Originally published 10/11/2015
It’s hard to believe how much can change in less than a decade! Since we posted the 2015 blog below, an exciting new imaging modality called PSMA PET/CT has entered the global prostate cancer diagnosis scene. When a short-lived positron emitting isotope called Gallium 68 is bonded to a molecule that is attractive to a specific protein found abundantly on the surface of prostate cancer (PCa) cells, the cells “light up” on PET/CT scans.
The surface protein is called Prostate Membrane Specific Antigen. Unlike the PSA (Prostate Specific Antigen) that is picked up by a blood test but does not necessarily indicate cancer, PSMA is picked up by imaging. The important news is that it can be detected virtually anywhere in the body, not just in the prostate gland. This includes lymph nodes, organs, and bones! Even when the cancer cells are just small, early clusters, their presence is revealed by the emitted radiation.
Why is this an important diagnostic contribution? There are two main reasons:
- A single scan makes it possible to stage PCa before primary treatment. The knowledge that PCa may have already escaped the gland—even if only outside the capsule, let alone remote spread elsewhere in the pelvic region or the rest of the body—influences the choice of treatment that best serves the patient’s life and lifestyle.
- If a patient has already been through treatment, but a subsequent PSA test shows a suspiciously high or rising PSA, it’s essential to know if his cancer is back. If so, where and how extensive is it?
Since prostate cancer is especially prone to skeletal involvement if it begins to spread, the PSMA PET/CT scan has been demonstrated to be significantly more accurate than previous conventional imaging methods at identifying PCa in bone. In fact, Fanti, et al. (2021) note that, generally speaking, the standard work up (CT and bone scan) fails in prognostic ability compared to PSMA PET/CT.[i]
Thus, not only has the traditional bone scan fallen out of favor, it’s being rapidly replaced by a more precise, sophisticated imaging modality. It’s a pleasure to post this new, lifesaving imaging update.
It wasn’t that long ago when it was routine to send a newly diagnosed prostate cancer patient for a bone scan (bone scintigraphy) to check for metastasis to the bone. When I say routine, I mean virtually all patients—even those with Gleason 6—had a bone scan to look for spots of metastasis in the pelvis, lower spine or other areas. Historically, there was good reason to do so. Until PSA screening began with FDA approval in 1994, there was no such thing as early detection. Over 90% of men who were diagnosed with prostate cancer (PCa) already had symptoms such as urinary difficulties, blood in the urine, lower back pain, etc. By the time these symptoms appear, it is inevitable that cancer has advanced beyond the gland.
The bones are a preferred site for prostate cancer metastasis, and are the main site of spread in about 80% of patients with metastatic disease. Twenty-five years ago, pain in the back or pelvis was a fearful sign that tumors had implanted in the bone marrow and were growing. Back then, complications from bone metastasis were the chief cause of morbidity and mortality, culminating in agonizing death.
Thankfully, much has changed with the advent of early detection. Now, the vast majority of tumors are diagnosed when they are low-to-intermediate risk. In terms of clinical factors, that means PSA is below 10, and Gleason score is less than 8. Expert recommendations, such as that expressed in a journal article called “Is There Still a Role for Computed Tomography and Bone Scintigraphy in Prostate Cancer Staging,”[ii] is trending toward bones scans only for high-risk patients.
The statistics justify this recommendation. For example, the well-respected British Journal of Radiology published a paper by Mcarthur et al. (2012) that contains persuasive data.[iii] They included 672 men in their study. All had bone scans, and the results were correlated with age, PSA level and Gleason score. Only 8% (54 patients) had evidence of spread to the bones. High PSA level (20 or higher) and Gleason score (8 or higher) were independent predictors of bone metastasis. The research team found that not a single patient with PSA level below 20 and Gleason score less than 8 had a positive bone scan. They concluded, “Staging bone scans in newly diagnosed prostate cancer patients with a PSA level of <20 and a Gleason score of <8 can be safely omitted, with these criteria having a negative predictive value of 100% in our series.” It is so rare to find a 100% negative predictive value that I found it compelling. (Negative predictive value means a test accurately predicts the absence of disease.)
For me, such research makes a solid case for eliminating bone scans for all but high-risk patients; the criteria suggested by the Mcarthur study are widely used in Europe. There is still a place for accurate tests to detect PCa that has spread to the bone, and today’s treatments can slow its growth and control pain far better than two decades ago. Reducing the stress of extra testing for newly diagnosed men, and saving medical dollars, are two positive results of eliminating needless bone scans.
NOTE: This content is solely for purposes of information and does not substitute for diagnostic or medical advice. Talk to your doctor if you are experiencing pelvic pain, or have any other health concerns or questions of a personal medical nature.
References
[i] Fanti S, Goffin K, Hadaschik BA, et al. Consensus statements on PSMA PET/CT response assessment criteria in prostate cancer. Eur J Nucl Med Mol Imaging. 2021;48(2):469-476. doi:10.1007/s00259-020-04934-4
[ii] Gabriele D, Collura D, Oderda M, Stura I et al. Is there still a role for computed tomography and bone scintigraphy in prostate cancer staging? An analysis from the EUREKA-1 database. World J Urol. 2015 Aug 15. [Epub ahead of print]
[iii] Mcarthur C, McLaughling G, Meddings R. Changing the referral criteria for bone scan in newly diagnosed prostate cancer patients. Br J Radiol. 2012 Apr; 85(1012): 390–394.