My HS for a long time was in my right armpit and both sides of my groin area. Now it's only in my left arm, which until a few years ago was scar free. The way HS moves around is actually really interesting and contradictory to a lot of beliefs. Like if stress, sweating, food, etc. triggers it, why does it pick particular areas and possibly move around overtime? Such a weird disease.

Oddly enough, you are right...yes, mine is predominately on my left side. Strange.

Not I... Started on my back, then under arms, then groin, butt, inner thigh and waist line. Interesting you only get it on your left side.

Yes. I've battled some of the worst bouts on the left side. From complete surgical removal of my left axilla, left inner thight, left lower leg and now, flare-ups every three months on the left side of the neck.... That's not to say, flare-ups don't occur on the right, but not a large and frequently than the Left. That's pretty Deep, for this pattern has existed for 48 yrs. of HS in me. I wonder why????

I don't know.. but it might be worth doctors looking into to see if there is a possible reason because that could lead to better test being run to find out exactly what causes it and why and maybe one day a cure.. I wasn't sure if anyone else made the observation that it was more unilateral than bilateral.

You are Wise, and many thanks, for I've never shared with anyone else accept doctors and surgeon's. Until now.....

That is a good question to ask Shane. I never thought about it before. For me I have it on both sides, but my most severe outbreaks are on my right side. I was also curious to ask if anyone has any other autoimmune disorders? This past year alone I have had eczema in certain spots, and I had shingles on my ribcage. Apparently people are getting shingles younger and younger (4 people alone that week my dr diagnosed), and I was curious if other auto immune disorders expedite that possibility of occurring.

as far as I know I do not have any other disorders at this time.. I do know that some people tend to get others when they have one already.. it's possible that they are somehow linked... I know a few people in the younger age bracket whom have had shingles.

Really good observation, Shane - thank you!

I think it may have to do with what bacteria land where, or where they like to live. Don't know where it is now but I'm sure I've seen materials and diagrams that talk about different bacteria being more likely to try to colonize different places on the body - not left/right but certainly upper and lower. Here's one reference
http://www.ncbi.nlm.nih.gov/books/NBK7617/

"Normal Flora of Skin
Skin provides good examples of various microenvironments. Skin regions have been compared to geographic regions of Earth: the desert of the forearm, the cool woods of the scalp, and the tropical forest of the armpit. The composition of the dermal microflora varies from site to site according to the character of the microenvironment. A different bacterial flora characterizes each of three regions of skin: (1) axilla, perineum, and toe webs; (2) hand, face and trunk; and (3) upper arms and legs. Skin sites with partial occlusion (axilla, perineum, and toe webs) harbor more microorganisms than do less occluded areas (legs, arms, and trunk). These quantitative differences may relate to increased amount of moisture, higher body temperature, and greater concentrations of skin surface lipids. The axilla, perineum, and toe webs are more frequently colonized by Gram-negative bacilli than are drier areas of the skin."

I've had almost zero involvement of the underarms even when I had Stage 3 down below - I think that really surprised my doctor the first time I stripped so they could have a look - but what I did have was in the underarm on the left side exclusively. Several very painful boils that went on about six months, shrinking and growing alternately then finally disappearing about six years ago.

Starrynight07, I think the bacteria that may have an exclusive association with Stage I when someone tries to look at the microbes in different stages of HS, is enough to do a number on a person's immune system. Staphylococci (and Streptococci) can even infect immune cells themselves.

Staphylococci, Streptococci, Prevotella / Bacteriodes and a few others that are often found in HS may actually have multiple toxins that foul up the normal workings of immune cells whose job is supposed to be cleaning up debris of various types, whether it's follicular debris or other damaged tissues, or bacteria.

Not only do some microbes or their toxins have the ability to interfere with that process (phagocytosis), some of these can also defeat another important aspect of immunity and that's where normally people and other creatures produce their own powerful antimicrobials (antimicrobial peptides, in humans most notably LL-37). Staphylocci can produce an enzyme (aureolysin) that can literally digests LL-37. Some of these critters have already worked out immunity to LL-37 and other natural host defenses (like lysozyme), but by degrading these host defenses, they can also help set up a host vulnerability to any microbes that would still be susceptible to them.

Note that phagocytosis and antimicrobial production are the immunological "pots of gold" at the end of the Vitamin D pathway "rainbow" - these are two very important immunological benefits we might expect from adequate Vitamin D and a working Vitamin D metabolism, but Staphylococci and some other bad nasties can cheat us right out of both, which then helps puts out the welcome mat for all sorts of opportunistic microbes. This may happen most in the affected tissues, but I'm sure it may easily have systemic effects also.

Here's a diagram of how this works in one of the more important immune cells, just substitute Staphylococcus for tuberculosis.
http://mpkb.org/_media/home/publications/marshall_autoimmunity_2010/2010ai_marshall_slide3.jpg?w=630
(In the diagram, "cathelicidin" is used instead of "LL-37" - the two are used somewhat interchangeably since cathelicidins are the category or family that LL-37 belongs to).

(By the way, that is NOT an endorsement of the Marshall Protocol for HS - It does happen to be the clearest diagram that I could find without a battle, though. That site has some remarkable info but I'm fairly sure our predicament is notably different from what they deal with. Upregulation + degradation of LL-37 may be entirely outside their realm in spite of how well versed they are in the general subject and phagosome defects may be as well).

So there sits Staphylococcus not only having possibly gained entry into a cell, but literally hanging out in the cellular garbage disposal (phagosome) intended for it and turning down the acidity that was supposed to help dissolve it and other debris... Just sitting there mocking us and printing out invitations for its little one-celled friends to come have a relaxing swim in the phagosome now that it's harmless.

Microbes taking up residence in host cells can also help to sheild those microbes from certain antibiotics. I'm guessing that in the complete remissions of HS that have been reported with antibiotics that this may not have been a big problem and they've probably done a good job cleaning out infected cells anyway in order to get the digestive powers of those cells back up and running so that we see the ability to digest bacteria and debris restored, resulting in the HS remissions that were obtained.

It's why I'm pretty emphatic about bacteriology with new posters even if it's probably rude of me - I'm sure a bacteriology lecture is the last thing anyone wants to walk right into, lol - but if HS can only be caught at Stage 1 when there may only be one organism that needs to be dealt with, it may be 50 times easier to stop than when any of 50 other microbes have gotten into the act now that the defenses have been impaired.

I still can't tell you much more about all that yet - I actually might have gotten a lead the other day from trying to look at how tuberculosis does that number on host cells that you see in the linked diagram but it would be way too soon to tell.

What I think is interesting is that following up that, could finally explain the an earlier success treating HS that Aude Nassif was involved in, which was a case of mastitis with rather different bacteriology.
http://www.researchgate.net/publication/26293521_Is_granulomatous_mastitis_a_localized_form_of_hidradenitis_suppurativa
If that instance isn't really different in terms of certain kinds of bacterial toxins even if it's very different bacteria, maybe I've stumbled onto something?

(What I'm thinking might imply that forskolin is not a good supplement with HS but I don't know if that proposal would really matche anyone's experiences or not. I've been passing on that one for one reason or other for quite awhile now although I was tempted by it several times when wanting to get in better shape).

It might also help explain why some bacteria more common HS in later stages seem to be able to come and go as if some of them are somewhat interchangable? The Staph species (S. lugdunensis) that's identified as possibly starting the process is maybe only still detectable in half of advanced cases, but other microbes may qualified to carry it on when that Staph departs, and so forth. Staph aureus has similar qualifications to foul the immune system and is often found in place of S. lugdunensis past Stage 1.

It may well be what needs to happen for a successful outcome in HS, is to get rid of anything that's capable of gumming up the phagocytosis garbage disposal like that. I don't where there's a proper list, but the larger it is the more important it may be to try to stop HS at Stage 1 whenever possible.

I'm at about the point where I have my own challenge to make to the accepted view of HS, wherein that 20 or 30 year accumulation of HS papers going on about follicles and apocrine and sebaceous glands, and obstruction of and debris from, seems to almost overlook the fact that Staphylococci are well known for being able to invade and damage some of these structures (folliculitis for example) and that they may easily have the required toxins to help prevent subsequent clean-up of that debris.

Since Staphylococcus lugdunensis may be that qualified to be the origin of HS, what other origin does it need exactly if infection actually proves to be enough in itself to account for the earliest detected events in the tissues?

Other than that, if there's some predisposition to that particular microbe, it may not be that unique depending on what it is. If it's inflammation, for example, which is one common denominator between contributors like smoking and obesity (and ruptured follicles), it may turn out to be a manageable enough predisposition to help keep the HS away, just like anti-inflammatories seem to be able to help in managing existing cases of HS.

BTW, the difference between S. aureus and S. lugdunensis probably would have eluded doctors as well as researchers writing in older literature, because S. lugdunensis wasn't named until 1988 when they used DNA to distinguish the two. Before that it probably would have been ID'd as Staph aureus, with which it's often been confused since they're similar in some respects. They can be distinguished, however, because lugdunensis should be positive for the ODC (ornithine decarboxylase) test
http://en.wikipedia.org/wiki/Staphylococcus_lugdunensis

I'm not sure, but that characteristic might turn out to have something to do with why it might be that S. lugdunensis has been consistently linked to Stage 1 HS, while S. aureus might never have been so far (I'm not 100% sure, I'm due for a review of the lit but I can't think of a clear exception offhand). Something about any predisposition to HS might involve somehow putting out a rather selective welcome mat for S. lugdunensis. Still no good ideas here on my part but there may be a clue in there somewhere.

I do tend to wonder, though, because various decarboxylases of bacteria are a likely origin of malodous aspects of HS - these putrefactive enzymes can turn amino acids into stink. It makes me go, "Hmmm..." to think a that Staph that has a unique putrefactive asset might happen to be hosting the party, but I don't have an answer to that.

The Prevotella that tend to dominate in the French studies as well as dominating the sore parts of my own person are probably pretty capable in that department, in addition to making enzymes that eat antibodies (degrading immunoglobins is a trait they share with a number of bacteria that still belong to Bacteroides, where the Prevotella used to be classified also.

I am always writing Prevotella / Bacteroides rather than Prevotella because Bacteroides has a bad reputation (including association with perianal symptoms) and Prevotella deserves one.

The two can be interchangeable in at least some respects and I'm very curious whether all of us Stage 2 & 3 cases will be riddled with Prevotella as in the French studies, or whether some of us could have Bacteroides infections instead. Either they really are rather interchangable or I may even have both myself since I have a confirmed Prevotella and significant perianal involvement.

I know I have Prevotella bivia since it's the one bacteria I've ever known the local lab to even name, and so I have some important similarities to those cases even though I couldn't be further from France geographically, but I have no idea if all us have significant colonization with Prevotella.

Sure do wish I'd been to med school, I'm sure this would be way easier. I'm trying though anyway, because dammit I'm sick and tired of being pushed around by things that aren't even big enough to be visible to the naked eye.

Probably not the rant you wanted... Sorry, I've been trying to figure out how to write this stuff up in case it helps anyone and it just all poured out here half-baked... May not do that again for awhile since that was everything I know right there.

But yeah - I'm pretty sure having HS can indeed make it easier to end up with more infections (and maybe some more persistent ones), and that's not just because having open lesions.

BTW, I really have to wonder if why it is that perspiration is such a no-no if you have HS, could be because healthy people's perspiration contain the necessary anti-microbial peptides to discourage bacterial growth, whereas if a number of important ones are being degraded by bacterial enzymes before they can be exported to the skin surface, it's maybe more like offering them food and water...???

I'm sure it would bug me to no end that people at the gym can sweat buckets and I dare not sweat two drops, if I thought about it very long. I'd love to know why that is.

And then after the doctor informs you that you can be hospitalized by perspiration, they want you to excercise. Get out Sweatin' To The Oldies and go for it... except the sweating part of course. Just because every other sucky thing about HS doesn't suck enough already.

I wonder though... I've seen some people use a sauna.. you know you really start sweating and then go to the cold dunk to open the pores if that would help... I know the sweating part isn't suppose to be good but maybe if you add that cold dunk after to open the pours it will leech the stuff out that you don't want causing a flare up...