Hemoglobin too high for t deficiency?

HighLevel

New Member
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?
 
Last edited:

madman

Member
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
















 

HighLevel

New Member
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
Hey man,

Thank you for taking the time to respond.

I don't believe she did CBC but here are some results from a blood test done by the end of 2019 that includes a lot of values. I'm not sure they qualifiy as CBC.

edit: EVF was at 0,5 on the test mentioned in OP. I'm looking at the notes from the Dr. digitally and only testosterone, hemoglobin and EVF is mentioned.

 
Last edited:

Vince

Super Moderator
Hey man,

Thank you for taking the time to respond.

I don't believe she did CBC but here are some results from a blood test done by the end of 2019 that includes a lot of values. I'm not sure they qualifiy as CBC.

edit: EVF was at 0,5 on the test mentioned in OP. I'm looking at the notes from the Dr. digitally and only testosterone, hemoglobin and EVF is mentioned.

Your TSH is 3.5, if not out of the range. But I will consider it too high. You definitely need a complete thyroid panel.
 

HighLevel

New Member
Your doctor has no clue what she’s doing.
Most likely.
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?
I got a hold of the results from bloodwork done about 6 weeks ago, if that changes anything. Again not sure this is CBC:

Analys

Resultat

Referensintervall

Om provet

P--Folat

9.3 nmol/L

7 - 45 nmol/L

 

P--Kobalamin

263 pmol/L

140 - 650 pmol/L

 

S-Ferritin


Saknar verifierad NPU-kod

120 µg/L

20 - 275 µg/L

-

P--TSH (Tyrotropin)

3.4 mE/L

0,40 - 4,00 mE/L

2021-02-19

P--Testosteron

8.6 nmol/L

  

B-SR (EDTA)


Saknar verifierad NPU-kod

1 mm

<15 mm

 

B-Hemoglobin


Saknar verifierad NPU-kod

170 g/L

134 - 170 g/L

 

B--Erytrocyter

5.4 10E12/L

4,2 - 5,7 10E12/L

 

B-EVF


Saknar verifierad NPU-kod

0.50

0,39 - 0,50

 

B--MCV

91 fL

82 - 98 fL

 

(B)Erc-MCH


Saknar verifierad NPU-kod

31 pg

27 - 33 pg

 

(B)Erc-MCHC


Saknar verifierad NPU-kod

342 g/L

317 - 357 g/L

 

B--Leukocyter

4.5 10E9/L

3,5 - 8,8 10E9/L

 

B--Trombocyter

214 10E9/L

145 - 348 10E9/L

 

P--Kreatinin (enz)

76 µmol/L

<100 µmol/L

 

Pt-eGFR(krea) relativ


Saknar verifierad NPU-kod

>90

>80

: 2021-02-19

P--Natrium

142 mmol/L

137 - 145 mmol/L

: 2021-02-19

S-Kalium


Saknar verifierad NPU-kod

4.3 mmol/L

3,6 - 5,0 mmol/L

: 2021-02-19

P--Calcium

2.30 mmol/L

2,15 - 2,50 mmol/L

: 2021-02-19

S-Ca, albuminkorrigerat


Saknar verifierad NPU-kod

2.25 mmol/L

2,15 - 2,50 mmol/L

: 2021-02-19

P--Albumin

46 g/L

35 - 50 g/L

: 2021-02-19

P--Bilirubin

5.2 µmol/L

<26 µmol/L

: 2021-02-19

P--ASAT

0.43 µkat/L

<0,76 µkat/L

: 2021-02-19

P--ALAT

0.46 µkat/L

<1,2 µkat/L

: 2021-02-19

S-ALP, Alkalisk fosfatas


Saknar verifierad NPU-kod

1.7 µkat/L

0,6 - 1,8 µkat/L

: 2021-02-19

P--GT

0.41 µkat/L

<1,4 µkat/L

: 2021-02-19

S-CRP


Saknar verifierad NPU-kod

1.9 mg/L

<5,0 mg/L

: 2021-02-19

P-Glukos


Saknar verifierad NPU-kod

5.2 mmol/L

4,0 - 6,0 mmol/L

2021-02-19


Your TSH is 3.5, if not out of the range. But I will consider it too high. You definitely need a complete thyroid panel.
Ok, thank you.
 

HighLevel

New Member
You should be tested for sleep apnea.
I don't think I have sleep apnea, I did a test by staying 2 nights in a sleep clinic about 10 years ago where they had a machine hooked to my mouth and nose that monitored breathing and they said nothing was wrong. Of course that could have changed.

Was it the testosterone in conjunction with the hemoglobin count that made you suspect that? Or only the hemoglobin count?
 

captain

Active Member
Sleep apnea would cause increase in hemoglobin and decrease in testosterone. If you add testosterone you may increase hemoglobin higher and make sleep apnea worse.
 

madman

Member
I just found out that EVF on my previously posted blood works means Hct, and it was at 0.5 which I assume means 50%.

1616947483833.png


post #3

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.


Need to look into underlying reasons why your hematocrit is on the higher-end.

As you need to be aware the use of exogenous T will result in driving up RBCs/hemoglobin/hematocrit within the first month of starting trt and can take up to 9-12 months to reach peak levels.

In many cases, levels can stabilize in due time but many will also struggle with high levels and try to manage with frequent blood donations.

In most cases running too high TT/FT levels will result in high hematocrit.


My reply from another thread:Daily Injection Experiment

Injectable T has been shown to have a greater impact on increasing HCT compared to transdermal T.

3–18% with transdermal administration and up to 44% with injection.

In most cases when using injectable T high supra-physiological peaks post-injection and overall T levels (running too high TT/FT level) will have a big impact on increasing HCT.

Manipulating injection frequency by injecting more frequently using lower doses of T resulting in minimizing the peak--->trough and maintaining more stable levels may lessen the impact on HCT but it is not a given.

As again running very high FT levels will have a stronger impact on driving up HCT.

T formulation, the dose of T, genetics (polymorphism of the AR), age all play a role in the impact a trt protocol will have on blood markers (RBCs/hemoglobin/hematocrit).

Other factors such as sleep apnea, smoking can have a negative impact on hematocrit.
 
Last edited:

HighLevel

New Member
View attachment 13514

post #3

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.


Need to look into underlying reasons why your hematocrit is on the higher-end.

As you need to be aware the use of exogenous T will result in driving up RBCs/hemoglobin/hematocrit within the first month of starting trt and can take up to 9-12 months to reach peak levels.

In many cases, levels can stabilize in due time but many will also struggle with high levels and try to manage with frequent blood donations.

In most cases running too high TT/FT levels will result in high hematocrit.


My reply from another thread:Daily Injection Experiment

Injectable T has been shown to have a greater impact on increasing HCT compared to transdermal T.

3–18% with transdermal administration and up to 44% with injection.

In most cases when using injectable T high supra-physiological peaks post-injection and overall T levels (running too high TT/FT level) will have a big impact on increasing HCT.

Manipulating injection frequency by injecting more frequently using lower doses of T resulting in minimizing the peak--->trough and maintaining more stable levels may lessen the impact on HCT but it is not a given.

As again running very high FT levels will have a stronger impact on driving up HCT.

T formulation, the dose of T, genetics (polymorphism of the AR), age all play a role in the impact a trt protocol will have on blood markers (RBCs/hemoglobin/hematocrit).

Other factors such as sleep apnea, smoking can have a negative impact on hematocrit.
Ok, cheers.
 

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