Did someone of you used Roaccutane/Accutane? Cause of POIS?

[Hopeoneday]

From this angle it seams that peoples who took accutane
could be the couse of theirs pois...

Me, after severe preumona as a teeneger i was treated with
antibiotics, after that i got severe cystic acne wich last for 6
years.. acne was a nightmare for me.. i do not remeber what i did
not taking i thouse time to get rid of acne, but i clearly remeber
that i order and drink  (set medication for acne, wich did conteined
red pils,, i am 100% sure it was accutane )

I noticed that thigs like acne, antibiotics gut problems
are randomly repeates by poisers... that leed to warisos
disorders.. lipids, fat suliable vitamines(eg D), liver problems etc

This man is man is "damaged by accutane" eg antibiotics..
https://inews.co.uk/news/health/roaccutane-acne-drug-poisoned-fitness-fan-228884

https://poiscenter.com/forums
/index.php?topic=107.msg37379#msg37379

https://poiscenter.com/forums/index.php?topic=2081.msg16476#msg16476

https://poiscenter.com/forums/index.php?topic=3713.msg40812#msg40812

https://poiscenter.com/forums/index.php?topic=3799.msg40406#msg40406

https://poiscenter.com/forums/index.php?topic=3799.msg40406#msg40406

https://www.reddit.com/r/POIS/comments/rzonck/woman_with_pois_symptoms/ (a woman probbly damaged
by accutane and antibiotics combo)

[BoneBroth]

I also had Acne accutane in my teens (maybe for some months), so did my gf. She dont have POIS now but shares many other synptoms, most distinctly low blood pressure. She also said her vision was harmed directly following the accutane treatment. After that she had to wear glasses and had since. I dont remember if I developed POIS before or after the accutane though, but yeah, it could be a contributing factor.

[Hopeoneday]

The size of potential damage form accutane is fascinating.

I now remebered that i losted my hair from it...

Internal organs damaged, panceras, liver, gut, pitury gland
increasing brain pressure, reduced blod flowe...

https://www.healthline.com/health/accutane-side-effects-on-the-body

https://www.medicalnewstoday.com/articles/accutane-side-effects

[berlin1984]

I had skin issues and I remember using some topical products that all didn't help so much.
I (or my mother) don't remember if I took any pills or which one it was.

Journey, interested in making a poll on Reddit? Seems that's an easy way to get a lot of replies.
[ ] Yes oral
[ ] Yes topical
[ ] I don't remember if I took it (oral, topical)
[ ] No and I had acne skin issues
[ ] No and I never had acne skin issues

[BoneBroth]

Perhaps my pancreas took a hit on the accutane, thats why I have symptoms like yellow stools, bloating etcetera. Check out this poll. Accutane is just a syntetic form of Vitamin A that is extremely potent and potential toxic (not to compare with Vitamin A pills you buy at the healthshop with natural betacarotene or retinyl palmitate).

[Progecitor]

Well, we may have fewer POISers here than we thought.
Objective: To investigate clinical reports of post-SSRI sexual dysfunction (PSSD), post-finasteride syndrome (PFS) and enduring sexual dysfunction following isotretinoin.
Serotonin reuptake inhibiting medications, including the selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and the serotonin reuptake inhibiting tricyclic antidepressants, as outlined in their datasheets, almost invariably affect sexual functioning and do so after a first dose. The 5a-reductase inhibitors, finasteride and dutasteride, according to their labels, commonly (5–9%) have acute effects on sexual functioning. Isotretinoin also has acute effects on sexual functioning, but the frequency of this change is unknown and is not mentioned in the medicine’s label.
While PSSD and PFS have been named in the clinical literature, post-retinoid sexual dysfunction (PRSD) has not.
Table 1 Treatments linked to enduring sexual dysfunction
The mean causality scores were 8.9 for serotonin reuptake inhibitors, 8.8 for 5a-reductase inhibitors and 8.5 for isotretinoin.
In many instances the sexual dysfunction only appeared or became significantly worse when treatment was stopped. There were 41 (18.6%) reports for serotonin reuptake inhibitors, 9 (16.7%) for isotretinoin, and 7 (28.0%) for 5a-reductase inhibitors. Three subjects on SSRIs reported an increasing loss of sexual function as the dose was tapered. For all three drug groups there were reports of profound dysfunction appearing within days of stopping. This has similarities to antipsychotic-induced tardive dyskinesia which can appear on treatment and remain afterwards, or only appear when the drug is stopped.
Finasteride and isotretinoin are usually stopped abruptly whereas antidepressants are often tapered over weeks or months due to a withdrawal syndrome. At present, it appears that PSSD is equally likely following abrupt or gradual discontinuation of an SSRI or SNRI.
Seventeen subjects reported having the syndrome for at least 10 years since stopping treatment with isotretinoin (n ?= ?8 ), serotonin reuptake inhibitors (n? = ?8 ) or finasteride (n?=?1). Of these, five subjects reported that it had been over 20 years since stopping isotretinoin (n?=?4) or fluoxetine (n?=?1). Subjects also reported fatigue (9%), muscle weakness (3%), and cognitive problems including brain fog (19%) and memory impairment (11%). These were worse on finasteride. The cognitive symptoms appear to be a meta-cognitive problem in that testing rarely reveals deficits on what are tests of higher order cognitive function. Other drugs such as statins are linked to comparable difficulties.
In cases of enduring dysfunction, finasteride and isotretinoin appear to induce genital effects comparable to those found with serotonin reuptake inhibitors. However, finasteride and isotretinoin do not routinely cause acute onset genital anaesthesia that patients we have questioned are aware of. In this series, the numbness sometimes developed while on finasteride or isotretinoin, and occasionally appears to have done so shortly after commencement, but more often this feature became apparent during later treatment or after stopping the drug.
Pleasureless or weak orgasm is also common to the three treatment groups. This is experienced as a reduction or loss of pleasurable feeling, so that orgasm becomes a set of rhythmic muscle contractions with little accompanying sensation. These muscle contractions can also be weaker than normal, and may be noticed in male subjects as reduced ejaculatory force.
Rodents given fluoxetine were found to have sustained desensitisation of 5-HT1A receptors after removal of the drug. In another study, a 5-HT1A antagonist was shown to reverse and prevent sexual dysfunction in rodents that were being administered with fluoxetine. However, PSSD sufferers through online support forums have tried and reported on the effects of all combinations of medicines acting on serotonin and dopamine systems, and medicines known to enhance function such as sildenafil, but without benefit. The problem is again similar to tardive dyskinesia in this respect, in that counter manipulations of systems on which triggering agents work do not seem to remedy the problem.
It was hypothesised that SSRIs may induce disturbances of transient receptor potential (TRP) ion channels. The serotonin reuptake inhibiting antidepressants all have effects on sodium currents and other ion channels, raising the possibility that enduring effects arise from this source rather than at conventional receptor sites.
In addition to clinical need and research opportunities, these syndromes raise philosophical questions. The most common initial clinical and research response is to think about brain function. It is equally possible the problems arise peripherally, consistent with the James–Lange theory of the emotions which sees affective states arising from the periphery and more of our cognitive functioning as stemming from the body than is ordinarily supposed.
https://content.iospress.com/articles/international-journal-of-risk-and-safety-in-medicine/jrs744

So just add some poison to the venom and everything will be alright.
In order to convey as many targets as possible to stop Covid-19, it is possible to use combinations of molecules and some are currently being studied. The first combination that we will spell out is the association of isotretinoin with tamoxifen. Isotretinoin is a drug that is currently used to treat acne because of its antiandrogenic effect. Indeed, isotretinoin diminishes the serum levels of dihydrotestosterone, which is an androgen that promotes the transcription of TMPRSS2. The effect of androgens on regulating the expression of TMPRSS2 was previously reported on lungs. For this reason, it is tempting to speculate that suppressing the activity of androgens (including testosterone and dihydrotestosterone) will lead to the reduction of the expression of TMPRSS2, which results in less viral infection and this suppression may be induced by isotretinoin. Beyond its antiandrogenic activity, Sinha et al. have found out recently that isotretinoin is a strong downregulator of ACE2 receptors, being the strongest one out of over 20000 molecules tested in vitro. Taken together, isotretinoin may have a protective role due to suppression of TMPRSS2 and ACE2 expression.
https://onlinelibrary.wiley.com/doi/full/10.1002/rmv.2290

3 a-diol G was also reported to be low in post-finasteride syndrome!
Serum samples were obtained at baseline, 8, 16, and 24 weeks, and assayed for precursor androgens -total testosterone (TT), free testosterone (free T), dehydroepiandrosterone (DHEA), dehydroepiandrosterone-sulfate (DHEA-S); and tissue androgens - dihydrotestosterone (DHT), and its metabolite, 3 a-androstanediol glucuronide (3 a-diol G). Isotretinoin had no meaningful effects on precursor androgens, except for producing an elevation of free T in women. In contrast, isotretinoin produced depressions in the serum levels of DHT and 3 a-diol G in women and in 3 a-diol G in men. These decreases are believed to be the result, rather than the cause, of a reduction in the size of the sebaceous glands: The magnitude of the observed decreases may represent the amount of tissue-derived androgens that sebaceous glands normally contribute to the circulating pool.
https://jamanetwork.com/journals/jamadermatology/article-abstract/549304

It could be worth mentioning that alfalfa may increase 3a-HSD activity.
13-cis-retinoic acid (isotretinoin), 3,4-didehydroretinoic acid, and 3,4-didehydroretinol, but not all-trans-retinoic acid or the synthetic retinoids acitretin and adapalene, were potent competitive inhibitors of the oxidative 3a-HSD activity of RoDH-4, i.e., reduced the formation of dihydrotestosterone and androstandione in vitro. Extrapolated to the in vivo situation, this effect might explain the unique sebosuppressive effect of isotretinoin when treating acne.
https://www.sciencedirect.com/science/article/abs/pii/S0006291X03003322

There was a significant fall in testosterone during treatment and a significant reduction in the 24 h urinary excretion of androsterone, tetrahydrocortisone (THE) and tetrahydrocortisol (THF) from week 8 onwards and for aetiocholanolone and allo-THF from week 12. Although pretreatment levels of urinary steroid metabolites were not abnormal, the ratios of the 5a/5B metabolites (androsterone:aetiocholanolone and allo-THF:THF) were at the upper limit of the reference range and were lowered after treatment, suggesting that 5a-reductase activity is sensitive to isotretinoin.
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2133.1991.tb00598.x

In vitro studies of testosterone metabolism in hamster flank organ showed lack of inhibition of 5a-reductase by isotretinoin, but in female rats isotretinoin treatment caused a decrease in steroid 5a-reductase activity in both skin and liver. In cultured human prostatic cells 5a-reductase can be inhibited by retinoic acid through competitive inhibition of cofactor action (NADPH) yet in men circulating dihydrotestosterone is unchanged throughout isotretinoin therapy. In the present study marked reductions in the major androgen and glucocorticoid metabolites were found at the same time as decreased levels of 5a-reduction. 5a-reduction of androgens occurs in the peripheral tissues as well as the liver while glucocorticoids are mainly 5a-reduced in liver. It is therefore unlikely that these changes can be accounted for solely by drug-induced reduction in the size of the sebaceous gland and a direct effect on liver 5a-reduction is postulated.
https://scholar.google.com/scholar?hl=hu&as_sdt=0%2C5&q=Isotretinoin+treatment+alters+steroid+metabolism+in+women+with+acne&btnG=

[Hopeoneday]

My first intention is ruined now...
I did made a new topic acne-accutane-antibiotics on porpes...
and i think it shouldnt been deleted(it is important i think) , and his
place is not in hormonal but in generall section.
Old topics "are dead", antibitocis-acuttane topic is ipmortant as new !
Antibiotics-accutane combo are making
general body damage not yust hormonall.

[Progecitor]

My first intention is ruined now...
I did made a new topic acne-accutane-antibiotics on porpes...
and i think it shouldnt been deleted(it is important i think) , and his
place is not in hormonal but in generall section.
Old topics "are dead", antibitocis-acuttane topic is ipmortant as new !
Antibiotics-accutane combo are making
general body damage not yust hormonall.

I am sorry if you feel so, however these changes usually go hand-in-hand and one can't really exclude the other. Dysbiosis apparently plays a part in practically all cases of POIS, however it can't be easily ascertained whether it is the source or the result of the disease. There is at least indication for both as far as studies count.

Propionibacterium acnes (PA) is frequently involved in acne and can be detected by PCR in 82.8% of lesions. Propionibacterium species may adhere to intestinal mucosa. They secrete hyaluronidase and can alter intestinal mucosa. Microbiomes may associate several aggressive bacteria such as PA or Acinetobacter species and lead to synergic destructive and atrophic effect on mucosa. Patients with acne may receive isotretinoin which mucosal side-effects profile is well documented.
Isotretinoin affects also stem-cells renewal. May an isotretinoin-induced mucosal atrophy occur, a long-term or even a permanent effect could be expected; leading to severe consequences, repeated consultations and explorations in gastroenterology, and therefore to health expenditures.
Group 2 (Isotretinoin-treated) presents with dysbiosis: higher levels of H2 (7.3 ppm +/- 7 versus 4.6 +/- 6.9) and methylacetate (5.4 +/- 2.6 versus 3.9 +/- 4.4) than in the control group. The difference was also significant between group 1 (antibiotic-treated) and group 2: 7.3 ppm +/- 7 versus 4.3 +/- 4.7. for H2 and 5.4 +/- 2.6 versus 3.9 +/- 2.4 for methylacetate.
Group 2 also presents more frequently with oral herpes simplex (30.4% versus 21.4%) or allergy (34.6% versus 15.7%) than the control group; which suggests dysimmunity.
Propionibacterium acnes (PA) is frequently involved in acne. Human enterotypes have been classified into three groups. PA belongs to the Prevotella-enterotype. PA secretes hyaluronidase and can alter intestinal mucosa. However, PA has not been associated with dysbiosis, malabsorption or colitis. The Prevotella-enterotype also includes Helicobacter pylori and Desulfovibrio species as well as Acinetobacter species. HP favours gastric mucosal atrophy without any jejunal involvement. Desulfovibrio favours ulcerative colitis.
Acinetobacter favours mucosal atrophy. Therefore, although PA cannot directly favour colitis, other associated bacteria belonging to the Prevotella-enterotype may induce mucosal inflammation. However, there is no argument for any jejunal adverse effect of PA or of any associated bacteria from the Prevotella-enterotype.
In addition, isotretinoin normalizes (lowers!) exaggerated TLR-2- mediated responses in acne patients. TLR2 regulates the production of neurotrophic factors in intestinal smooth muscle cells and promotes survival of enteric neurons and glial cells. TLR2 controls mucosal renewal. TLR2 enables local tolerance via Bacteroides fragilis. It discriminates between pathogens and symbiotic bacterial molecules in a process that engenders commensal beneficial colonization. TLR2 controls indigenous bacteria proliferation in the upper alimentary tract. Lack of TLR-2 contribute to the settlement of undesirable bacteria, especially Gram-positive, or candida.
Isotretinoin is known to impair stem cells renewal and TLR2 expression in the mucosa of the small gut. These pharmacological effects, explaining the efficacy of the medication on acne ("the metabolic syndrome of the pilosebaceous gland") may induce the progressive atrophy of the jejunal mucosa and its long-lasting consequences.
https://pdfs.semanticscholar.org/aa42/f3e7260c399337f8e74faac8f8899ccce5ee.pdf

As a comparison to finasteride-induced changes:
Indeed, immediately after drug treatment an increase in Bacteroidetes phylum as well as in Prevotellaceae family was reported; after discontinuation of the finasteride, a decrease in Ruminococcaceae family, Oscillospira and Lachnospira genus was observed. Changes in gut microbiota could be ascribed to different factors, such as changes induced by finasteride in plasma and/or brain neuroactive steroid levels.
For instance, rats with depressive-like behavior show an increase in Bacteroidetes.
https://www.sciencedirect.com/science/article/pii/S235228951930061X

[Hopeoneday]

Somebody gaslighting us 
Somebody sticked 11 year old topic, and glued my new topic on that topic..
My new topic isnt attention to question - "did someone use accutane"
Topics like that existed, one of them is 11 years old..

[berlin1984]

Nothing was deleted.
It was me who merged the topic and also made it sticky so more people would notice it when browsing the forum

It's no use if one topic (accutante) has 5 threads with the same topic. Poiscenter has already too many threads, if we reddit-style open new posts for everything there won't be any cohesive threads..

Maybe I misunderstood your intention of making a new thread?
Can you explain?

I see it positive that an idea that came 11 years ago is getting some fresh air by you collecting links to other threads with same topic.
I also proposed for Journey to make a poll on Reddit so we can get more data. So I fully support your idea.

[Hopeoneday]

Berlin.. you killed my modjo 
Topic like this questionare should be pull??
I agree with you, but on the odher side we are tini mini comunity..
a micron. So.. i do not think that we hawe to much post here..
And sometimes new topic is needed to spin the wheels, ewen this
forum sugesting that for you when you replay on old topic..
i using a search on this forum wery suscesifully. Reddit is different
platform. But more on the other side i agree that we need tickened plot
with toppics. My inetention is Acne-ucuutane-antibiotcs-sibo and
tematic what can be damaged by tat...
Ok but i will write here my findings as it is pinned toppic...

[Hopeoneday]

Poisers coud hawe mucosal membrane damaged (a leaking)..
https://pubmed.ncbi.nlm.nih.gov/19492487/

Isotretinoin can affect all mucous membranes, causing multiple disorders of varying severity, affecting: the eyes (conjunctivitis); ear, nose and throat (epistaxis); respiratory tract; gastrointestinal tract (colitis); and urinary tract; (4)


Isotretinoin-induced inflammatory bowel disease
https://pubmed.ncbi.nlm.nih.gov/16517990/

Arthritis precipitated by isotretinoin treatment for acne vulgaris
https://pubmed.ncbi.nlm.nih.gov/8371229/

[Journey]

Never

[Hopeoneday]

Severe acne-antibiotics-havy metals exposure?

[Hopeoneday]

NEUTROPENIA AND THROMBOCYTOPENIA IN A PATIENT USED
ISOTRETINOIN FOR ACNE VULGARIS

https://dergipark.org.tr/tr/download/article-file/521027

[Hopeoneday]

https://www.reddit.com/r/SIBO/comments/pwgov5/new_study_accutane_causes_abdominal_adhesions/

[Progecitor]

Accutane and antibiotics really do have a connection.

A vitamin A derivate used in acne therapy (isotretinoin) has been inconsistently associated with the onset of IBD. However, what needs to be considered is the previous treatment of acne patients with antibiotics that are also associated with the development of IBD, thus representing a crucial confounding factor. Here, we studied whether doxycycline (acne therapy), metronidazole (IBD therapy) or isotretinoin are able to induce alterations in DNA methylation and microRNA expression patterns in murine colonic intestinal epithelial cells (IECs).
As for changes in DNA methylation, we found isotretinoin to have strong demethylating effects, while antibiotic treatment had only a moderate impact.
Regarding microRNA and mRNA expression, isotretinoin and doxycycline, but not metronidazole, potentially induce long-term changes in microRNA/mRNA expression profiles towards the down-regulation of immune responses.
In contrast, isotretinoin had a strong impact on DNA methylation with 234 hypomethylated targets compared to the vehicle. Previous treatment with isotretinoin resulted in eight hypermethylated targets, indicating a resolution of the direct effect on demethylation, and thereby pointing to a short-term effect of isotretinoin on DNA methylation. In total, 308 mRNAs were up-regulated and 136 mRNAs down-regulated after isotretinoin-washout, while treatment with metronidazole and doxycycline up-regulated the expression of 23 and 59 mRNAs, respectively, and down-regulated the expression of 59 and 91 mRNAs, respectively. These results point to possible long-term changes on mRNA expression levels after isotretinoin treatment in murine colonic IECs.
Treatment with the vitamin A derivate isotretinoin led to the demethylation of targets that were involved in IL-12 signaling and developmental processes, including the hypomethylated target IL-12rb1 and the corresponding up-regulated IL-12-dependent pathway in the transcriptome analysis directly after isotretinoin treatment in IECs. Although epigenetic marks such as DNA methylation are long-lasting and inheritable modifications, isotretinoin-induced demethylation was resolved after the washout phase of 4 weeks, indicating short-term effects on IL-12rb1. Furthermore, isotretinoin did not affect IBD-associated microRNAs in IECs neither directly after treatment cessation nor after the washout phase.
https://www.mdpi.com/2075-4655/1/3/24/htm

HDAC1 is overexpressed in prostate, gastric, colon, and breast cancers, and HDAC2 is overexpressed in colorectal, cervical, and gastric cancers.
Direct effects may be caused by drugs that affect chromatin architecture or DNA methylation, whereas indirect effects may be caused by drugs that affect transcription. For example, hydralazine directly affects the epigenome by inhibiting DNA methylation, and isotretinoin indirectly affects the epigenome by altering transcription factor activity. Drugs that indirectly affect the epigenome initially influence signaling pathways, thereby altering transcription factor activity at gene promoters and subsequently altering expression of receptors, signaling molecules, and other proteins. One study postulated that cells will ultimately adopt more permanent modifications to DNA methylation and chromatin structure, leading to enduring epigenetic changes. Thus these effects could persist after the drug is discontinued.
https://sci-hub.se/https://accpjournals.onlinelibrary.wiley.com/doi/abs/10.1002/phar.1408

[Vandemolen]

Did someone of you used Roaccutane/Accutane against acne? It also know as Isotretinoin? I had that 10 years ago against acne. It is a very heavy medicine and doctors warned me. But I asked and asked for it, because it was the only medicine which could get the acne get away. It is bad for the liver. It could be that my hormones were messed up by this medicine and caused POIS.

This will sound a bit weird for you but I am using Roaccutane right now. My POIS doctor desrcribed it to me. But in a very low dose (10 mg a day). If I have side effects I have to skip it taking it for a day. I have less acne now. I take it since almost 3 months. Because I only take a very low dose it is ok to take it even more than a year. The key is taking a low dose. Because of that if will take a longer time before the acne goes away for good.

[Hopeoneday]

Vander, i wouldnt recomended this medicine to my worst enemy!
Who hawe no luck in life, it would be damaged permanently from this medicine...

[Vandemolen]

I only use 10 mg a day. So I do not have any side effects.