Low Testosterone

I had low T for years because of a pituitary condition, and the damm gel is expensive. I got some osteopenia in my spine several year back. When I started pred, I was worried my bones would crumble. But this year's bone density test was normal, so the T-gel and regular vitamins (no extra calcium supplement because of kidney stone history) seemed to have taken care of my bones.

So do get checked, but it is usually a manageable condition. (besides, my risk of prostate cancer is lower because of the lower T.)

Max89 said...
You mean mesalamines in general or just Asacol? Also, any sources for this bit of info?

Yes, mesalamines in that enemas were implicated as well.

I searched but could not find any references although the clinician noted that the information was just beginning to be made available. He sent a message to both my GI as well as my GP to make sure they knew of this issue so others could benefit. He called it something specifically but I'm unable recall the term.

I'll see him again in about six weeks so I can ask him then.

Hmmm....I've been taking Mesalamine for 16 years and was diagnosed with Hypogonadism (Low T) 5 yrs ago. I've been on Testosterone Injections since and it has helped SO MUCH...helped me maintain my weight, muscle and strength and also improved my mood....as well as libido .....I could not imagine living without it.

While I would be keen to hear more about this, if only to facilitate a literature search, I am skeptical at the moment.

I take this position because the report here has the form of a 2nd hand rumor, and at least one other member's initial search did not turn up anything, and a lit search I just did in Web of Science did not turn up anything of concern (in fact there was some reassurance). Also, I wonder if this is a garbling of older/known short term and reversible effects of sulphasalazine on male sperm count.

I use the word "rumor" because we have the hearsay report of an ambiguously credentialed "clinician" at a urology center saying something (vaguely remembered) about testosterone and 5-asa (& Remicade). The clinician speculated this based on some symptoms, but not on an actual test of T levels (which is now scheduled). Further, google and Web of Science searches do not hit on this, excepting some old (e.g., 1988) reports of lower (but still normal) T levels with 5-asa.

Influence of Salazosulphapyridine and 5-Aminosalicylic Acid on Seminal Qualities and Male Sex Hormones

1988, Vol. 23, No. 9 , Pages 1100-1104
P. M. J. Zelissen1†, J. Van Hattum1, H. Poen1, P. Scholten1, R. Gerritse1 and E. R. Te Velde1

Seminal abnormalities are a common side effect of Salazosulphapyridine (SASP) treatment. We evaluated semen qualities and sex hormone concentrations in 11 patients with inflammatory bowel disease (IBD) during SASP treatment and 4 months after replacing SASP with an oral slow-release preparation of 5-aminosalicylic acid (5-ASA). Significant improvement in sperm count (p < 0.01), morphology (p < 0.02), and motility (p < 0.02) could be observed during 5-ASA therapy, in comparison with SASP treatment. Three pregnancies occurred during the study period. The serum concentrations of gonadotrophins, prolactin, and sex hormone-binding globulin were normal in all patients and not significantly different in the two treatment periods. The mean total testosterone concentration decreased significantly (p < 0.02) after 5-ASA substitution, together with serum albumin (p < 0.005), although all values remained within normal limits. The apparent free testosterone concentration was not significantly different in the two treatment periods. It is concluded that a significant improvement in semen quality can be obtained in male patients with IBD after replacing SASP with 5-ASA.

Read More: http://informahealthcare.com/doi/abs/10.3109/003655288090901

There is some literature showing Remicade (a TNF antogonist drug) not influencing T (or other hormone) levels.

Ernestam, S., I. Hafstrom, et al. (2007). "Increased DHEAS levels in patients with rheumatoid arthritis after treatment with tumor necrosis factor antagonists: Evidence for improved adrenal function." Journal of Rheumatology 34(7): 1451-1458. (PMCID:

Objective. To determine if major reduction of inflammation with longterm tumor necrosis factor (TNF) antagonist treatment has any influence on the adrenal and gonadal axes in patients with rheumatoid arthritis (RA). Methods. Forty-eight patients with RA were treated with infliximab or etanercept for 2 years. Disease activity, clinical response, and physical function were evaluated and serum levels of high sensitivity C-reactive protein and interleukin 6 were analyzed before start of treatment and after I and 2 years. At the same timepoints adrenocorticotropic hormone (ACTH), cortisol, and dehydroepiandrosterone sulfate (DHEAS) were analyzed; luteinizing hormone (LH), estradiol, and testosterone were analyzed as well in 18 male patients. Results. DHEAS increased (p < 0.05) after 1 and 2 years of treatment with TNF antagonists. No change in serum levels of ACTH, cortisol, LH, estradiol, or testosterone was recorded during the 2 years. The increased levels of DHEAS correlated with improved physical function measured by Health Assessment Questionnaire (p < 0.01). There was no correlation between hormone levels and clinical response or inflammatory markers. A longitudinal stability in individual hormone levels was found between baseline and 2 years, most markedly for DHEAS levels (r(s) = 0.90, p < 0.01). A female subgroup characterized by low levels of DHEAS had a lower age at disease onset. Conclusion. The increased DHEAS levels may indicate an improved adrenal function during 2 years' treatment with TNF antagonists. Improved physical function, correlated to increased DHEAS levels, may be an effect of better adrenal function during powerful anti inflammatory treatment. The stability in individual hormone levels suggests a stable hormonal homeostasis, independent of inflammatory activity.

Of course the effect might take longer than 2 years to show. ... So ***this is a good topic for critical discussion***, but it would be very very premature to just accept an imprecise recounting of some clinicians comments as facts. Just the fact that 5-asa and anti TNF drugs are so different, I am immediately curious about a comment that patients treated with either (?) or both (?) display low T for their age.

.... and even if the correlation of low T and certian IBD drugs was established as fact, this would not mean there was a causal relation. Other commonly used drugs (like steroids) or something related to IBD might ultimately be found to be the root cause. Perhaps more disconcerting, we then have another member, who has been seen to have a great fear of medicine, immediately embrace the rumor, and declare he KNEW 5-asa had to be bad stuff. I am not sure if the uncritical acceptance is more saddening, or if it is the potential for other board readers to "catch" the uncritical acceptance. Either way, it would be nice if such an important discussion remained free of premature and/or over-reactions.

As for Low T, it can be FREE or TOTAL. There are a number of conditions, some disease, and some human genetic variation, that bind  T in our systems. in response to this bound (unusable) T, the system makes more T. SO, in most cases it is the FREE T that needs to be looked at. In this case, we do not even know if a test was ordered for TOTAL or FREE or both.

As noted above, one study I found did see a drop in TOTAL T, but did not see any drop in FREE T. ("The mean total testosterone concentration decreased significantly (p < 0.02) after 5-ASA substitution, together with serum albumin (p < 0.005), although all values remained within normal limits. The apparent free testosterone concentration was not significantly different in the two treatment periods"). So, there is some possibility 5-asa binds some T, decreasing total T showing in tests, but the necessary free T, seems unaffected. Of course, further study would be reassuring.

The mean total testosterone concentration decreased significantly (p < 0.02) after 5-ASA substitution, together with serum albumin (p < 0.005), although all values remained within normal limits. The apparent free testosterone concentration was not significantly different in the two treatment periods


Read More: http://informahealthcare.com/doi/abs/10.3109/00365528809090175

.... and it would be great to get the exact term the clinician used. 

 

Post Edited (DBwithUC) : 2/15/2012 10:07:55 AM (GMT-7)

Gonk said...
Kolitis, do you attribute your low T to the mesalamine? Is there any way to know really? And what prompted you to have your T levels tested? Curious as I am your age and have been on the mesalamines (Asacol and now Lialda, plus Canasa, Rowasa) for about 11 years now. Looks like your T took a hit after 10 years on this stuff.

Hard to tell, but perhaps so. I was also taking alot of prednisone at high doses for a while which may have brought T-levels down. Stress, I'm sure depletes testosterone as well.

I stumbled upon the term that the clinician was using: hypogonadism. According to Pubmed Health "Hypogonadism is when the sex glands produce little or no hormones. In men, these glands (gonads) are the testes; in women, they are the ovaries."

Searching with this term I was able to encounter the following document that states that ulcerative colitis (inflammatory diseases in general) can cause Secondary Hypogonadism (pituitary failure).

www.utasip.com/tracker.cfm?file=files/articlefiles/pdf/ASP_3_4p142_148.pdf&aid=138

Like I said earlier I will ask him next time I see him what he based his comments on with respect to mesalamine and Remicade usage.

Interesting read. Thanks. I had encountered a lot of this information in bits and pieces since I have had pituitary problems for over two decades. But, it was nice to see things tied together, and linked to other diseases, and distinguished as primary vs secondary, and cause vs effect.

tap said...
I stumbled upon the term that the clinician was using: hypogonadism. According to Pubmed Health "Hypogonadism is when the sex glands produce little or no hormones. In men, these glands (gonads) are the testes; in women, they are the ovaries."

Searching with this term I was able to encounter the following document that states that ulcerative colitis (inflammatory diseases in general) can cause Secondary Hypogonadism (pituitary failure).

www.utasip.com/tracker.cfm?file=files/articlefiles/pdf/ASP_3_4p142_148.pdf&aid=138

Like I said earlier I will ask him next time I see him what he based his comments on with respect to mesalamine and Remicade usage.

When they spoke of secondary hypogonadism secondary to  hyperprolactinemia, that's me. It increased my BMI and aided in the development of type-II diabetes. The low T also increased insulin resistance, and exacerbated the diabetes.

This is the 1st time I have seen hyperprolactinemia and low T listed as causal for autoimmune like RA and UC. Very interesting.

 

Anyway, in all of this, the UC is caused by the low T and not the other way around, so this would not be connected to reports of UC drugs causing low T. Like I said above, the causal direction can be crucial for understanding the sense of things.

 

I did have an appointment with my endocrinologist yesterday. I asked him about these drugs and low T. He said he had not hear of anything like that. I asked if he thought it might be recycled info based on old/dated problems with the sulfasalamides used before 5-asa, and he thought that was likely - but he said he would keep an ear out, and let me know when I come back in 3 months.

Post Edited (DBwithUC) : 2/16/2012 8:06:16 AM (GMT-7)

DBwithUC said...
Anyway, in all of this, the UC is caused by the low T and not the other way around, so this would not be connected to reports of UC drugs causing low T. Like I said above, the causal direction can be crucial for understanding the sense of things.

I believe that you are mistaken.

I don't read Table 1 the way you are reading it. It notes the acquired causes not the acquired disorders. For instance, does castration cause hypogonadism or does hypogonadism cause castration?

I did some more searching...

These references were from the first document I included above:

11. Grant NN, Anawalt BD. Male hypogonadism in the primary care clinic. Prim Care. 2003;30:743-763. www.propeciahelp.com/forum/download/file.php?id=41&sid=df7d57be347eab07f33b375b2c62a50d>

It notes that Corticosteroids are associated with male hypogonadism (see box 5). The ones that I have used are Prednisone are Hydrocortisone.

14. Oh JY, Barrett-Connor E, Wedick NM, Wingard DL. Endogenous sex hormones and the development of type 2 diabetes in older men and women: the Rancho Bernardo study. Diabetes Care. 2002;25:55-60 www.ncbi.nlm.nih.gov/pubmed/11772901

"CONCLUSIONS: Low testosterone levels in men and high testosterone levels in women predict insulin resistance and incident type 2 diabetes in older adults." This might explain my prediabetes status.

I also ran into the following article that gives a potential explanation for an Asacol concern:

"Science linking environmental contaminant exposures with fertility and reproductive health impacts in the adult male", Hauser www.prhe.ucsf.edu/prhe/prhe_articles/16.FertSter2008.Sup1.Hauser.pdf

This 2007 article dicusses the need for more reseach into reproductive toxicants such as phthalates and notes: "Several of the phthalate containing medications (such as Asacol) are prescribed for many thousands of individuals with inflammatory bowel disease."

Here is another article I found on phthalates. www.environmentalhealthnews.org/ehs/news/prescription-drugs-can-deliver-high-doses-of-phthalates (NOTE: remove the < strong > < /strong > that is inappropriately added by the forum's software in the word "prescription".

I agree drugs with this kind of enteric coating may not be best for pregnant women. Or, they should max out on the rectal 5-asa and take no (or very low dose) oral 5-asa. I also think there are some 5-asa that use a molecular bond and do not rely on an enteric coating.

It has been well known that steroids, including Prednisone, lower testosterone. It is one of the several reasons it is recommended to taper off as soon as possible, or to use 6mp to spare the use of Prednisone. If I recall, the levels usually normalize some time after steroids are discontinued. The period of low T may have harmed bones, so having a density screening is not a bad idea.

It has also been long known that low T can lead to (or worsen) diabetes. Been there, done that, taking the insulin. I am not sure what this has to do with the original suggestion that 5-asa and/or Remicade cause low T. We have drifted rather far from that part of the discussion.

We were talking about 5-asa and Remicade, not steroids. The entric coating on some 5-asa may be a problem for male children of women taking enteric coated drugs - but this is far form any link to problems in males taking the drug. Also, Remicade has no coating. Still, taking fewer pills (e.g., Lialda), or using a 5-asa that does not use an enteric coating, might be a good idea for any male concerned about phthalates. ... and the rectal meds have no enteric coating at all.