Audrea Teal
|Subscribers
About
Given the clinical and commercial testosterone landscape, the American Urological Association (AUA) identified a need to produce an evidence-based document that informs clinicians on the proper assessment and management of patients with testosterone deficiency. If you’ve been on testosterone therapy for 3–6 months without significant improvements, consult your healthcare provider. If those things don’t work, you might be a candidate for testosterone therapy. RCTs, however, showed that menopausal hormone therapy increased the risk of heart attacks and stroke.150–153 It is likely that healthier women chose to take menopausal hormone therapy, but menopausal hormone administration did not improve health. Another retrospective cohort study using Veterans Administration data showed a lower rate of all-cause mortality, myocardial infarction, and stroke among testosterone-treated men whose testosterone concentrations "normalized" after treatment. Testosterone increases muscle mass, but not strength, and while some improvement is seen in some surrogate markers of cardiovascular risk, there is little evidence of clinical benefit.
PSA should be measured in men over 40 years of age prior to commencement of testosterone therapy to exclude a prostate cancer diagnosis. Men with testosterone deficiency who are interested in fertility should have a reproductive health evaluation performed prior to treatment. The diagnosis of low testosterone should be made only after two total testosterone measurements are taken on separate occasions with both conducted in an early morning fashion.
An overview of the assays available to aid in the diagnosis of testosterone deficiency is available in Table 4 (See button below). Given these inconsistences, prevalence of low testosterone has varied dramatically among studies, with statistics reporting %.5-8 A summary of findings from four large-scale contemporary prevalence studies can be found in Table 3 (See button below). Across the prevalence literature, the cut-off values used to define low testosterone vary widely, heterogeneity exists in the populations studied, the forms of testosterone used to measure testosterone (total and/or free) are not consistent, and the assays utilized to measure testosterone differ.
In men with elevated Hct and low/normal on-treatment testosterone levels, measuring a SHBG level and a free testosterone level using a reliable assay is suggested. In men with elevated Hct and high on-treatment testosterone levels, dose adjustment should be attempted as first-line management. Several validated questionnaires are used as screening tools to identify men at high risk for testosterone deficiency, but there is an absence of concordance among the questionnaires as to what symptoms are related to low testosterone or to what extent these symptoms improve with treatment. Another study showed no effect of IM testosterone enanthate on ejection fraction, although there was an improvement in a Doppler-based myocardial performance index. Intramuscular (IM) testosterone treatment for 12 weeks improved exercise capacity and reduced heart failure symptom scores without identifiable effects on left ventricular size or ejection fraction (EF). There was a decreased incidence of silent MI with testosterone treatment in 1 study. The remaining eight studies evaluated treatments of 2 to 24 weeks in duration.1, 3, 10, 11, 13–17 The 3 studies that looked at time to ST-segment depression found a benefit of testosterone supplementation.1, 14, 16|Most authors with an interest in 17β-estradiol have suggested that the effectiveness of testosterone, when it has shown effectiveness, is due to aromatization to 17β-estradiol. Treatment of men with suspected or diagnosed Alzheimer disease or cognitive impairment was reported in five studies, two of which had a Jadad score above 3. Another injection study found no effect of supplementation on memory in hypogonadal men. The response of depression and dysthymia to testosterone was mixed and inconsistent. The study that used hostility assessments by undergraduate judges found no change in personality as assessed by the Gough and Heilbrun Adjective Check List. Twenty-nine of these studies focused on men without psychiatric disorders, and 16 on men with psychiatric disorders.}
The long-term impact of exogenous testosterone on spermatogenesis should be discussed with patients who are interested in future fertility. Patients with persistently high prolactin levels of unknown etiology should undergo evaluation for endocrine disorders. When sufficient evidence existed, the body of evidence for a particular treatment was assigned a strength rating of A (high), B (moderate) or C (low) for support of Strong, Moderate, or Conditional Recommendations. Measure your levels for the 3 main thyroid hormones plus thyroid antibodies
Exogenous testosterone therapy has been shown to interrupt normal spermatogenesis and can put patients in severely oligospermic or azoospermic states and should not be used in men trying to conceive. At baseline, 22 patients had total testosterone 375 For further information on the testosterone therapy and the risk of MACE, please see Appendix D (in the Appendix D section in the left menu). A meta-analysis of RCTs developed in support of this guideline indicate that there is no significant difference in MACE in men on testosterone therapy when compared to placebo. RCTs have failed to categorically define if testosterone therapy increases the incidence of MACE when compared to placebo.
Of the outcomes included in the protocol of this systematic review, data were available on quality of life (QoL), sexual function, cardiovascular events, anemia, bone health, insulin resistance, cardiovascular risk factors, mood, cognitive function, body composition, and numerous adverse events. Clinicians should inform testosterone deficient patients that low testosterone is a risk factor for cardiovascular disease. The use of validated questionnaires is not currently recommended to either define which patients are candidates for testosterone therapy or to monitor symptom response in patients on testosterone therapy. Clinicians should use a total testosterone level below 300 ng/dL as a reasonable cut-off in support of the diagnosis of low testosterone.