JimJimJimJim Posted August 14, 2013 Share Posted August 14, 2013 Jim Marshall (not a doctor) said ... Your doctor will be wary of early studies in a topic. That's because most of them will be proven not to be true when a proper trial is done (with half men with real treatment, half with dummy treatment). These early studies are important because they suggest things that should be looked at carefully with good studies. The press, however, has no qualms about using alarming headlines about early studies. Thanks to members Snowy and Joan for drawing my attention to such an alarming headline. The article below, which clearly states, in words clear to your doctor and the scientific community (for whom this article is written): "These findings require replication in other well-designed studies as well as further investigation of their clinical importance." In common language that translates as something like: "This is just a suggestion that this might be a problem. Proper studies should be done to see whether this is real, and whether it is something a doctor should be concerned about." Instead, the press and internet gave it headlines like: Prostate cancer hormonal therapy tied to kidney risks and wrote things like: Hormone therapy for prostate cancer may dramatically increase a man's risk of kidney failure, according to a new study. You often had to look a long way down the text to find more accurate sentences like this: "These results are suggestive that an association may exist, but they are not definitive," Brooks said. "There will need to be other research looking at this." As always, ask your doctor if you are concerned. If there is not a strong case for you to be on hormone therapy, and you have kidney problems, your doctor may take into account this suggestion of possible problems with hormone therapy and kidneys. They will note that the possible connection happened with combination therapy (standard hormone therapy like Zoladex, Lucrin or Eligard) plus continuing use of an antiandrogen tablet (Like Cosudex or Androcur), and that the problem stopped when the treatment did. Single hormone therapy most often uses a drug called an LHRH agonist (or sometimes a GnRH antagonist). Mostly these are given by injection or implant, and last from one month to several months. They lower the sex hormones, particularly testosterone. Common LHRH agonists (LHRHa) are: Zoladex (Goserelin), Lupron (leuprorelin), Eligard (leuprolide), Lucrin (leuprorelin acetate), Suprefact (buserelin), Suprecor (buserelin), Synarel (nafarelin), histrelin (Supprelin), Suprelorin (deslorelin), Ovuplant (deslorelin), Triptorelin GnRH antagonists (GnRHa) include: Abarelix, Firmagon (degarelix) Combined androgen blockade (CAB) adds a continuing, often daily anti-androgen tablet to give a more complete lowering of the sex hormones. This continuing use of an androgen should not be confused with the one-time use of an anti-androgen before you start on an LHRH agonist (like when you have Cosudex for a few weeks before you start Zoladex). Common anti-androgens (AA) include: Cosudex/Casodex (bicalutamide), Anandron/ Nilandron (Nilutamide), Eulexin (Flutamide), all nonsteroidal, and Androcur (Cyproterone, a steroid). Nizoral (Ketoconazole), and Zytiga (abiraterone acetate) and Xtandi (enzalutamide) are sometimes regarded as anti-androgens, but are stronger and have much wider effects. ... end Jim JAMA. 2013 Jul 17;310(3):289-96. doi: 10.1001/jama.2013.8638. Androgen deprivation therapy and risk of acute kidney injury in patients with prostate cancer. Lapi F, Azoulay L, Niazi MT, Yin H, Benayoun S, Suissa S. Source Centre for Clinical Epidemiology, Lady Davis Institute, Jewish General Hospital, Montreal, Quebec, Canada. Abstract IMPORTANCE: The use of androgen deprivation therapy (ADT) in the treatment of advanced prostate cancer has been shown to delay the clinical progression of the disease. However, the testosterone suppression associated with this therapy may lead to a hypogonadal condition that can have detrimental effects on renal function, thus raising the hypothesis that ADT-induced hypogonadism could potentially lead to acute kidney injury (AKI). OBJECTIVE: To determine whether the use of ADT is associated with an increased risk of AKI in patients newly diagnosed with prostate cancer. DESIGN AND SETTING: A nested case-control analysis using medical information extracted from the UK Clinical Practice Research Datalink linked to the Hospital Episodes Statistics database. PARTICIPANTS: Men newly diagnosed with nonmetastatic prostate cancer between January 1, 1997, and December 31, 2008, were selected and followed up until December 31, 2009. Cases were patients with incident AKI during follow-up who were randomly matched with up to 20 controls on age, calendar year of prostate cancer diagnosis, and duration of follow-up. MAIN OUTCOMES AND MEASURES: Conditional logistic regression was used to estimate odds ratios (ORs) with 95% CIs of AKI associated with the use of ADT. ADT was categorized into 1 of 6 mutually exclusive groups: gonadotropin-releasing hormone agonists, oral antiandrogens, combined androgen blockade, bilateral orchiectomy, estrogens, and combination of the above. RESULTS A total of 10,250 patients met the study inclusion criteria. During a mean follow-up of 4.1 (SD, 2.9) years, 232 incident cases of AKI were identified (rate, 5.5/1000 person-years). Overall, current use of any ADT was associated with an increased risk of AKI when compared with never use (OR, 2.48 [95% CI, 1.61-3.82]), generating a rate difference of 4.43/1000 persons per year (95% CI, 1.54-7.33). This association was mainly driven by a combined androgen blockade consisting of gonadotropin-releasing hormone agonists with oral antiandrogens (OR, 4.50 [95% CI, 2.61-7.78]), estrogens (OR, 4.00 [95% CI, 1.06-15.03]), other combination therapies (OR, 4.04 [95% CI, 1.88-8.69]), and gonadotropin-releasing hormone agonists (OR, 1.93 [95% CI, 1.20-3.10]). CONCLUSIONS AND RELEVANCE: In a cohort of patients with newly diagnosed nonmetastatic prostate cancer, the use of ADT was significantly associated with an increased risk of AKI. These findings require replication in other well-designed studies as well as further investigation of their clinical importance. PMID: 23860987 Link to comment Share on other sites More sharing options...
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