Verneuil's disease AKA Hydradenitis Suppurative

SeekinTruth said:

That's interesting about the zinc, Laura. I wonder if it's also connected to copper toxicity? Zinc deficiency and copper toxicity/overabundance tend to be associated.

About the fistulas, I read years ago that it's related to gut issues. I actually had one on my tailbone starting in the last couple of years in high school (my brother had it also and my father had it when he was young and had some kind of surgery that took care of it for the rest of his life). Now, from my brother (and my father's experience he related) and a bunch of other people who had this in the same area -- on or around the tailbone, everyone else would have periods where it would swell with lots of pain, and then a wound would open and drain. And then it would close for a while.

In my case, when it was in the very early stage of starting, I actually banged my tailbone on a hard surface, and then the swelling and pain started. For a couple of years, mine never opened and drained. Then, it opened and never closed -- it was pretty much perpetually draining, but the pain was much less. After almost two years of the open wound, and the whole time my mother kept nagging me to go to a doctor and get it taken care of (she kept fearing that I'd get "blood poisoning") I finally scheduled a surgery to cut it out. Well when the surgeon went in to cut out what was an open wound of a 1/4 inch and surrounding slight swelling of about 3/4 inch diameter, he ended up cutting huge amounts of flesh and muscle on the very lower back and right on the top part of my butt. It was real hell for the next couple of weeks.

I had to go a couple of times for the doctor to check on the healing. After the stitches were taken out, he "burned the open flesh" with nitrogen a couple of times that was supposed to help it heal faster. Well, in my case, it never came back again and healed well. The thing is, that years later, when I was 39, I got prostatitis, which is treated with high doses of zinc for several months, among other things. And it has a large component of severe biochemical imbalances that start the process which could be cured with dietary changes and supplements for about 6 months. What I'm thinking now is, I wonder if the lack of zinc/too much copper was already a problem that manifested in the fistula in my late teens-early twenties.

At the time I was doing research on prostate problems, there was a statistic that at least 50% of men age 40 or over are expected to have enlarged prostate, which is a precursor of prostatitis. Well, I'm convinced that such alarming numbers, like so many other things, are connected to a lifetime of the totally wrong diet, and probably stress, toxic buildup, and chemical imbalances, etc.

Just a note. About ten years or so ago, a second cousin of mine who also had the cyclical fistula opening/closing told my brother that he read somewhere that black pepper was a culprit. And he (and my brother) used to eat large amounts of black pepper. When my cousin cut it out completely, it went away in a month or two. My brother tried just cutting down to almost complete abstention from black pepper and his also went away. But for years if he had a considerable amount of black pepper for a couple of days, the irritation and pain would start again. Then after several years of totally avoiding black pepper it resolved completely and now he eats black pepper regularly (though more sparingly) and has no problems. I don't know what the mechanism behind is, but thought I'd mention it as something for others to consider/look into.

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loreta said:

How interesting about black pepper.

I had the same problem with a fistula in my tailbone some years ago. A very suffering situation, took antibiotics, went to urgency to opened it 3 times! Finally my doctor told me that the best solution was an operation. I accepted it because I was living literally hell. I was put in a waiting list. And then she gave me again antibiotics....for the third time. Before taking it I went to see an homeopathic specialist, a friend of mine. She asked me not to take again the antibiotics, instead take Silicea 9CH and to put green clay on my fistula almost 3 times a day. And miracle: my fistula disappeared after 2 months of this treatment. Later it came again, I follow the same treatment and it worked. In my case I think it was related with big big stress situation, it was like an emotional response. I believe also that fistulas can be cured with clay, with the help of Homeopathic medicine. The clay absorbs the fistula (I don't know how to express this but you understand). And Silicea helps.

This is my experience with the worst fistula I had in my life. Maybe this can help.

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Laura said:

I think that ya'll need to understand what a fistula is as opposed to a boil. A fistula is when a boil forces a connection between an internal organ and the abcess. It can also force a passageway between the internal organ and the outside of the body. A channel coming out from a simple boil could be said to be a sort of fistula, but it generally means an abnormal passageway that is created by the forcing of the abcess. That is, the abcess may find it easier to burrow into the body and infect other organs, than to burrow its way out, to drain as a normal boil would do. (Though boils really aren't normal!) These abcessing processes can force numerous channels in several directions, with branches, causing large scale infection within the body in various organs, interstitial places, cavities, etc. In women, fistulas can be forced between the rectum and the vagina so that fecal matter can leak constantly through. It's a very, very, very unpleasant condition and it's no wonder that people who have it don't talk about it. A fistula can be forced between the inner chamber of the apocrine gland/anal glands to the interior of the colon and constant leaking from the infected gland will pour into the colon and fecal matter can leak into the gland. If it is a double fistula, fecal matter can leak through the channel to another opening that the infection has created to the outside of the body. We've read a few papers about it and looked at the images. It really can get awful.

What we have learned is that it is due to blockage of apocrine glands and the blockage is due to the fact that these types of glands empty into hair follicles and the hair follicles appear to be hyper-active in the production of keratin/skin cells. This is useful if you spend a lot of time in water because the skin is constantly being replaced and the apocrine glands are lubricating the skin appropriately to protect from the washing away of skin cells. But if you are not spending enough time in water, the system backs up. And it has nothing to do with scrubbing or soap or anything like that, nor does it have anything to do with any particular bacteria on the skin since the process begins INSIDE the body. It can crank up in several places at once, start forcing channels through the tissue, and the person can end up, as SeekinTruth and Atriedes have done, with a whole lot of tissue having to be surgically removed en masse. Atriedes has already had three such surgeries and we hope that this last one will be the last though he now has to have the surgeries to close the channels. These types of surgeries leave huge, gaping, wounds that take weeks or months to close. Basically, you can end up with having half of your butt surgically removed or a big chunk of your neck, or a big chunk under your arm, from the front/groin area, up into the lower abdomen where fistulas can be forced.

Apocrine glands are found in the neck, under the arms, in the groin and ano-rectal area. The condition is supposedly more common in women than in men. It's genetic. There is no cure, only control.

Stress appears to be a significant factor since the adrenals stimulate the apocrine glands to secrete.

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What is hidradenitis suppurativa?

Hidradenitis suppurativa is a chronic skin disease characterized by recurrent boil-like lumps (nodules) under the skin. The nodules are inflamed and painful. They tend to break open, causing abscesses that drain fluid and pus. As the abscesses heal, they produce significant scarring of the skin.

Nodules are most likely to form in the armpits and groin. They may also develop around the anus, on the buttocks, or under the breasts. In some cases, nodules appear in other areas, such as the nape of the neck, waist, and inner thighs.

The signs and symptoms of hidradenitis suppurativa appear after puberty, usually in a person's teens or twenties.

The recurrent nodules and abscesses cause chronic pain and can lead to self-consciousness, social isolation, and depression. Less common complications of hidradenitis suppurativa include severe infections, restricted movement caused by a buildup of scar tissue (fibrosis), and a type of skin cancer called squamous cell carcinoma.

How common is hidradenitis suppurativa?

Hidradenitis suppurativa was once thought to be a rare condition because only the most severe cases were reported. However, recent studies have shown that the condition affects about 1 in 100 people when milder cases are also considered. For reasons that are unclear, women are about three times more likely than men to develop the condition.

What genes are related to hidradenitis suppurativa?

The cause of hidradenitis suppurativa is unknown, although it probably results from a combination of genetic and environmental factors. Originally, researchers believed that the disorder was caused by the blockage of specialized sweat glands called apocrine glands. However, recent studies have shown that the condition actually begins with a blockage of hair follicles in areas of the body that also contain a high concentration of apocrine glands (such as the armpits and groin). The blocked hair follicles trap bacteria, leading to infection and inflammation. It remains unclear what initially causes the follicles to become blocked and why the nodules tend to recur.

Researchers have studied many possible risk factors for hidradenitis suppurativa. Obesity and smoking both appear to increase the risk of the disorder, and obesity is also associated with increased severity of signs and symptoms in affected individuals. Studies suggest that neither abnormal immune system function nor hormonal factors play a significant role in causing the disease. Other factors that were mistakenly thought to be associated with this condition include poor hygiene, the use of underarm deodorants and antiperspirants, and shaving or the use of depilatory products to remove hair.

Genetic factors clearly play a role in causing hidradenitis suppurativa. In one large family, researchers determined that the condition was related to a gene on chromosome 1 (although they were not able to identify the specific gene). Researchers are looking for additional genetic factors that are associated with hidradenitis suppurativa.

How do people inherit hidradenitis suppurativa?

Hidradenitis suppurativa has been reported to run in families. Studies have found that 30 to 40 percent of affected individuals have at least one family member with the disorder, although this finding may be an underestimate because affected individuals do not always tell their family members that they have the condition.

In some families, hidradenitis suppurativa appears to have an autosomal dominant pattern of inheritance, which means one copy of an altered gene in each cell is sufficient to cause the disorder. However, the specific gene or genes have not been identified.

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Hidradenitis Suppurativa: A Treatment Challenge

NIPA SHAH, M.D., University of Illinois College of Medicine, Chicago, Illinois

Am Fam Physician. 2005 Oct 15;72(8):1547-1552.

Patient Information Handout

Hidradenitis suppurativa is a chronic, recurrent, debilitating disease that presents with painful, inflamed lesions in the apocrine-gland–bearing areas of the body, most commonly the axillary, inguinal, and anogenital areas. Etiology traditionally has been attributed to occlusion of the apocrine duct by a keratinous plug; however, defects of the follicular epithelium also have been noted. Contributing factors include friction from axillary adiposity, sweat, heat, stress, tight clothing, and genetic and hormonal components. Multiple treatment regimens are available, including antibiotics, retinoids, corticosteroids, incision and drainage, local wound care, local excision, radiation, and laser therapy. However, no single treatment has proved effective for all patients. Radical excision of the defective tissue is the most definitive treatment. The psychological impact on the patient can be great, encompassing social, personal, and occupational challenges. This impact should be addressed in all patients with significant disease.

Hidradenitis suppurativa (from the Greek hidros, sweat, and aden, glands), is also known as Verneuil’s disease or acne inversa, and occasionally is spelled hydradenitis. It is a common disorder, but its exact prevalence in the United States is unknown. A Danish study1 noted a prevalence of 4 percent in women. However, the diagnosis of hidradenitis suppurativa often is overlooked by physicians and therefore may be more common than is recognized. Hidradenitis suppurativa affects more women than men, with a female-to-male predominance as high as 4:1.2 This painful, disfiguring, and at times debilitating disease is marked by periods of inflammation with occasional secondary infection, and intermittent remissions that can last several years. The disease almost always occurs after puberty and before age 40, leading to the theory that there is a hormonal component to the pathogenesis. Flare-ups have been linked with menses3; shorter menstrual cycles and longer duration of menstrual flow are associated with the disease.1 There also seems to be a genetic component, and in one study3 of 110 patients, 38 percent reported a family history of this disease. This may reflect a familial form with autosomal dominant inheritance.4

Diagnosis

The clinical presentation of hidradenitis suppurativa indicates the diagnosis. A thorough history and physical examination are recommended at the initial visit. Early symptoms may include discomfort, itching, erythema, burning, and hyperhidrosis. Hidradenitis manifests most commonly as tender, nodular lesions in the axillae (Figure 1), although other parts of the body also may be affected (Table 1 and Figure 2). If a single nodule appears, it may indicate one of several other skin lesions that manifest in a similar fashion, and distinguishing hidradenitis can be difficult. A differential diagnosis is given in Table 2.5–7 Nodules may have malodorous, superinfected drainage. Rarely, the patient has a fever or is septic, or both. In these instances, further work-up is based on laboratory findings. Complete blood count, blood cultures, and routine chemistries should be considered. Culture of the drainage is a reasonable option to help direct treatment.

As the disease progresses, the diagnosis becomes more apparent, especially if the patient presents with frequent recurrences, scarring, fistulous tracks, and incomplete healing. The clinical course varies from occasional axillary lesions to diffuse abscess formations in multiple sites leading to chronic draining sinuses, as well as indurated, scarred skin and subcutaneous tissues. Some areas may coalesce to form tender, raised, violaceous dermis.

Symptoms of hidradenitis may be associated with several other conditions (Table 3).8,9 In perianal hidradenitis, biopsies should be performed to exclude the possibility of coexisting cancer.10 Crohn’s disease should also be considered.

Complications

Potential complications of hidradenitis suppurativa include dermal contraction, local or systemic infection resulting from the spread of microorganisms, arthritis secondary to inflammatory injury, squamous cell carcinoma (in indolent sinus tracts), disseminated infection (rare), restricted limb mobility from scarring, lymphedema caused by lymphatic injury from inflammation and scarring, rectal or urethral fistulas, systemic amyloidosis, and anemia from chronic infection.11

Treatment

There is no cure for hidradenitis suppurativa. However, several treatment options are available, including preventive, medical, surgical, and psychological strategies (Table 4). Because of the variety of ways in which the disease can manifest and progress, treatment should be based on the patient’s presentation and circumstances. Few high-quality randomized controlled trials or systemic reviews have addressed treatment of this condition.

Although an abundance of anecdotal advice for the prevention of hidradenitis suppurativa exists, few methods have proved to be effective for all patients. In one study,3 24 percent of patients found nothing to help their condition, despite an average disease duration of almost 19 years.

For unknown reasons, women are more affected than men. Deodorants, shaving, and depilation have not been supported as a cause for this discrepancy in at least one study.12 However, these should be avoided if they cause irritation. Warm compresses, topical antiseptics, and antibacterial soap may help in patients with folliculitis. To help alleviate patient anxiety about the condition, physicians should emphasize that hidradenitis suppurativa is not caused by poor hygiene and is not contagious.

The progression of hidradenitis may be advanced by excessive underarm adiposity because this creates an ideal environment for bacterial growth and also produces friction. Therefore, one method of prevention may be weight loss. However, although losing weight improves symptoms, it does not provide a cure. Friction from clothing increases pain and discomfort, and patients should avoid wearing tight, synthetic clothing near the affected areas. Heat and humidity also have been associated with flare-ups, and prolonged exposure to hot, humid climates should be avoided if possible. Stress management methods may be useful because the disease can be aggravated during times of increased psychosocial stress.

MEDICAL TREATMENT

Initial treatment of hidradenitis suppurativa can begin with conservative measures such as warm baths, hydrotherapy, and topical cleansing agents to reduce bacterial load.13 Nonsteroidal anti-inflammatory drugs may alleviate pain as well as inflammation. Antibiotics, although not proven to be effective, are the mainstay of medical treatment, especially for lesions suspected of being superinfected.

There is no evidence that chronic suppressive antibiotic therapy alters the natural history of hidradenitis. In a study3 of 110 patients with hidradenitis, the average duration of painful nodules was 6.9 days—about the duration of an average course of antibiotics. Therefore, the perceived response of hidradenitis suppurativa to antibiotics may be explained by the natural history of the condition itself, calling into question the routine use of antibiotics.3 One option is to culture the drainage from a large nodule and treat based on the results. Staphylococcus commonly is isolated; other pathogens include Escherichia coli and β-hemolytic streptococcus. Enteric flora may be found in cultures from perianal regions. Multiple organisms, including anaerobic bacteria, also may be found.8

Empiric antibiotic treatment may be given when conservative measures with several days’ observation have not improved symptoms. However, when superinfection is suspected it is best to treat based on culture results of drainage. Treatment can begin with topical or systemic antibiotics, or both. The only topical antibiotic that has been proven effective in a randomized controlled trial is clindamycin (Cleocin).1 Antistaphylococcal agents are best for axillary disease, and more broad-spectrum coverage is better for perineal disease. Dicloxacillin (Dynapen; 1 to 2 g daily), erythromycin (1 g daily), tetracycline (1 g daily), and minocycline (Minocin; 1 g daily) have been used. Cephalosporins may be helpful for concurrent active cellulitis. For severe, recurrent disease, anecdotal evidence suggests that two months or more of antibiotic therapy may be needed to prevent progression and worsening of concomitant infection.

Other medical treatment options address the possible hormonal etiology of hidradenitis; these options include oral contraceptive agents that contain a high estrogen-to-progesterone ratio and low androgenicity of progesterone.14 Two patients with severe, long-standing disease benefited from finasteride (Proscar) at a dosage of 5 mg daily.15 In Europe, the antiandrogen cyproterone acetate (Cyprostat) has been successful in some studies,16 but it currently is not approved for use in the United States.

Oral retinoids, which work by inhibiting sebaceous gland function and abnormal keratinization, also have been used. Pre-treatment with isotretinoin (Accutane) at a dosage of 0.5 to 1.0 mg per kg daily for a few months before surgery has been recommended to reduce the inflammatory components.17 No consensus on the dosing and duration of isotretinoin therapy has been reached by the few studies that have investigated it as a possible therapeutic option. Side effects of isotretinoin remain a major issue and include birth defects, hepatotoxicity, pseudotumor cerebri, and aggression.

Corticosteroids and immunosuppressants are other treatment possibilities. Topical tri-amcinolone (Aristocort) may be an option, but insufficient research has been conducted for it to be recommended routinely. Oral cyclosporine (Sandimmune) has shown some benefit, but chronic treatment can cause serious toxicity.18

SURGICAL TREATMENT

For early, limited disease that presents with a fluctuant abscess, incision and drainage may be a good first option. However, this procedure provides only short-term relief and has little impact on the disease course. When hidradenitis sinus tracks are well established but relatively superficial, they can be unroofed or laid open.19 Because these tracks are lined by epithelium, the floor of the track can be preserved; this facilitates rapid healing and minimizes scarring.10

Early, rather than delayed, wide excisional therapy has been recommended by some experts as the treatment of choice because repeated failed treatments lead to the disease being more widespread and severe at presentation, making surgical options more difficult.17,20 Patients should be advised that surgery treats only the disease that is present at the site of the excision; recurrence at a new site is possible. In one study21 of 82 patients treated with wide excision, recurrence rates were zero percent for perianal disease, 3 percent for axillary disease, and 37 percent for inguinoperineal disease. Obesity, insufficient excision, significant skin maceration, and chronic skin infection may increase the incidence of recurrence.21 In another study,20 the overall complication rate was 17.8 percent; most complications were minor, such as suture dehiscence, postoperative bleeding, and hematoma. The rate of recurrence in this study was 2.5 percent and was related to the severity of the disorder.20

OTHER TREATMENT OPTIONS

Radiotherapy has been investigated as a potential treatment option. In a study22 of the effects of radiotherapy in 231 patients, 38 percent had complete relief, and 40 percent showed clear improvement of symptoms. However, the possibility of long-term side effects must be discussed thoroughly with the patient.

Cryotherapy also has been considered. In one small study,23 10 patients who did not respond to systemic antibiotics were given one cycle of cryotherapy; eight patients reported improvement. However, patients also experienced significant pain, prolonged healing time (average, 25 days), and post-treatment infection. A carbon dioxide laser used in conjunction with second-intention healing provided relief for a few patients.24

Counseling

In addition to treating the physical illness, it is crucial that physicians acknowledge and treat the psychological burden associated with the disease. Because of the areas of the body that are affected, the malodorous discharge, the chronic discomfort, and the general unsightliness of the disease, hidradenitis suppurativa poses many challenges for patients in their personal life. Sexuality can be negatively affected. Unforgiving societal attitudes regarding inappropriate body odor (especially for those who choose not to wear deodorants), as well as years of inadequate treatment, may lead to frustration, depression, and isolation. For patients at increased risk for these outcomes, early surgical intervention should be strongly considered.17

Final Comment

Hidradenitis suppurativa remains a challenging disease for patients and physicians. Because there has been no significant research comparing treatment options, the choice of therapy should depend on the patient’s circumstances and preferences, the outcome of previous treatments, the experience of the physician, local expertise (e.g., a surgeon or dermatologist who specializes in treatment of the disease), and the chronicity and severity at presentation. Further research should be conducted not only on the etiology of this disease but also on the optimal treatment regimen.

The Author

NIPA SHAH, M.D., is director of predoctoral education at the University of Illinois College of Medicine, Chicago, where she received her medical degree. She completed a family medicine residency at the University of New Mexico Department of Family and Community Medicine, Albuquerque.

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Zinc salts effective in treating Verneuil's disease (hidradenitis suppurativa)


A pilot study published in the journal "Dermatology" shows that zinc salts can provide an effective treatment for Verneuil's disease (hidradenitis suppurativa).

Verneuil's disease is a chronic, suppurative dermatosis involving the apocrine glands with a severe impact on the quality of life.

There is no standard treatment for this disease, and the drugs usually prescribed are often poorly effective. Therefore, a new therapeutic approach based on zinc salts was investigated with 22 patients, mainly from grade I or II in Hurley’s clinical staging.

All patients included had previously been prescribed a treatment (antibiotic, isotretinoin, surgery or anti-androgens), which was inefficient. The patients were treated with 90 mg of zinc gluconate per day (15 mg zinc, 6 times per day).

A clinical response in all patients was observed, with 8 complete remissions and 14 partial remissions. When complete remission was obtained, the treatment was progressively decreased; however, relapses occurred when reaching 2-4 capsules per day, depending on the severity of the disease. Recurrence disappeared when the dosage was increased again, suggesting that the treatment is suppressive rather than curative.

The treatment was well tolerated (4/22 patients experiencing side-effects, mainly gastro-intestinal), and this is crucial in the context of a chronic disease strongly affecting quality of life.

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Hidradenitis suppurativa and zinc: a new therapeutic approach. A pilot study.
Brocard A, Knol AC, Khammari A, Dréno B.
Source

Department of Dermatology, INSERM U601, CHU Hôtel-Dieu, Nantes, France.
Abstract
BACKGROUND:

Hidradenitis suppurativa (Verneuil's disease) is a chronic suppurative dermatosis involving apocrine glands with a severe impact on the quality of life, which is enhanced by the fact that the drugs usually prescribed are poorly effective.

OBJECTIVE:

We discuss a new therapeutic approach based on zinc salts.

METHODS:

We performed a pilot study on 22 patients, mainly from grade I or II in Hurley's classification. All included patients had previously been prescribed a treatment (antibiotic, isotretinoin, surgery or anti-androgens), which was inefficient. They were then treated with 90 mg of zinc gluconate per day (15 mg zinc per Rubozinc capsule).

RESULTS:

We observed a clinical response in all patients, with 8 complete remissions (CR) and 14 partial remissions (PR). When CR was obtained, the treatment was progressively decreased (average of 3.5 capsules/day); 4/22 patients experienced side-effects, mainly gastro-intestinal.

CONCLUSION:

Zinc salts could provide a new therapeutic alternative for the treatment of hidradenitis suppurativa.

2007 S. Karger AG, Basel

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Quote from: SeekinTruth on Today at 09:15:35 AM

That's interesting about the zinc, Laura. I wonder if it's also connected to copper toxicity? Zinc deficiency and copper toxicity/overabundance tend to be associated.

About the fistulas, I read years ago that it's related to gut issues. I actually had one on my tailbone starting in the last couple of years in high school (my brother had it also and my father had it when he was young and had some kind of surgery that took care of it for the rest of his life). Now, from my brother (and my father's experience he related) and a bunch of other people who had this in the same area -- on or around the tailbone, everyone else would have periods where it would swell with lots of pain, and then a wound would open and drain. And then it would close for a while.

In my case, when it was in the very early stage of starting, I actually banged my tailbone on a hard surface, and then the swelling and pain started. For a couple of years, mine never opened and drained. Then, it opened and never closed -- it was pretty much perpetually draining, but the pain was much less. After almost two years of the open wound, and the whole time my mother kept nagging me to go to a doctor and get it taken care of (she kept fearing that I'd get "blood poisoning") I finally scheduled a surgery to cut it out. Well when the surgeon went in to cut out what was an open wound of a 1/4 inch and surrounding slight swelling of about 3/4 inch diameter, he ended up cutting huge amounts of flesh and muscle on the very lower back and right on the top part of my butt. It was real hell for the next couple of weeks.

I had to go a couple of times for the doctor to check on the healing. After the stitches were taken out, he "burned the open flesh" with nitrogen a couple of times that was supposed to help it heal faster. Well, in my case, it never came back again and healed well. The thing is, that years later, when I was 39, I got prostatitis, which is treated with high doses of zinc for several months, among other things. And it has a large component of severe biochemical imbalances that start the process which could be cured with dietary changes and supplements for about 6 months. What I'm thinking now is, I wonder if the lack of zinc/too much copper was already a problem that manifested in the fistula in my late teens-early twenties.

At the time I was doing research on prostate problems, there was a statistic that at least 50% of men age 40 or over are expected to have enlarged prostate, which is a precursor of prostatitis. Well, I'm convinced that such alarming numbers, like so many other things, are connected to a lifetime of the totally wrong diet, and probably stress, toxic buildup, and chemical imbalances, etc.

Just a note. About ten years or so ago, a second cousin of mine who also had the cyclical fistula opening/closing told my brother that he read somewhere that black pepper was a culprit. And he (and my brother) used to eat large amounts of black pepper. When my cousin cut it out completely, it went away in a month or two. My brother tried just cutting down to almost complete abstention from black pepper and his also went away. But for years if he had a considerable amount of black pepper for a couple of days, the irritation and pain would start again. Then after several years of totally avoiding black pepper it resolved completely and now he eats black pepper regularly (though more sparingly) and has no problems. I don't know what the mechanism behind is, but thought I'd mention it as something for others to consider/look into.

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In the 1950s, pilonidal sinus disease was thought to be of congenital origin rather than an acquired disorder. The pilonidal sinus and abscess were thought to be secondary to a congenital remnant of an epithelial-lined tract from postcoccygeal epidermal cell rests or vestigial scent cells. Sinuses to the neural canal can occasionally extend to the dura, but these are rare and are located in the lumbar region rather than in the sacral region. Pilonidal disease is now widely considered to be an acquired disorder, based on the observations that congenital tracts do not contain hair and are lined with cuboidal epithelium. The recurrence of the disorder after complete excision of the disease tissue down to the sacrococcygeal fascia and the high incidence of chronic pilonidal sinus disease in patients who are hirsute further support an acquired theory of pathogenesis.

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SeekinTruth said:

About the fistulas, I read years ago that it's related to gut issues. I actually had one on my tailbone starting in the last couple of years in high school (my brother had it also and my father had it when he was young and had some kind of surgery that took care of it for the rest of his life). Now, from my brother (and my father's experience he related) and a bunch of other people who had this in the same area -- on or around the tailbone, everyone else would have periods where it would swell with lots of pain, and then a wound would open and drain. And then it would close for a while.

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What is Pilonidal Disease?

A nest of hairs

Pilonidal disease is not a cyst (an epithelial-lined sac), it is an abscess (a cavity filled with infected fluid and/or debris). The fluid, if present, is infected fluid called purulent material or pus, and the debris is usually loose hair. In fact pilonidal means “nest of hairs.” Around half of all pilonidal abscesses contain hairs. The hairs have been shed from other parts of the body (such as the scalp, back etc.) and then become lodged in an unusually deep cleft near the tailbone. They are not ingrown hairs. This is why shaving the affected area is usually of little help.

Symptoms of pilonidal disease

Pilonidal disease can cause a variety of symptoms which may happen all the time, may come and go, may be mild, or may be severe. These symptoms include:

• Pain/discomfort or swelling above the anus or near the tailbone that comes and goes
• Opaque yellow (purulent) or bloody discharge from the tailbone area
• Unexpected moisture in the tailbone region
• Discomfort with sitting on the tailbone, doing sit-ups or riding a bike (any activities that roll over the tailbone area)

Be aware that most physicians are not trained to differentiate pilonidal disease from a perianal abscess or buttock abscess. If you suspect that you have pilonidal disease, it is important to consult a Colon and Rectal Surgeon for a proper exam.

Why there?

Pilonidal disease affects a very specific area of the body called the natal cleft. The natal cleft is the 2-3 inch valley under the tailbone that is hidden by one’s buttock cheeks when standing. It is bracketed above by the coccyx (tailbone), and below by the anus.

Formation of abscesses

The abscess is believed to start when skin in the natal cleft stretches during sitting, breaking hair follicles and opening a pore or ‘pit’. As one stands up, the movement causes a suction that pulls loose hair and debris into the now open ‘pore/pit’. Once lodged, the hairs can cause irritation if not expelled by the body or removed in time. Chronic infection can develop in this hidden area and lead to the formation of tunnels (sinuses) from under the skin to areas outside the natal cleft. Additional ‘pits’ can then develop leading to persistent or recurrent symptoms of pain, swelling, drainage, and even odor. Many people with pilonidal disease have or develop ‘divots’ in their natal clefts, which further encourage the deposition of debris and the formation of more ‘pits’.

The deep clefts of people with pilonidal disease

Pilonidal disease typically develops in people with very deep natal clefts that have poor air circulation as a result of the deep cleft. The only way to see pilonidal disease in these individuals is to part the buttock cheeks enough to visualize the pores or sinuses within the valley of the natal cleft.

Age and pilonidal disease

Pilonidal disease is common among young people. The disease most often affects teens and young adults. For unclear reasons, many, but not all, affected people will stop having symptoms of untreated disease by their 40s.

When pilonidal disease affects normal life

Pilonidal disease or failed surgical procedures aimed at treating the disease can lead to many months or years of discomfort, disability, and suffering. Due to severe symptoms of pain or discharge, affected individuals may have trouble sitting for long periods of time, miss school or work, refrain from sports, or avoid close contact with friends. Embarrassment from the condition may prevent individuals from using common locker rooms or wearing a bathing suit. Unsuccessful surgical procedures may force individuals to remain at home and pack wounds in areas they can’t see or easily reach.

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Instead of looking for a single pathogen or simple cause of HS, I have begun to consider a complex of diseases or conditions that could lead to or be related to HS.

At this point in time, I feel that the cause of the actual HS inflammations is an inappropriate autoimmune response that is localized in the apocrine sweat gland-bearing skin (either in the apocrine gland itself or the adjacent follicle).

I feel this inappropriate autoimmune response may cause the gland to become blocked, and may result in the accumulation of fluid inside the gland. Swelling naturally follows.

I feel that this inappropriate autoimmune response may initially be triggered by activity in the apocrine glands, which do not seem to become active in most people until puberty.

I feel that infections in the site of inflammation caused by bacteria and other pathogens, such as yeast, fungus, viruses, or microorganisms are most likely “secondary”, and while they may make the situation worse, I do not necessarily consider them to be directly related to the initial cause of inflammation in most cases.

I feel that the inappropriate autoimmune response is a genetically inherited condition.

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It seems to me, based on information I have read on many websites, that a factor common to many Hidradenitis Suppurativa sufferers may be what is sometimes known as “leaky gut syndrome”. This is mentioned in many of the texts I have found that describe symptoms of Irritable Bowel Syndrome, Crohn’s Disease, Diabetes, Chronic Fatigue, Thyroid problems, Autoimmune disorders (such as Graves Disease, and Celiac Disease) and others.

<skipped long bit about Leaky Gut>

As you can see from the information above (and I highly recommend visiting the website to read the full text) it is consistent with much of what has been said regarding symptoms and diseases often associated with HS. Furthermore, the causes of Leaky Gut Syndrome listed here seem to be consistent with conditions that are often cited as “triggers” for flare ups by HS sufferers. The effects of Leaky Gut Syndrome include autoimmune disorders, which may also be consistent with HS. These are the primary reasons why I feel Leaky Gut Syndrome may be a factor in HS.

Another reason I feel Leaky Gut Syndrome may be a condition involved in the development of HS has to do with my personal treatment. I am not a doctor and I have no medical background, but I suspected that Candida albicans (a yeast/fungus) and/or Pityrosporum ovale (another yeast/fungus) played a major role in my HS due to the similarities between symptoms I experienced and those of Candidiasis (also called Candidiosis, or Candida overgrowth). Candida is often said to cause leaky gut syndrome. Though this is not a scientific study, and the anecdotal evidence of my response to a self-prescribed anti-candida treatment can not be considered conclusive, it supports the possibility that this theory is not without merit. More information on Candida will be presented later on this site.

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The autoimmune connection often mentioned by HS sufferers is supported here as well. Through extensive reading of reputable websites about autoimmune disorders, Celiac Disease (also spelled “Coeliac Disease”, also called “Celiac Sprue”) became my focus for two reasons: First of all, it may be the only autoimmune disorder for which the triggering agent and mechanism is known, and secondly, many of the symptoms associated with Celiac Disease were consistent with those of many HS sufferers, including myself.

<skip long bit about Celiac>

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This information sheds considerable light on the nature of autoimmune disorders in general. While I do not necessarily consider Celiac (or often related “Dermatitis Herpetiformis”) as a cause of HS, there are considerable similarities between the symptoms of each. I mention Celiac only to show how the human body can have very non-specific autoimmune reactions to a specific set of food sources.

If we consider the possibility that Leaky Gut Syndrome allows foreign substances from food (as well as pathogens) into our bloodstream, we can see how an autoimmune response could result. In the case of Celiac, the autoimmune response to Gluten can actually damage the intestines, and may be a precursor to Leaky Gut Syndrome. A damaged intestine could provide a place for Candida or other pathogens to grow.

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So this line of thinking leads us in circles, because each condition [Leaky Gut Syndrome, Candidiasis, and Celiac (or a similar “inappropriate” autoimmune-type response to a food source or pathogen)] seems to be able to lead to the others. However, each one may be able to be present in the absence of the others. This makes it very difficult to list any one of these conditions as a “cause” and the others as “effects”.

If we consider a pure definition of Hidradenitis Suppurativa, excluding the related symptoms and diseases, such as:

(Source: http://dictionary.reference.com/search?q=Hidradenitis+Suppurativa)

1. Inflammation of the apocrine sweat glands of the perianal, axillary, and genital areas, producing chronic abscesses or sinuses.

2. a chronic suppurative inflammatory disease of the apocrine sweat glands

several questions arise.

Exactly what is contained in the inflammations, and what causes apocrine glands (* or follicles, depending on where you believe the actual inflammation occurs) to become blocked is the real heart of the question. It would seem that if we could find a way to prevent blockage of the apocrine glands (or follicles), we would not have the painful swelling, but might instead just have drainage of fluids. If we could prevent the fluid that is contained in the inflammations from forming or being deposited there by our body, there would be no swelling....

As you can see, only the apocrine glands are implicated in the definition here. On numerous websites, the follicle is considered to be the location of these inflammations. According to what I have learned so far, apocrine sweat glands typically do not open to the skin surface, but to a follicle (see diagram below). As such, I feel it is a minor point to consider whether the inflammation occurs in one or the other. Due to the overall structure, I feel that either way, both the apocrine sweat gland and the follicle are likely to be involved. I have not chosen to pursue this difference of opinion any further, for the time being.

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As for the question of what causes the blockage of the apocrine gland (or follicle), that is not known either. Some possible causes revealed by a Google search for “blocked sweat glands” revealed the following:

(Source: http://www.wdxcyber.com/nvulva03.htm)

“Epithelial inclusion cysts result when a duct is plugged up and the skin cells, squamous cells, that are usually sloughed as they naturally die off, cannot get out of the duct. New cells keep forming, however and a cyst filled with cells forms under the skin. If those cysts are opened surgically, a cheesy -like contents are extruded.

Some women may form these as a result of surgery or an episiotomy during delivery. Others just seem to have a tendency for the vulvar skin ducts to get plugged up. The only treatment for these is to surgically open the cysts with a needle or scalpel wide enough not to get replugged up, or to actually surgically excise the cyst and close the skin with a stitch.

Remember that epidermoid cysts are usually not infected with bacteria unless you have been squeezing them and the cyst breaks up into the skin rather than to the surface of the skin.

If the vulvar sweat glands become swollen, inflamed and sometimes drain like severe acne, what can be done?

The first step is to be absolutely sure of the diagnosis. If there are draining, reddened cysts like a pustular acne, a biopsy usually has to be performed in order to confirm what type of lesion in present. Fox-Fordyce disease and hidradenitis suppurativa are very similar. They can both affect the arm pits (axilla) as well as the vulva. Fox-Fordyce disease is a chronic blockage of the sweat gland ducts with a secondary, non bacterial inflammatory response to the secretions and cellular debris in the cysts. Hidradenitis is very similar but tends to have a secondary bacterial infection so that pus draining sinuses are formed. It is a very devastating skin disease that does not have universally curative treatments. Often surgery with complete excision of the gland bearing skin under the arms or across the entire vulva may need to be performed. Irradiation therapy may also be used and antibiotics are used to reduce the inflammatory response.

Since hidradenitis suppurativa is such a chronic devastating disease, large support groups have been formed and help disseminate the latest information about the disease. Some women respond with treatment to antibiotics, Accutane®, or hormonal treatment (e.g., Lupron®) but the mainstay treatment is surgical removal of the skin tissue containing affected sweat glands.”

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This prompted a little search of “Fox-Fordyce disease”, which revealed the following:

(Source: http://www.emedicine.com/derm/topic160.htm)

“Background: Fox-Fordyce disease is an infrequently occurring chronic pruritic papular eruption that localizes to areas where apocrine glands are found. The etiology is currently unknown. The eponym is based on the 1902 report by G. Fox and J. Fordyce.

Pathophysiology: Fox-Fordyce disease is a disease of the skin alone. In 1956, Shelley and Levy proposed apocrine miliaria as the cause. The observed pathophysiology is a keratin plug in the hair follicle infundibulum obstructing the apocrine acrosyringium and producing an apocrine anhidrosis. Histologically, a rupture of the apocrine excretory duct occurs, and spongiotic inflammation results. Extravasation of sweat and inflammation is postulated to cause the intense itching. Ranalletta et al found that the acrosyringium of the eccrine glands was similarly involved.

In 2003, Kamada et al published a histopathologic analysis from which they concluded that the 2 types of this disease are (1) an apocrine (follicular) type and (2) an apocrine (nonfollicular) type.”

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Given that information, it seems to be very possible that at least a small percentage of people may have been misdiagnosed. ...

This misdiagnosis could be the cause of a great deal of confusion regarding HS. While it is mentioned several times in old posts on the Yahoo HS forum, there is not a clear connection between the two, although it has been said that someone could suffer from both at the same time. So the anecdotal information gathered from (especially “self-diagnosed”) HS sufferers may be incorrect if they actually only suffer from Fox Fordyce. As you can see, this could cause a lot of confusion, especially since the additional symptoms often associated with HS are not typically considered to be associated with Fox-Fordyce.

WebMD had this to say about Fox-Fordyce:

(Source: http://my.webmd.com/hw/womens_conditions/nord941.asp#)

“Fox-Fordyce Disease is a rare disorder that occurs almost solely in women. It is characterized by the development of intense itching usually in the underarm area, the pubic area, and around the nipple of the breast. Perspiration becomes trapped in the sweat gland and in the surrounding area causing intense itching, inflammation, and enlargement of the glands. Skin in the area may become darkened and dry; raised patches develop. Hair follicles in the area dry out resulting in loss or breakage of hair.”

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Getting back to the possible sources of plugged up apocrine glands (or follicles), they are often said to be blocked by Keratin, so I found the following definition of keratin:

(Source: pop-up definition provided by selecting the word “keratin” in the text on the site: http://www.emedicine.com/derm/topic160.htm)

keratin

Pronunciation: (ker'a-tin)

Collective name for a group of proteins that form the intermediate filaments in epithelial cells. Keratins have a molecular weight between 40 kd and 68 kd, and are separated one from another by electrophoresis and isoelectric focusing; thus separated, they are sequentially numbered from 1-20, and also subdivided into low, intermediate, and high molecular weight proteins. According to their isoelectric mobility they are either acidic or basic. In general, each acidic keratin protein has its basic equivalent with which it is paired to form the intermediate filaments; some keratin proteins, however, occur unpaired. Various epithelial cells contain different keratin proteins, in a tissue-specific manner. Antibodies to keratin proteins are widely used for histologic typing of tumors, and are especially useful for distinguishing carcinomas from sarcomas, lymphomas, and melanomas.

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Overall, this definition is mostly just overwhelming, but the part that states “Antibodies to keratin proteins are widely used for histologic typing of tumors” alerted me to the possibility that the human body may be capable of attacking it's own keratin with antibodies. This re-enforces the notion that an inappropriate autoimmune response may be responsible for HS.

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So we can not draw any definite conclusions as to why apocrine sweat glands may become blocked. It might not be as important to know exactly how or why an apocrine gland (or follicle) becomes blocked as it is to know why the swelling occurs. While this whole line of questioning has not enabled me to draw any conclusions, it sheds light on the degree of confusion surrounding HS and provides at least a slight glimpse of the physical mechanisms involved.

Leaps of Faith

Because the information regarding these conditions and diseases is so scarce, and the causes of some of them are unknown, it requires a leap of faith to try to draw any sort of conclusions. Please note that here, in this “Leap of Faith” portion of this website, I am putting forth ideas and theories that are my own thoughts and hypotheses. They may not be rooted in fact or backed by scientific data. As such, I will not be quoting other websites or listing sources very much here. These are just my thoughts regarding possibilities that have occurred to me. Some of these I intend to research online at a future date, as needed.

*** THESE ARE NOT OBJECTIVE STATEMENTS! ***

Scenario 1: I BELIEVE it may be possible that an inappropriate autoimmune response to a keratin (type of protein produced in the epithelial layer of our skin) or other substance found in active apocrine glands may cause the apocrine glands or follicles to become plugged up with dead cells. As our body continues to produce this keratin or other substance, our immune system continues to attack it, resulting in more and more dead cells. The accumulation of these cells inside the plugged apocrine gland or follicle would cause swelling. Swelling could result in rupture of the structure of the apocrine gland or follicle. If this rupture occurs at the skin surface, drainage would occur. If this rupture occurs beneath the skin surface, fluids would leak into nearby tissue, causing additional inflammation.

Cause: In this scenario, a (most likely) hereditary autoimmune disorder would be solely responsible. Inflammations would be sterile, unless bacteria or another pathogen was previously present within the apocrine gland or follicle, or invaded after inflammation ruptured. HS inflammation would be the only symptom or disease present unless this autoimmune disorder caused the immune system to attack other organs in the body as well.

Treatment: There are not many effective known treatments for autoimmune disorders. If bacterial infection is present, antibiotics might be effective for alleviating the additional irritation caused by the bacteria, but will not affect HS. A culture would be required to determine which bacteria are present, and the appropriate antibiotic would have to be used. If the infection does not contain bacteria, other pathogens could be considered. If a yeast or fungus is found to be present, an antifungal medication could be used to alleviate additional irritation, but will not affect HS. To reduce the occurrence of HS inflammations, it may be possible to suppress the immune system to some degree, but this may be dangerous and could cause other problems.

Conclusion: If this scenario applies, there is no cure or viable treatment for HS. The only available remedy would be to use simple, basic techniques to prevent the apocrine glands or follicles from forming or retaining keratin plugs, possibly by bathing in warm, soapy water several times a day and/or applying hot compresses often. This may keep the skin supple enough to release the plugs so that swelling does not occur. It would also be advisable to wear loose clothing and avoid the use of products that could irritate the skin or clog pores and follicles, such as deodorant and oil-based lotions and ointments. Topical antibiotic and antifungal cremes and soaps could be used as needed to prevent or treat secondary infection, unless these infections are severe. If secondary infection is severe or has become systemic, prescription antibiotics or antifungal medication may be necessary.

Scenario 2: I BELIEVE that it may be possible for a yeast/fungus type pathogen to infect an apocrine gland or follicle. Toxic waste products produced by the pathogen, as well as dead cells from within, could plug the apocrine gland or follicle. An immune system response could result in an accumulation of dead cells within the apocrine gland or follicle, causing swelling. Swelling could result in rupture of the structure of the apocrine gland or follicle. If this rupture occurs at the skin surface, drainage would occur. If this rupture occurs beneath the skin surface, fluids would leak into nearby tissue, causing additional inflammation.

Cause: In this scenario, the yeast/fungus type pathogen would be primarily responsible, with the immune response (appropriate or inappropriate) contributing to the swelling. Affected apocrine glands or follicles might also contain bacteria, which could further irritate the site of inflammation. HS inflammation would be the primary symptom, but other symptoms might be present, such as those normally known to be caused by the pathogen.

The nature of the body’s immune response to the pathogen should be considered. In most cases of HS, this response would most likely be considered an inappropriate response, thus indicating an autoimmune disorder, (though it might be possible for a normal immune response to result in HS inflammation under certain conditions). As such, additional autoimmune disorders may be observed if the disorder causes the immune system to attack other organs in the body as well. If infection by the yeast/fungus pathogen is systemic, this autoimmune response may be observed in any tissue where the pathogen can be found. This makes it very difficult to discern whether the immune response is appropriate or inappropriate. Further research into why some people are more susceptible to the pathogen than others may be required in order to support this scenario.

Treatment: If a yeast/fungus type pathogen were to be the cause of apocrine glands or follicles becoming plugged and eliciting an immune response, then a topical antifungal cream (as a treatment for current inflammation and preventatively) should essentially cure HS, but this has rarely, if ever, been found to be the case. Given the possibility that bacteria could also be present, it might be necessary to treat the inflammation sites with both topical antibacterial and antifungal agents. If severe, prescription antibacterial and antifungal medications may be required simultaneously. If yeast/fungus type pathogen infection has become systemic, additional measures would have to be taken to kill the pathogen internally. Also, damage caused by the pathogen would have to be repaired and normal health restored. Changes in diet and herbal supplements are considered effective (primarily by manufacturers and sellers of these supplements, and by writers and purveyors of diet books, but evidenced occasionally on medical and scientific websites) to some degree, but prescription medications might prove to be more effective and work much faster. However, medications may have side effects, and aside from eliminating the pathogens, may do little more than promote healing, unless they are also anti-inflammatory. Additional measures may also be needed to promote healing. If the intestines are infected, normal beneficial flora may be damaged or impaired. Restoring this flora would be important to restoring health, and to prevent future re-infection by the pathogen.

Conclusion: If this scenario applies, it might seem possible to cure or at least treat HS effectively by ridding our body of the offending yeast/fungus and bacterial pathogens and restoring damage done by them. While this is extremely unlikely to cure HS, if additional symptoms of Candidiasis or other pathogenic fungal infection are present, some improvement in HS might be observed by effectively by ridding our body of the offending yeast/fungus. But if the cure was this simple, I’m fairly certain it would have been discovered by now. The possibility of an inappropriate autoimmune response to a pathogen should really be considered and could weigh heavily in this scenario. Perhaps the yeast/fungus type pathogen is merely a trigger for the autoimmune response. Given this scenario, antibiotics would only be effective at removing or reducing the effects of a (secondary) bacterial infection (which may or may not be present), but would not improve the condition of HS because they do not address the problem of the fungal infection, nor do they address the autoimmune issue in any way. The possibility that antibiotics might contain anti-inflammatory agents could partially account for the temporary relief some have experienced in their HS symptoms while using antibiotics. As such, anti-inflammatory medications might be useful for reducing the overall swelling and pain, but would not be a cure. Side effects of the medication could also be a problem, especially if long-term use is required. Additionally, to decrease overall swelling and pain, it might be advisable to use simple, basic techniques to prevent the apocrine glands or follicles from forming or retaining plugs, possibly by bathing in warm, soapy water several times a day and/or applying hot compresses often. This may keep the skin supple enough to release the plugs so that swelling does not occur. It would also be advisable to wear loose clothing and avoid the use of products that could irritate the skin or clog pores, such as deodorant and oil-based lotions and ointments. Topical antibiotic and antifungal cremes and soaps could be used as needed to prevent or treat infections, unless these infections are severe. If infection is severe or has become systemic, prescription antibiotics or antifungal medication may be necessary.

Scenario 3: I BELIEVE it may be possible for much of the theory contained in Scenario 2 to be true, but with one major difference: a food substance, environmental pollutant, microorganism, or chemical could be the triggering agent instead of a fungal pathogen. As such, the presence of fungal and bacterial infections would be considered secondary. In the case of Celiac disease, Gluten (contained primarily in wheat, barley, rye and oats) would be the offending triggering agent, but there are certain to be other possible agents that could cause an inappropriate autoimmune response. As the “cause, treatment and conclusion” paragraphs listed in scenario 2 state, the primary treatment would be to identify and eliminate any triggering agents from the body. While allergy tests might be helpful, intolerance of certain agents may not be provable in this way. Celiac disease is not necessarily indicated in most cases of HS, though there may be a connection. In at least one case of HS found on an HS forum, the HS sufferer had been diagnosed with Celiac disease and has been gluten-free since the age of 4, yet still developed HS at the age of 14. That person said, “Cant say Ive noticed much correlation between the two...” regarding Celiac and HS. So the triggering agent is not likely to be as simple as Gluten.

Scenario 4: I BELIEVE that leaky gut syndrome could cause extreme immune reactions ultimately resulting in our immune system attacking our own cells and organs. Without knowing a lot more about how the immune system works on a chemical and molecular level, I can only form a loose theory regarding this possibility. In the event of a “leaky gut”, foreign substances from the intestines could enter the bloodstream where they don’t belong. This could include food in various states of digestion or decomposition, contaminants of a bacterial, fungal, viral or other microbial organism nature, stomach acid, antibodies that normally only exist in the intestines - not normally found in the blood, and dead cells from the lining of the intestines. This would most likely prompt a significant immune reaction. If the immune system begins to identify dead cells from the lining of the intestines or antibodies from the intestines (not normally found in the blood) as “not self”, it will attack them, bind to them and attempt to remove them through normal procedures. This is where we have to take a leap of faith in this scenario - what if our immune system identifies these cells or antibodies from the intestines as “not self”, creates and releases specific antibodies into our blood to bind to and destroy these cells and antibodies (from the intestines) and in doing so, has created an antibody that can also bind to certain other tissues in our bodies? If the new antibodies were structurally created to bind with cells and antibodies from our intestines, could it be possible that they would also be able to bind with cells of certain other tissues in our body and damage them? If they can bind with cells in the pancreas and damage them, Type 1 Diabetes could result. Please consider the following quote:

(Source: http://www.islet.org/3.htm)

“In order to understand a potential cure for diabetes, it is necessary to look briefly at the cause. In insulin-dependent diabetes, the diabetic's body fails to make insulin, a hormone essential to the metabolism of glucose. Glucose enters the blood stream from the food that we eat and, in the presence of insulin, is taken up and "burned" by cells that require this essential fuel. In the absence of insulin, however, glucose accumulates in the blood causing the condition known as high blood sugar (hyperglycemia), while the cells starve for fuel. Without taking insulin injections, the diabetic will slowly starve to death despite abnormally high blood sugar levels.

Why does a diabetic's body fail to produce insulin? Within the pancrease, the Islets of Langerhans produce insulin in response to blood glucose. These islets are tiny insulin factories that sense the level of glucose in the blood stream, and produce insulin in precise proportion to that level. Therefore, following a meal, blood sugar levels will rise significantly, and the islets will release a large amount of insulin. This insulin will cause body cells to take up the sugar, causing blood sugar to quickly return to its normal range. Once blood sugar is in the normal range, the islets will reduce the output of insulin to an idling state. In this way, the islets adjust their production of insulin on a minute-by-minute basis, always producing just enough insulin to deal with the amount of blood sugar presently in the blood stream.

In insulin-dependent diabetes, the islets are destroyed by the person's own immune system, which mistakenly identifies these essential cells as foreign invaders. This self-destructive mechanism is the basis of many so-called autoimmune diseases. Once the islets are killed, the ability to produce insulin is lost, and the overt symptoms and consequences of diabetes begin.”

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The site quoted here does not seem to be essentially commercial-based, and may be of great interest to diabetics.

So at least part of this can be shown in existing research, in that the body is most likely capable of having an inappropriate autoimmune response where it kills our own vital cells. As for the possibility that leaky gut syndrome could initiate this autoimmune response, that is not known, nor is it known why the autoimmune system would attack the apocrine glands, resulting in HS. As I said, this scenario requires a leap of faith because there might not be enough information available to prove or disprove it. I offer it merely as a possibility for consideration, and I do not expect to be right.

In terms of a treatment for this scenario, the cause of a person’s “leaky gut syndrome” would have to be found and corrected. The damage done would have to be healed, and even still, HS might persist. I do not know how the immune system works, but somehow the production of self-destructive antibodies would have to be stopped, because even though the original “foreign materials” that leaked from the gut may no longer be present in the bloodstream, the immune system may continue to fight our own healthy tissue since it has been identified as a foreign substance (or “not self”) in the past. The basic question is: Can cells or antibodies from our own body that are not normally found in the bloodstream cause an (possibly irreversible) autoimmune disorder when they are somehow deposited in the bloodstream? That is a question I can not answer.

Scenario 5: Come out on the ledge with me. It’s a little scary, but there’s a wonderful view. Okay, this one may seem too far-fetched for most people, but I consider it important because of the way it relates to me personally. I BELIEVE that a toxic substance (in my case, mercury) may play a role in some cases of HS. Despite research I have pursued on the internet, there is very little data available, and too much conflicting information to determine whether or not the harmful effects of mercury, other heavy metals or chemicals play any role at all. I just wanted to mention this remote possibility in case anyone else had considered it. I will try to find out more about mercury and post any important information I can find here at a later date.

Conclusion: As you can see, there are common threads and overlaps in these scenarios. Even though I have not found the answers, perhaps they are suggested in here somewhere. I certainly hope someone gets to the bottom of this and finds a cure or at least a viable treatment soon.

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curious_richard said:

If an auto-immune system problem is part of this disease, it seems to me that vitamin D could help. And vitamin C.

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Laura said:

curious_richard said:

If an auto-immune system problem is part of this disease, it seems to me that vitamin D could help. And vitamin C.

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Vitamin C and vitamin D3 and K2 and zinc are being taken religiously.

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Scenario 3: I BELIEVE it may be possible for much of the theory contained in Scenario 2 to be true, but with one major difference: a food substance, environmental pollutant, microorganism, or chemical could be the triggering agent instead of a fungal pathogen. As such, the presence of fungal and bacterial infections would be considered secondary. In the case of Celiac disease, Gluten (contained primarily in wheat, barley, rye and oats) would be the offending triggering agent, but there are certain to be other possible agents that could cause an inappropriate autoimmune response. As the “cause, treatment and conclusion” paragraphs listed in scenario 2 state, the primary treatment would be to identify and eliminate any triggering agents from the body. While allergy tests might be helpful, intolerance of certain agents may not be provable in this way. Celiac disease is not necessarily indicated in most cases of HS, though there may be a connection. In at least one case of HS found on an HS forum, the HS sufferer had been diagnosed with Celiac disease and has been gluten-free since the age of 4, yet still developed HS at the age of 14. That person said, “Cant say Ive noticed much correlation between the two...” regarding Celiac and HS. So the triggering agent is not likely to be as simple as Gluten.

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