30 Years Cushing’s Free!

 

Today is the 30th anniversary of my pituitary surgery at NIH.

As one can imagine, it hasn’t been all happiness and light.  Most of my journey has been documented here and on the message boards – and elsewhere around the web.

My Cushing’s has been in remission for most of these 30 years.  Due to scarring from my pituitary surgery, I developed adrenal insufficiency.

I took growth hormone for a while.

When I got kidney cancer, I had to stop the GH, even though no doctor would admit to any connection between the two.  Even though I’m when I got to 10 years NED (no evidence of disease) from cancer, I couldn’t go back on the GH.

However, this year I went back on it (Omnitrope this time) in late June.  Hooray!  I still don’t know if it’s going to work but I have high hopes.  I am posting some of how that’s going here.

During that surgery, doctors removed my left kidney, my adrenal gland, and some lymph nodes.  Thankfully, the cancer was contained – but my adrenal insufficiency is even more severe than it was.

In the last couple years, I’ve developed ongoing knee issues.  Because of my cortisol use to keep the AI at bay, my endocrinologist doesn’t want me to get a cortisone injection in my knee.

My mom has moved in with us, bring some challenges…

But, this is a post about Giving Thanks.  The series will be continued on this blog unless I give thanks about something else Cushing’s related 🙂

I am so thankful that in 1987 the NIH existed and that my endo knew enough to send me there.

I am thankful for Dr. Ed Oldfield, my pituitary neurosurgeon at NIH.  Unfortunately, Dr. Oldfield died a couple months ago.

I’m thankful for Dr. Harvey Cushing and all the work he did.  Otherwise, I might be the fat lady in Ringling Brothers now.

To be continued in the following days here at http://www.maryo.co/

Giving Thanks, Day 4: October 21, 2017

Adapted from this post: http://www.maryo.co/giving-thanks-day-4-october-21-2017/

 

 

I am so thankful for all my doctors but today I am thankful for Dr. Amir Al-Juburi who saved my life by removing my kidney cancer (renal cell carcinoma).

 

In 2006 I picked up my husband for a biopsy and took him to an outpatient surgical center. While I was there waiting for the biopsy to be completed, I started noticing blood in my urine and major abdominal cramps. I left messages for several of my doctors on what I should do. I finally decided to see my PCP after I got my husband home.

 

When Tom was done with his testing, his doctor took one look at me and asked if I wanted an ambulance. I said no, that I thought I could make it to the emergency room ok – Tom couldn’t drive because of the anesthetic they had given him. I barely made it to the ER and left the car with Tom to park. Tom’s doctor followed us to the ER and became my new doctor.

 

When I was diagnosed in the ER with kidney cancer, Tom’s doctor said that he could do the surgery but that he would recommend someone even more experienced, Dr. Amir Al-Juburi.

 

Dr. Amir Al-Juburi has been so kind to me, almost like a kindly grandfather might be, and he got rid of all 10 pounds of my kidney and cancer.

 

I owe him, the original doctor, and my Cushing’s doctors (who will be featured later!), my life.

 

Targeted drug shows promise in rare advanced kidney cancer

Some patients with a form of advanced kidney cancer that carries a poor prognosis benefited from an experimental drug targeted to an abnormal genetic pathway causing cancerous growth, according to research led by a Dana-Farber Cancer Institute scientist.

The drug, savolitinib, showed clinical activity in patients with metastatic papillary renal cell carcinoma (PRCC) whose tumors were driven by overactivity of the MET signaling pathway, but was not effective for patients whose tumors lacked the MET abnormality, said the investigators, led by Toni Choueiri, MD, director, Lank Center for Genitourinary Oncology, and director, Kidney Cancer Center, both of Dana-Farber.

These results from a single-arm, multicenter phase II clinical trial, reported in the Journal of Clinical Oncology, suggest that savolitinib holds promise as a personalized treatment for a subgroup of patients with metastatic papillary renal cell carcinoma, the researchers said.

In the US alone, about 6,400 cases of PRCC are expected to be diagnosed in 2017, compared to a total of 64,000 cases of kidney cancers. The majority of them are classified as clear cell renal cell cancers. Papillary renal cell carcinoma are non-clear cell kidney cancers. No good treatments exist for advanced or metastatic PRCC.

The current trial tested savolitinib, a potent and selective MET inhibitor, in 109 patients with locally advanced or metastatic PRCC. Of the 109 patients, 40 percent had tumors driven by MET, 42 percent had tumors that did not rely on MET, and MET status was unknown in 17 percent of patients.

When the results were analyzed, 18 percent of patients with MET-driven cancers had significant shrinkage of their tumors, and 50 percent had stable disease. By contrast, none of the patients with MET-independent tumors had shrinkage response, and only 24 percent had stable disease.

In addition, the length of time after treatment before the cancer began growing was significantly longer in the MET-driven tumor group – 6.2 months versus 1.4 months.

“These data support the hypothesis that savolitinib has antitumor activity in patients with MET-driven papillary renal cell carcinoma,” the authors wrote. “Our study identified a defined molecular group and highlights the prevalence of MET-driven disease in this rare population of RCC patients.”

Although some patients had their dosage of savolitinib reduced and two patients discontinued treatment because of side effects, the researchers said the drug was generally well-tolerated.

Explore further: New models of kidney cancer may drive immunotherapy research

Journal reference: Journal of Clinical Oncology search and more info website

Provided by: Dana-Farber Cancer Institute

Read more at: https://medicalxpress.com/news/2017-06-drug-rare-advanced-kidney-cancer.html#jCp

Adventures with Human Growth Hormone

I’ve been dealing with Cushing’s since 1983.  The after effects of pituitary surgery since 1987, kidney cancer since 2006.  It’s time I felt better, already!

From 1999 to today,  not-so-quick recap from my bio:

1999 ~ Many people are now finding that they need HgH after pituitary surgery, so an Insulin Tolerance Test was performed. My endocrinologist painted a very rosey picture of how wonderful I’d feel on Growth Hormone. It sounded like a miracle drug to me!

I was only asked to fast before the ITT and to bring someone with me to take me home. There is no way I could have driven home. I got very cold during the test and they let me have a blanket. Also, though, lying still on that table for so long, my back hurt later. I’d definitely take – or ask for – a pillow for my back next time. They gave me a rolled up blanket for under my knees, too.

I don’t remember much about the test at all. I remember lying very still on the table. The phlebotomist took blood first, then tried to insert the IV (it took a few tries, of course). Then the endo himself put the insulin in through the IV and took the blood out of that. I remember the nurse kept asking me stupid questions – I’m sure to see how I was doing on the consciousness level. I’d imagine I sounded like a raving lunatic, although I believed that I was giving rational answers at the time.

Then everything just got black…I have no idea for how long, and the next thing I knew I was becoming aware of my surroundings again and the doctor was mumbling something. They gave me some juice and had me sit up very slowly, then sit on the edge of the table for a while. When I thought I could get up, they gave me some glucose tablets “for the road” and called my friend in. I was still kind of woozy, but they let her take me out, very wobbly, kind of drunk feeling.

My friend took me to a close-by restaurant – I was famished – but I still had trouble with walking and felt kind of dazed for a while. When I got home, I fell asleep on the sofa for the rest of the day.

But the most amazing thing happened. Saturday and Sunday I felt better than I had for 20 years. I had all this energy and I was flying high! It was so wonderful and I hoped that that was from the HgH they gave me to wake me up.

2001 ~ I had the ITT this morning. I don’t get any results until a week from Thursday, but I do know that I didn’t recover from the insulin injection as quickly as I did last time. The endo made a graph for my husband of me today and a “normal” person, although I can’t imagine what normal person would do this awful test! A normal person’s blood sugar would drop very quickly then rise again at about a right angle on the graph.

I dropped a little more slowly, then stayed very low for a long time, then slowly started to rise. On the graph, mine never recovered as much as the normal person, but I’m sure that I did, eventually.

The test this time wasn’t as difficult as I remember it being, which is good. Last time around, I felt very sweaty, heart pounding. I don’t remember any of that this time around. I do know that I “lost” about an hour, though. The phlebotomist took the first blood at 9:15, then the endo injected the insulin and took blood every 15 minutes after that. I counted (or remembered) only 4 of the blood draws, but it was 11:30 when they told me that my sugar wasn’t coming up enough yet and I’d have to stay another 30 minutes. It actually ended up being another hour.

Kim, the phlebotomist, asked me if I got a headache when they “crashed me” and I have no recollection of any of that.

Like last time, I was very, very cold, even with the blanket and my left arm – where the heplock was – fell asleep. Other than that – and my back hurting from lying on one of those tables all that time this wasn’t as bad as I remembered.

So, I waited for 10 days…

September 2004 ~ My new doctor was wonderful. Understanding, knowledgeable. He never once said that I was “too fat” or “depressed” or that all this was my own fault. I feel so validated, finally.

He looked through my records, especially at my 2 previous Insulin Tolerance Tests. From those, he determined that my growth hormone has been low since at least August 2001 and I’ve been adrenal insufficient since at least Fall, 1999 – possibly as much as 10 years! I was amazed to hear all this, and astounded that my former endo not only didn’t tell me any of this, he did nothing. He had known both of these things – they were in the past records that I took with me. Perhaps that was why he had been so reluctant to share copies of those records. He had given me Cortef in the fall of 1999 to take just in case I had “stress” and that was it.

The new endo took a lot of blood (no urine!) for cortisol and thyroid stuff. I’m going back on Sept. 28, 2004 for arginine, cortrosyn and IGF testing.

He has said that I will end up on daily cortisone – a “sprinkling” – and some form of GH, based on the testing the 28th.

October 2004 ~ I had cortrosyn and arginine-GHRH stimulation test at Johns Hopkins. They confirmed what the doctor learned from reading my 4 year old records – that I’m both adrenal-deficient and growth hormone-deficient. I started on my “sprinkle” (5 mg twice a day) of Cortef now and my new doctor has started the paperwork for GH so maybe I’m on my way…

November 2004 ~ Although I have this wonderful doctor, a specialist in growth hormone deficiency at Johns Hopkins, my insurance company saw fit to over-ride his opinions and his test results based on my past pharmaceutical history! Hello??? How could I have a history of taking GH when I’ve never taken it before?

Of course, I found out late on a Friday afternoon. By then it was too late to call my case worker at the drug company, so we’ll see on Monday what to do about an appeal. My local insurance person is also working on an appeal, but the whole thing sounds like just another long ordeal of finding paperwork, calling people, FedExing stuff, too much work when I just wanted to start feeling better by Thanksgiving. I guess that’s not going to happen, at least by the 2004 one.

As it turns out the insurance company rejected the brand of hGH that was prescribed for me. They gave me the ok for a growth hormone was just FDA-approved for adults on 11/4/04. The day this medication was approved for adults was the day after my insurance said that’s what is preferred for me. In the past, this form of hGH was only approved for children with height issues. Am I going to be a ginuea pig again? The new GH company has assigned a rep for me, has submitted info to the pharmacy, waiting for insurance approval, again.

December 2004 ~ I finally started the Growth Hormone last night – it’s like a rebirth for me. I look forward to having my life back in a few months!

January 2005 ~After a lot of phone calls and paperwork, the insurance company finally came through at the very last minute, just as I needed my second month’s supply. Of course, the pharmacy wouldn’t send it unless they were paid for the first month. They had verbal approval from the insurance, but the actual claim was denied. Talk about a cliff hanger!

Later January 2005 ~I’ve been on the growth hormone for 7 weeks now, and see no change in my tiredness and fatigue. A couple weeks ago, I thought there was a bit of improvement. I even exercised a little again, but that was short lived.

I feel like my stomach is getting bigger, and Tom says my face is looking more Cushie again. Maybe from the cortisone I’ve been taking since October. I can’t wait until my next endo appointment in March to increase my GH. I want to feel better already!

March 2005 ~ My IGF-1 was “normal” so I can’t increase the GH.

September 2005 ~ I don’t see any benefit with the growth hormone.

January 2006 ~A new year, a new insurance battle. Once again, they don’t want to pay so I have to go through the whole approval process again. This involves phone calls to Norditropin (the company that makes the GH), my endo, iCore Specialty Pharmacy (the people who prepare and ship the meds) and my insurance company. This is turning into a full-time job!

April 14, 2006 ~I just went to see my endo again on Thursday to see how things are. Although I know how they are – I’m still tired, gaining a little weight, getting some red spots (petechiae) on my midsection. He also noted that I have a “little” buffalo hump again.

My endo appointment is over. Turns out that the argenine test that was done 2 years ago was done incorrectly. The directions were written unclearly and the test run incorrectly, not just for me but for everyone who had this test done there for a couple years. My endo discovered this when he was writing up a research paper and went to the lab to check on something.

So, I’m off GH again for 2 weeks, then I’m supposed to be retested. The “good news” is that the argenine test is only 90 minutes now instead of 3 hours.

April 27, 2006 ~ Wow, what a nightmare my argenine retest started! I went back for that. Although the test was shorter, I got back to my hotel and just slept and slept. I was so glad that I hadn’t decided to go home after the test.

The next day I felt fine and drove back home, no problem. I picked up my husband for a biopsy and took him to an outpatient surgical center. While I was there waiting for the biopsy to be completed, I started noticing blood in my urine and major abdominal cramps. I left messages for several of my doctors on what I should do. I finally decided to see my PCP after I got my husband home.

When Tom was done with his testing, his doctor took one look at me and asked if I wanted an ambulance. I said no, that I thought I could make it to the emergency room ok – Tom couldn’t drive because of the anesthetic they had given him. I barely made it to the ER and left the car with Tom to park. Tom’s doctor followed us to the ER and became my new doctor.

They took me in pretty fast since I was in so much pain, and had the blood in my urine. They thought it was a kidney stone. After a CT scan, my new doctor said that, yes, I had a kidney stone but it wasn’t the worst of my problems, that I had kidney cancer. Wow, what a surprise that was! I was admitted to that hospital, had more CT scans, MRIs, bone scans, they looked everywhere.

My open radical nephrectomy was May 9, 2006, in another hospital from the one where the initial diagnosis was made. My surgeon felt that he needed a specialist from that hospital because he believed preop that my tumor had invaded into the vena cava because of its appearance on the various scans. Luckily, that was not the case.

My entire left kidney and the encapsulated cancer (10 pounds worth!) were removed, along with my left adrenal gland and some lymph nodes. Although the cancer (renal cell carcinoma AKA RCC) was very close to hemorrhaging, the surgeon believes he got it all. He said I was so lucky. If the surgery had been delayed any longer, the outcome would have been much different. I will be repeating the CT scans every 3 months, just to be sure that there is no cancer hiding anywhere. As it turns out, I can never say I’m cured, just NED (no evidence of disease). This thing can recur at any time, anywhere in my body.

I credit the argenine re-test with somehow aggravating my kidneys and revealing this cancer. Before the test, I had no clue that there was any problem. The argenine test showed that my IGF is still low but due to the kidney cancer I cannot take my growth hormone for another 5 years – so the test was useless anyway, except to hasten this newest diagnosis.

August 19, 2006 ~ I’ve been even more tired than usual now that I’m off GH.  But I also had cancer.

October 2006 ~ I went to see my Johns Hopkins endo again last week. He doesn’t “think” that my cancer was caused by the growth hormone although it may well have encouraged the tumor to grow faster than it would have.

I was so stupid way back in 1987 when I thought that all my troubles would be over when my pituitary surgery was over.

2016/2017 ~ So.  My 10 year kidney cancer anniversary passed, then 11.

May 4, 2017 ~ My endo at Hopkins and I talked about maybe trying growth hormone again.  We tested my levels locally and – surprise – everything is low, again.

So, we started the insurance routine again.  My insurance rejected the growth hormone I took last time around.  I just love how someone, a non-doctor who doesn’t know me, can reject my person endocrinologist’s recommendation.  My endo who specializes in Growth Hormone, who runs clinical trials for Johns Hopkins on “Control of growth hormone secretion, genetic causes of growth hormone deficiency, consequences of growth hormone deficiency.”

That insurance person has the power over the highly trained physician.  Blows my mind.

But I digress.  My doctor has agreed to prescribe Omnitrope, the insurance-guy’s recommendation.

June 14, 2017 ~ I got a call from my insurance.  They “may” need more information from my doctor…and they need it in 72 hours.

My doctor’s nurse says that they have to refer this to their pharmacy.

June 15, 2017 ~ I got a call from the Omnitrope folks who said they will need approval from my insurance company <sigh> but they will send me a starter prescription of 30 days worth.

June 16, 2017 ~ I got a call from the Specialty Pharmacy.  They’re sending the first month supply on Tuesday.  Estimated co-pay is $535 a month.  I may have to rethink this whole thing 😦   We sure don’t have an extra $6000.00 a year, no matter how much better it might make me feel.

June 19, 2017 ~ The kit arrived with everything but the actual meds and sharps.

June 20, 2017 ~ The meds and sharps arrived along with the receipt.  My insurance paid nearly $600 – and they took my copay out of my credit card for $533.

I still have to wait for the nurse’s visit to use this, even though I’ve used it in the past.

I’ve been doing some serious thinking in the last 24 hours.  Even if I could afford $533 a month for this, should I spend this kind of money on something that may, or may not, help, that may, or may not, give me cancer again.  We could do a couple cruises a year for this much money.  I’ve pretty much decided that I shouldn’t continue, even though I haven’t taken the first dose of this round.

What will happen?

Stay tuned!

Perioperative Systemic Therapy for Kidney Cancer: Current Data and Ongoing Trials

Kidney Cancer

 

Chicago, IL (UroToday.com) Dr. Uzzo gave the third and final talk in this excellent session highlighting systemic therapy in the management of kidney cancer. Focusing specifically on the role of perioperative systemic therapy (neoadjuvant [NAC] and adjuvant [AC]), he adeptly covered the prior literature and the future directions of this important intersection between surgery and systemic therapy. While his talk was extensive, below we will review the major highlights and key points.

Ultimately, in Dr. Uzzo’s eyes, we are all managers of health care risk. We seek to “understand, predict and prevent future health care events.” As such, from the time of diagnosis, the key steps in managing a patient are: identify risk (screening, etc), utilize risk tools to risk stratify, communicate this risk to the patient, and finally, mitigate risk with intervention.

Looking at biomarkers in the kidney cancer space, he highlights the key point that biomarkers have been few and far between for RCC. At the end of the day, commonly used biomarkers such as stage, grade, and histology still remain the standards for risk stratification. While numerous biomarkers (genetic, epigenetic, etc) have been evaluated, none have been demonstrated to be superior to stage, grade and histology. As biomarkers have failed to improve upon these factors, we also looked to different models to help stratify patients. In the localized RCC disease space, these include the UISS, MSKCC, SSIGN, and Mayo clinical models (among others) to predict recurrence, but the C-index for these tests ranged between 0.76-0.89. However, all the models shared common features that are easily identified clinically – stage, grade, tumor size, performance status, presentation, age, gender, and coagulative necrosis. Models for metastatic RCC are even less capable of predicting cancer-specific mortality (C-indices ~0.6). At this point, biomarkers and models give way to common patient and pathologic characterizations for risk stratification.

Neoadjuvant Therapy (NAT)
Dr. Uzzo provided a very nice comparison of the “Halstedian” model and “Fisheresque” model of cancer progression. Dr. Halsted, a legend in oncologic surgery, believed in stepwise progression of disease from stage 1 -> stage 2 -> stage 3 -> stage 4, which supported utilization of adjuvant therapy rather than NAT. However, Dr. Fisher was a strong proponent of the idea that a subset of patients were likely metastatic at inception, which better supported the need for NAC.

When looking at NAT, there are some key questions:

1) Does it work? (does it shrink the tumor? Can it work as a “litmus test” prior to cytoreduction? Can it control distant disease?)
2) Is it safe?
3) Are there translational signals?

In terms of tumor shrinkage, based on retrospective series and phase II trials, it results in approximately 25% tumor volume reduction, with an objective response rate (ORR) in 30-40% of patients. So, if patients are referred for that indication, that is what a medical oncologist can cite to a surgeon. However, the implications of this are heavily surgeon dependent, and as Dr. Uzzo states, it is a “function of judgment and experience” – if they feel that this will allow for partial resection vs. radical nephrectomy, or make a non-operative patient operative, then it may be worthwhile to proceed. This is difficult to quantify in clinical studies, and selection bias is an unavoidable issue. In his review of NAT to facilitate partial nephrectomy (PNx), there were <200 cases amongst 7 series.1 Similarly, there have primarily only been case reports/series demonstrating tumor thrombus reduction (25-40%), but rarely does it change the level of thrombus without a concomitant risk of toxicity.

In terms of efficacy, he reviewed a few clinical trials of neoadjuvant targeted therapies, including pazopanib.2 While many of these had some tumor size reduction, they often had high rates of patients not making it to surgery due to adverse events. Importantly though, a significant portion did not make it to surgery due to progression of extrarenal disease. As such, he emphasizes that NAT may be utilized as a litmus test for patient response. Patients progressing on NAT likely wouldn’t have benefited from surgery anyway.

No biomarkers have correlated with ORR in NAT trials.

In summary, NAT is not in the guidelines, high quality guidelines are limited, and there is no long-term data. While newer therapies (cabozantinib, immune checkpoint blockage) may change management, clinical trials are the recommendation for now.

Three clinical trials in NAT space:
CARMENA – activated in 2009, still accruing but having difficulty. Testing the importance of surgery – comparing surgery + adjuvant sunitinib vs. sunitinib alone.
SURTIME – testing sequencing (sunitinib -> surgery vs. surgery -> sunitinib). While initially expecting 440 patients, they have modified study to accrue 98 patients (study closed). In data analysis phase now.
ADAPT – SUO CTC joint effort, they have accrued 713/1133 patients in 3 years. Tests sequencing, including the use of autologous dendritic cell immunotherapy and sunitinib.

Adjuvant Therapy (AT)
Recent publications on adjuvant trials have increased interest in this treatment option. However, there are still no approved ATs for RCC. Dr. Uzzo breaks down the history of AT in RCC into three time periods: the “dark ages”, the “middle ages” and “the future.”

In the “dark ages” of AT, numerous trials were done but it combined “ineffective surgery with completely ineffective systemic therapy.” None of them showed significant benefit, though many had significant flaws.3

More recently, we have come into the “middle ages”, where we utilize “ineffective surgery with more effective systemic therapy.” As is well known, S-TRAC4 and ASSURE5, presented conflicting results regarding disease-free survival outcomes in the adjuvant setting. Dr. Uzzo did highlight the key differences in the studies (only cT3-4 disease in S-TRAC, primarily clear-cell histology in S-TRAC) that may have contributed to the discrepancy. However, even when the clear-cell subset of the ASSURE cohort was analyzed, there was no DFS benefit. Two ongoing trials for whom results are pending are PROTECT (pazopanib) and SORCE (sorafenib). The PROTECT trial investigators should be presenting their results later in the meeting.

He very nicely looked at the role of adjuvant therapy in other malignancies (breast cancer, colorectal cancer, melanoma and GIST) and found DFS benefit to be 4-11% (modest), often times with significant monthly cost. As such, he makes a good point, that adjuvant therapy touted as standard of care in other malignancies doesn’t have as much of a benefit as we often put faith in.

Adjuvant therapy is only marginally effect because of
1) Poor timing and patient selection
2) Bad biology
3) Ineffective therapies

In RCC, based on prior literature regarding growth kinetics, tumor doubling time, and presentation of metastatic disease, micrometastases typically present as visible disease between 6-11 years later. Perhaps we are not giving systemic therapy at the right time?

So, while it has not been shown to be highly effective in RCC yet, he recommends:
1) Improving timing (using CTCs and biomarkers)
2) Attacking tumor stem cells (yet to be identified)
3) Attack less promiscuous upstream targets (balance toxicity for specificity)

The future is promising. The “New” Age hopes to combine “incompletely effective surgery with potentially more effective systemic therapy.” He cites two trials, the ECOG PROSPER trial (nivolumab) and the SUO-CTC INmotion trial (atezolizumab), as upcoming studies with novel therapies that may provide new standards.

Overall, in terms of perioperative systemic therapy for RCC, there are no approved options. However, clinical trials with more effective therapies and better patient selection represent the future.

Presented By: Robert G. Uzzo, MD, FACS, Fox Chase Cancer Center, Philadelphia, PA

Written By: Thenappan Chandrasekar, MD, Clinical Fellow, University of Toronto, Princess Margaret Cancer Centre
Twitter: @tchandra_uromd

at the 2017 ASCO Annual Meeting – June 2 – 6, 2017 – Chicago, Illinois, USA

From https://www.urotoday.com/conference-highlights/asco-2017/asco-2017-renal-cancer/96168-asco-2017-perioperative-systemic-therapy-for-kidney-cancer-current-data-and-ongoing-trials.html?utm_source=newsletter_4518&utm_medium=email&utm_campaign=asco-2017-day-2-highlights

Kidney Cancer Symptoms: 12 Early Warning Signs of the Life-Threatening Disease

 

More than 12,000 people in the UK are diagnosed with kidney cancer each year, according to 2014 statistics.

And although 42% of cases are deemed “preventable”, only 50% of patients survive kidney disease for 10 or more years.  I will celebrate 11 years next month, on May 9!

It’s the seventh most common cancer in the UK and is much more prevalent in males.

But do you know the warning signs of the potentially deadly disease?

Here we reveal the 12 main symptoms of kidney cancer:

1. Blood in your pee  Not until the day I was diagnosed.

You may notice your pee is darker than normal or reddish in color. This could also be a sign of chronic kidney disease and bladder cancer.

2. A persistent pain in your lower back or side, just below your ribs No

3. A lump or swelling in your side (although kidney cancer is often too small to feel) No

4. Extreme tiredness (fatigue) Possibly, although I assumed it was from Cushing’s

5. Loss of appetite and weight loss No

6. Persistent high blood pressure Yes

7. A high temperature of 38C (100.4F) or above No

8. Night sweats No

9. In men, swelling of the veins in the testicles Nope

10. Swollen glands in your neck No

11. Bone pain No

12. Coughing up blood No

If you are concerned about any of these symptoms you should see you GP, they will carry out a series of tests, including urine and blood tests, in order to get an accurate diagnosis.

What are the treatment options?

The treatment will depend on the size and severity of the cancer and whether it has spread to other parts of the body.

These are the five main treatments:

1. Surgery to remove part or all of the affected kidney Yes, all plus some other stuff

This the main treatment for most people

2. Ablation therapies No

Where the cancerous cells are destroyed by freezing or heating them

3. Biological therapies No

Medications that help stop the cancer growing or spreading

4. Embolisation No

A procedure to cut off the blood supply to the cancer

5. Radiotherapy No

Where high-energy radiation is used to target cancer cells and relieve symptoms

For more information go to nhs.uk/Conditions/Cancer-of-the-kidney

Adapted from http://www.dailystar.co.uk/health/605586/Kidney-cancer-symptoms-treatment-males-females-early-warning-signs

Go for new cancer treatments

WHEN it comes to cancer, many healthcare professionals advocate early detection to increase the chances of successful treatment. In reality, this is hardly the case. Although there are no Malaysian-centric statistics, research has shown that almost 50% of cancer patients in Britain are diagnosed late, making treatment less likely to succeed and reducing their chances of survival.

What this means is we need to ensure that patients with late diagnosis are able to access treatment without compromising their quality of life.

Renal cell carcinoma (RCC) or kidney cancer is often diagnosed late. This is because the symptoms for RCC are similar to those of other diseases and may only surface in the late stages. In fact, 49% of patients in Malaysia are diagnosed with RCC when the cancer is in the final stage (Stage IV). A study showed that the five-year survival rate of patients with Stage IV RCC was only 13%.

Kidney cancer is among the top 10 cancers in Western communities. According to the 2007 Malaysia National Cancer Registry Report, RCC accounts for 43.8% of new kidney cancers. However, these statistics are quite dated as it has been nine years since the data was collected.

Advances in medical research have led to new treatment modules. A revised healthcare policy should ideally be aligned with innovation in cancer treatments. Despite new targeted therapies being approved for use in the US and Europe, these therapies are still limited in most parts of South-East Asia, including Malaysia. And even if they are available in the market, patients have to purchase the drugs from private medical facilities, excluding the majority of Malaysians (75%) who seek treatment at government hospitals.

In the treatment for RCC, there is only one drug approved in the government formulary. More options are needed because a single drug may not be right for every patient. For those who are not able to respond to this particular treatment, access to an alternative drug is often a lengthy and uncertain process. For some patients, the options available to them are so dismal, there is almost a case of no option at all.

In developed countries, drug choices are fully funded by the government, leading to patients having equal access to various drugs of treatment that best suit them. In Malaysia, drug choices are limited. Patients may have to pay out-of-pocket to access these treatments, putting them in a financial dilemma of cost versus survival.

In fact, a recent study by Universiti Malaya showed that 5% of cancer patients and their families were pushed into poverty, and that cancer resulted in “financial catastrophe” for almost half of the patients who suffered from economic hardship.

The policy of approving new drugs is based on an analysis of the quality of life years patients gain versus the cost of the drug. Unfortunately, drug affordability is determined by pharmaceutical companies based on the affordability of developed countries. This leads to a mismatch in drug affordability in a country like Malaysia, where Malaysians have a diverse range of economic situations. Furthermore, no matter how clinically effective a drug is touted to be, no drug has been approved in the government formulary in recent years.

Cancer is set to be a major burden of disease worldwide and the leading cause of morbidity and mortality. It is imperative for policy makers to review and update the targeted cancer therapy treatments currently available in the national formulary so that efficacious medicines are accessible to the majority of the population in public hospitals.

We hope increased funding will be made available to assist patients in their treatment, allowing them to live longer with a better quality of life and without putting them at risk of financial catastrophe.

While Malaysia’s public healthcare system continues to evolve to meet the needs of a growing and aging population as well as alarming rate of non-communicable diseases (NCD), let us be aware of the imperative need for this country to also keep abreast of breakthrough therapies available for patients and to champion for these therapies to be accessible at our public hospitals.

Cancer does not discriminate. Every patient, regardless of their economic status or cancer stage, deserves access to treatment.

DATUK DR MOHD IBRAHIM ABDUL WAHID

Medical Director, Beacon International Medical Centre

Vice President of College of Radiology (COR) Malaysia