My ritux experience so far

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But 90% of American doctors to this day (2018) still label me with a "CFS" diagnosis. And it is not just me. There is clearly a misdiagnosed group, some severely ill like I was, who are labeled with CFS and basically told to fuck off and die by the traditional medical establishment in the US (so I can only imagine what is happening in other countries).

We have an illness yet to be formally named and it usually involves having multiple autoantibodies. The volume of PM's that I was receiving from people similar to me was insane and every last one had been given a "CFS" diagnosis by at least one doctor (and usually multiple doctors).



I have spoken to them and don't know why you would assume otherwise? I spoke to hundreds of Rituximab patients as part of my research. Some from OMI, some from Center for Complex Diseases, some from Kolibri, and many with private doctors across not just the US but worldwide. Many from PR, some from Facebook, some from other medical groups. Almost every single one had been given a "CFS" diagnosis as I was.

I continued to dig deeper since 2013 and with each layer, it brought me to my current treatment. I do not deny or sugar coat that there can be major risks like anaphylaxis or very rarely PML. It also should not be done if you are at risk of reactivating hepatitis or TB (which I was not b/c never had either).

But if I were to name the top 100 things that have injured or harmed me in my pursuit to get better, Ritux would not even make the list (for me).
I'm very interested in your analysis, it's impressive you talked to so many patients. Can you send me a PM with a summary of what you learned(from talking to them), and which antibodies you tested positive for? I myself have doubts about ME/CFS, im diagnosed with POTS but 1) being unable to access a 2 day cardiopulmonary testing 2) no joint pain whatsoever and 3) my PEM symptoms being mostly cognitive i can't tell if my PEM is "actual" PEM or just increased autoimmunity/inflammation in the brain.

Thanks a lot and i'm glad you are better!
 

Gingergrrl

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Most doctors throughout the world I think are very badly trained when it comes to ME/CFS diagnosis, and probably have never heard of the exacting Canadian consensus criteria. I would think in the mind of many doctors, ME/CFS is just a vague waste-bin diagnosis that they conveniently use when nothing else fits.
I have never in my entire life (not once) met a doctor who has mentioned the Canadian Consensus Criteria to me and the only place I have ever heard of it is here on PR (or other ME/CFS boards).

If I remember rightly, a few years ago I think it was the NIH that set up a department for dealing with mystery illnesses that no other doctors or specialists could fathom. I can't remember the name of it, but that's ideally how patients should be treated when their symptoms match no known disease: they should be investigated by some very high level researchers.
I have no idea if this NIH dept still exists but if it does, my guess is that they are extremely selective with how many patients they can see/choose and that no insurance company in the US would pay for this and would consider it a wild goose chase.

Did those other people you were in contact with have a symptomatically identical condition to you, or did they each have their own idiosyncratic symptoms which just happened to be labelled as ME/CFS?
I have never met anyone who is symptomatically identical to me and each person has their own idiosyncratic symptoms. This is my experience of PR as well. I have several very close friends from PR (back to 2014) and of the four who I consider to be like family (some of them no longer post but we remain in regular contact), their illnesses (including the initial triggers, their current symptoms, and their treatments) are dramatically different. And yet all of them have an ME/CFS diagnosis.

I am just wondering if you might have a new unknown syndrome that others also have.
While this is in the realm of human possibility, I find it unlikely that I have a new unknown syndrome that no one else has. The triggers of my illness were a combination of severe Mono/EBV, toxic mold exposure, and neurotoxic reaction to an antibiotic (all within a 2-3 year period until my immune system lost control). It then shifted from viral to autoimmunity. I have rock solid diagnoses of POTS/Dysautonomia and MCAS except the MCAS is in remission. I also have Hashimoto's. The mystery was the level of muscle and breathing weakness which my doctors now attribute to the autoantibodies.

So it's these considerations of how much risk is involved, weighed up against the chances of improvement (which are poor in the case of ME/CFS).
It is high risk with MCAS as well (allergic reactions/anaphylaxis and even third spacing of normal amounts of fluid leading to pulmonary edema which happened to me several years prior to Rituximab) but I felt the risk was worth it (in my case).

That's great that you fared so well, though one cannot judge the safety of a drug via the effects of only one patient, and you may be the only patient with your mystery condition that's ever been treated with rituximab.
I absolutely do not judge the safety of a drug based on one patient but I also cannot fathom that I have a mystery condition that no one else on earth has. Even for my most obscure autoantibody (the N-type calcium channel Ab), there is a FB group with people all around the world who have this autoantibody and many of them are very similar to me. Doing IVIG and Ritux as treatment is much more common in that group and there seems to be much more willingness to try treatments b/c the level of desperation is much more extreme (in my experience as a participant in both places).
 

Gingergrrl

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Can you send me a PM with a summary of what you learned(from talking to them), and which antibodies you tested positive for?
I apologize but I cannot do this right now. My mom is dying of cancer and I am with her almost every day and I am no longer able to keep up with PM's and already got three new ones just today that I have not read yet. I feel incredibly guilty that I cannot reply to PM's so I wrote in my thread, my avatar, and my signature that I cannot do it in the hopes that people would read it. I apologize but I am unable to type up a summary of what I learned from other Ritux patients right now. Maybe in future months I will be able to and I would love my case to help others in the future.
 

Sushi

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I have no idea if this NIH dept still exists but if it does, my guess is that they are extremely selective with how many patients they can see/choose and that no insurance company in the US would pay for this and would consider it a wild goose chase.
As far as I know it still exists.
Undiagnosed Diseases Network launches online application portal
A friend of mine went through their program (she also had severe dysautonomia). As far as insurance, I don't believe there is any charge for patients in this program. However, this is not a "to dream for" program. My friend found that none of them many specialists who examined her, consulted with each other! In the end she found her week there a waste of time that only made her more sick due to PEM.
I cannot reply to PM's so I wrote in my thread, my avatar, and my signature that I cannot do it in the hopes that people would read it.
You can turn off the receiving of PMs or a moderator can do it for you.
 

Gingergrrl

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As far as I know it still exists.
Undiagnosed Diseases Network launches online application portal
A friend of mine went through their program (she also had severe dysautonomia). As far as insurance, I don't believe there is any charge for patients in this program. However, this is not a "to dream for" program. My friend found that none of them many specialists who examined her, consulted with each other! In the end she found her week there a waste of time that only made her more sick due to PEM.
I think you might have mentioned this friend to me before @Sushi (although I might be mixing her up with someone else)! Either way, this does not surprise me whatsoever and I can only imagine that the level of disorganization at the NIH far exceeds that of a regular hospital (re: trying to get doctors to consult with each other, etc). I am sorry about your friend's experience.

You can turn off the receiving of PMs or a moderator can do it for you.
If I turned off PM's but people did not know and sent them to me anyway, would they get an alert telling them that I have the PM function off or would they think that I had received it and was just ignoring them? I would feel bad if people felt I was ignoring them and this is not something that I would do. Also, when I turn the PM function back on in a few months, if people sent me PM's, would I be able to view them later or would I never know that they existed? My closest long-term (and newer) PR friends all know how to reach me by e-mail, text, phone, etc.

Thanks in advance @Sushi and I am sorry to sidetrack this thread from discussing Rituximab (which I feel continues to be a very important topic).

Edit: Sushi, if you want to reply to my questions re: turning off PM's via PM, I promise I will read it and reply! I just don't want to take this thread further off track.
 
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Hi Desertstorm,
I don't post to this forum much any more but I would like to answer here. In case you are not aware, I was the physician who introduced the use of rituximab for rheumatoid arthritis and vasculitis etc. in 1998. I thought the early results in ME/CFS were interesting and my group have worked closely with the Norwegian team but I am now clear that rituximab is not a sensible option for ME/CFS per se. Basically the results show it does not work.

However, rituximab is known to produce good results in various types of vasculitis, including forms affecting kidney and lung. It is a much better option than steroids.

What is not clear to me from your post is exactly what illness you have. If you have vasculitis then that is something quite different from Gulf War illness. The two would not be confused by a competent physician.

So for vasculitis rituximab is good treatment. For ME/CFS it is not. I have no reason to think it is useful for GWI. Vasculitis is not caused by viruses or insecticides or nerve gases as far as I know (except in some very specific infections chiefly in children). Vasculitis can produce severe fatigue. So I think it all depends on whether you have vasculitis. If so the answer is in the textbooks. If not, then rituximab is not something to try without very good reason.
GWI is not a disease per se but rather a term used to describe a bunch of conditions and unexplained multi symptom illnesses that run the gamut from CFS, FM, rashes, neurological stuff, foggy thinking, joint pain, various auto immune and inflamatory conditions to weird effects of semen on partners. My condition in terms of vasculitis and systemic inflammation Was DX at both Stanford and Mayo plus the VA. My fatigue started after a virus in the Middle East in 1991. With that came rashes that never have been DXed, a couple years latter a kidney inflamatory condition that was biopsied and thought to be from exposures. Then my bronchial passages started to become inflamed resulting in massive coughing attacks. Mayo put me on steroids in 2008 which work for for everything but the fatigue. The vasculitis shows up as purpura rashes along with the other mentioned symptoms as soon as I taper down on steroids. I used to get kennolog shots, but now am on between 100 and down to 60 mg of hydrocortisone at which point the symptoms reappear. Not a doctor but I have puzzled more than my share over the past 25 years. Like most patients I don't REALLY know what I have other than what I am told...and that I have the same thing as many (tens of thousands) of fellow vets have from that time period, including one local Army vet here who's medical history from 1991 on mirrors mine in a remarkable fashion. What I do know is that for every doctor there is an opinion and a counter opinion. For instance at one point I was told "definitively" I had lymphoma which as in Unrest made us happy to know what it was. Except it was not. Same with Lymes disease, PTSD, you name it. Vasculitis being an Autoimune condition is just one condition amongst the others I am told. There is also the possibility that is could be steroid induced. But given the history and timing of all these "unexplained multi symptom illnesses" as the Congress mandated the VA recognize my conditions follow a defined trend line (for lack of a better term) and that nobody really knows anything about CFS or the cause of the other Autoimune conditions it is all we vets have to go on...thus GWI incapsulates the wide spectrum of illnesses. The best research on GWI was complied in the Kansas NG study. The VA's War Related Illness and Injury Study Center seems to think that pyridostigime bromide pills in combination with other exposures such as insecticides or oil fumes caused the autoimmune condition. That said, as was the case with Agent Orange, the VA itself and the military denies any connection. My guess is that as nobody will make public who or why exactly decided PB pills should be used as a nerve agent preventative without any any real research we shall never know. Not in my lifetime.


My current civilian doc tried methotrexate which did not work at all. The next suggestion is rituximab to replace the steroids. I traded my soul (skin and bones) years ago to retain functionality via the steroids. To be clear, he is treating me for the autoimmune/inflammation process not CFS. I was reading about any possible improvement in terms of CFS may have transposed the conditions, given that to me they are all linked.

Sorry about rambling on. Thanks for your input doc. Any further advise would be wonderful.
 

Wonkmonk

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@Hip and @Gingergrrl, thank you letting us take part in this very interesting discussion which I think makes some very interesting points.

I can understand both standpoints. I think Hip is correct to point out that adverse events can occur and indeed have occurred in a number of CFS patients who took Rituximab. I also agree that from what we know, the risk-benefit expectation is not very favorable. Still, from what I know (correct me if I'm wrong) it seems like most CFS patients who try it have no meaningful effect at all - neither positive nor negative.

The case of Olaf Bodden, which is very prominent in Germany, is also something that should give everyone who thinks about Rituximab pause. Here is the last major report I found from 2016, at that time he had still not improved from Rituximab and was taking Gamma-Interferon and high-dose vitamins. Google translator works very well if you'd like to read it fully:

https://sportbild.bild.de/bundeslig...den-so-ist-das-kein-leben-45133844.sport.html

BUT: I can also understand Gingergrrls point that some of us are in such a bad situation that doing nothing is just not an option. Some people have benefitted from Rituximab, even if they might be few. I am among those people. I do consider trying Rituximab, but I am still undecided, because there are so few positive reports and if it worked even for only a small percentage of people, there should be a number of positive reports. But there are very few, actually Gingergrrl is the only one I know of plus those in the first Rituximab trials.

At this time, it seems likely that I will end up trying Rituximabm because what else can I do? And if I do so and it makes me worse, I won't blame anyone but myself.

By the way, this is also Olaf Bodden's mindset. Of course in retrospect, he regrets taking Rituximab, but despite this terrible experience, he says he'd try a new study anytime. Quoting from the article above:

„Ich gehe jedes Risiko ein. So ist das ja kein Leben“, spricht Bodden, der Kämpfer. „Meine Situation ist so grauenhaft, da sterbe ich lieber an einer Studie.“
("I'd be willing to take any risk, because this is no life at all. My situation is so terrible, that I'd rather die while taking part in another study")

Doing nothing is not an option.
 

Wonkmonk

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In this very interesting lecture (Feb 20, 2018), Dr Montoya gives a possible explanation why Rituximab seems to only work in few patients (if any): It targets a too narrow part of the immune system whereas immune system abnormalities are very broad and wideranging in CFS. (see after 39:00)

This could also be an explanation why Cyclophosphamide seems to work better, because it is nonspecific and targets a broader part of the immmune system.

 

Joh

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Doing IVIG and Ritux as treatment is much more common in that group and there seems to be much more willingness to try treatments b/c the level of desperation is much more extreme (in my experience as a participant in both places).
I can't imagine that their higher desperation is the reason and find this quite insulting and unfair. You are the lucky ones with lab abnormalities that can be targeted by treatments. I envy everybody with autoimmunity and I would start treatments tomorrow because there's a range of possible treatment options (IVIG, Rituximab, plasmapharesis) and it's even possible to fight the insurance over it. Imagine you feel like dying for decades every day, but have no interesting lab abnormalities - nothing you can do, nothing you can fight your insurance over, no lead for doctors. Welcome to the world of ME/CFS. The reason is not, that these people are not as daring or proactive, as your group smugly seems to think. I find this really insulting and you apparently have no idea how it feels to not have your level of misery reflected in lab tests and no one to believe you because of the lab tests and to regularly ask yourself if you're crazy because nothing shows up and to not have Cell Trend and doctors interested in your case because it's so special. Ever wondered why the suicide rate is so high in ME?
 
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Gingergrrl

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I can't imagine that their higher desperation is the reason and find this quite insulting and unfair.
The reason is not, that these people are not as daring or proactive, as your group smugly seems to think.
I just logged on here b/c I am in tears over my mother being near dying to find your post. What in the fuck are you talking about? The group I referred to is not "smug" and nothing could be further from the way you just characterized them. They are are group of people from literally around the planet who have a rare autoantibody and almost every single one of them has been dismissed by doctors (as I was) and treated like human garbage. My words about the people in that group getting IVIG and Rituximab were MY WORDS. I find what you just said about them to be insulting, especially because you do not even know them or their stories.

I would say that at least 50% of the people in that group have cancer b/c the autoantibody we have is a paraneoplastic autoantibody that often links to small cell lung cancer. Some of the people in that group have died since I joined it. None of them were handed their treatments on a silver platter and they fought like hell to get them. Many paid privately and were denied all levels of appeal by their insurance companies.

I have been dropped by my insurance company a total of FIVE times. It happened again to me on March 1st and I did not even bother to post about it b/c it is just my life. They take my full payment and then drop me. I have fought to the core of my being to get these treatments approved and I went into the treatments prepared for death. I have never said that ANY person on this board (or any board) was not "daring or proactive" and you have literally put words in my mouth.

I have continued to post here in the hopes of helping other people. Every single time I have tried to stop my Rituximab thread people have sent me PM's begging me to continue it. I have been attacked for promoting treatments when I am just reporting on my own experience. Nothing in my post was meant to be insulting and I am truly sorry that you took it that way. I am baffled to be honest.

Edited to add: I have lost count of the number of times that Dr. Edwards has referred to my doctors, my treatments, Cell Trend labs, etc, as "fake" or "bullshit" but no one seemed upset when these words were directed specifically at me. I just had to take it and either defend myself or keep quiet. I was not insulting anyone and was only reporting on my own experience as I have lived it.

It was quite a bit of effort to send my blood from Los Angeles to Cell Trend in Germany and I paid over $600 including the bank transfer which I had to do in person. I chose to do these things b/c I felt they were worth the risk. I do not know why I am being criticized for it? I think you are directing anger at me that has nothing to do with me to be honest.
 
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Gingergrrl

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What is anti mog is it relevant A different topic
I think it is an autoantibody that has been linked to MS and other demyelinating diseases but I am not certain how it may or may not respond to Rituximab (if that is what you are asking)? Others would probably know better than me.
 

Gingergrrl

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I really appreciate you saying that @Wonkmonk and it was a good reality check for me b/c I started to question myself and wondering if had done something wrong! It is never my intention to hurt another person on this board (or anywhere). I have spent hours every single week replying to PM's asking me about my treatments and I answer them from my heart, from my own experience, with the goal to be helpful.

It is now 3 am here but I am still awake b/c I am so shaken by @Joh's comments and I have to get up early to be at the SNF with my mom. I am not looking for an apology but I definitely do not think I deserved to be attacked like that. I re-read every single thing that I have written in this entire thread and remain completely confused as to what I did wrong. The point I was trying to make (if this is the offensive one, I am still not sure?) is that in the other boards that I belong to (for LEMS, for MCAS, for POTS, for IVIG, for autoimmunity, etc), the people seem to try a wide variety of treatments and to inquire about things that are similar to your questions in this thread where I can tell that you are really struggling with whether or not to try Rituximab (and ultimately only you can make that decision and there is no right or wrong answer). I was a newbie (in those other groups) and they answered my questions with great patience which I appreciated very much.

In kind, I have tried my best to answer every single question that I have been asked here. This board seems more focused on only doing treatments that have been proven in double-blind research studies and if they are not, then the treatments are dismissed. Whereas, to me, there is a grey area and I believe there are sub-groups or mis-diagnosed groups who could still benefit from some of these treatments. This is my opinion. If my insurance had denied me, I would have found another way. And my insurance may still deny me and I may end up in medical bankruptcy some day.

I was just trying to explain that to me it was worth it and no matter how many people told me that it was too risky, or it I could get PML, or that it should not be done outside of a double-blind study, etc, I did not care. I was near death in 2015 and it was worth the risk. But that is just me. I am not imposing this belief system onto anyone else. I often get tagged into these discussions on Rituximab so I share my experience. But after Joh's attack on me, I will be much more hesitant to talk about Rituximab or anything else b/c I just do not need this kind of negativity right now.
 
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Wonkmonk

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@Gingergrrl I think it should be clear and obvious to anyone who is following you on this board that you are trying to help other members wherever possible and that you are not seeking to disparage any other individual or group of patients. To be honest, I think that is an absurd accusation that I can only imagine must have been some kind of misunderstanding on @Joh's part.

In the end, we are all in this mess together and our situation is difficult enough. It is known that psychological stress can make CFS (and other things) worse, so I think everyone of us should be very careful in how we deal with each other and how we voice disagreements. That of course, includes myself, too.
 

Learner1

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@Gingergrrl, please do not stop posting on this subject. You have been generous with your time and have gone to great effort to provide detailed information about your situation, which is quite helpful in putting the treatments you have chosen in context.

Not every treatment will be right for all of us, so it is incredibly important to understand why people are doing what they're doing, the context, and what the results are.

Thank you and hope you get some much needed rest.
 
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In this very interesting lecture (Feb 20, 2018), Dr Montoya gives a possible explanation why Rituximab seems to only work in few patients (if any): It targets a too narrow part of the immune system whereas immune system abnormalities are very broad and wideranging in CFS. (see after 39:00)

This could also be an explanation why Cyclophosphamide seems to work better, because it is nonspecific and targets a broader part of the immmune system.

How does cyclophosphamide compare to high dose systemic cortisone?
 

Learner1

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How does cyclophosphamide compare to high dose systemic cortisone?
From Wikipedia:
Cyclophosphamide is used to treat cancers and autoimmune diseases. It is used to quickly control the disease. Due to its toxicity, it is replaced as soon as possible by less toxic drugs. Regular and frequent laboratory evaluations are required to monitor kidney function, avoid drug-induced bladder complications and screen for bone marrow toxicity.

...

Cyclophosphamide decreases the immune system's response, and although concerns about toxicity restrict its use to patients with severe disease, it remains an important treatment for life-threatening autoimmune diseases where disease-modifying antirheumatic drugs (DMARDs) have been ineffective. For example, systemic lupus erythematosus with severe lupus nephritis may respond to pulsed cyclophosphamide.

...

Adverse drug reactions from cyclophosphamide are related to the cumulative medication dose and include chemotherapy-induced nausea and vomiting, bone marrow suppression, stomach ache, hemorrhagic cystitis, diarrhea, darkening of the skin/nails, alopecia (hair loss) or thinning of hair, changes in color and texture of the hair and lethargy. Other side effects may include easy bruising/bleeding, joint pain, mouth sores, slow-healing existing wounds, unusual decrease in the amount of urine or unusual tiredness or weakness
Also from Wikipedia:

Therapeutic immunosuppression

Glucocorticoids cause immunosuppression, and the therapeutic component of this effect is mainly the decreases in the function and numbers of lymphocytes, including both B cells and T cells.

The major mechanism for this immunosuppression through inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κB). NF-κB is a critical transcription factor involved in the synthesis of many mediators (i.e., cytokines) and proteins (i.e., adhesion proteins) that promote the immune response. Inhibition of this transcription factor, therefore, blunts the capacity of the immune system to mount a response.[2]

Glucocorticoids suppress cell-mediated immunity by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and IFN-γ, the most important of which is IL-2. Smaller cytokine production reduces the T cell proliferation.[24]

Glucocorticoids, however, not only reduce T cell proliferation, but also lead to another well known effect - glucocorticoid-induced apoptosis. The effect is more prominent in immature T cells still inside in the thymus, but peripheral T cells are also affected. The exact mechanism regulating this glucocorticoid sensitivity lies in the Bcl-2 gene.[25]

Glucocorticoids also suppress the humoral immunity, thereby causing a humoral immune deficiency. Glucocorticoids cause B cells to express smaller amounts of IL-2 and of IL-2 receptors. This diminishes both B cell clone expansion and antibody synthesis. The diminished amounts of IL-2 also cause fewer T lymphocyte cells to be activated.

The effect of glucocorticoids on Fc receptor expression in immune cells is complicated. Dexamethasone decreases IFN-gamma simulated Fc gamma RI expression in neutrophils while conversely causing an increase in monocytes.[26] Glucocorticoids may also decrease the expression of Fc receptors in macrophages,[27] but the evidence supporting this regulation in earlier studies has been questioned.[28] The effect of Fc receptor expression in macrophages is important since it is necessary for the phagocytosis of opsonised cells. This is because Fc receptors bind antibodies attached to cells targeted for destruction by macrophages.

Anti-inflammatory

Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2, thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events (epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes. They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase/PGE isomerase (COX-1 and COX-2),[29] the latter effect being much like that of NSAIDs, potentiating the anti-inflammatory effect.

In addition, glucocorticoids also suppress cyclooxygenase expression

Side effects
Glucocorticoid drugs currently being used act nonselectively, so in the long run they may impair many healthy anabolic processes. To prevent this, much research has been focused recently on the elaboration of selectively acting glucocorticoid drugs. Side effects include:

Immunodeficiency (see section below)
Hyperglycemia due to increased gluconeogenesis, insulin resistance, and impaired glucose tolerance ("steroid diabetes"); caution in those with diabetes mellitus
Increased skin fragility, easy bruising
Negative calcium balance due to reduced intestinal calcium absorption[38]
Steroid-induced osteoporosis: reduced bone density (osteoporosis, osteonecrosis, higher fracture risk, slower fracture repair)
Weight gain due to increased visceral and truncal fat deposition (central obesity) and appetite stimulation
Hypercortisolemia with prolonged or excessive use (also known as, exogenous Cushing's syndrome)
Impaired memory and attention deficits[39]
Adrenal insufficiency (if used for long time and stopped suddenly without a taper)
Muscle and tendon breakdown (proteolysis), weakness, reduced muscle mass and repair[40][23]
Expansion of malar fat pads and dilation of small blood vessels in skin
Lipomatosis within the epidural space[41]
Excitatory effect on central nervous system (euphoria, psychosis)
Anovulation, irregularity of menstrual periods
Growth failure, delayed puberty
Increased plasma amino acids, increased urea formation, negative nitrogen balance
Glaucoma due to increased ocular pressure
Cataracts
Topical steroid addiction
In high doses, hydrocortisone (cortisol) and those glucocorticoids with appreciable mineralocorticoid potency can exert a mineralocorticoid effect as well, although in physiologic doses this is prevented by rapid degradation of cortisol by 11β-hydroxysteroid dehydrogenase isoenzyme 2 (11β-HSD2) in mineralocorticoid target tissues. Mineralocorticoid effects can include salt and water retention, extracellular fluid volume expansion, hypertension, potassium depletion, and metabolic alkalosis.

Immunodeficiency Edit
Glucocorticoids cause immunosuppression, decreasing the function and/or numbers of neutrophils, lymphocytes (including both B cells and T cells), monocytes, macrophages, and the anatomical barrier function of the skin.[42] This suppression, if large enough, can cause manifestations of immunodeficiency, including T cell deficiency, humoral immune deficiency and neutropenia.

Main pathogens of concern in glucocorticoid-induced immunodeficiency:[42]
Bacteria
Enterobacteriaceae
Legionella micdadei
Listeria monocytogenes
Mycobacterium tuberculosis
Nontuberculous mycobacteria
Nocardia asteroides
Rhodococcus equi
Salmonella species
Staphylococcus aureus
Streptococci
Fungi
Aspergillus
Blastomyces
Candida albicans and nonalbicans species
Coccidioides immitis
Cryptococcus neoformans
Fusarium species
Histoplasma capsulatum
Penicillium marneffei
Pseudallescheria boydii
Zygomycosis
Viruses
Adenovirus
Cytomegalovirus
Herpes simplex virus
Human papillomavirus
Influenza/parainfluenza
Respiratory syncytial virus
Varicella zoster
Other
Cryptosporidiosis/Isospora belli
Pneumocystis carinii
Strongyloides stercoralis
Toxoplasma gondii