .5 cm focal nodular hyperplasia), HIPEC

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Robino1
Posts: 463
Joined: Fri Aug 11, 2017 12:09 pm
Facebook Username: Robin.lawthers
Location: Florida

Re: Monitoring Stage IV

Postby Robino1 » Wed Mar 07, 2018 9:54 am

Following this thread since I'm currently considering HIPEC. I do hope you continue posting on your wife's progress. I find very few success stories with the HIPEC procedure.
At 54 2014 1st colonoscopy colon cancer detect
Colon resect margins clear. No chemo Stage II
2017
Distend abd, pain in intestines.
CT scan seeding & Ascites
Lap diag - cancer on the omentum
CEA 217; 219
FOLFOX started 6/17
CEA 202
8/29/17 CT melting of tumor.
Latest CT scan shows 2 new tumors and return of ascites.
CEA: (2017)9/30 -109; 10/12 -99.1; 11/4 -90.7; 11/30 -70.7; 12/14 -83.4; (2018)1/4 -73.3; 2/1-84.2; 89.2; 89.8; 88.5; 81.8: 93.5; 107; 119
BRAF V600e

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betsydoglover
Posts: 978
Joined: Mon Aug 14, 2006 2:31 pm
Facebook Username: Betsy Lindh Williams
Location: Maryland - outside DC

Re: Monitoring Stage IV

Postby betsydoglover » Wed Mar 07, 2018 11:26 am

Personally, I would like (and have) a much more proactive follow up plan. I don't want to scare you, but HIPEC is often not successful in the long term. I really question your oncologist's recommendation. A year between scans is pretty long for someone who is in the early stages of being Stage 4.

Take care,
Betsy
diag. Stage IV, 5/05, liver met
lap sigmoid colectomy, 6/05
6 cycles Xeloda/oxaliplatin/Avastin (NED after 2)
11/08 9x13mm right lower lobe lung nodule; removed via VATS 4/09
NED
6 cycles Xeloda + Avastin
Avastin only 10/09-5/11
Still NED 06/18

rp1954
Posts: 1540
Joined: Mon Jun 13, 2011 1:13 am

Re: Monitoring Stage IV

Postby rp1954 » Wed Mar 07, 2018 4:30 pm

I'm very critical of most "standard" cancer monitoring regimes. I've lost personal friends whose standard monitoring programs were patently defective in retrospect, whose recurrence (not CRC) would have been easily detected much sooner if they had done better, more frequent blood tests after nominally curative treatments. I'm 100% sure we would be long done if we had just followed NCCN/ASCO recs too.

Our experience is that intensive blood monitoring is more sensitive to some growth or changes, at near zero cancer activity following a curative surgery. With low residual cancer mass(es) on metronomic treatment fully suppressing cancer activity, clear changes in terms of standard deviations from baseline were in detailed blood tests first, for us. Our experience was that the scans more picked up stuff disappearing later that wasn't supposed to....

After curative treatment, you have some non-standard options: (1) intensify the blood tests for common labs, more labs/more frequently; (2) attack more indirect markers of cancer environment and precursors like cytokine panels with possibly preventive, off label chemistry; and (3) "liquid biopsies" for cancer activity. With a budget, #1 has worked well for us. Your CEA, CA199 and CA125 look like potentially viable markers for a good measurement series (btw great first post, I missed it earlier. More posts mean more eyes on and wider world views).

The real issues are buffering patients from worries with excessive uncertainty of more frequent tests, and having an actual, viable biochemical tx plan for unclear or non-imaged progression and earlier treatment. Handled well, having frequent blood tests at the outset is actually one way to reduce alarm, and to gain more confidence later even if things initially go south.
watchful, active researcher and caregiver for stage IVb/c CC. surgeries 4/10 sigmoid etc & 5/11 para-aortic LN cluster; 8 yrs immuno-Chemo for mCRC; now no chemo
most of 2010 Life Extension recommendations and possibilities + more, some (much) higher, peaking ~2011-12, taper to almost nothing mid 2018, mostly IV C

StDrogo
Posts: 25
Joined: Thu Jun 08, 2017 7:54 pm

Re: Monitoring Stage IV

Postby StDrogo » Wed Mar 07, 2018 10:07 pm

Thank you for all for your responses. You're certainly not bursting my bubble, Betsy; I think I've read nearly all the published French, Italian, and English literature on treating peritoneal disease in the context of colorectal cancer. (I only felt comfortable playing Pollyanna when no one else would.) That said, I am curious about the scientific rationale for the oncologists' and surgeons' newfound optimism. Throughout this ordeal, I have unfortunately had a very hard time finding any comparable presentations to my wife. On this board, for example, I can't even find a single case of massive ascites that wasn't caused by either extensive carcinomatosis or liver failure. (Nicopia's is probably the closest case to my wife's, although her met was metachronous, followed by Skifletch and rheaeliza, although her cancer's spread was much more extensive and cytoreduction more extreme; alan b's case has similarities, but the signet cell ring histology makes comparison difficult.) The only substantial literature reviews of pseudo-Meigs' syndrome in colorectal cancer I've found are the following: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5109729 and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5061673. (I have a hard time even finding solidly documented case reports of CRC patients diagnosed with isolated ovarian metastases.) Remarkably, among the vanishingly few reported cases of pseudo-Meigs', a majority of those with long follow-ups (i.e., a handful, which obviously isn't much to go on) remained alive without disease. (Maybe that means there's something unique about the biological and pathophysiological features of cancers that provoke this rare syndrome . . .)

The real question is, Where is my wife likely to recur and will conventional imaging modalities be able to detect a recurrence in a therapeutically timely fashion? Before my wife's exploratory laparotomy and HIPEC in December, I conjectured that her remaining ovary and peritoneum were the most vulnerable potential sites of metastasis. My wife had a normal transvaginal ultrasound about a year before the 22 cm mass was discovered in her left ovary (which was a well-differentiated adenocarcinoma), so it stands to reason that metastasis occurred not long before her dx and grew prodigiously in a short span of time and therefore the ovary represents a preferential site of metastasis in her disease. As her right ovary appeared normal at second-look laparotomy over eight months after her previous operation, if the metastatic pathway to her left ovary was transcoelomic (which is likely since the primary was t4 and the spread was unilateral) rather than hematogenous, there should be a very high likelihood that her right ovary is not microscopically infested. What's more, while not discounting the possibility that pelvic/abdominal adhesions might have insulated the remaining ovary, the fact that her remaining ovary was not obviously infested may have further prognostic significance and serve as an indication that her abdominal/pelvic cavities are largely free from any residual cancer cells—and it's to be hoped that the HIPEC wash eliminated any remaining cells. Even still, if she were to recur in her right ovary, past experience suggests that CA-125 would be markedly elevated, so quarterly serum testing should be at least as effective as pelvic CTs.

Since my wife's PCI turned out to be 0 in her second-look laparotomy, I'm not especially concerned right now about the possibility of peritoneal mets. Preliminary results from trials on prophylactic HIPEC (as well as, I believe, Sugarbaker's anecdotal observations in Peritoneal Carcinomatosis: Principles of Management) indicate that patients who are macroscopically free of peritoneal surface malignancy at second-look laparotomies scheduled six months or more after primary intervention are very unlikely to subsequently develop carcinomatosis (see, e.g., https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5291843). At any rate, CT, PET, and MRI are astonishingly bad at identifying carcinomatosis while it is still surgically treatable, so I'm not convinced that more frequent scans would make a meaningful difference at the end of the day.

Then there's the possibility of liver mets, which is easily the most daunting. But there, too, my wife's case is a bit unusual. First, there has never been any indication of hepatic involvement (unlike, say, rheaeliza or perhaps even Skifletch, who reported that his surgeon discovered friable necrotic material on the dome of his liver). Second, my wife's HIPEC surgeon thoroughly palpated her liver (which can be more effective than radiology in identifying very small superficial lesions) and did discover what he thought was a lesion in her left lobe, so he ended up performing what turned out to be an unnecessary wedge resection, which afforded an opportunity for microscopic evaluation. Third, my wife's one possibly affected lymph node from her primary resection was infested through direct invasion. While the issue is somewhat contentious, there is a good case to be made that direct-invasion-only lymph node status is prognostically intermediate between N0 and N1 status. Last, assuming a clean scan in May, she will be 13.5 months NED. For the sake of assessing the probably of hepatic recurrence, since my wife only had an isolated intraperitoneal met, it makes most sense to compare her odds with stage IIIa patients. If memory serves (I'd have to go through my files to find the precise studies), at least 40 percent of recurrences (at any location) for colon cancer (not rectal cancer) occur within a year. Since only around 15 percent of stage IIIa patients with my wife's tumor histology and the like (although obviously without the ovarian met) will ever develop hepatic metastases, my wife's odds of belonging to the cohort of patients who will never develop hepatic metastases is still somewhat better than even when one widens the confidence interval to account for the admittedly prejudicially skewed data. It's conceivable that this consideration combined with the aforementioned other factors is enough to substantiate the opinion that my wife's probable oncological outcome is at least as good as a stage IIIa patient and justify treating/monitoring her accordingly.

Last, there's a possibility of lung mets, but I think that's fairly remote with my wife's primary location and nodal status. Are six-monthly chest CTs appreciably better at detecting lung mets in a therapeutically timely manner than annual CTs and quarterly serum panels? If my wife were to get a lung met, since her primary was a well-differentiated adenocarcinoma, I would expect it to be pretty slow growing. It's hard to know for sure if CEA is a reliable marker for my wife (owing to the ascites/pleural at the time of her dx), but I tend to think it probably is since it isn't usually elevated with normal Meigs' syndrome, and her level promptly plummeted upon resection of the primary even though she remained septic and her inflammation markers were through the roof.

So, in conclusion, I suppose I'm coming around on this annual CT scan idea. I do like rp1954's idea of adding more indirect markers and have been prevailing upon my wife's doctor to add back in the CA19-9 test (which they don't want to do primarily because it's expensive and probably superfluous—the slightly elevated but still "normal" CA19-9 value at dx can easily be chalked up to peritoneal/pleural irritation); we have something like two dozen biochemical, cytokine, and endocrine panels (still haven't been able to work out why a colonic primary would significantly elevate her testosterone levels) from the months leading up to her diagnosis that were taken in the context of an infertility workup. We will probably be going back to the fertility doctor in the coming months, so it will be easy to add some complementary blood work.
Wife Age 33
02/17 dx Ovarian mass, ascites, pleural effusions
03/17 Resection of 16 x 20 cm ovarian mass; CEA = 10, CA125 = 180, CA19-9 = 36
04/17 Emergency surgery, diastatic perforation, purulent peritonitis, extended right hemicolectomy, well-differentiated adenocarcinoma in splenic flexure, 1/16 lymph
11/17 CT = NED, CEA < 1
12/17 CRS (peritoneal nodules of foreign body giant cell reaction, no evidence of malignancy; liver resection—1 cm FBGCR and .5 cm focal nodular hyperplasia), HIPEC

rp1954
Posts: 1540
Joined: Mon Jun 13, 2011 1:13 am

Re: Monitoring Stage IV

Postby rp1954 » Thu Mar 08, 2018 1:28 pm

Regular chemo and RFA certainly distort CA199 for a while during treatment and after, along with potential confounders or alternate sources of elevation. We had tight CA199 data with a standard deviation of approximately 1 unit in a year of data with daily immunochemo and IV C. More analysis is likely possible with mild treatments and a quality series of CA199 measurements with expanded blood chemistry, a "Chem30", than is commonly recognized. A good CA199 series can enable you to see met activity, and treatment effects not observed with CEA, at critical moments. About 8 years in, CA199 and AFP are active treatment markers, CEA has returned to baseline.

- One set of problems with CA199 concern single point data, timing, inappropriate cutoffs and interpretations for CRC already dx'd. This is a skill and information problem.
- Tissue staining is an important part of the opportunity with CA199. Matsumoto (2002) and related papers show that CA199 and some CD15s antibodies (e.g. CSLEX1) are unusually good companion markers, predictive for cimetidine use with oral 5FU. No gallbladder in the CRC met itself...
- Many of the CA199 interference can be indentified and monitored for invariance, background changes ameliorated, perhaps controlled, or maybe corrected by adjustment transform.
- Although multiple potential medical conditions can be involved, a critical area of CRC CA199 measurements and interpretation, is in the range 19 - 37 with potential overlaps. This yields partial or probabilistic information in a cumulative, total information approach. Ultralow readings (single point needed) and undistorted elevated readings can have particular information of use.
- An adequate data set can be analyzed or discarded, no data means no opportunities.

My thought for your wife is to establish a CA199 populated statistical baseline now, or even 1-2 post surgical values.
watchful, active researcher and caregiver for stage IVb/c CC. surgeries 4/10 sigmoid etc & 5/11 para-aortic LN cluster; 8 yrs immuno-Chemo for mCRC; now no chemo
most of 2010 Life Extension recommendations and possibilities + more, some (much) higher, peaking ~2011-12, taper to almost nothing mid 2018, mostly IV C

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Robino1
Posts: 463
Joined: Fri Aug 11, 2017 12:09 pm
Facebook Username: Robin.lawthers
Location: Florida

Re: Monitoring Stage IV

Postby Robino1 » Thu Mar 08, 2018 2:13 pm

What amount of cimetidine does your wife take? I just started with Tagamet and do one pill a day.
At 54 2014 1st colonoscopy colon cancer detect
Colon resect margins clear. No chemo Stage II
2017
Distend abd, pain in intestines.
CT scan seeding & Ascites
Lap diag - cancer on the omentum
CEA 217; 219
FOLFOX started 6/17
CEA 202
8/29/17 CT melting of tumor.
Latest CT scan shows 2 new tumors and return of ascites.
CEA: (2017)9/30 -109; 10/12 -99.1; 11/4 -90.7; 11/30 -70.7; 12/14 -83.4; (2018)1/4 -73.3; 2/1-84.2; 89.2; 89.8; 88.5; 81.8: 93.5; 107; 119
BRAF V600e


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