Hello gentlemen,
A big thank you to all those that contribute on this board!
I visited a Dr. and had a talk about low t since I have many of the symptoms. She granted a blood work and it showed a hemoglobin level of 170 g/l while t was at 8.6nmol/l (247 ng/dl).
She said that the hemoglobin levels were too high which meant there was no risk for t-deficiency. She was following a template which she had been trained in by endocrinologists.
Is this legit or bs?
Obviously I know the t-levels are extremely low for my age of 30ish.
Thank you.
Edit: I'm not sure of the exact word she used, I believe it was defiency. She acknowledged that 8.6 was under reference level of 10. What is the explanation for this?
Your TT 8.6 nmol/L (247 ng/dL) is horribly low and more importantly, your FT level would be in the gutter!
Although TT is important to know keep in mind that FT is what truly matters as it is the active unbound fraction of testosterone responsible for the positive effects.
Your levels definitely merit treating your t-deficiency but there are some contraindications:
*If the Hct exceeds 50%, clinicians should consider withholding testosterone therapy until the etiology of the high Hct is explained.
Can you post your labs including full CBC?
EVALUATION AND MANAGEMENT OF TESTOSTERONE DEFICIENCY: AUA GUIDELINE (2018)
Guideline Statements Diagnosis of Testosterone Deficiency
1. Clinicians should use a total testosterone level below 300 ng/dL as a reasonable cut-off in support of the diagnosis of low testosterone. (Moderate Recommendation; Evidence Level: Grade B)
2. 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. (Strong Recommendation; Evidence Level: Grade A)
3. The clinical diagnosis of testosterone deficiency is only made when patients have low total testosterone levels combined with symptoms and/or signs. (Moderate Recommendation; Evidence Level: Grade B)
4. Clinicians should consider measuring total testosterone in patients with a history of unexplained anemia, bone density loss, diabetes, exposure to chemotherapy, exposure to testicular radiation, HIV/AIDS, chronic narcotic use, male infertility, pituitary dysfunction, and chronic corticosteroid use even in the absence of symptoms or signs associated with testosterone deficiency. (Moderate Recommendation; Evidence Level: Grade B)
5. 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. (Conditional Recommendation; Evidence Level: Grade C)
Adjunctive Testing
6. In patients with low testosterone, clinicians should measure serum luteinizing hormone levels. (Strong Recommendation; Evidence Level: Grade A)
7. Serum prolactin levels should be measured in patients with low testosterone levels combined with low or low/ normal luteinizing hormone levels. (Strong Recommendation; Evidence Level: Grade A)
8. Patients with persistently high prolactin levels of unknown etiology should undergo evaluation for endocrine disorders. (Strong Recommendation; Evidence Level: Grade A)
9. Serum estradiol should be measured in testosterone deficient patients who present with breast symptoms or gynecomastia prior to the commencement of testosterone therapy. (Expert Opinion)
10. Men with testosterone deficiency who are interested in fertility should have a reproductive health evaluation performed prior to treatment. (Moderate Recommendation; Evidence Level: Grade B)
11. Prior to offering testosterone therapy, clinicians should measure hemoglobin and hematocrit and inform patients regarding the increased risk of polycythemia. (Strong Recommendation; Evidence Level: Grade A)
12. PSA should be measured in men over 40 years of age prior to commencement of testosterone therapy to exclude a prostate cancer diagnosis. (Clinical Principle)
GUIDELINE STATEMENTS
11. Prior to offering testosterone therapy, clinicians should measure hemoglobin and hematocrit and inform patients regarding the increased risk of polycythemia. (Strong Recommendation; Evidence Level: Grade A)
Polycythemia, sometimes called erythrocytosis, is generally defined as a hematocrit (Hct) >52%. It is categorized into primary (life-long), often related to genetic disorders; and secondary (acquired), which is attributed to polycythemia vera, living at high altitude, hypoxia (e.g., chronic obstructive pulmonary disease, obstructive sleep apnea, tobacco use), paraneoplastic syndromes, and testosterone therapy.187 188
Prior to commencing testosterone therapy, all patients should undergo a baseline measurement of Hb/Hct (Appendix C). If the Hct exceeds 50%, clinicians should consider withholding testosterone therapy until the etiology of the high Hct is explained.187 While on testosterone therapy, a Hct ≥54% warrants intervention. In men with elevated Hct and high on-treatment testosterone levels, dose adjustment should be attempted as first-line management. In men with elevated Hct and low/normal on-treatment testosterone levels, measuring an SHBG level and a free testosterone level using a reliable assay is suggested. If SHBG levels are low/free testosterone levels are high, dose adjustment of the testosterone therapy should be considered. Finally, men with elevated Hct and on treatment low/normal total and free testosterone levels should be referred to a hematologist for further evaluation and possible coordination of phlebotomy.
Androgens have a stimulating effect on erythropoiesis and elevation of Hb/Hct is the most frequent adverse event related to testosterone therapy.189-191 During testosterone therapy, levels of Hb/Hct generally rise for the first six months and then tend to plateau.192, 193
Among 5 randomized, placebo-controlled trials that evaluated Hb and Hct levels in men (mean baseline testosterone <300 ng/dL) using either gel, solution, or IM testosterone therapy for 12 weeks to 1 year, a significant increase in the incidence of elevated Hct was observed in those using testosterone (OR=6.46; CI: 1.86, 22.40) compared to those on placebo.194-201 The calculated odds ratio belies the number of polycythemia events in absolute terms; 19 events in 1,094 patients occurred in the treatment arm as compared to 1 event in 1,093 patients in the placebo group.
While the incidence of polycythemia for one particular modality of testosterone compared to another cannot be determined, trials have indicated that injectable testosterone is associated with the greatest treatment-induced increases in Hb/Hct. In the current meta-analysis of RCTs, long-acting IM testosterone resulted in a mean increase in Hb levels of 1.4 mg/dL compared to 1.6 mg/dL with short-acting IM testosterone, 0.9 mg/dL with transdermal preparations, and 0.7 mg/dL with topical patches.150, 182, 194-196, 201-218
This is likely due to the high and sometimes supra-physiological levels of testosterone that occur in the early days after injection.219 A retrospective comparative series involving 175 men with testosterone deficiency who used different modalities of testosterone therapy reported that 19% of men receiving IM testosterone experienced polycythemia compared to 12.5% with testosterone pellets and 5.4% with gels.220
It is unclear if the risk of polycythemia is greater in men with comorbid disorders that predispose to hypoxia, such as chronic obstructive pulmonary disease or obstructive sleep apnea.188 It is also currently unknown if rates of polycythemia are associated only with short-acting injectable agents or occur with equal frequency when using the longer-acting testosterone undecanoate.221
