Category Archives: Uncategorized

by | November 30, 2018 · 12:22 pm

“Have you reviewed your medical records? You should”

…and I’m not alone in saying this.  Often I am a voice in the wilderness, asking/demanding that we all have easy and complete access to our health records–all of them and as soon as they are created.  This article posted by Pinnacle Care sites multiple reasons why.   Get your records, read them, make sure they are correct, and that they really ARE your records.  Look through the medication lists; read those imaging reports, get the details of your diagnosis, and let your family know where your copy is stashed.  Important stuff for all.

November 13, 2018 in Health Risk Management

medical records review

Thanks to HIPAA, you have the right to get a copy of your medical records and review them. There’s a good reason to take the time to read over your records in detail. A study published in BMJ Quality and Safetyfound that 29% of the study participants who reviewed their doctors’ visit notes found information they believed was incorrect.

OpenNotes, a non-profit that advocates for the sharing of medical visit notes with patients, says nearly 29 million Americans and Canadians currently have online access to their notes. While checking these records for accuracy is important and can lower your risk of misdiagnosis, duplicate testing and procedures, and inappropriate care, and even provide evidence of medical identity theft, there are a number of other important reasons you should review this information regularly.

  • Information from previous visits can help you prepare for an upcoming appointment. Reviewing past notes can help you figure out what questions you’d like to ask your doctor or issues you’d like to revisit during your next appointment. For example, if your doctor recommended weight loss as a first step to control high cholesterol, you can ask if your levels have improved enough or if you should consider cholesterol-lowering medication.
  • Notes can help make sure you and your doctor are on the same page. What you heard at your appointment and what your doctor meant to convey may not be the same. Reviewing the information in your medical records and visit notes gives you the chance to read what your doctor said at a time when you’re less likely to be anxious, distracted, or feel rushed. In addition, if you’ve received a serious diagnosis, you may not remember everything that was said at your appointment, so reviewing the notes gives you the opportunity to better understand your diagnosis and treatment plan.
  • Reviewing your records gives you the chance to clear up misunderstandings. If your doctor used terminology that you didn’t understand at your visit, you can use your notes to identify any terms or information you didn’t understand and get in touch with your doctor to ask for clarification in plain English.
  • If you forgot to mention something, now’s the chance to get it added to your record. There’s a lot going on at a doctor’s appointment and even the well-prepared patient can forget to share important information. After reviewing your medical records, if you realize you didn’t share information such as family history, allergies, previous diagnosis or treatment, current medications, or symptoms you’ve been experiencing, contact your doctor and provide the missing information so your doctor can develop a personalized risk management plan for you.
  • Access to your medical records allows you to share information with all your doctors: If you see more than one doctor, reviewing your visit notes and sharing them with all the doctors who are treating you can be another way to lower your risk of overtreatment, medication interactions, and duplicate testing.
  • Checking your records can help prevent billing errors. When you review your visit notes, make sure that the care that’s recorded in your record matches the care you received. For example, if the note says you underwent an EKG but your doctor didn’t perform that test, contact the office to correct the error so you and your insurance carrier are billed only for the care you received.

Leave a Comment

Filed under Uncategorized

by | October 28, 2018 · 8:39 am

Patient ToolKit–Prepare for your doctor appointment

Patient_Toolkit_v4A_Fillable Format

The Patient’s Toolkit for Diagnosis prepares patients for medical appointments. We patients know that being engaged in our care helps figure out a “working diagnosis”. That “working diagnosis” may change as more information is gathered.  We recognize that a diagnosis can be certain or uncertain.  But communication between patients and medical providers leads most efficiently to the most accurate diagnosis.

The Toolkit help the patient be part of this process.  As you fill out the form, think through the problems which concern you. Then you can discuss them well with the medical team.  Use it during the appointment so your questions are addressed.  After the appointment, it reminds you what was said or forgotten(!) and to prepare for any tests or treatments recommended.  You can give a copy of the form to the doctor before the actual appointment, while you take notes on your copy.  Don’t be surprised if he sets it aside, as he really should listen to you above all!

The Four Parts of the Toolkit:

      1.  Prepare for My Appointment

      2.  My Symptoms or Pain

      3.  My Medications

      4.  After My Doctor’s Visit: What’s Next?

 Prepare for your appointment so you can remember what made you want to see the doctor.  Think about your symptoms and what you have done to care for yourself.  Think about the medications you take—or forget to take, and bring them with you.  Decide what you want to get from this appointment in terms of your symptoms.  Write down what the doctor might need to know about your health history or that of your family.

The Toolkit reminds you to ask, “What else can it be?” or “What is the purpose of this test?” These questions remind us and the doctor that getting a diagnosis comes from process of gathering information at the outset. If you understand the doctor’s thinking and need for the tests, you will likely be able to continue to help in this process.  Remember it is a process in which both you and the doctor participate, so continue to take an active role.


WHY USE THIS TOOLKIT?

How in the world does a patient really prepare for an appointment with the doctor when there is a new problem…or not?  Often we are not sure how to answer the doctor, when he asks, “What seems to be the problem?”  We might have vague symptoms, be embarrassed, have an odd and worrisome pain that has gotten worse, think that it just ‘getting old’ or ‘being fat’ or ‘being stressed’.  Plus, what if we are really sick?  That might make us downplay some symptom or feel silly talking about  being worried.

The Patient ToolKit helps the patient tell his story to the doctor and in a way that MIGHT get the doctor to hear your complete story.  It can help you organize your symptoms, prompt you to remember the timing, what has helped, what hasn’t, the meds you are taking and so on.  As a minimum, it can get you to THINK about your symptoms in a more clear way.

Too often, it seems you are asked the same questions by the receptionist or then the nurse. When you see the doctor, you may think he has read all their notes and that you should not repeat what you have said.  In fact, the doctor needs to hear your story in your words, and how you explain your concerns.  To have all your thoughts organized and in writing might help that conversation be more effective, and can help you both to focus on the issue at hand.

 

 

 

 

Leave a Comment

Filed under Uncategorized

by | June 11, 2018 · 3:32 pm

What Do You Mean “No Nephrectomy?” An ASCO Study to Question & Answer

The headlines announced (or pounced upon) a study from ASCO (American Society Clinical Oncologists), with MedScape’s 6/2/2018 example: “In Advanced Kidney Cancer, Surgery No Longer Sole Standard of Care”.

Is there value to surgery in advance of treatment with Sutent(sunitinib) for the patient with metastatic clear cell carcinoma? The study author,  Dr. Arnaud Mejean from France claimed, “Cytoreductive nephrectomy should no longer be consider the standard of care in metastatic renal cell carcinoma.” My own doctor said it, “flips the existing paradigm” of treatment.  Typically, a patient with metastatic kidney cancer has a nephrectomy, likely followed by medications or even more surgery to remove metastases.

What the heck does this mean to patients? How will the less-experienced urologists and oncologists interpret this?  Is there a comparison  with treatments in the US to used in this trial?  What are the important DETAILS?

Stunned at headlines, I studied the original NEJM article.  Since 425 of the 450 in the trial were from France, I tried to compare mRCC  stats in France to the US stats as available.  Should this study alter diagnosis and care of metastatic RCC patients? No trial never gives the whole picture, and quick headlines add confusion.  Earlier studies have concluded that there is benefit to an upfront nephrectomy, even when there are metastases.  Officially, that is a  cytoreductive nephrectomy (CN)–removal of the affected kidney with mets in place.

This study says NOTHING about patients who have NO METASTASES, but do have malignant tumors.  A tumor,  large or small, can create metastases. Some doctors don’t look for metstases before or after the surgery, but they may still be there.  The “Got it all” message is a comfort but is no guarantee that the cancer has not spread, or is  not visible to the surgeon as he operates. Of course, mets may be found away from the site of the surgery, so an ‘all clear’ signal does not cover bones, liver, lungs, etc.

Note also that this is for clear cell kidney cancer patients only: there are other subtypes of RCC, so those cases were not permitted in this trial.

Trial patients can vary  from ‘real world’ patients.  Depending on the time to find the disease, they may be quite sick.  They may be referred to a trial when their case is too difficult to manage locally, and perhaps after a lengthy delay as to the diagnosis. Usually they are seen by a general practitioner, eventually receive a CT scan, likely are referred to a urologist or oncologist.   A urologist who might remove a large 8-10cm tumor (3-4 inches), but may not want to do for many causes.  Thus it is important to understand the non-surgical options for those rarer cases. This is true in the US and well as France.  Although 425 of the 450 patients were from France, there may be broad differences in general access to CTs and the referral pattern for these patients.

With more unanswered questions, this trial should NOT change the entire approach to a nephrectomies for mRCC patients.

Missing Data and Blocks of Patient Time to Treatment?  

Time lost without care for cancer patients is lost opportunity for longer survival. This can be common: the patient has a complaint–anemia, cough, blood in urine, pain in his flank, concern of a general sort of failing health.  He may be examined and given blood tests, internal exams, etc and eventually a CT scan. He then may be referred to a specialist, even to get a referral for the CT scan.  With the finding of a kidney mass, the patient may then see an oncologist or urologist.  How long these patients were sick until there was a final diagnosis is unknown.

From the initial diagnosis and eventual recommendation to the CARMENA trial, the patient was without care.  We do not know how long it was for the recommendation until the actual enrollment in the trial.  To be enrolled, the patient must first have the recommendation to do so, be set up to see the trial physicians, and have a biopsy before enrollement can happen. With the large tumors found, such biopsies likely did not happen until referral to the trial.  The trial accepted only clear cell RCC, thus the biopsy was necessary. We do not know if the biospies were reviewed by one central pathology lab, or if there were many opinions from various labs.  Was it days, weeks or months from referral to biopsy to actual enrollment and randomization into one of the two arms of the trial.

These steps can delay treatment, adding weeks or months from initial diagnosis until either surgery or Sutent.  Remember that all these patients were definitely found with metastatic disease prior to trial recruitment

According to the trial, all the enrolled patients were in intermediate or poor risk categories.  Everyone had recognized risk factors. The ECOG performance status (PS) of 0-1, so able to care for themselves, not bed-ridden.  That means that they could function fairly normally.  In the Surgery First group, about 70% of the patients had tumor Stages 3 & 4.  Only 50% of the Sutent Alone group with in Stages 3 & 4.  As to the tumors themselves?   The aggressiveness of the tumors were also measured from the biopsies, with about half having more aggressive disease at Furhman grade 3 and 4.

The trial protocol indicates that the surgery first patients do so within 28 days. Though the median time to to so was 19 days.  However, some obviously had surgery much later, up to 50 days post randomization.  It would have been valuable to know if delay of surgery played a role in outcome.

We are not told where the patients had surgery. This is important, as there is clear survival advantage to patients who have that surgery at a “High Volume” institution.

The patients  randomized to “Sutent Alone” group also had the initial diagnosis, and were sent to the trial site, which may have delayed their treatment.  Medication was to start within 21 days of randomization, which seemed to have happened in a timely manner.  They got the 4weeks on/2 weeks off regimen, which is the standard of care.  Again, no sense of how quickly they were into treatment post diagnosis.

Back to the “surgery-first, then medication” group:  their Sutent treatment was to begin 3 to 6 weeks post surgery.  (Some doctors would not do a nephrectomy that quickly, as Sutent can interfere with healing post-surgery. )

By final randomization, there are 226 Surgery First, then Sutent patients, and 224 Sutent Alone patients.  But of the 226 surgery patient 40 did not receive Sutent, so down to 186 patients, which was furthered diminished by 20 patients.   Post their surgery &  Sutent time, 114 received ‘futher lines of therapy’.

In the Sutent alone group of 224 patients, 11 did not get Sutent, leaving 213. Of those patients 38 (17%) did undergo nephrectomy due to ”control of symptoms”, and at about 11 months after randomization.  After leaving Sutent for reasons of toxicity and/or disease progression, 115 received additional therapies.

Questions Unanswered

How sick were these patients, how big were their tumors, where else did they have metastases?  The stats between the two group are pretty similar, in most factors.  But I note that the primary tumor sizes, although matched, are generally big.  The median is 8.8 centimeters.  Bad enough, but the measure of ‘tumor burden’, which includes metastases, generally in two groups is pretty stunning.  That is described as 14cm, with sizes up to 39.9cm in the Surgery First group, and 31cm in the Sutent Alone.  With the large percentage (70%) of Stage 3 & 4 patients in the surgery group, the range of sizes of tumors was considerally greater–up to 33.9cm.  Only 50% of the Sutent only group were in Stage 3 & 4, with the maximum tumor burden about 31cm.  One could argue tha the groups were not well-balanced as to the level disease found in the separate groups.

Despite what appears to me to be high tumor burden of both primary and metastatic disease, the authors claim that patients with either “a poor performance status, minimal primary tumor burden and high volumes of metastatic disease” are “not generally recommended to undergo a nephrectomy”. This is apparently the general standard of care in the participating institutions.  This seems contradictory to me!  There is no clarity here.  If ‘minimal primary tumor” means a 1-3cm tumor, that is understandable, but the 4-8cm tumor would seem to be the typical nephrectomy patient.  The issue of no nephrectomy for patients with ‘high volumes of metastatic disease’ seems to describe the patients in this study very accurately.  Or does the French experience of RCC patients vary so much from the US experience?

How well did they tolerate Sutent?  Of the surgery first group, over 30% had dose reductions, and in the Sutent alone group, it was quite similar–all done to manage adverse events.  Grade 3 or 4 events–really tough kind–were more common in the Sutent only group, with 43% reported thus, and 33% in the surgery/Sutent group.

  1. The ratio of deaths from RCC patients in France compared to those diagnosed in year 2013 is about 1 in 3. The same ratio in the US is about 1 in 5.  Rough stats, but that makes me wonder if getting a cancer diagnosed sooner and treated sooner might have something to do with that.  These trial details make me question whether the typical French patient is diagnosed and begins treatment early enough to make a difference in outcomes.

Happy to share my documents and would love to hear comments/complaints, esp from the EU and UK people who may have a different view.

3 Comments

Filed under Uncategorized

by | June 3, 2018 · 2:42 pm

ABSTRACT from ASCO & Impact for Patients: “Alterations in key clear cell renal cell carcinoma (RCC) genes to refine patient prognosis”

This abstract title reflects important changes about kidney cancer. It is not about “kidney cancer”, but clear cell RCC, with a  focus on changes or genomic alterations (GAs) in the genes.  The study goal was to see if patient the prognosis related to those GAs in genes that are found in RCC.  It describes ccRCC in a very detailed way–as to its gene expressions/changes.  (Abstract and Take-Home messages from Dr. Monty Pal are found below, with my comments to follow.

Session: Genitourinary (Nonprostate) Cancer Saturday June 2, 8:00 AM–11:30 AM
4516 (http://abstracts.asco.org/214/AbstView_214_229517.html) Alterations in key clear
cell renal cell carcinoma (RCC) genes to refine patient prognosis.

D Bossé, W Xie, Y Ged,et al
Take-Home Message
In this study of 308 patients with clear cell mRCC treated with VEGF-TKI therapy in the
first line, the researchers wanted to determine the prognostic value of genomic
alterations leading to loss of function. Genomic alterations in BAP1 were significantly
associated with a worse IMDC risk group and worse overall survival. Longer overall
survival was significantly associated with genomic alterations in KDM5C and PBRM1.
Significantly worse overall survival was reported in IMDC intermediate–risk patients
with PBRM wild-type tumors that also harbored genomic alterations in BAP1.
The researchers suggest that genomic alteration assessment may be predictive of
survival in IMDC intermediate–risk patients.

A prognostic study is about the likely progression of the disease, and the related risk factors.  With a more precise diagnosis of the disease, the prognosis will be better understood, which should guide treatments accordingly. (Sad that we still need prognostic studies vs comparative effectiveness studies!)

But first, a quick lecture on the background issues…

Patients might never know if their RCC subtype is clear cell (ccRCC),  papillary (pRCC) or chromophobe RCC (chRCC) until their tumor cells are seen under a microscope.  Until recently, most metastatic RCCs were treated similarly. Treatment was limited at best, with few options beyond surgery. When RCCs had spread, even surgery was not always recommended.  Diagnosis occurred when a mass was found, often fairly large, with about 1/3 of patients having metastatic disease.

It was wrongly assumed was that very small tumors  carried little risk, that they could not grow quickly and were unlikely to spread malignant cells. They could be ‘watched’. If removed surgically or ablated with radiation, there would be no real risk of spread and the patient needed no follow up treatment.

However, some small tumors are aggressive, grow quickly and spread to other organs. Surgery will not ‘get it all’, as the spread can occur well before the discovery of the mass. In addition, a “small” kidney tumor can be up to 7cm (2 3/4″) in size and have had years of silent growth.

Why do these tumors act so differently?  They arise from a mix of genomic changes in the kidney cells. Genomic alterations (GAs) vary in ccRCC patients, and those variations were thought to reveal aggressiveness and impact patient outcomes.

Earlier researchers found they could group ccRCC patients into categories based on the molecular characteristics of their tumors.  Those newly defined patient/tumor groups had every different Overall Survival (OS) statistics.  One subgroup had more aggressive disease, with OS of 2.5 years, while others had OS of over 8 years.  The more aggressive tumors needed to be identified and treated more appropriately. This abstract gives greater insight into those defining characteristics and the drivers of growth of those tumors.

Back to GAs–genomic alterations, or mutations/changes. Cells can change or mutate, due to age,  to family tendencies, or to environmental causes.  Cancer cells don’t follow the rules of normal growth, possibly due to these previously unrecognized GAs in the genes.  Most mutations in our genes do not cause problems, but some GAs in some genes drive tumor growth that endanger lives.

These genes –VHL, PBRM1, BAP1, TP53 and KDM5C–are often found in metastatic RCC. Each gene may have different GAs and at different frequencies.  Those characteristics define the tumor more carefully, and create greater risk of aggressive disease.  The abstract reviews the GAs and survival statistics in the patient population.

This is a study of 308  patients with metastaticRCC, previously treated with tyrosine kinsase inhibitors (TKIs), such as  Sutent and Votrient.  The patients were  grouped into ‘favorable’, ‘intermediate’ or ‘poor’ risk groups, a reflection of disease impact.  Their tumors were sequenced for GAs in the named genes.  Tumors have varying degrees of GAs within those genes, so were examined by those GAs and combinations of GAs. Then those GAs were compared with patient risks and their outcomes.

Those patients with GAs in the genes BAP1 and PBRM1 wt  had the worse OS.  Patients with GAs in the BAP1 gene had poorer survival, even if they were in the intermediate risk group.   The presence of GAs in three genes, VHL, TP53 and KCM5C did not seem to play a negative role in outome.  Indeed, the GAs with KDM5C seemed to improve OS stats.

What does this mean for the current patient with  metastatic ccRCC?  Perhaps a genomic analysis will give some guidance as to the aggressiveness of the disease, or reassurance that there to watch a tumor and decide the next step.  If the patient has alterations in BAP1 and PBRM1, which is associated with greater risk, he will need more aggressive care.

This information does not tell patients and doctors what treatment to use.  It does demonstrate the value of having one’s tumor sequenced to see the GAs, and help judge risk.  Those patients most at risk of aggressive disease may benefit from earlier treatment and  increased monitoring. Since about one-third of all patients not metastatic at diagnosis will indeed develop metastases, so that sequencing to discover these GAs would be a consideration for all.

This abstract gives a picture of the prognosis for the group of mRCC patients–not of any single patient–who have these gene alterations in theor tumors.  Other details will be found inthe complete study.  There may be comparisons as to how long the patients had been ill before diagnosis, the time until emergence of metastases, the length of time until TKI treatment, the length of response to the TKIs and time, if any, without treatment post the TKI until the sequencing.  There is no similar comparison to patients who were not treated at all, or who were treated with other agents.  The abstract does report a meaningful way to judge risk for patients with metastatic RCC with the use of gene sequencing, and that alone, can have impact on treatment decisions.

 

Leave a Comment

Filed under genomics, Genomics & Genes, Guidelines, Medical Conferences, Uncategorized

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

1 Comment

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

by | June 2, 2017 · 6:06 pm

Genetic Differences in Kidney Cancer? So What or What’s UP?

A few years back, I attended a kidney cancer conference with a highly eminent kidney cancer doctor.  He opened his talk by saying he was no longer treating kidney cancer!  The room was stunned, patients already wondering where to go for the next appointment when he finished his statement. “From now on, I will be treating cancers of the kidney.”

Not a small distinction, and a great way to confuse the patient and the newly diagnosed, but is critical.

Just because some growth lands in the kidney, that growth is not the same person to person, and even not from kidney to kidney in one person. In the link below, CURE magazine, May 5, 2017,  interviews Dr. Marston Linehan who expands upon the history and future of this work, which I have used as the basis for this report.  This research started in the 1980s, when doctors and researchers noted that some families were at greater risk l to develop some growths and tumor, some of which ‘landed’ in the kidney.  The early work defined that disease, Von Hippel Lindau hereditary cancer syndrome as to its genesis–an inherited mutational tendency in the VHL gene.

http://www.curetoday.com/articles/expert-stresses-significance-of-genetic-differences-in-kidney-cancer

This research started in the 1980s, when doctors and researchers noted that some families were at greater risk l to develop some growths and tumor, some of which ‘landed’ in the kidney.  The early work defined that disease, Von Hippel Lindau hereditary cancer syndrome as to its genesis–an inherited mutational tendency in the VHL gene.  Given that clue, patients with kidney cancer but from this inherited tendency, most often had mutations in that same gene.  These were ‘sporadic’, out of the blue mutations, but that opened the door to treatment improvements.  About 90% of patients with the more common clear cell kidney cancer have a mutation in the VHL gene–but not due to any inherited tendency.  Much work has been done for these patients and less for those with the rarer cancers of the kidney.

AND…there are more inherited kidney cancers which also enlightened research.  One is PRCC, Papillary Renal Cell Carcinoma, defined in the 1990s.  The gene that drove this kidney cancer was MET, wh0se mutations make those patients “highly likely to develop bilateral, multifocal, Type I papillary kidney cancer,” per Dr. Marston Linehan of the National Cancer Institute.

Research is being done for these people, as well as those who are affected by the similar disease which is NOT inherited. There disease also comes from sporadic mutations, these from the same MET gene.  This work is critical, as the generally available treatments are not as effective with the rare RCCs.

Still another and challenging rare kidney cancer is HLRCC, or hereditary leiomyomatosis with renal cell carcinoma. Linehan says it is not uncommon, and can make the patient vulnerable to develop leiomyomas–particular kinds of growths–and an aggressive form of Type 2 papillary kidney cancer.  Quite different genes make this happen, which can be referred to as Krebs cyle enzyme mutation cancers.  Obviously, still quite different that the garden-variety clear cell RCC (ccRCC) and requiring quite a different approach as to treatment.

Though there are currently studies underway to find more appropriate therapies for these rarer forms of RCC, some with combinations of agents that have been developed earlier in the decade, and with agents that were not originally envisioned to be used with kidney cancer–oops, cancers of the kidney.

If you don’t really know the pathology of your tumor and its genetic drive, you don’t have a complete diagnosis.  And if you relatively young for kidney cancer, the 46 and under group, this is time to discuss it with your kidney cancer cancer of the kidney specialist.

PS According to Linehan, there are at least 13 different types of inherited kidney cancers, and at least 16 known genes that can cause cancer in the kidneys…lots to learn and to discuss with your doctors!

 

 

 

 

Leave a Comment

Filed under genomics, Genomics & Genes, Newly Diagnosed, Rarer RCC Cancers, RCC Basics, Uncategorized

by | May 28, 2017 · 10:25 pm

New “NEWS!” for Non-Clear Cell re NIVO or NOT? Limited data or a light along the way?

With the headline, “Nivolumab Shows a Substantial Objective Response Rate in Refractory Non-Clear-Cell Renal Cell Carcinoma”, the article should be welcome to all of those in the  in the non clear cell RCC world.  Clear cell  is the most common, the garden variety of renal cell carcinoma.  This is welcome news, as the non clear cell patients get very little attention from the research world. Though the patient with nccRCC might interpret this as, “Good news! Now that they know what to do for me!” , it is just not the case.  Rarely is the news all that good or all that simple.

Let’s back up here and lay the groundwork.  Clear cellRCC, or ccRCC is the most common of about 10 RCCs.  They all land in the kidney, but can vary widely. ccRCC may be about 65% to 85% of the cases of kidney cancer,  with the rarer non-ccRCCs making up the rest.  Maybe 15-35% of the RCCs are considered rare, with the most common Papillary Type I, Papillary Type II, chromophobe, clear cell papillary, collecting duct/Bellini’s, medullary,  translocational (not to be confused with transitional, etc, etc.) and to make it still more confusing, unclassified RCC. But when the most common is described as either 65% of the whole or 85% percent, you have to question if there is clarity in that category!

Clinical trials for RCC have usually only included patients who had clear cell. The reasons are simple; it is the biggest group, the patients can be more readily found, and that is the largest group in need of the medications.  But the patients with nccRCC are really also terribly underserved.    Back in the day, none of us had many options beyond surgery, so little distinction was made.  The prognosis was grim all around, once the cancer had spread.

But the new world of precision medicine, in its name alone, reminds us that the meds need to be developed more precisely, that they be given to the right patients at the right time.  The general crap shoot or “wild-ass guessing”, as a friend says, still remains.  The latest (not necessarily greatest) group of meds are the newish immune therapies.  You have seen their ads, no doubt.

One of those is Opdivo or nivolumab, its research name.  It tries to unblock some of the inhibiting mechanisms that prevent the immune system from doing its job, but it has been tested in trials only with clear cell patients.  BUT,  that does not mean that only clear cell patients are being prescribed the meds–this, thanks to the slightly wild west of the US medical system, that can truly go beyond the FDA approved medication guidelines.

This study, which will be formally presented at ASCO in June, 2017 was announced with the headline above, “Nivolumab Shows a Substantial Objective Response Rate in Refractory Non-Clear-Cell Renal Cell Carcinoma”.  The researchers are NOT in charge of the headlines, so we must dig deeper and see what this study really means to the patients with nccRCC

I tried to sort out what it means–or does not mean. My quick review is that it does not give a great deal of clarity to the majority of those nccRCC patients. A more complete report may improve upon this.  Based on this link, I offer the following:

http://www.practiceupdate.com/news/16132/67/10?elsca1=

“I am always concerned that these new study reports are characterized carefully. They are always more complex and incomplete than I would like. A patient in a forum says this tells of  ‘good’ responses, and especially so for the non clear cell group, but s does ‘good’ really mean generally a benefit to those rarer nccRCCs? Until a fuller report emerges, I can only note the following:

There were 23 patients, from three centers, with a median age of 59. Surprisingly 30% were African -American. This may tell us that there are more African-Americans with the rarer non-clear cell RCCs, or  could reflect the local population of the three centers.  Only 23 patients and with a mix of diseases will never meet the statistically critical requirements to reach the level of excellent evidence–but it may be all we have at this point.

All 23 had non-clear cell, but nearly half had ‘unclassified’ RCC, quite a high rate.  Usually that is considered to represent between 1 to 4% of renal tumors. Most of the rest were papillary, but they generally make up the largest percentage of nccRCCs. No distinction is made here between Papillary Type I or Type II, which are really quite different diseases. Papillary Type I and II are the most common of the uncommon, non clear cell RCCs, and are readily distinguished from each other.  This would be valuable info, and wonder if this was noted in the fuller report. 

Only 3 of 4 patients had nephrectomies before the trial treatment. Were 1 of 4 patients too sick to be given the standard of care of surgery or were their doctors unaware of that? How does this affect the study, and were the no nephrectomy patients from one center or with one subtype?   We do not know the reason for this high rate of no surgery, and at a time in which it is clear that the removal of the tumor is a great benefit to the patient, metastatic or not.

Two-thirds had metastatic disease at the time of diagnosis. Of the total 23, 74% had a prior treatment, mostly Sutent or Votrient. Of these patients with prior treatments, 26% had TWO such treatments.  Thus these patients had already received treatments that were not directly approved for their subtypes.  This is not too rare in the US, where we have greater leeway from our prescribing doctor than do patients elsewhere.  But how does this fit in with the relatively low rate of nephrectomies?

This report does not say how quickly they were treated, i.e., how long from initial diagnosis until treatment with Nivolumab?A patient with Papillary Type II found to have no metastatic disease at the time of diagnosis, but who received a nephrectomy, was monitored for a year or so, then went on one or more systemic therapy is quite different from the patient with an unclassified RCC,  metastatic at the time of diagnosis, not given a nephrectomy, though treated quickly with Nivolumab.  What can be learned when there are such wide variations in just 23 patients that would be helpful to the Papillary Type 1 patient?

The follow up period was a median of 6.5 months, which seems very short, especially when the median Progression Free Survival of the responders was 4.2 months. The median OS is not given. That certainly may reflect an ongoing study situation, or a failure to provide a longer period of follow up.

As to objective response, 6 of  the 21 evaluable patients (29%) had a Partial Response, which would likely be a 30% reduction in metastases. Another 4(19%) had Stable Disease. Two of the 23 patients died, but not from the treatment. (Assume that had to be due to the disease, but certainly indicates that for nearly 10% of the patients, this was not at all effective.)

When the final analysis was done, nine patients were still receiving Nivo. Newly recruited patients might still be in treatment at that time, but those recruited earlier may have gone out of the trial at the same time.  It is important to not that Nivolumab treatments were stopped in three patients due to intolerance, and six more had postponed treatment, i.e., 9 of the 23.

Certainly we need to find meds which create responses for nccRCC patients. However,  I am concerned we draw any certain conclusions from this study.  Indeed, it is “good” to know that the treatment was tolerable for the majority of the participants, but not so good to read that 6 of the 21 patients had to postpone treatment, and three were removed from treatment due to intolerable/toxic side effects.  We also do not know which subtypes seem to have shown responses, which would have been qutie easy to report.  Did the group with Papillary Type II do generally better that the majority “unclassified” group?  No answer from this stury report. And in the back of my head, I keep wondering why in the world there were so many unclassified patients in this small study?  Was there a standard pathology review, or could these patients been misdiagnosed by one pathologist. Typically there is a single pathologist which can standardize the reporting.  Were all these patients properly diagnosed?

Just wishing there were greater clarity and hoping to get a fuller report, post ASCO.

Without a doubt, the ‘good’ that comes from this sort of report begins with the recognition that the nccRCC group is underserved by the research community> They probably have the poorest outcomes, rarely have a clear diagnosis, and must wait for the ever popular “further research is warranted.”  But all must be aware that these very small observational studies must be reviewed very carefully for what they show or do not show.  Again, one to watch at ASCO, but not enough to make a major change in treatment for any one with a non clear cell RCC.

PS.  Does your doctor know that there are at least four subtypes of clear cell–the big ‘common’ group–which have clearly different survival patterns?  Thought so.

 

2 Comments

Filed under Basics, Clinical Trials, Immune Therapies Old & New, Rarer RCC Cancers, Surgery, Therapies, Uncategorized

by | May 19, 2016 · 1:21 pm

Kidney Tumors & Diagnosis? Size Matters–Big Surprise

Kidney cancer is generally a very silent disease. It is sneaky, hides out for years, and is often assumed to be something else.  In my case, my doctor essentially decided I was just a menopausal women with the ever-popular “stress” as a an extra.  The stress of carrying about a 10 cm tumor and wasting away  was probably part of it.

That slow diagnosis, often delayed for years is far too typical.  Only the greater use of CT scans has been significant in finding kidney cancer at an early stage. And just what is early or small? Looking for a cracked rib, or the dislocated shoulder has often revealed kidney cancer, and in the case of the shoulder, lung mets.  And then the hunt is on!  By the time this diagnosis is made, nearly 30-40% of kidney cancer is already metastatic.

The ‘classic triad’ of symptoms, are 1) blood in the urine, 2) flank pain, and 3) palpable mass in the abdomen. There are doctors who will consider kidney cancer only when the patient has these three symptoms, but that happens in fewer than 10% of patients.  The cancer has to be pretty far along to be found this way.  Meeting a pair of new doctors who were aware of my kidney cancer, they were obviously bewildered to hear that I had had none of the these symptoms.  “But those are the usual symptoms,” one said.  Maybe ‘classical’, but not ‘usual’.  Unfortunately that expectation is a barrier to good diagnosis.

Beyond the diagnosis and the staging of the disease is the pretty obvious question of what to do next. (Staging: another of those words used one way in English, and quite another in medicine No wonder we are confused.)  Getting treatment is derived from that ‘staging’.  To be told your cancer is at Stage I seems the only  bright spot of a cancer diagnosis,  but not so reassuring with kidney cancer.  The  “SMALL” Stage I kidney tumor is one which is confined to the kidney (good news) and is 7 centimeters or less.  Maybe Europeans react with the required, “Yipes!”, but few Americans would until they know that this is almost 3 inches in size!

Ain’t so small in my world, or in my kidney!, or anywhere else. In my previously-naive patient world, I thought a ‘small’ tumor was the size of a pea, or maybe a peanut.  In any case, these so-called small tumor are Stage I, of four Stages.  Don’t even ask about Stage V.  Calling a near-three inch tumor small reflects the history of many very large tumors being found in the early days.  Even in 1997 there was discussion about whether a 5cm (2 inch) tumor should be the ‘small’, and in the 1987 system, it had to be 2.5cm to be small, ie, about one inch a T1 stage.  I do not understand why this basic staging was so dramatically changed, but it may well be that there were so few truly small tumors found in this early CT era.

In any case, we now have a system which lumps all tumors 7 cm or smaller into TI category, re-divided into T1a if under 4cm, and T1b, up to 7cms.  This minimizes the sense of risk that comes with these larger Stage I tumors, despite clear evidence of much greater risk at about as they grow.  That shift to a more aggressive tumor, capable of having metastatic potential, seems to start just over 1 inch, about 2.8cm.  There is a measurable increase in risk of about 62% at this size, so waiting around for a mass to be palpable (ie, it can be felt) puts us all at risk.  And of course, that metastatic potential has likely started even earlier, prepping the body to accept new cancer in new locations.

Thus, the absolute need to monitor patients who have had large ‘small’ tumors far more carefully and for a longer time.  The reality is that even truly small tumors have the ability to start the metastatic process.  Tiny and invisible even to a CT, they can grow unnoticed for several years.  There is no magic ‘five years/safe at home’ for kidney cancer patients, sad to say.

So, if your doctor tells you not to worry, that he got it all, that it was small, that there is no need for further monitoring, you might just find another doctor who keeps up with the kidney cancer literature.  If you got this far with this post, you may be ahead of your doctor.

Re the above risk stats, seehttp://www.cancertherapyadvisor.com/renal-cell-carcinoma/renal-cell-carcinoma-larger-tumors-high-grade-pathology/article/415189/

22 Comments

Filed under Guidelines, Newly Diagnosed, Patient Engagement, Patient Resources, RCC Basics, Uncategorized, Your Role

Tagged as

by | November 13, 2015 · 10:04 pm

Immune Therapies: Headlines, Hype or Hope?

Recent headlines called a new medication, Nivolumab, both a miracle or breakthrough and more.  Is it hype or hope?Why is it so hard to sort out the reality?

Let’s go through the facts from the New England Journal of Medicine and ignore the headlines. First, its being  in the NEJM is important, as it has passed review by other researchers.  (Sadly missing in too many ‘breakthroughs”).

The new med, Nivolumab was compared against Everolimus, a second-line treatment. Therefore Evero is thought to be of lesser effectiveness than the first line meds.  Second-line meds are generally used when others meds quit helping or their side effects are too hard. Automatically NOT the miracle cure, but another option when first-line treatments fail.

Should Nivo have been compared to the first-line meds?  Being better in the first-line would be bigger deal, but we need more approved meds. Second-line treatments usually are easier to ‘beat’, as the new med must be better or less toxic.  Again, more likely to be approved!

PATIENT CHARACTERISTICS

The study had 821 patients 24 countries, half using Nivo and half Evero. Patients were similar, 90% having had a nephrectomy, removing the tumor and some or all the kidney. Then the cancer spread, making metastases, (mets, for short). These patients had 1-3 treatments, first-line drugs like Sutent, a targeted therapy, and a few had used cytokines or even chemotherapy.  Having had an mTOR inhibitor like Everolimus was not acceptable. Most had lung mets (67%), followed by liver(12%) and then bone mets (18%). Most with 2 or more sites of mets.

To enter the trial, the patient had to have had disease progression after their last treatment, within six months of enrolling in the trial. No doubt, some patients had greater disease progression than others, but had relatively good performance status, not completely bed-ridden or unable to function.

The median time from initial diagnosis of kidney cancer at any stage to entering the trial was 31 months;  half had been diagnosed less than 31 months ago, and half more than 31 months before the trial. That range of time from diagnosis to trial was 1 to 392 months. That means that for some patients, they went a long time either fighting the disease since diagnosis, having a later recurrence, being treated, yet having disease progression years after the intial diagnosis.  At least one person was diagnosed 392 months earlier. This is a good reminder to patients who have been told, “I got it all”. This darn stuff can return, so having a plan B is important. Again, the previous treatment failed and these patients got directed into this trial.

GENERAL RESULTS

Median Overall Survival (OS) is a measured when one-half of the total number in the group dies. Median OS for Nivo was 25 months with some patients still surviving at time of report, beyond the 25 months. For Evero, OS was 19.6 months, some of who were also likely surviving, as well.  The OS of 25 months was clearly better with the Nivo group by this analysis. Nevertheless, half of all the 821 patients total died while on this trial from progressive disease.  Of  183 of the 410 Nivo patients, 183 has died by 25 months, and 215 of the 411 Evero patients had died at 19.6 months. 

 

There is no report of ongoing response here, but many went on to other meds, as explained below. 

Median Progression Free Survival (PFS), measurable growth of disease,  was 4.6 months for Nivo, 4.4 months for Evero.  The median shows that half of each group, roughly 200 each had return of disease in less than 5 months!  Again, these trial patients were pretty sick or at risk. All had been treated earlier, and had to stop previous treatments due to recurrence of disease. However, this shows a pretty quick return of disease or new growth from the base CT scan for nearly  65-70% of all patients.

One subgroup did a bit better than the 4 1/2 months median PFS.  At six months after the start of treatment, there was a special subgroup was noted,  about 1/3 of those patients–145 pts (35%) with Nivo, and 129 (31%) with Evero. Obviously they did not die or have Progressive Disease until after six months.  The Nivo group had eventually had a median PFS of 15.6months, and the Evero group, 11.7 months.  Their success pushed the median OS higher, especially for the Nivo group.

Obviously, there were some patients with far more aggressive disease in both groups, some dying before six months, and others not progressing to more disease until after six months.  In contrast, nearly 1/3 of all the patients had PFS of 12-15 months, and much longer OS. What is the common characteristic in the most successful two groups in both arms of treatment?  Not answered by this trial report.

The duration of treatment was longer with Nivo, and likely easier to tolerate. Since Nivo was given by IV every two weeks, the doses were most consistently received. Even so, 51% of them had dose delays, but no per dose reductions.  Those people were seen by the medical team every two weeks.

The Evero group took oral meds, and 66% had dose delays or interruptions with 26% with at least one dose reduction. This would indicate that these meds could be hard to take, or perhaps lacking the same interaction with their medical team.  Of course the Evero patients may have underreported how much of the medication they actually took!

However, the reported types of side effects were generally similar, but the more severe grade 3 and 4s effects in the Evero group.There were 2 treatment related deaths in the Ever group, none in the Nivo group.

POST PROGRESSIVE DISEASE

Even after the disease did progress, about half of  patients in both groups stayed with their meds–despite ‘failing’, the researchers hopes that would continue to benefit, perhaps slowing the disease.  In a local clinic setting or with a less experienced docs, their meds might have been stopped or changed. Afterall, those meds were no longer “working” and  mets are growing. This approach is significant to consider, especially after multiple treatments.  (The decision to keep giving a medication or increasing its dosage where tolerable is causing some changes in treatment in a number of the targeted therapies.)

Perhaps because of being in a trial or getting care than was more expert than most, one-half of  patients chose to keep on the trial meds.  Others crossed over to the med in the other arm or returned to existing non-trial meds. In some countries, there were likely fewer choices than in the US.  There are no real stats as to survival for those on those who stopped taking the meds. It is reported that indicate that 55% of the surviving Nivo group and surviving 63% of the Evero group went on to other agents. About one-quarter of the Nivo group shifted to  the Evero. Of the Nivo group, 36% shifted to axitinib.

Sadly, as per the chart in the New England Journal of Medicine, all these patients had died by 30-33 months post enrollment.  However, it is again not clear what was effect, if any on that period from the non-trial drugs.  Of the 227 who stopped Nivo for any reason, nearly half shifted to Evero. Of those who stopped Evero, 140 went to Axitinib.

DURABLE RESPONSES?  HOW LONG? FOR HOW MANY?

The writers of the study say that there was a higher number of objective responses with Nivo vs Everolimus, and that many (of the Nivo group) “were durable”.  There is no definition of ‘durable’.  My question is “What equals durable?”.  We patients really want a cure, but are very grateful for anything that pushes the cancer back, slows it, stops in from growing any further. Nevertheless, we do want those responses to last.  The clearest reference to durable responses is a note that 32 of the Nivo patients and 6 of the Evero patients had a response that lasted more than 12 months.  But in an unexplained statement, the median duration of treatment was just 5.5 months for the Nivo patients, 3.7 for the Evero group.  It seems that there was not an extension available, or that the patients moved on to a different treatment or passed away.

CONCLUSIONS AND EDITORIALIZING AGAIN

It seems that Nivo is more helpful for some patients than others in this group previously been treated with other TKIs. This is NOT A SILVER BULLET.  There would be greater value to know more about the molecular nature of  the tumors of the responding and the non-responding patients.  We desperately need to know for whom any of these drugs is likely to be more effective.  The headlines that don’t discuss that challenge underserve us, as does the design of the trial that does not elicit the more nuanced, genomic data that could be forthcoming!

We all know that headline claims are more wonderful  than the reality.  The story of RCC medication development is that of more and more help in a difficult disease, making mixed progress, while the other researchers find out that RCC is really many diseases.  Clear cell is probably better defined as being made up of four types, Papillary Type 1 and Type 2 being further divided into three Type 2, then there is chromophobe, clear cell papillary and the really odd versions of RCC.  I known this, and so do you.  But why don’t the researchers incorporate those definitions and monitor the patients with those various subtypes as they go forward?

Good luck to all of us.

 

1 Comment

Filed under Clinical Trials, genomics, Genomics & Genes, Immune Therapies Old & New, Newly Diagnosed, Patient Activism, Therapies, Uncategorized

Link

We hear of “patient engagement” as a topic, but it can be misused in a self-serving way! For some hospitals, it comes in the form of a survey that asks your opinion of the newly-remodeled lobby, but never asks if you were properly treated while in the hospital.  That is my least favorite and most cynical use of ‘patient engagement’ efforts.

We patients must be engaged, especially needed in this cancer world.  But that is a huge challenge when we have not be taught by experience or the medical world to do so.  Just how does the nervous or bewildered patient do that when the problem is confusing or terrifying?

Starting with what we know about ourselves and knowing HOW to explain it is obvious, but not easy.  Just how to do that?

See what doctors are learning, as in the following short article.  There is a link to a Patient ToolKit  http://www.patient-experience.org/PDFs/Patient_Toolkit_v4A_Fillable-Format.aspx developed by others who work with me to improve diagnosis.  This is available for anyone to use, can be filled in online or printed out as needed.

Simply, it helps the patient organize his symptoms, concerns and history in a way that MIGHT be more acceptable to the doctor.  It can remind you well ahead of the appointment what to do so that the appointment is more useful and efficient.

Your ideas gratefully requested.

http://www.patient-experience.org/Resources/Blogs/DM-Blog/Blogs/July-2015-(1)/Engaging-Patients-Before-You-Even-See-Them-Tools-t.aspx

2 Comments

by | July 30, 2015 · 9:58 am