ok got it thx
Thanks for all the material, I am studying the question. I apparently don’t have symptoms of autoimmune ganglionopathy, apart from a possible autonomic dysfunction but I’m taking a look.
Yes, I’ve had a finding of abnormal pituitary activity when I was a “mild” case. At that time I only had physical problems, e.g. muscle wasting/worsening with exercise, until rechallenge years later after which I severely crashed and developed severe neurological and sexual symptoms, and progressive atrophic changes. I have not had an MRI since.
I’ve given some thoughts in the literature review awor and myself provided in 2020 if you’re interested. O’Reilly et al. provided an important paper determining a role of androgen signaling in CSF pressure in IIH patients, and further demonstrated this in animal cell modelling:
"A central and potentially causative role of androgen signaling was recently demonstrated in idiopathic intracranial hypertension (IIH), which entails an increase of CSF pressure. O’Reilly et al. identified a pattern of androgen excess in female IIH patients. Like human choroid plexus, rat cells expressed AR along with androgen-metabolising enzymes. It was demonstrated that testosterone drove CSF output in rodent choroid plexus cells (O’Reilly et al., 2019). O’Reilly et al. noted that while a determinant role for androgens in IIH may seem biologically implausible considering IIH occurs less frequently in men, androgens are now known to exert sexually dimorphic effects on metabolism. The metabolic phenotype of hypogonadal men resembles that of women with androgen excess, including an increased risk of type 2 diabetes, non-alcoholic fatty liver disease and cardiovascular mortality (Ding et al., 2006; Kautzky-Willer et al., 2016). O’Reilly et al. suggest epigenetic modifications to local androgen action or differences in AR signaling in both sexes as a plausible explanation, with IIH potentially representing a distinctive manifestation of these sex specific differences (O’Reilly et al., 2019).
Interestingly, male IIH patients are more likely to have symptoms typically associated with androgen insufficiency including obstructive sleep apnoea, erectile dysfunction and loss of libido (Fraser et al., 2010). As well, androgen deprivation therapy or hypogonadism can induce IIH symptomatology (Valcamonico et al., 2013). Although in males the metabolic parabola of AR signaling is shifted far to the right compared with females (Ding et al., 2006; Morford et al., 2018), significant increases in AR signaling in men are likely to recapitulate this symptomatology, and we therefore consider it plausible IIH occurs in PFS and contributes to commonly reported symptoms, including feelings of intense pressure in the head.
In this context, it is of interest that the pilot study of Melcangi et al. evaluating CSF methylation in PFS patients and controls found only one member of the control group with methylation of SRD5A2, and this patient had normal-pressure hydrocephalus. The majority of PFS patient samples exhibited variable methylation of this gene (Melcangi et al., 2019)."
citations in original text.
Also @tab, please could you complete the survey? It’s important symptoms like yours are recorded in this data set, and every submission really helps. You can take it by clicking the graph icon in the top right of the forum when on a desktop or laptop. Thank you very much.
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About 6 months ago. I have not had a hormonal blood test done since, but at the time my prolactin was increasing. Perhaps it would be wise to do another blood test soon as my symptoms have not really changed much over time and to see if my prolactin levels have significantly increased since and if a new MRI is warranted.
Have you been prescribed medication for the hyperprolactinoma, like cabergoline? I’ve heard people mention (short-term) increase in libido and sexual functioning while taking cabergoline. Although in my view taking cabergoline would be symptom relief instead of actual treatment.
If you have a similar condition to mine, I have taken many prolactin tests during the years, I also took a prolactin curve test.
I have seen it vary from normal to 97 ng/ml (near prolactinoma limit). Sometimes it is down, sometimes it is up. I couldn’t find any clue on this behavior. My sexual condition too is not stable, I sometimes have problems keeping it up, sometimes I’m pretty hard. I have no clue why these changes happen from day to day. In my limited knowledge of erectile physiology, there probably is something fkdup in the hypotalamus too as when I experience ejaculation the penis immediately softens during ejaculation. I can see this only as nervous mediated effect from the hypotalamus, through the spine and then to the penis. But this again is only my hypothesis as I’m not an MD I’d have to study much more in order to be fairly sure about that.
So yes, if I were you, I would take a prolactin test from time to time just to understand what is it’s behavior.
I only made a short cabergoline cycle many years ago. I restarted a cycle a couple months ago. Prolactine goes down, T increases, but honestly the benefits seem to be limited. I hope that by waiting a bit more the symptoms will fade. Howver considering the recent finding from the MRI I’m not all that positive anymore as the pituitary compression probably hinders all other pituitary hormones. That being said, I don’t like cabergoline as it brings risks of heart fibrosis and similar, at least at higher dosages. But who trusts leaflets anymore? Big Pharma is a joke and they should go and fk themselfes. I don’t think I’m going to take it lifelong. You might try it out to check if it does something for you.
Either way, at least in my case, I don’t have a lot of hopes for a real healing treatment anymore. As you can see the problems are many. I will do all what I can anyway and I’m still prone to holistic/behavioral therapies. I’m reconsidering my workout and diet routine as in these years I wasn’t able succeed in the body fat/muscle recomposition, and I have muscle wastage and gynoid fat deposits from Fin that surely act as hormonal organ. Not to mention my real gynecomastia (another gift from FIn). I’m getting some results with the new routine but it’s too early to tell if this translates into stable improvements.
Thanks for the elaboration on your experience. I will push to get a new hormone measurement.
I do agree with axolotl though: Would you please contribute to the survey, because it’s not going to be open for much longer and it’s very important that as many patients as possible contribute to the data.
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I do not feel to complete the survey as I took also an antipressant and benzos during my finasteride therapy. The data I can provide would probably be misleading. Also more than 10 years have passed since the start of Fin. It’s very hard for me to recall the answer to many questions which are very detailed. I think my survey would only be misleading to researchers.
I have been found a few days ago to have very high semen leukocytes. Leukocytospermia is a sign of infection/inflammation in seminal vescicles/prostate. I will do a seminal colture and see what happens.
I am pretty sure that PFS is nothing more than an antibody that somehow attacks the androgen receptors and in the worst cases, even estrogen receptors, preventing them from binding to the hormone. I can’t understand why the researchers don’t want to move in this direction. The answer to PFS would be around the corner.
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Anti-AChR antibodies disrupt communication between nerve fibers and skeletal muscles, inhibit muscle contraction and prevent activation of acetylcholine receptors, resulting in rapid muscle fatigue. The action of the anti-AChR antibodies is threefold:
Binding antibodies bind to exposed receptors on nerve cells and can cause inflammation that destroys the receptors;
Blocking antibodies can “mask” the receptors, preventing acetylcholine from binding to them;
Modulating antibodies cause cross-reactivity between receptors, with consequent internalization of receptors within muscle cells and elimination from the neuromuscular junction
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This is the most interesting part, because in the first PFS studies the researchers found an increase in the density of the androgen receptor. It seems to me a fairly rational mechanism: The antibody binds to the receptors, preventing them from working, but without destroying them. The body is not responding to the hormone and what is the most logical move? It produces other receptors, which are blocked again. This would also explain why partial recoveries last so short. It seems really crazy to me that no research has moved in this direction. It seems too obvious.
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Interesting theory… There is a test for Anti-AChR antibodies in my country for like 20-30 bucks, maybe you can find the same in yours. Haven’t done it but maybe I might in the future
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Sounds leggit!
If it’s that cheap you should get checked them asap and share your results with us, I don’t have that test unfortunately in my country , so wondered whats going on .
These are different antibodies from the one I mentioned.
This is what I tested positive for,
neuronal achr ganglionic (alpha-3)
It will probably cost more then 20 or 30 bucks Im guessing.
The other is used to help diagnose Myasthenia gravis, but they are not the same antibodies even though they look similar.
I am going to have some more time and money in the near future and I might follow-up on this antibody.
How rare is autoimmune autonomic Ganglionopathy?
Approximately 100 Americans are diagnosed with AAG per year. AAG is a treatable antibody-mediated disorder of autonomic ganglionic synaptic transmission.
How is it treated and are you going to treat it?
Did any of you guys had a spermiogram and did it turn high in leukocytes? As I found this evidence on me(more than double the limit), I am now wondering if it is bacterial induced or if it is autoimmune. Will do the seminal colture tomorrow, but if it turns negative, I guess it can only be autoimmune. And in that case I’ll probably check as you did.
It could be both, I also wouldnt call some of these possibilities an infection per se, but maybe a type of shift in balance or triggering event. You see all of these thoughts are within the past couple of years.
I still think this could be the closest organic (or non-drug) type of treatment that could be coming.
Otherwise those antibodies are sometimes treated with IVIG, which wont even be an option for most people.
Why gut bacteria are becoming key suspects in autoimmune …
Feb 2, 2021 — Many patients with PSC have other autoimmune diseases, and some of the genes associated with the condition are also linked to autoimmunity .
Bacterial infections are associated with many autoimmune diseases involving chronic inflammation and demyelination. The possible mechanisms of bacterial involvement as aetiological agents or in the exacerbation of these diseases have been investigated intensively.
Could a bacteria-stuffed pill cure autoimmune diseases?
https://www.nature.com › outlook › article
](https://www.nature.com/articles/d41586-020-00197-z)
Jan 29, 2020 — Could a bacteria -stuffed pill cure autoimmune diseases? Researchers are investigating how the community of microbes living in the gut might …
Triggers of Autoimmunity: The Role of Bacterial … - Frontiers
https://www.frontiersin.org › fimmu.2019.02608 › full
](https://www.frontiersin.org/articles/10.3389/fimmu.2019.02608/full)
by CC Qiu · 2019 · Cited by 20 — Moreover, bacterial infections can release bacterial DNA associated with other bacterial molecules, complexes that can elicit autoimmunity by acting as innate stimuli of pattern recognition receptors and activating autoreactive B cells through molecular mimicry.
Researchers Discover New Link Between Autoimmune …
https://www.infectioncontroltoday.com › view › researc…
](https://www.infectioncontroltoday.com/view/researchers-discover-new-link-between-autoimmune-diseases-and-gut-bacterium)
Oct 29, 2018 — The culprit in this case is called Bacteroides fragilis, a bacterium that normally lives in the human gut. The Queen’s team has shown that this …
The enemy within: Gut bacteria drive autoimmune disease …
https://news.yale.edu › 2018/03/08 › enemy-within-gut…
](https://news.yale.edu/2018/03/08/enemy-within-gut-bacteria-drive-autoimmune-disease)
Mar 8, 2018 — Bacteria found in the small intestines of mice and humans can travel to other organs and trigger an autoimmune response, according to a new …
Gut bacteria may hold key to treating autoimmune disease
https://researchfeatures.com › Health & Medicine
](https://researchfeatures.com/gut-bacteria-key-treating-autoimmune-disease/)
May 31, 2018 — Emerging research supports that the gut bacteria influence various immune cells in autoimmune diseases. The precise mechanisms of how and …
How rare this antibody is btw,
Ganglionic Acetylcholine Receptor Autoantibody
Oncological, Neurological, and Serological Accompaniments
Of 15 000 patients tested on a service basis, 1% were seropositive
Other Autonomic Neuropathies Associated with Ganglionic Antibody
The identification of the acetylcholine receptor ganglionic (G-AchR) antibody by Vernino et al. in 1998 and especially following the comprehensive study in 2000 opened a new era in the diagnosis, evaluation, and treatment of the autonomic neuropathies.
The autoimmune disorder was suspected in the original description (Young et al., 1969, 1975) when it was considered as an autonomic variant of Guillain-Barre’ syndrome. The view was sustained in the Mayo Clinic experience, where we demonstrated selective involvement of C fibers, an inflammatory, presumed immune attack of nerve and possible response to immunotherapy
This could be another possible marker.
Antiphospholipid Syndrome as a Neurological Disease
Neurologic disorders are among the most comum and important clinical manifestations associated with the antiphospholipid syndrome (APS), mainly those that affects the central nervous system (CNS). These include sroke, transient ischemic attack, Sneddons syndrome, convulsions/epilepsy, dementia, cognitive deficits, headaches/migraine, chorea, multiple sclerosis-like, transverse myelitis, ocular symptoms and Guillain-Barre syndrome.
Anti-phospholipid antibodies in serum from patients with Guillain-Barré syndrome
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Of 15,000 patients evaluated at the Mayo Clinic for paraneoplastic autoantibodies in a 27-month period, α3-AChR Ab values exceeded 0.02 nmol/L in 155 patients
Mine was 0.07
It didnt copy and paste too well but you see how getting a few simple blood tests run could maybe start to paint a picture or help diagnose when most are saying there is nothing wrong with you.
“Since incorporating the α3-AChR Ab assay into the standard Mayo Clinic serological evaluation for paraneoplastic autoimmunity in 2005, we have observed that this Ab has broader oncological and neurological associations than originally recognized.”
Neurological Associations in 155 α3-AChR Ab–Seropositive Patients by Titer
|Neurological Manifestation
|Peripheral nerve, autonomic(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3764484/table/T2/?report=objectonly#TFN8)|17 (20)b|6 (10)b|
|Limited dysautonomia|20|3|14|3|
|GI dysmotility|10c|1|8|1|
|Orthostatism|5|1|3|1|
|Anhidrosis|3|1|1|1|
|Sicca syndrome|2|0|2|0|
|Pandysautonomia|13|7|3|3|
|Peripheral nerve, somatic|44 (28)|0|31 (36)|13 (22)|
|Sensorimotor polyneuropathyd|28|0|22|6|
|Small fiber sensory neuropathy|7|0|5|2|
|Polyradiculopathy|4|0|2|2|
|Cranial neuropathy|3|0|1|2|
|Sensory ganglionopathy|1|0|0|1|
|Multifocal motor neuropathy|1|0|1|0|
|Neuromuscular junction|4 (3)|0|1 (1)|3 (5)|
|Myasthenia gravise|4 (3)|0|1|3|
|Central|26 (17)|1 (8)|20 (24)|5 (9)|
|Cortical and/or neuropsychiatric|15|1|11|3|
|Movement disorderf|5|0|5|0|
|Demyelinating CNS disorders|5|0|3|2g|
|Stiff-man syndrome|1|0|1|0|
|Nonautoimmune disorder or noneh|48 (31)|1 (8)|16 (19)|31 (54)|
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Anyway this could explain how guys can take massive amounts of steroids and still not feel muscular or sexual effects?
Yes they diagnosed high dose white blood cell in my urine and I though it is prostatitis, must be anything important.
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