Category Archives: Making a Plan

by | October 16, 2017 · 11:51 am

Clinical Trial for NEWLY DIAGNOSED–Surgery Now or Later with an Immune Therapy Option

Kidney cancer patients are stunned by their diagnosis, anxious to make a treatment decision, and  simply not know what to expect.  If you are struggling with the issue of surgery to remove the tumor/kidney or to start with a med, you need to read this.  Deb Maskens, Kidney Cancer Patient and Patient Advocate, our guest writer is a valued member of our disease community and currently serves on the Renal Task Force for the National Cancer Institute.  A series of links below will also be helpful.  (My extra comments will be in italics, like this. )Welcome aboard, Deb! 

Clinical Trial Opportunity for Newly Diagnosed (Non Metastatic) Kidney Cancer

As a community of kidney cancer patients, we  hear from newly diagnosed patients  looking for treatment options. This is written for those patients, and for patient advocates who help patients navigate through their treatment decisions.

The challenge: this clinical trial is available at many locations across the U.S. and Canada, but patients must ask about it BEFORE they have a nephrectomy. Their own doctors may be unaware of the trial and how to work with the trial centres.  In many places, patients get booked for surgery prior to learning about this option.  That would be too late for a trial like this–it gives a drug therapy before the surgery for a brief period.  (In one of the t wo arms, there is medication before the surgery.)

Why Might Patients Consider this Trial?

For years, the standard of care for early stage kidney cancer has been to remove the tumour surgically, sometimes with the entire kidney–either a partial or full nephrectomy. That was the end of treatment and the beginning of surveillance to watch for any signs of recurrence.  (And early stage tumors can be quite large–up to 7cm or about 2 3/4″.)

Now we hope to prevent a recurrence of disease. Since advanced or metastatic kidney cancer is still incurable for the vast majority of patients, this is a worthy goal. With preventive or ‘adjuvant’ treatments, maybe we can stop the disease before it gets to the lungs, liver, bones — to those places where it begins to threaten our lives.  Other cancers use this approach and offer patients a real chance to avoid recurrence.

Adjuvant – and Perhaps One Step Better to Neo-Adjuvant

We’ve seen trials for “Adjuvant” (or preventative) therapy which hope to prevent recurrence (treatments given immediately after nephrectomy). But one trial goes one step better – it’s for “Neo-Adjuvant” (before nephrectomy) as well as Adjuvant (after).

Patients may want to rush to surgery to “get it out”. In reality, those tumours have generally been  growing slowly, undetected for many years. Kidney cancer surgery is rarely an emergency. There is usually time for a second opinion and to check out any newer approaches.

Here’s the thought: given that the tumour cells have gone undetected and tolerated by the immune system for so long, can put those millions of cells to work and make them “show their calling cards” to our immune system before we take them out?

Combining Neo-Adjuvant and Adjuvant Treatment – PROSPER-RCC

The Phase 3 clinical trial called PROSPER-RCC (NCT03055013) is  for patients whose tumors are 7cm (2 ¾”) and larger in size, but not spread beyond the kidney area.  These patients are at greater risk of spread of the cancer than those with Stage I or with smaller tumors.

Based on earlier studies, nivolumab (Optivo) is now approved for advanced kidney cancer. This is a trial to test whether there is a benefit when nivolumab is given immediately before and after a nephrectomy when tumor cells might have spread outside the kidney but are too small (microscopic) to see on scans.  (Typically a patient without spread of disease would not be treated, but monitored.)

The Rationale for PROSPER-RCC: Why It Might Be Helpful

Here’s what I’ve learned:

  • Checkpoint inhibitor treatments with PD-1 blocking drugs like nivolumab seem to work best when the immune system may be being turned off by this cellular growth pathway. Cancer is deceptively clever and some tumours can express a protein, PD-L1. This protein can turn off our immune cell responses that recognize and fight the cancer.  There was a hint of this  with some positive data that indicates that these drugs work best in patients whose tumors were “PD-L1 positive”.  (PD means Programmed Death and PD-L Programmed Death Ligand or connector.  Death to the cells, and the signalling loop that hinders the immune response.)
  • In theory, when the kidney tumour is in place, there are millions of cancer cells. All of those tumour cells send off multiple negative signals to the immune system to stop it from working. However, if a checkpoint inhibitor was used and stopped those blocking signals, the immune system would have a big wake-up call – e.g., lots of targets with which to build an army of T cells. In theory, these newly educated T cells would later turn into memory cells. (If the body can maintain these memory cells, they would continue to fight any return of disease.)This is much like what happens when we are exposed to certain bacteria or viruses. Once we get exposed to the bug, we don’t usually get it again. Our immune cells have learned (“immunity”) how to kill it more quickly the next time before it turns into a full blown cold. Similarly, if these anti-RCC immune cells ever see one of these tumor cells anywhere in our bodies again, they would know to attack and kill them even if there is no drug in the patient and has not been for some time.
  • Surgery is still the main treatment to control early stage kidney cancer. But it will also remove the majority of targets (PD-L1) that the checkpoint drug uses to rev up the immune system. Giving the checkpoint inhibitor before surgery may maximize/optimize the drug’s ability to wake up the immune system and build that T cell army.
  • So the surgery is important. But let’s assume a few cells might be still circulating and have gone undetected for some time. They could still show up later on a scan as an enlarged lymph node or spot somewhere. A boost of the same checkpoint inhibitor right after the surgery could then be used to remind the immune system to continue to look for those cells and kill/eliminate them when they are small. In theory, the immune system will remember what the past “trouble” was: “Hey, haven’t I seen you before?”

From what I understand, this theory worked well in mice. The checkpoint inhibitors worked better if the primary tumour was there to help provide “a target” to activate the immune system first before the tumor was removed.  While we’re not mice, this  makes sense, no?

Trial Design: What Really Happens to the Patient in the Trial

PROSPER-RCC will place patients randomly into two groups:

  • Group One gets two infusions of nivolumab before surgery (at about 28 days and 14 days before surgery). Following that nephrectomy, the patient will receive more infusions of nivolumab. This is for 9 months post-surgery altogether, with 12 more doses.
  • Group Two gets the usual standard of care: upfront nephrectomy, partial or radical nephrectomy, and will be followed by close observation at an expert centre.
  • Two arms/groups:  BLUE arm with surgery  and monitoring by the trial team, the standard of care; the RED arm with  medication before to surgery, followed by more after the surgery.

It is important to note that no patient on this trial receives any intravenous placebo/inactive treatment. Every patient is treated.  Each patient will have either the experimental treatment or the standard of care.  All are under close observation at the trial centre. This trial has been designed and discussed with patient advocates and is supported by the NCI.

For More Information

Patient-friendly explanation here – http://www.10forio.info/clinical-trials/prosper-rcc

For contact information at over 100 trial sites, dig a bit in the site below:

https://clinicaltrials.gov/ct2/show/NCT03055013

or call the office of the Principal Investigator, Dr. Lauren Harshman, at: 617-632-2429

Deb’s Disclaimer:

As a patient and advocate for kidney cancer patients, I have been delving into the world of clinical trials and trying to understand as much as I can. I’m not a scientist, but I am a patient with this disease, so I bring that lens, along with some abilities to translate science into understandable terms. As a volunteer, I have no financial interest in this trial or any specific medications. @DebMaskensKCC; dmaskens@rogers.com

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Filed under Clinical Trials, FDA Medications, Immune Therapies Old & New, Making a Plan, New Trials, Newly Diagnosed, Patient Resources, Surgery, Therapies, Uncategorized

by | May 7, 2015 · 12:06 pm

Younger Patients & Kidney Cancer: Your Genes or Your Luck?

Once you reach a ‘certain’ age, you are horrified, but not surprised to get a cancer diagnosis, or hear about it in a loved one.  That same cancer in a young person is even more horrifying, we instinctively know.

Most kidney cancers (and there are more types than we previously knew) are found in people in their 60s and 70s.  Bad enough, but a cancer called by the same name and found in a younger person is often a very different cancer, with a very different prognosis.

Some new research recognizes that special attention should be paid to those RCCs found in patients 46 years of age and younger.  Why is this?

The quick answer is that this may represent a more aggressive kidney cancer and/or be of a familial or hereditary nature.  That important distinction has researchers strongly recommending that young patients be referred for genetic testing.  This can explain those special risks and create more appropriate treatment plans, and alert other family members as to special monitoring. Critically it may change the approach to any removal of the kidney and/or tumor.

Typically a small renal mass might be monitored or removed by either surgery or some laser ablation.  If removed, the tumor can be assessed by a pathologist–a look under the microscope.Without a prior biopsy, the ablated tumor will not be examined, and no genetic testing can be done.

BIG HOWEVER HERE: even with a good pathology report, that may tell only what that tumor looks like–not what pushed it to grow, i.e., the genetic drivers. And those genes don’t go away with the tumor, so the risk remains that more tumors will grow, maybe in the second kidney, or in the partially removed kidney.  Plus the rest that can happen with cancer…

An 75 year old whose small renal mass is removed will likely function well with one kidney.  That same tumor  in a 35 year old creates another challenge.  If that tumor is driven by familial genes–not just by sheer bad luck–more tumors on the other kidney may be in the works.  A partial nephrectomy   must be considered. The risk of more tumors emerging in that kidney AND the other kidney is high.  The younger patient needs decades of good kidney functioning, but those decades carry the risk of the emergence of more mets.

What else should trigger a genetic testing?

Quick answer: anything that doesn’t look like the senior  citizen with a single tumor in one kidney.  More officially below:

Early onset of kidney cancer is 46 years or less.

Bilateral (two-sided) or Multifocal (many locations) kidney tumors

Family history of kidney cancer, 1 or more close relative, 2 or more in more distant relatives

Kidney cancer with either a mix of other tumor types roughly related to kidney cancer or with lung cysts or pneumothorax (air leaking out of lung into chest cavity)

Personal or family history of kidney cancer syndromes.

The above list is from Yale  School of Medicine, Professor Brian Shuch, who work includes dealing with heredity forms of kidney cancer.

More small renal masses found at an earlier age in more patients, as our imaging techniques improve and more CTs scans are done. Not all will be hereditary, and many will be sporadic or out-of-the-blue kidney cancers.  Those are likely due to the sheer chance. Things go wrong as trillions of cells divide and make DNA mistakes along the way. Years of environmental damage may overwhelm the body’s ability to correct those DNA mistakes–i.e., the immune system gets overwhelmed, tricked, tired, etc.

Kidney cancer found at an early age or with the bilateral/multifocal tumors simply must be tested as to it genetic origins.  This gives information critical to protect the rest of the kidney(s) and to participate in treatment that is more helpful.  Finding an effective treatment will still be a challenge, but proper treatment requires knowing exactly which kidney cancer you have.  From there, a real plan can be developed.

Just as I remind all readers to work with an experienced RCC oncologist–not just a surgeon and/or urologist (sorry guys, we need a team)–those who fall into this early and hereditary renal cell carcinoma category must also work with super specialists.

The person to contact at NIH is genetic counselor Lindsay Middelton at (301) 402-7911. She is with the National Cancer Institute’s Urologic Oncology Branch.  An introductory link is below to the NCI and two other rare kidney cancer organizations.

http://www.cancer.gov/cancertopics/causes-prevention/genetics/genetic-testing-fact-sheet

Birt-Hogg-Dubé syndrome:
http://www.bhdsyndrome.org/for-families/what-is-bhd/

Other syndromes causing kidney cancer:
http://www.bhdsyndrome.org/for-families/kidney/other-causes-of-hereditary-kidney-cancer/

 

 

 

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by | February 7, 2014 · 12:15 am

Molecular Marker for RCC/ Papillary RCC. Molecular

One of the many challenges in fighting kidney cancer is knowing where it all got started.  This research indicates that a gene gone astray, the MET gene, is part of the problem from some patients.  It is this type of study that will change the treatment for us, as there will be greater clarity as to the “target” to be reached by “agents of change”.  (Nothing political intended, but seems to work here!)  Especially of interest to patients who have the variant of papillary RCC, about 10% of us.

 MET Variant as a Prognostic Marker in Clear Cell Renal Cell Carcinoma

 Dr. Ari Hakimi of Memorial Sloan-Kettering Cancer Ctr.,New York USA

ASCO GU Congress 2014

eCancer reporter Peter Goodwin’s questions are in italics. Where I was not certain of the lecture, I added a (?) to show that. Link below to the actual lecture.

Ari, you have been looking at prognosis or prognostic features, or actually, molecular features of renal cell carcinoma. Can you tell me what you were doing in the study you’ve just been talking about?

There was a great paper that was published by the people at Harvard and Lancet (?) Oncology last year. It found for the first time a prognostic marker that was associated with poor survival in kidney cancer, a molecular marker. This was a variant, a normal variant in the gene, the MET gene. In that study they had several hypotheses they generated from that study, but they didn’t really have enough genetic data to try to figure out what was going on here with this variant in the genes. So what we did was, we took that same concept, that same variant, in the Cancer Genome Atlas Study, which has both patient information and then a host of genomic information. We tried to validate their finding and explore the biology of that marker.

It sounds like a needle in the haystack but you’ve but you become quite familiar with this variant called RS11762213. What you know about it so far?

 We know about that it is a variant in the MET oncogene, a very important gene in a lots of different cancers, particularly in papillary renal cell cancer. It’s a gene not thought to be very important in clear cell renal cell carcinoma, but we found that it is, and we explored the variant in an exonic region of the gene–meaning the coding region of the gene.  Because the variant is in a coding region of the gene, we thought it might be more than just a prognostic marker. It might also have some biological implications.

Biological implications?  What sort of biological implications?

 We think the marker may be; we figured out through computational methods, exploring the TCGene data(?) that it might be in the region of enhancement,  meaning the variant leads to higher activation of the MET oncogene.  In turn, this might explain why these patients have a poorer outcome.  It might also have potential therapeutic implications.

So what have you found so far then, about the level of additional risk if you happen to have this variant gene?

Great question.  We took about 270 patients from the cohort who had available information.  We genotyped them, meaning we determined what percentage of these patients had the risk variant, which is about 10 %, consistent with prior studies.  We showed that when these patients had that risk, in addition to the current prognostic features, they had about a 3-4 fold increased risk of cancer-specific death, or tumor recurrence after surgery.

That’s really quite powerful!  Am I right that there wasn’t any clear kind of molecular feature to give you some help in the past?

Until this study, which was published last year, there were really only tumor features and patient features that were associated with poor survival in kidney cancer. This is the first study that really showed, that they published last year, to show in two different cohorts that had a molecular feature that added to the prognostic models.  We showed, augmented their findings, that if you took the best current prognostic models and stratified patients, added to that model, meaning it improved the predictive accuracy of even the best post-surgical models that are out there.

You are looking actually disease mechanisms–mechanisms of cancer production. You established prognosis, but what about predicting response to therapy?

That’s a great question. Our goal now– that we’ve established that this is a valid biomarker, truly multiple cohorts now showing this marker can stratify patients for aggressive behavior, we can now explore—hopefully–whether this has therapeutic implications because it is in a gene that is a known cancer gene.  Because there are multiple drugs that target this gene, and because we think that this variant that is activating this gene, it stands to reason that an inhibitor for these patients with this variant might work. These patients might have another option.

So theoretically a new drug which is an inhibitor for this variant might work.  What about existing cancer drugs? Do you have any ideas about if any these do influence that variant?

We don’t know yet. We are trying to find it in cell lines, meaning cell lines that are derived from tumors that are used in the lab, to see MET inhibitors that currently exist and are in phase I or II trials in kidney cancer could potentially be used against patients against this variant. That could be a very powerful tool, and a kind of the precision medicine that were looking for.

This is an amazing achievement, actually going through the Cancer Genome Atlas to find information like this, information about expression. In the realm of the everyday cancer doctor with patients to treat today, tomorrow, what you think the doctor should take home from this development?

The exciting thing about this is to genotype the patient, that is to determine that this patient carries this risk variant, is something you can detect from the patient’s blood or even a swab from the cheek. It’s a very inexpensive. It costs about $10-$70 to get this information for a patient. You can have what is called a liquid biopsy, meaning you need any tissue. You can get it from their own normal cells, because this is germline variant. You can find out this information very affordably and very quickly to determine risk for these patients. Obviously, if we are able to show that it has implications for therapy, that as a whole opens a whole new avenue.

How much hope to have that this it will be possible to manipulate this gene expression by using this kind of drug to target this?

I think that the data there is quite strong for other types of cancers. We know that other genes that are overexpressed or mutated in activated fashion respond quite well to inhibitors. This exists in multiple cancer types, lung cancer, breast cancer, for example. It stands to reason that this would work as well in kidney cancer, and the hope would be that this variant would be actually an activating factor and that we could use that also.

We’re also hearing, and especially at this GU meeting here in San Francisco, about the heterogeneity of the tumors. In fact, you may have tracked down one particular cause of cancer, but there’s another five going to rear their ugly heads at the same time. What you make of that?

 Well, that’s definitely a major factor, particularly in kidney cancer, where heterogeneity was really first described in the clinical setting two years ago in the New England Journal. What the nice thing is about this variant is, is that it is germline. It exists in every cell. Thus heterogeneity does not exist in this situation. The variant is present in all cells, including the tumor cells. So if our data does hold up, and it is a therapeutic target, it will not be affected by tumor heterogeneity.

Give me a message to take home for the community cancer doctor very briefly..

The messages that we have truly validated this important finding that was published last year and we truly believe that this is a new prognostic marker and adds to the existing prognostic markers.  Time will tell if it will actually help guide treatment of metastatic disease and really change the paradigm for kidney cancer.

Thank you very much.

 http://ecancer.org/video/2663/met-variant-as-a-prognostic-marker-in-clear-cell-renal-cell-carcinoma.php

 

 

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by | January 21, 2013 · 9:58 pm

Drug Interactions; Don’t Be Surprised!

At a City of Hope Medical Center, teaching hospital/research center, a pharmacist spoke to our patient group about drug interaction.  She reminded us that we are responsible to follow the dosages, to alert our doctors to ALL the medications we take–prescribed and over the counter, herbals and supplements. “Remember that diet and its fat content affect our drug’s efficacy”, she added.

 Pharmacists consider three types of interactions, which can happen between drug and another, with drugs and food or beverages, and drugs and conditions under which a drug is taken.  They are described as follows:

 1)     Pharmokinectic issues of absorption, distribution, metabolic and excretion—how does the body bring it in, how long is it in the system, and where does it get absorbed?  Does one drug slow down the effect, or prevent its use?

2)     Pharmocodynamic effects occur when drugs with similar properties to one another are used together.  They may interact with one another; such interactions might cause one or more to be ineffective, or too effective, or with side effects that are unexpected.

3)     Toxicity may happen if the combinations of drugs have a toxic effect on an organ that would not occur with just one of the drugs. 

For example, soranfenib (Nexavar) should be taken without food, while Sutent is recommended to be taken with food—but never with grapefruit juice. 

 Some drugs cannot be taken with NSAIDS; some are platelet inhibitors, for example.  Sutent’s efficacy may be impaired by taking St. John’s wort, or when taken with barbiturates.

 How do you keep track of all of this?  Speak with the pharmacist whenever you have a change in medication—or right now, since you probably have not done that! Make an appointment to have the time cover all the questions. Bring in ALL the medications you use, even those you feel are “probably” safe or those you are embarrassed to admit you take!  Pharmacists have access to extensive data bases, not only of the prescribed drugs, but also many of the supplements and herbals on the market.

 As to herbals and supplements, she reminded the group that there are no controls as to the quality and quantity of active ingredients in the non-FDA approved supplements, and they can vary dramatically. Meningitis caused by a fungus in steroids produced by a US-company has caused the death of 44 and sickened at least 600 just last year.   

It was fascinating to hear that, “Pharmacists don’t take medications”, but she emphasized that she rarely uses anything. It’s harder to convince her mother! Anticipating problems in the future with family-related conditions, she eats properly and exercises, for example. 

Trust your gut about your body’s reactions.  If something seems amiss, talk to your pharmacist or doctor to be sure you are not having a drug interaction.

Read the labels and follow the instructions.  Not sure when and how much to take? Go back to the pharmacist or doctor for clear instructions.

 Bring a “brown bag” of meds and such to your pharmacist to get a review of your meds. You know you should have already done this, so get going!

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by | September 8, 2012 · 7:44 pm

A Second Opinion: How the Heck Do I Do That? And What If?

Second opinion? How do I  dare ask my doctor?  He seems so nice, he helped my mother, what makes me think he is wrong, what if he gets mad at me, how will it affect my care, what if the other doctor says the same?  All this goes through your head when you question the diagnosis or treatment plan you have just been given.  But the failure to ask for that second opinion will always haunt you, and may cost you a better treatment, or your life.

Nothing is more frightening than a cancer diagnosis–except perhaps the fear that you do not have the best advice or the best doctor. At minimum we want options and some control. You mayonder if your doctor really knows what he is talking about–you certainly have no way to judge, except to judge how he handles your request for a second opinion.

If the doctor proclaims that only he is qualified to treat you, and that no one else could possibly offer you anything else, the decision is easy.  Just stand up and walk out, getting all your records as you exit.  Your records are yours legally, of course, and should be in hand even when you work wonderfully with your doctor.

You may value your doctor’s advice, but know that your disease is rare and difficult, and that new information may have relevance to your case.  Can your doctor possibly have all the latest information at his finger tips?  And what about that article which you read on the internet or that your friend sent you from his hospital?

First of all, your doctor cannot possibly be up-to-date on all aspects of care and research into your disease.  One doctor estimated that if read two medical journal articles per evening, by the end of the year, he would be only 400 years behind!  And that was several years ago.

One patient friend through ACOR and its kidney cancer list serv has shared his approach, which has been effective and let him work closely with his doctor, while pursuing questions and potential treatments not readily available through his doctor in Australia.  I have made tiny changes to his letter, as it follows.  Good advice and the results, all relevant to us.

Tony starts: ” I’ll  outline how I start “delicate” discussions and get involvement from the likes of the hospital pharmacist. After working out exactly the treatment I want, I kick-start with a simple email, usually to my (general) oncologist. Importantly, I always attach one only medical study –  which is either current or past year.

My request for a treatment is always based on the conclusion in my cited study. I never offer my own opinion or view. I always keep the email short, logical and free of any argumentative material. This leaves the oncologist in the position of having to either (1) meet my request or (2) find grounds to reject the study itself or (3) to call in experts from other disciplines.

  I  learned that the medical decision making process mirrors life outside the medical profession where business managers and bureaucrats want that proverbial piece of paper in case something goes wrong – in this case it’s the well selected medical study (but finding exactly the right study can sometimes involve a lot of work). I find that
these general non-RCC specialists do respect precise RCC studies as they have no hope of keeping up with everything in every cancer type. Simple logic on basis of a reasonably current medical study is the art.

My simultaneous important method is little known fine print I found in our Oz hospital system where every patient is entitled to a second opinion from every relevant discipline. (Tony is in Australia.)

So where, an issue is complex, I respectfully ask for my med-onc’s opinion on whether we should get a second opinion. That gets a much wider team involved where the med-onc doesn’t want sole responsibility for decision making. All just normal human stuff where it’s not smart to make a decision contrary to a current medical study.

So far, I have pulled off four little feats:

The first was getting the urology department to reverse their initial decision to not neph me (they wanted to try to “reduce” my 10cm tumour with systemic drugs and otherwise reckoned I was at risk of karking it on the table).

Then, I got a thoracic surgeon involved with agreement for a rib resection that would have made me disease free (but surgery was called off the day before the scheduled date for sudden emergence of liver and lung mets).

Then, I got the hospital itself to pay for a shot of the very important zoledronic acid (Zometa) – Unbelievably, it is not on our PBS for RCC unless the patient has high blood Ca. Discussion continues on whether they will pay for the shot.
More recently, after one week into first Sutent round, I discovered from doing my own due diligence that another drug I must take for an unrelated condition dilutes the efficacy of the Sutent by about 50% which is unacceptable. My now well practised email / study / second opinion request procedure got the ball rolling resulting in an embarrassment of riches in a big team my med-onc pulled together.

Next week, for the first time I meet with a further member of my expanded team – an oncology radiation expert.”

 

Tony is obviously engaged in his own treatment, comfortable and motivated to read through medical articles, and choosing those which have impact on his treatment options.  He has done his homework  carefully and backs up the request with the medical article, i.e., in the physician’s language.  Tony puts himself in the equation, by asking if “we” should get a second opinion from an expert, partnering with his doctor in this request.  He has wisely calculated the needs of the doctor, and the system requirements. His results speak for themselves, and can have impact for the next patient the doctor sees!

You may think that this is a laborious process, and one which should not be necessary, but the reality is that it is both necessary and effective.  Getting the best possible treatment and making sure that your doctor supports you in this quest may save your life.

As a friend said, doing these kinds of things may save you someday from waking up dead…

 

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