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A beer a day keeps stones away

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This month the Twitter-based International Urology Journal Club #urojc made a bold move away from cancer to discuss kidney stones. The paper entitled ‘Soda and other beverages and the Risk of Kidney Stones’ by Ferraro et al. was published online on 15th March 2013. Open access to the article was generously provided by the Clinical Journal of the American Society of Nephrology. The lead author, Pietro Manuel Ferraro, was kind enough to actively participate within the Twitter discussion.

This particular study looked at a total of 194 095 participants amalgamated from the Harvard-based Health Professionals Follow-Up Study and The Nurses Health Studies I and II. These individuals all filled in biennial questionnaires regarding their diet, general health and kidney stone pain for a median follow up period of 8 years. It is interesting that the event rate was relatively low with only 4462 cases identified, however it is important to note that the study looked only for new stone formers and persons who had previously had a kidney stone were excluded from the trial. At the outset this begs the question as to whether these results are in any way applicable to the recurrent stone former population.

 

So what did they find? The referent is the consumption of less than one drink per month, so with respect to daily consumption of one or more sugar sweetened colas there was a 23% increased risk in the incidence of renal calculi. Other beverages to show a statistically significant increased risk of stones included:

Sweetened non-cola soft drinks 33% increased risk
Artificially sweetened non-cola soft drinks 17% increased risk (p=0.05)
Punch (sugar sweetened fruit drink) 18% increased risk

 

And what decreases your risk?   % risk reduction        
Coffee 26%                 
Decaffeinated coffee 16%
Tea 11%
Red Wine 31%
White Wine 33%
Beer 41%
Orange Juice 12%          

 

Missing my poison of choice, diet cola? While there was a trend towards a decreased risk, this was not found to be statistically significant. But not an increased risk….so I may just keep drinking it for the time being. I am not alone.


There were certainly more than one of the so called Urological ‘Twitterati’ who seemed delighted that the study findings justified their habits:

   

There are undoubtedly limitations with any cohort questionnaire analysis. The authors have acknowledged that while they tried to control and adjust for variables including age, BMI, diabetes, race, BP and dietary intake, there are variables that simply cannot be accounted for on the basis of a simple questionnaire. Fructose, for example, is purported to be a potential contributor to the increased risk of stones by increasing calcium, oxalate and uric acid excretion. There are many other dietary sources of fructose, including fruits, cereals and processed foods and sauces that are not accounted for and are potential confounders. Along the same lines, coffee is a relatively broad category of beverage. When one compares an espresso with a teaspoon of sugar to a Starbucks Frappuccino the difference in sucrose, and thus fructose, content is extraordinary. The caffeine content of these beverages, while purported to decrease the risk of stones through diuresis, is variable and thus also a potential confounder.

Manuel Ferraro importantly acknowledged that the study observed ‘associations, not causal effects’. Harder evidence such as 24 hour urines, stone analysis and imaging data would be useful to draw more significant conclusions as to causality.
 

The population studied was also somewhat limited. As mentioned by Jason Lee, Henry Woo and Matt Bultitude the study included male health professionals and female nurses, who were generally white, an older population with a relatively low BMI and potentially prone to dehydration. There was also limited control of comorbidities.

As suggested by Christopher Bayne, the only evidence as yet in randomized controlled trials is that water consumption as reflective of hydration status and urinary volume is the only substance known to reduce the risk of stone formation.
 

An astute observation by one of my fellow Australian trainees Janice Cheng noted the relatively dehydrated status of the study subjects.


This won the best Tweet prize, kindly donated by European Urology @EUplatinum.

Increased water intake has been reviewed on the Cochrane Database in 2012, however the consensus drawn was that there is currently insufficient evidence that increased water intake specifically, as opposed to other fluids, prevents the formation of urinary calculi.

So what conclusions should we draw? A patient with his first presentation kidney stone actually asked me yesterday whether he could keep drinking his favourite drink….beer. I simply replied that there was no current evidence that this would increase his risk of stones, however that moderation was key. We must remember that many of these calorific drinks have significant impact on comorbidities outside of the world of kidney stones. #a(lotof)wateradaykeepstheurologistaway

The overall participation in #urojc continues at a solid rate, with 39 participants and 178 total tweets over the 48 hour period. The next #urojc will be on the first Sunday or Monday of July (depending on your time zone).

   

Dr Helen Nicholson is an Australian Urology Trainee, currently based at The Sydney Adventist Hospital, NSW. Tweeted initially under duress, now a voluntary convert @DrHLN

 

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Early Prostate Cancer Detection. One Canadian Urologist’s Perspective

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After seventeen years as a practicing urologist and a further six in training, it amazes me that we still regard prostate cancer as a mystical science and view the issue of screening through the opaque prism of controversy. For so long it seems that the advanced stage disease that I learned about in the mid 1980s in medical school was irreversibly altered by early detection and treatment. Of course we now know that much of this early detection was simply a lead-time bias and that many men who were treated required only observation and were left with many potential compromises to quality of life. “Doctor, my cancer is gone, why am I so miserable?”

At the recent annual meeting of the American Urological Association in San Diego, new guidelines on prostate cancer screening were unveiled. In the past, routine testing at age 50 was recommended with age 40 being the threshold for those at risk. Essentially they can be summarized as:

  • Avoid screening under 40
     
  • Do not routinely screen between 40 and 54 for average risk men. For those at risk screening should be individualized.
     
  • For those between age 55 and 69 there is possibly some benefit and shared decision-making with a patient should be the rule.
     
  • Finally no routine screening after 70.
     
  • PSA should be considered every two years

The motivation for this more cautious recommendation stems for the fact that many men have indolent disease. Many of these men don’t require treatment. Treatment brings with it the potential to harm and therefore casts into doubt the value of any treatment.

The problem of course is while that may represent a possible, cost-effective strategy across the wider population, there is little doubt in my mind that this will lead to many younger and even older men falling through the cracks. It will be justified as too high a number needed to treat to make sense to find these men. Policy makers and health economists may shrug. My own experience is that we have much to learn about risk factors and that many men present seemingly without warning with significant disease.

 

This email from a patient illustrates the concern. Identifiers of course are removed. Both men had disease beyond the capsule of the prostate. Neither man had risk factors. Our patients are very wise and quickly become experts in the disease.

In Canada, the Canadian Urological Association has taken the view for some time that we should look at multiple factors as we “build a case” for prostate biopsy. Its own guidelines reflect this. This paper that we published speaks to the use of nomograms to make better biopsy decisions. Many calculators are available on the web.

So what is shared, informed decision-making? The assumption after the AUA meeting is that somehow patients and their primary care doctors will somehow know. What sort of conversation is happening if urologists themselves don’t seem to provide clear guidance? I suspect it will go something like “PSA doesn’t work, prostate cancer is not lethal and you will likely die from something else” Many family doctors have much of their time rightfully diverted to treating important disease entities such as hypertension, depression and diabetes. A not insignificant number of primary care doctors don’t necessarily even do a DRE anymore. If the urological community conveys the message that prostate cancer is not worth the effort it will further fall down the priority list.

In my view I am a little dismayed by the rhetoric that has started since these guidelines were presented. Much of this is well intentioned and a reaction to years of potential over-treatment. This earlier 2012 piece from the highly respected @OtisBrawley of the American Cancer Society illustrates the false promise of screening message that is being told. It will only be amplified after San Diego. In my view PSA itself is a blood test. It is harmless. It is the treatment machinery that it often initiates that potentially gives it a bite and needs careful reflection.

To many, prostate cancer is simply a benign disease in aging males along the lines of male pattern baldness. This would be a disaster in my view. We have definitely shifted the curve to the left but in addition to lowering overall mortality have greatly lessened the burden of disease complications. Men presenting with hematuria, urinary retention and renal failure has significantly diminished. It is rare that we get asked to insert nephrostomy tubes for advanced disease. This was a common clinical scenario when I was a resident in the early 1990s. I think we will see much more of that if we massively abandon screening.

I think as urologists we have a big responsibility to lead within our local communities. This comment from Dr. A Partin speaks to this very well. In the absence of the perfect pre-test conditions that predict meaningful disease my view is that we have to cast a wide net. In doing so we will uncover disease that does not need to be treated. We must then be prepared to separate diagnosis from treatment and carefully counsel our patients in a way that takes much detail and effort. It is not a five-minute discussion you can have in the middle of a busy clinic. Active Surveillance does work for low-risk disease. Our patients are sophisticated and will not blindly ask for treatment out of overwhelming anxiety. In parallel, we must continue to improve. The risk of biopsy, which has greatly increased over fifteen years, must be modified. Biopsy accuracy to find “real” disease can perhaps be improved with technology such as MRI. Techniques that lessen quality of life issues need to be modified. Robotic surgery can’t be a marketing free-for-all. In other words the onus is on us experts to get it right and do better.

Prostate cancer is a very significant disease and the source of pain and suffering for men and their families. We must continue to be vigilant of its implications, respectful of patient desires and hopeful ultimately of a cure. A benign disease it most certainly is not.

Dr. Rajiv K Singal is a Urologist at Toronto East General Hospital and Assistant Professor in the Department of Surgery at the University of Toronto.

Follow him on Twitter at @DrRKSingal

 

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Editorial: Androgen deprivation therapy: further confirmation of known harms

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Androgen deprivation therapy (ADT) has been an established and effective treatment for men with asymptomatic metastatic prostate cancer for decades. Randomized trials have shown significant survival benefits when ADT is used, coupled with radiotherapy, for patients with locally advanced disease; however it is often used in patients where the benefits are less clear, such as for a rising serum PSA level after radical prostatectomy, and among patients who elect to take a more conservative approach to treatment for low-risk disease. In addition to the absence of data proving benefit, there are a number of adverse consequences attached to androgen deprivation which should be given serious consideration before beginning treatment. Most of the side effects of ADT are linked to its induced hypo-androgenic, and consequently hypo-oestrogenic, state. These include fatigue, vasomotor flushing, loss of muscle mass, weight gain, hyperlipidaemia and insulin resistance.

Osteoporosis and fracture are additional known consequences of ADT with a trend toward greater fracture risk with a higher number of doses of a GnRH agonist and/or longer duration of use. Studies indicate that men with non-metastatic prostate cancer treated with ADT experience an annual loss in bone mineral density of up to nine times that of men in the general population. The use of intermittent ADT, as opposed to continuous use, as a strategy to reduce the negative cardiometabolic and osteoporotic effects is unresolved; however, a report indicating that more recent treatment was associated with a greater risk of fracture, irrespective of cumulative dose, suggests the potential for some reversibility in bone loss post-treatment.

In the present issue of the BJU International, Lu-Yao et al. add to the literature in this area. In a study of nearly 76 000 men with prostate cancer, using data gathered as part of the National Cancer Institute’s Surveillance, Epidemiology and End Results (SEER) cancer registry linked to Medicare claims data, the authors reported that patients at high risk for skeletal complications were, not surprisingly, more likely to experience a fracture associated with ADT use over a 12-year period compared with patients receiving ADT but at low risk for developing such complications. Furthermore, men who experienced a fracture were 40% more likely to die during follow-up than those without fracture. Patients were sorted into risk groups using an index which summed the number of known risk factors for incident fracture identified from Medicare claims in the 12 months before their prostate cancer diagnosis. Unfortunately, owing to the relatively small number of patients with more than one risk factor, the study was limited in its ability to establish a dose – response relationship between the baseline index and fracture risk. SEER-Medicare is an excellent resource to investigate both outcomes and treatment-related expense associated with cancer diagnoses in the USA; however, in this particular study, the reliability of behaviours included in the baseline index (i.e. smoking) is questionable as it would require both patient report of tobacco use as well as physician documentation as a billable claim. Still, one might argue that the heaviest smokers, whose behaviour would most likely be captured as part of a claim, would also be the most important group to capture in an index intended to predict fracture risk.

Interestingly, it was reported that patients at high risk for skeletal complications were significantly more likely to receive ADT than patients at low risk. This was driven in part by the use of primary ADT among elderly men (aged ≥80 years) with prostate cancer and consistent with the notion that when curative treatment is contraindicated (i.e. older patients and those with pre-existing comorbidities) treatment with ADT is more common. Lastly, these findings do not suggest any modification of fracture risk associated with ADT according to baseline risk index, which is consistent with reports of the impact of comorbid conditions and ADT on the risk of incident diabetes and cardiovascular events. This is an important observation in that it says, there is no group that is immune to the adverse effects of ADT – all men are at risk. In absolute terms, however, the men at the greatest risk of an ADT side effect (i.e. a fracture or diabetes) are the men who are at greatest risk of having that side effect even if they were not receiving ADT. The findings of Lu-Yao et al. reinforce the need for careful monitoring of all men receiving ADT. Moreover, when these data are combined with an earlier study that showed that primary ADT was associated with poorer survival than that for men with low-risk prostate cancer who were managed conservatively with observation alone, it should be a wake-up call for us to stop treating non-lethal cancer with lethal and toxic treatments, including ADT.

Jennifer L. Beebe-Dimmer*† and Stephen J. Freedland‡§
*Wayne State University School of Medicine, †Karmanos Cancer Institute, Detroit, MI, ‡Durham VA Medical Center, and §Duke University School of Medicine, Durham, NC, USA

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The new AUA PSA Testing Guidelines leave me scratching my head

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The fact that Otis Brawley describes the new PSA testing guidelines of the American Urological Association (AUA) as “wonderful”, should immediately raise a red flag at AUA headquarters. Dr Brawley, Chief Medical Officer of the American Cancer Society, and the most vocal anti-prostate cancer screening voice in the USA over the past decade, has enthusiastically welcomed the new document and “commended” the AUA for bringing its policy closer to that of his Society. The Guidelines have also been compared to those of the United States Preventative Services Task Force (USPSTF) which completely opposes PSA testing in any situation – a position which the AUA called “inappropriate and irresponsible” just a few months ago. Oh dear – where has it all gone wrong? ?

For those who haven’t yet seen the document, here are the five statements issued by the Guideline committee at the Annual Meeting of the AUA in San Diego this week along with some of my thoughts in italics:

  1. The Panel recommends against PSA screening in men under age 40 years. This appears reasonable.
  2. The Panel does not recommend routine screening in men between ages 40 to 54 years at average risk. I have some problems with this (as do many others). In addition to this statement, the AUA highlights its view that the likelihood of causing harm is high and that any benefit is marginal. It appears to have completely dismissed evidence (and its own previous view), that a baseline PSA in men in this age group is highly predictive of future prostate cancer, metastasis and death. In my view, there is considerable value in having a baseline PSA in this age group and I am disappointed that the AUA has not recognised the evidence to support this.
  3. For men ages 55 to 69 years the Panel recognizes that the decision to undergo PSA screening involves weighing the benefits of preventing prostate cancer mortality in 1 man for every 1,000 men screened over a decade against the known potential harms associated with screening and treatment. For this reason, the Panel strongly recommends shared decision-making for men age 55 to 69 years that are considering PSA screening, and proceeding based on a man’s values and preferences. I agree with the emphasis here on shared decision-making, although the concept can be somewhat nebulous and difficult to achieve in real-life. However, I think that this statement somewhat over-emphasises the harms associated with PSA testing in this group. Rather than portray the reduction in prostate cancer mortality as being very minor (1 in 1000), men should know that when compared with a man who chooses not to have PSA testing in this age group, those who do have regular PSA testing have a 44% reduction in prostate-cancer mortality over a 14 year period. Furthermore, the numbers needed to screen (293) and number needed to treat (12) to save one life stack up very well when compared with other screening modalities such as mammography (Hugosson et al). Why has the AUA instead chosen to over-emphasise the harms? This is disappointing.  
  4. To reduce the harms of screening, a routine screening interval of two years or more may be preferred over annual screening in those men who have participated in shared decision-making and decided on screening. As compared to annual screening, it is expected that screening intervals of two years preserve the majority of the benefits and reduce over-diagnosis and false positives. This appears reasonable.
  5. The Panel does not recommend routine PSA screening in men over age 70 years or any man with less than a 10 to 15 year life expectancy. Yes, but this strong advice not to offer PSA testing in men greater than 70 belies the fact that many men in this age group have a long life expectancy (eg in Australia a male who reaches 70 has a 15 year life expectancy (www.abs.gov.au), and an early diagnosis of prostate cancer may prevent their untimely death from this disease. Clearly, not all men in their 70’s are the same but following this advice to the letter could deny many men the option of avoiding death from prostate cancer in later life.

Therefore, it appears that the only circumstances under which the AUA currently recommend a PSA test be performed is for men between the age of 55 and 69 following a weekend seminar so they can be adequately informed (or thoroughly confused).

These statements have led to headlines such as these in the mass media today:

  • Urology Group Stops Recommending Routine PSA Test (USA Today)
  • Looser Guidelines Issued on Prostate Cancer Screening (New York Times)
  • Urologists No Longer Support Routine Prostate Cancer Screening (Minn Post)
  • Most men don’t need PSA test (Arizona Star)
  • AUA No Longer Recommend Routine PSA Testing For Prostate Cancer (Huff Post)

I think it is reasonable to say that this AUA document adds more confusion than clarity to the debate around prostate cancer testing. It has certainly provoked some anger among prominent members of the AUA who voiced their displeasure to the Committee during the plenary and also through social media. Dr Catalona was first to the microphone asking why AUA members were not more widely consulted prior to publication and in particular, challenging the guidance around men aged 40-54 (reported on Twitter):

 

 

Dr Stacy Loeb also voiced her concerns at various sessions during the day:

 

Much progress has been made in the last few decades with a 30% reduction in prostate cancer-specific mortality since the introduction of PSA testing. And while we accept that this has led to a large amount of over-treatment of less aggressive disease, it is clear that (at least outside the USA), active surveillance is being enthusiastically embraced for appropriate patients. Any return towards the pre-PSA era would likely lead to a reversal in these mortality gains and we would again see many more men presenting to our rooms with incurable disease.

As Dr Smith editorialized in the Journal of Urology following the publication of the ERSPC and PLCO trials in 2009, “Treatment or non-treatment decisions can be made once a cancer is found, but not knowing about it in the first place surely burns bridges”. It is clear that many urologists consider these new AUA PSA Guidelines to be in danger of burning these bridges. However, rather than burn bridges, it is likely that urologists and others will ignore these guidelines and continue to counsel men in a more balanced fashion about the pros and cons of PSA testing. The AUA will then need to consider whether ignored guidelines are failed guidelines.

 

Prof Tony Costello is a Director and Professor of Urology at the Royal Melbourne Hospital, Melbourne, Australia.

Twitter: @proftcostello

 

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