Prevention of bone-related and metabolic complications of treatment for men on ADT


A new article from an Australian clinical research group in the journal Andrology addresses “the effectiveness of implementing standardized guidelines to mitigate metabolic and bone side effects of androgen deprivation therapy (ADT) in men with non-metastatic prostate cancer.”

In an ideal world, one would want to minimize risk for side effects of ADT in such patients while optimizing the possibility that early ADT would delay the onset of evident metastasis (and perhaps extend survival).

Cheung et al. carried out a relatively short-term (2-year-long), prospective, pilot study at their tertiary teaching institution in Heidelberg, Victoria. Here are the findings of that study:

  • 236 men (with an average [mean] age 69.8 ± 7.1 years) started ADT for non-metastatic prostate cancer at their clinic between 2007 and 2011.
  • 113/236 patients were eligible for follow-up and had data available for analysis after 2 years on continuous ADT.
  • At baseline,
    • 87 percent of patients were overweight or obese.
    • 61 percent had hypertension.
    • 56 percent had hypercholesterolemia.
    • 27 percent had a history of cardiovascular disease.
    • 11 percent had osteoporosis.
    • 40 percent had osteopenia.
  • After 2 years of continuous ADT,
    • There was a significant average increase in waist circumference (+2.8 ± 6.3 cm; p = 0.002).
    • There was a significant increase in HbA1c levels in men without diabetes (+0.13 ± 0.34 percent; p = 0.019).
    • There was a significant decrease in total cholesterol level (–0.35 ± 1.00 mmol/l, p < 0.001).
    • There was a significant decrease in blood pressure levels (systolic, –7.6 ± 19.3 mmHg; diastolic, –4.7 ± 11.6 mmHg; p < 0.001).
    • Prevalence of anemia increased from 13.8 to 32.5 percent.
  • Also after 2 years of ADT, in men not receiving anti-resorptive therapy (i.e., bisphosphonate or similar therapy),
    • There was a significant decrease in lumbar spine bone mineral density (–0.042 ± 0.134 g/cm2; p = 0.012).
    • There was a significant decrease in total hip bone mineral density (–0.026 ± 0.036 g/cm2; p < 0.001).
  • By contrast, after 2 years of ADT, in men receiving bisphosphonate therapy, bone mineral density was stable compared to baseline levels.
  • Older age independently predicted a greater drop in hemoglobin levels (p = 0.005).

The authors conclude that “a structured approach to assess and treat men undergoing ADT effectively improves cardiovascular risk factors and prevents bone decay” and go on to recommend that “Larger studies are needed to determine effects on cardiovascular outcomes, fracture prevention and survival.”

There is considerable diversity about the use of a variety of different agents to manage risk for metabolic and bone-related complications of treatment with ADT (in non-metastatic and metastatic men with progressive forms of prostate cancer). This is both right and proper in some ways (because treatment needs to be tailored to the individual issues affecting each individual patient) but it is also problematic because we have little concrete guidance available as regards “best practices” in the management of such men. We could certainly do with much better data from much larger studies that might allow the development of such “best practices”.

One Response

  1. Here’s some information about “best practices.” I was on ADT for 3 years. Two years into its use, an oncologist friend in another country told me I was getting “very good” treatment. He then asked me if I had gotten a bone mineral density (BMD) test. I asked him why, and he told me about the osteoporosis risk with LHRH agonists. They can — but need not — induce osteoporosis between 6 months and 1 year after one starts on ADT, yet I was not told about this and have reason to suspect that other men were not told. I demanded the test, which is not included in several guidelines as a part of treatment but is mentioned in at least one regional care programme (that of my region has not one word about it), was told it’s not in the national tradition, was persistent, and got the test. I have osteoporosis (but cannot prove that it originated from the treatment) and was promised regular tests in future. Now, 2 years later, it’s held in check by use of vitamin D + calcium tablets and D-enriched milk. At two points my BMD has increased and at no point has it decreased. I cannot say how, but I managed to end this local informal “understanding”. All men who are scheduled for ADT are now warned as early as possible, and are advised to take what I now take from the start. Doing this might — but need not — reduce the severity of the disease. Most of the papers I and some specialists I influenced read, recommend this. I know that the doctors I spoke with at length desired this change. I think they needed some forcible motivation.

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