Hidradenitis Suppurativa Support Group
Hidradenitis suppurativa (hi-drad-uh-NIE-tis sup-yoo-ruh-TIE-vuh) is rare, long-term skin condition that features small, painful lumps under the skin. The disease manifests as clusters of chronic abscesses or boils, sometimes as large as baseballs, that are extremely painful to the touch and may persist for years with occasional to frequent periods of inflammation,...
I know HS gets blamed on tobacco a lot... There may be some anomalies there, along with a possible lack in the literature of a good explanation for the association. It's okay, I haven't really been able to come with a good one myself why tobacco should be linked to HS and it isn't for lack of trying.
I'm feeling the weirdo because my HS seems to flare, even dangerously, because of withdrawal from cigarettes. This maybe shouldn't have surprised me because I've read that withdrawal can be an inflammatory process and I am highly sensitive to inflammation, there may be hormones involved in the process of cravings of different kinds (i.e., leptin) that can work synergistically with inflammation and infection to make them worse, and there may even be anti-inflammatory properties in tobacco (in addition to inflammatory ones) that a person might become increasingly responsive to and dependent on as an anti-inflammatory, the more inflammation they are suffering from.
The largest consensus in HS literature on any abnormal inflammatory markers in HS patients may be that there is elevated IL-10 (Interleukin-10) in lesional tissues - possibly more consensus than that which points out elevated TNF-a or any other inflammatory markers that have led to therapies (biologics) involving antibodies to neutralize excessive TNF-a (Humira etc) in HS patients. Schlapbach, Hunger, Kelly and van der Zee all reported elevated IL-10 in HS patients.
One paper that goes into generous detail about elevated Interleukin-10 in HS goes so far as if to "blame" it on smoking as if it's a bad thing - Wolk et al wrote: "Nicotine, which is likely to be present in most AI patients because of the high prevalence of smokers, may be another reason for the increased IL-10 production." http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0020385
(I don't know why seem to they credit IL-10 with RAISING TNF-a in that paper, that may well be a mistake and it is contrary to other literature here that sees things differently).
There are other papers that go into great detail about the possibilities of therapies that deliberately elevate IL-10
http://pharmrev.aspetjournals.org/content/55/2/241.full
Interleukin 10 can act as an anti-inflammatory that counteracts the inflammatories TNF-a and IL-6. Irritability and depression, fog and fatigue might make good aliases in my experience although that took awhile because they're a duet. Both are very typically elevated inflammatory markers in the presence of infection.
From the last link:
"More concretely, IL-10 inhibits the production of proinflammatory mediators by monocytes and M, such as endotoxin- and IFN--induced release of IL-1, IL-6, IL-8, G-CSF, GM-CSF, and TNF-"
This article on kidney disease attempts to sort them out as "The Good, the Bad, and the Ugly"...
"Like the characters in the Clint Eastwood Western movie from the 1960s The Good, the Bad and the Ugly, the roles of these three cytokines and their soluble receptors are quite different. Whereas the first cytokine that will be discussed, IL-10 (the good one) appears to have a critical role in suppressing the inflammatory response the other two cytokines, IL-6 (the bad one) and tumor necrosis factor-alpha (TNF-alpha) (the ugly one), seem to have proinflammatory and proatherogenic properties"
http://www.nature.com/ki/journal/v67/n4/full/4495166a.html
Although I really should emphasize that TNF-a and IL-6 seem to provide inflammation that normally has an important immunological role in healthy people, helping gear up the immune system for defense. It's when it becomes a vicious cycle of inflammation and infection and these go through the roof, or when they never stand down but instead remain elevated and create chronic inflammation because whatever is causing them isn't yet resolved, that they become harmful. This seems to be though why if I take something that raises either of them, I have a nasty flareup, whereas medications that lower them cause improvement in HS management in general in studies and trials.
That is all I know about that, though. I don't know of anything else offhand that raises IL-10 and I don't know of anything I'm currently ingesting except tobacco that raises it. I don't know if it's a good idea to deliberately raise it and I don't think the authors of that HS paper did either. I just hope someday to be able to figure that out if that is what is making tobacco so hard for me to live without and if getting that straightened out would make it any easier. Possibly not coincidental
This is not an endorsement of possible medicinal properties of tobacco - that is absolutely horrible to be held hostage by the proposition that if I don't keep smoking as I normally do I may be bound for the hospital that quick. Cigarettes aren't all healthy I guarantee you. I'm not fond of them anymore and I'm embarrassed by the habit and pretty disturbed that I've been able to give up anything else that might be causing me HS but not cigs.
So this is what I'm wondering, if it isn't the case generally speaking that the more inflammation, the harder it may be for some of us to quit? - and some of that might have to do with why? Or it might also have to do with different microbes and how they fit into it - some might be particularly inflammatory and I might have at least one of the nastier ones?
Also I don't know if I should get into this, but I've just learned what may be another nasty Streptococcal trick that I need to find out more about it. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC108217
"The pore-forming toxins streptolysin O and E. coli hemolysin have also been shown to induce the release of IL-6R from human monocytes and macrophages (55).... Because up to 50% of the IL-6R can be liberated by low concentrations (nanograms per milliliter) of the toxins within 10 min of exposure, the biological consequences would be expected to be dramatic. Not only would normally unresponsive cells be rendered responsive to IL-6 but also cells from which the IL-6 had been shed may no longer be capable of reacting to the cytokine."
I don't know but I'm afraid that may mean that this trick may end up harming healthy cells and preventing infected immune cells from getting the signal to give up the cause when they're not able to digest the bacteria infecting them?
van der Zee proposes that HS involves "pyroptosis (a highly inflammatory form of cell death)"
http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0625.2012.01552.x/full
Is that how that comes about is having some vile nasty Strep move your inflammatory receptors around so that inflammation does in the wrong cells? I don't know if this is really a sound picture of what is happening but I guess it would go a long way to explain my discomforts.
At least it's been suggested that Streptolysin O can be inhibited by allicin in garlic
http://www.ncbi.nlm.nih.gov/pubmed/20538890
Now if I could only explain why garlic seems to make my HS worse after about the third day... sigh... And one of the things I need to try to find out is if Staph or others can play the same dirty trick or not.
Meanwhile, I've come up with a question, and that's whether HS should be linked to smoking or to tobacco - I've begun to wonder if there's a difference between the two.
Tobacco had been around a long time before HS, and we are able to do things like look back in history and see the likely effect of tobacco snuff on one of the people (Thomas Harriot 1560-1621, compatriot of Sir Walter Ralegh) who was probably among the very enthusiastic for King James to invest in growing tobacco...
http://en.wikipedia.org/wiki/Thomas_Harriot
But I don't know of HS making an appearance before 1839.
I don't know the history of tobacco that well, but Wikipedia sort of makes it sound as if HS makes its appearance within only 10 years of cigarettes?
"By 1830, the cigarette had crossed into France, where it received the name cigarette; and in 1845, the French state tobacco monopoly began manufacturing them."
http://en.wikipedia.org/wiki/Cigarette
"In 1839, Velpeau identified and described hidradenitis suppurativa"
http://en.wikipedia.org/wiki/Hidradenitis_suppurativa
I don't know what is different about cigarettes except that eventually potassium nitrate (saltpeter) and glycerine are added to cigarette papers to help keep cigarettes burning and to burn more evenly, but I don't know when that practice started and I'm not sure if it extended to the cigars. Maybe it hadn't started before HS, not sure of it. (I did find a really old book that says a little potassium nitrate in the lungs is good for you, but really old books say all kinds of things). It might require that the practice was extended to cigars also, since I think one famous HS sufferer used tobacco that way, so I'm not sure what to think.
I don't suppose anyone has ever had their HS go into remission from finding another way to get nicotine than cigarettes or cigars, or knows of anyone who got HS from nicotine or tobacco other than cigarettes? Do we have any Nicorette-induced HS? (All of the sudden I just realized I never paid attention whether the distinction was made between tobacco and cigarettes in all those papers I'm going to have to read all over again now, groan...)
I guess I could ask too if anyone's had anti-TNF-a therapies make it seemingly easier to quit smoking?
Hope I'm not making too much out of nothing, but I wish I knew what this meant. I'd love to be able to milk a helpful suggestion or two out of it, or maybe a further insight, but I guess it might take some really detailed tobacco history to try to look further into it?
It tries to sound like switching to a pipe might make an improvement that I cannot bring myself to quite believe is going to happen. Could that really be true???
Anyway, I hope it cheers any of us up that someone is trying to beat the secrets out of HS, even if it's only the likes of me. If I just keep stumbling long enough, I'm bound to stumble over something... probably the coffee table, but that wasn't my point. :-)
I'm feeling the weirdo because my HS seems to flare, even dangerously, because of withdrawal from cigarettes. This maybe shouldn't have surprised me because I've read that withdrawal can be an inflammatory process and I am highly sensitive to inflammation, there may be hormones involved in the process of cravings of different kinds (i.e., leptin) that can work synergistically with inflammation and infection to make them worse, and there may even be anti-inflammatory properties in tobacco (in addition to inflammatory ones) that a person might become increasingly responsive to and dependent on as an anti-inflammatory, the more inflammation they are suffering from.
The largest consensus in HS literature on any abnormal inflammatory markers in HS patients may be that there is elevated IL-10 (Interleukin-10) in lesional tissues - possibly more consensus than that which points out elevated TNF-a or any other inflammatory markers that have led to therapies (biologics) involving antibodies to neutralize excessive TNF-a (Humira etc) in HS patients. Schlapbach, Hunger, Kelly and van der Zee all reported elevated IL-10 in HS patients.
One paper that goes into generous detail about elevated Interleukin-10 in HS goes so far as if to "blame" it on smoking as if it's a bad thing - Wolk et al wrote: "Nicotine, which is likely to be present in most AI patients because of the high prevalence of smokers, may be another reason for the increased IL-10 production." http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0020385
(I don't know why seem to they credit IL-10 with RAISING TNF-a in that paper, that may well be a mistake and it is contrary to other literature here that sees things differently).
There are other papers that go into great detail about the possibilities of therapies that deliberately elevate IL-10
http://pharmrev.aspetjournals.org/content/55/2/241.full
Interleukin 10 can act as an anti-inflammatory that counteracts the inflammatories TNF-a and IL-6. Irritability and depression, fog and fatigue might make good aliases in my experience although that took awhile because they're a duet. Both are very typically elevated inflammatory markers in the presence of infection.
From the last link:
"More concretely, IL-10 inhibits the production of proinflammatory mediators by monocytes and M, such as endotoxin- and IFN--induced release of IL-1, IL-6, IL-8, G-CSF, GM-CSF, and TNF-"
This article on kidney disease attempts to sort them out as "The Good, the Bad, and the Ugly"...
"Like the characters in the Clint Eastwood Western movie from the 1960s The Good, the Bad and the Ugly, the roles of these three cytokines and their soluble receptors are quite different. Whereas the first cytokine that will be discussed, IL-10 (the good one) appears to have a critical role in suppressing the inflammatory response the other two cytokines, IL-6 (the bad one) and tumor necrosis factor-alpha (TNF-alpha) (the ugly one), seem to have proinflammatory and proatherogenic properties"
http://www.nature.com/ki/journal/v67/n4/full/4495166a.html
Although I really should emphasize that TNF-a and IL-6 seem to provide inflammation that normally has an important immunological role in healthy people, helping gear up the immune system for defense. It's when it becomes a vicious cycle of inflammation and infection and these go through the roof, or when they never stand down but instead remain elevated and create chronic inflammation because whatever is causing them isn't yet resolved, that they become harmful. This seems to be though why if I take something that raises either of them, I have a nasty flareup, whereas medications that lower them cause improvement in HS management in general in studies and trials.
That is all I know about that, though. I don't know of anything else offhand that raises IL-10 and I don't know of anything I'm currently ingesting except tobacco that raises it. I don't know if it's a good idea to deliberately raise it and I don't think the authors of that HS paper did either. I just hope someday to be able to figure that out if that is what is making tobacco so hard for me to live without and if getting that straightened out would make it any easier. Possibly not coincidental
This is not an endorsement of possible medicinal properties of tobacco - that is absolutely horrible to be held hostage by the proposition that if I don't keep smoking as I normally do I may be bound for the hospital that quick. Cigarettes aren't all healthy I guarantee you. I'm not fond of them anymore and I'm embarrassed by the habit and pretty disturbed that I've been able to give up anything else that might be causing me HS but not cigs.
So this is what I'm wondering, if it isn't the case generally speaking that the more inflammation, the harder it may be for some of us to quit? - and some of that might have to do with why? Or it might also have to do with different microbes and how they fit into it - some might be particularly inflammatory and I might have at least one of the nastier ones?
Also I don't know if I should get into this, but I've just learned what may be another nasty Streptococcal trick that I need to find out more about it. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC108217
"The pore-forming toxins streptolysin O and E. coli hemolysin have also been shown to induce the release of IL-6R from human monocytes and macrophages (55).... Because up to 50% of the IL-6R can be liberated by low concentrations (nanograms per milliliter) of the toxins within 10 min of exposure, the biological consequences would be expected to be dramatic. Not only would normally unresponsive cells be rendered responsive to IL-6 but also cells from which the IL-6 had been shed may no longer be capable of reacting to the cytokine."
I don't know but I'm afraid that may mean that this trick may end up harming healthy cells and preventing infected immune cells from getting the signal to give up the cause when they're not able to digest the bacteria infecting them?
van der Zee proposes that HS involves "pyroptosis (a highly inflammatory form of cell death)"
http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0625.2012.01552.x/full
Is that how that comes about is having some vile nasty Strep move your inflammatory receptors around so that inflammation does in the wrong cells? I don't know if this is really a sound picture of what is happening but I guess it would go a long way to explain my discomforts.
At least it's been suggested that Streptolysin O can be inhibited by allicin in garlic
http://www.ncbi.nlm.nih.gov/pubmed/20538890
Now if I could only explain why garlic seems to make my HS worse after about the third day... sigh... And one of the things I need to try to find out is if Staph or others can play the same dirty trick or not.
Meanwhile, I've come up with a question, and that's whether HS should be linked to smoking or to tobacco - I've begun to wonder if there's a difference between the two.
Tobacco had been around a long time before HS, and we are able to do things like look back in history and see the likely effect of tobacco snuff on one of the people (Thomas Harriot 1560-1621, compatriot of Sir Walter Ralegh) who was probably among the very enthusiastic for King James to invest in growing tobacco...
http://en.wikipedia.org/wiki/Thomas_Harriot
But I don't know of HS making an appearance before 1839.
I don't know the history of tobacco that well, but Wikipedia sort of makes it sound as if HS makes its appearance within only 10 years of cigarettes?
"By 1830, the cigarette had crossed into France, where it received the name cigarette; and in 1845, the French state tobacco monopoly began manufacturing them."
http://en.wikipedia.org/wiki/Cigarette
"In 1839, Velpeau identified and described hidradenitis suppurativa"
http://en.wikipedia.org/wiki/Hidradenitis_suppurativa
I don't know what is different about cigarettes except that eventually potassium nitrate (saltpeter) and glycerine are added to cigarette papers to help keep cigarettes burning and to burn more evenly, but I don't know when that practice started and I'm not sure if it extended to the cigars. Maybe it hadn't started before HS, not sure of it. (I did find a really old book that says a little potassium nitrate in the lungs is good for you, but really old books say all kinds of things). It might require that the practice was extended to cigars also, since I think one famous HS sufferer used tobacco that way, so I'm not sure what to think.
I don't suppose anyone has ever had their HS go into remission from finding another way to get nicotine than cigarettes or cigars, or knows of anyone who got HS from nicotine or tobacco other than cigarettes? Do we have any Nicorette-induced HS? (All of the sudden I just realized I never paid attention whether the distinction was made between tobacco and cigarettes in all those papers I'm going to have to read all over again now, groan...)
I guess I could ask too if anyone's had anti-TNF-a therapies make it seemingly easier to quit smoking?
Hope I'm not making too much out of nothing, but I wish I knew what this meant. I'd love to be able to milk a helpful suggestion or two out of it, or maybe a further insight, but I guess it might take some really detailed tobacco history to try to look further into it?
It tries to sound like switching to a pipe might make an improvement that I cannot bring myself to quite believe is going to happen. Could that really be true???
Anyway, I hope it cheers any of us up that someone is trying to beat the secrets out of HS, even if it's only the likes of me. If I just keep stumbling long enough, I'm bound to stumble over something... probably the coffee table, but that wasn't my point. :-)
Here is one my main references on what may raise inflammation
http://www.anaturalhealingcenter.com/documents/Thorne/articles/Cytokine.pdf - I had forgotten some of what was in it.
Those results are listed as in vitro, but they do seem to match what goes on my body.
You'll see a number of my suspected herbal triggers listed under TNF-a as causing an Increase in TNF-a: Ginseng (Panax ginseng), Echinacea, Milk Thistle (Silybum marianum)...
A lot of obscure herbs there, though... There's another reference that's really good but the only source of a free read that I could find got pulled.
I just find it very curious in looking back at that reference says that Garlic (Allium sativum) lowers TNF-a and IL-6 and actually raises IL-10. On paper it looks very useful like that, but my experience doesn't match. Others might have better luck? I hope so, that will be my first constructive suggestion :-)
Unfortunately, maybe smoking is even harder than I thought to untangle from an inflammatory mess - I don't think garlic has ever helped me to smoke less.
The other article is
Anti-inflammatory activity of extracts from fruits, herbs and spices
Monika Mueller, Stefanie Hobiger, Alois Jungbauer
Here's the abstract but this site charges for the full article
http://www.sciencedirect.com/science/article/pii/S0308814610003158
More of my triggers there like Pomegranate, which on paper (and probably in my experience) is one of the worst.
I'm not just talking about food allergies or cross-reactive antibodies here though, the triggers that raise TNF-a and IL-6 for me may do it for anybody just like bacteria may raise anyone's TNF-a and IL-6, it may depend on how much inflammation you have whether you tolerate an additional source well?
So far, at least for me, these materials has been more useful for spotting triggers ahead of time, than for do-it-yourself anti-TNF therapy and I've had only rather limited results with trusted things like reserveratol or quercitin that are listed as lowering TNF-a in vitro, similar to the limited results that may come from anti-TNF-a therapy with biologics. By now I've mostly given up on cytokine management as any kind of cure - I think they're treating symptom and not cause, personally - but who knows who might benefit?
I thought it was interesting though that turmeric (Curcuma longa) also seems to be in that lit as lowering TNF-a. It may not be an ideal HS remedy (I get only mixed results), but it may have that quality going for it. It may also have some impact on Staphylococcus? There's something else I really need to brush up on is alternative antimicrobials...
Chili pepper looks very good in that paper, as does black pepper, as anti-TNF-a although other lit says that certain spices (possibly including those two) increase intestinal permeability and may result in inflammation.
I suppose there may be an explanation for this that involves some of the same cytokines: there is something that happens when I exercise that helps calm the craving for nicotine so that I smoke way less when I'm walking (on the other hand, it's not really practical to take a 25-miler every day to constantly be suppressing a nicotine fit).
Sorry, I thought sure I was onto something more sound than that turned out to be. Guess garlic may not save me from the ole demon nicotine after all, back to the drawing board on that one.
Suffice it that for now I'm way more worried about the nasty Strep that I'm pretty sure I have than I am about tobacco, I guess. I don't think I've ever had a near hospitalization because of tobacco before... infection is another story.
I hope any of that turns out to be helpful to anyone, as muddy as it still is.
Don't know if that helps any.