My thoughts on Hidradenitis Suppurativa

Site updated Saturday, September 10, 2005

Hidradenitis Suppurativa - Thoughts and Theories

by Jason Cameron

Latest Theory:

This new theory essentially takes into account my previous theories and attempts to correct any information that may have been wrong. It also puts forth some new ideas based on my latest research on the internet. This research applies to my own specific set of symptoms most of all, but I try to consider as much information from the HS Forums as I can, as well as scientific and/or clinical information available online, regarding medical studies. In other words, I am the only test subject I have at my disposal upon which I can base my research and treatment , but I look for information that either supports or contradicts my ideas in posts made on the forums and in scientific and/or clinical reports. I had not considered the information from forums as much in the past because the information is sporadic and anecdotal.

I have also tried to show my research sources more than I have in the past. This takes a lot more time, but I want to be sure that everyone can see the sources I am drawing from. I try never to rely on information given by sources that are selling products (there are advertisements on some pages, but that is the nature of the internet. I try not to cite pages where the purpose of the information provided is to sell a particular product or products). I encourage everyone to view the sources in order to gain a greater understanding of the ideas I am putting forth. Do not accept my ideas blindly. These are only my own personal thoughts, theories and opinions. They are not to be accepted at face value. It is up to every individual to question them and decide what they feel is true, and decide how they may or may not apply to themselves.

In the past, I was naļve enough to believe that a single non-bacterial pathogen could be entirely responsible for HS and all of the related symptoms and diseases. Originally, I considered Candida albicans, a yeast that lives in and on most people, to be the cause. Empirical and anecdotal evidence is sometimes contrary, and that fact should be considered to be very important. However, in HS forums, some (admittedly 2-5 people, an extremely small percentage of HS sufferers - information gathered from a search of 55,853 forum posts) have stated that they or family members with HS have experienced positive results from treating themselves for Candida. I am amongst them. My personal anti-Candida (to be more precise, “anti-fungal”) treatment plan has resulted in a dramatic decrease in “related symptoms”, but has not (yet) cured me of HS. As of this writing (8/30/05), my HS lesions show signs of improvement, but are not completely healed. I can not conclude anything from my personal treatment in terms of curing or treating HS. Six weeks is not enough time to come to a conclusion, and my self-treatment is FAR from scientific. I am a terrible test subject. I have not committed to a complete anti-fungal diet (*), and that fact definitely affects any anecdotal information I can report regarding my own treatment. In one sense, it complicates matters, but on a personal level, I do try to observe the effects of my deviations from my own prescribed treatment and diet. While these effects are often subtle, I try very hard to be “in-tune” with my body and observe these effects. While this approach is very unscientific, it may not be completely without merit. Many effects can be observed almost instantaneously, while some are not apparent right away.

(*) I am referring to the “Anti-Candida” diet. There is a lot of contradictory information as to what foods should be restricted from the diet in order to treat Candida albicans, the pathogen said to be responsible for Candidiosis (also referred to as “Candidiasis”). Rather than trying to treat Candida (and other funguses) through dietary changes alone, I have chosen to take herbal supplements that some (scientists and supplement suppliers) claim can fight systemic fungal infections (I take Olive Leaf Extract, Garlic, and Oil of Oregano for this purpose. Due to the nature of my unscientific self-treatment, I can not state conclusively that any of these supplements are of any value whatsoever. Please view my treatment diary for more specific anecdotal information regarding my use of these supplements). I also decided to take a probiotic supplement to re-colonize my internal flora with beneficial bacteria.

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.

Given the statements above, I have selected several diseases or conditions that I feel, based largely on symptomatic similarities to HS, may be important. This is not a complete list by any means, but hopefully it is enough to illustrate the possible need to look at each individual case of HS as a “complex” involving multiple conditions or diseases. I feel that HS may present as an independent inappropriate autoimmune response alone, or in conjunction with other diseases or conditions. That is to say that these and other additional diseases and conditions are not necessarily a prerequisite to HS, nor are they necessarily caused by HS.

I consider it to be possible that a (somewhat rare) inherited genetic trait or set of traits could be responsible for HS and other diseases (especially autoimmune diseases) concurrently, so that all, some, or none of the disorders associated with these genetic traits may manifest in various people (in varying degrees) who share these genetic traits. Without a great deal of research into genetics and heredity, I can not confirm this, so I list it strictly as a possibility.

Diseases or conditions that I feel, based largely on symptomatic similarities to HS, may be important:

Leaky Gut Syndrome

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. “Leaky Gut Syndrome” is described as:

(Source: http://www.afpafitness.com/articles/LEAKGUT4.HTM)

“The leaky gut syndrome is the name given to a very common health disorder in which the basic organic defect (lesion) is an intestinal lining which is more permeable (porous) than normal. The abnormally large spaces present between the cells of the gut wall allow the entry of toxic material into the bloodstream that would, in healthier circumstances, be repelled and eliminated. The gut becomes leaky in the sense that bacteria, fungi, parasites and their toxins, undigested protein, fat and waste normally not absorbed into the bloodstream in the healthy state, pass through a damaged, hyperpermeable, porous or "leaky" gut. This can be verified by special gut permeability urine tests, microscopic examination of the lining of the intestinal wall as well as the bloodstream with phase contrast or darkfield microscopy of living whole blood.”

“The inflammation that causes the leaky gut syndrome also damages the protective coating of antibodies of the IgA family normally present in a healthy gut. Since IgA helps us ward off infections, with leaky gut problems we become less resistant to viruses, bacteria, parasites and candida. These microbes are then able to invade the bloodstream and colonize almost any body tissue or organ. When this occurs in the gums, periodontal disease results. If it happens in the jaw, tooth extraction or root canals might be necessary to cure the infection.”

“Leaky gut syndrome also creates a long list of mineral deficiencies because the various carrier proteins present in the gastrointestinal tract that are needed to transport minerals from the intestine to the blood are damaged by the inflammation process. For example, magnesium deficiency (low red blood cell magnesium) is quite a common finding in conditions like fibromyalgia despite a high magnesium intake through the diet and supplementation. If the carrier protein for magnesium is damaged, magnesium deficiency develops as a result of malabsorption. Muscle pain and spasms can occur as a result. Similarly, zinc deficiency due to malabsorption can result in hair loss or baldness as occurs in alopecia areata. Copper deficiency can occur in an identical way leading to high blood cholesterol levels and osteoarthritis. Further, bone problems develop as a result of the malabsorption of calcium, boron, silicon and manganese.”

“The Causes

The leaky gut syndrome is basically caused by inflammation of the gut lining. This inflammation is usually brought about by the following:

· Antibiotics because they lead to the overgrowth of abnormal flora in the gastrointestinal tract (bacteria, parasites, candida, fungi) · Alcohol and caffeine (strong gut irritants)

· Foods and beverages contaminated by parasites like giardia lamblia, cryptosporidium, blastocystis hominis and others

· Foods and beverages contaminated by bacteria like helicobacter pylori, klebsiella,

· citrobacter, pseudomonas and others

· Chemicals in fermented and processed food (dyes, preservatives, peroxidized fats) · Enzyme deficiencies (e.g. celiac disease, lactase deficiency causing lactose intolerance)

· NSAIDS (non-steroidal anti-inflammatory drugs) like ASA, ibuprofen, indomethacin,

· Prescription corticosteroids (e.g. prednisone)

· High refined carbohydrate diet (e.g. candy bars, cookies, cake, soft drinks, white

· bread) Prescription hormones like the birth control pill

· Mold and fungal mycotoxins in stored grains, fruit and refined carbohydrates.”

“Prescription broad spectrum antibiotics, especially when taken for extended periods of time, wipe out all the gut friendly bacteria that provide protection against fungi and amoebic (parasitic) infections, help the body break down complex foods and synthesize vitamins like B12 and biotin. Since this friendly bowel flora is killed off, the body now has no local defence against the parasites or fungi that are normally held in check. This then causes an inflammatory reaction leading to the leaky gut syndrome. Food allergies quickly develop and these may trigger the signs and symptoms of arthritis, eczema, migraines, asthma or other forms of immune dysfunction. Other common symptoms of this bowel flora imbalance and leaky gut syndrome are bloating and gas after meals and alternating constipation with diarrhea. This set of symptoms is usually labelled as IBS (irritable bowel syndrome) or spastic bowel disease and treated symptomatically by general practitioners and gastroenterologists with antispasmodic drugs, tranquilizers or different types of soluble (psyllium) and insoluble (bran) fiber.”

“The mainstream thinking on IBS is that it is caused by stress. Irritable bowel syndrome is the number one reason for general practitioner referrals to specialists. In well over 80% of the cases, tests like the intestinal permeability test (a special urine test involving the determination of absorption rates of two sugars called lactulose and mannitol), CDSA or livecell darkfield microscopy reveal the presence of an overgrowth of fungi, parasites or pathogenic bacteria. The one-celled parasite, blastocystis hominis and different species of candida are the most common microbes seen in IBS. The only stress associated with IBS is that which is generated by infection and the leaky gut syndrome. If allowed to persist without the correct treatment, IBS can progress into more serious disorders like the candidiasis syndrome, multiple chemical sensitivities, chronic fatigue syndrome, many autoimmune diseases and even cancer. If treated medically, IBS is rarely cured. To treat it correctly, natural treatments work best and must include the removal of the cause, improvement of gastrointestinal function and healing the lining of the gut.”

“How to Reverse Leaky Gut Syndrome

Band-aid treatments with corticosteroids, prescription antibiotics and immuno suppressive drugs may be temporarily life-saving for acute episodes of pain, bleeding or severe inflammation as occurs in lupus or colitis. In the long run, however, none of these treatments do anything to heal the leaky gut problem. To reverse the leaky gut syndrome the diet must be completely changed to one which is as hypoallergenic as possible. Sugar, white flour products, all gluten-containing grains (especially wheat, barley, oats and rye), milk and dairy products, high fat foods, caffeine products, alcohol and hidden food allergies determined by testing must all be eliminated for long periods of time (several years in the most severe cases).

Treatment might also include the use of natural antibiotics (echinacea, *colloidal silver, garlic), antiparasitics (cloves, wormwood, black walnut) and antifungals (taheebo, caprylic acid, grapefruit seed extract) depending on the type of infection which shows up on objective tests. It is rare that victims require prescription drugs for these infections and they should be discouraged. The drugs are usually expensive, have unpleasant side effects and are best reserved for life-threatening conditions.”

(* - Please note that this treatment option, Colloidal silver, is NOT my own recommendation, but a treatment option put forth by the creator of the information quoted from the “source” website listed above.)

“Leaky gut syndrome patients can help themselves by chewing their food more thoroughly, following the basic rules of food combining, eating frequent small meals rather than three large ones and taking more time with their meals. Gastrointestinal function can be improved with a juice fast or a hypoallergenic diet and supplements like lactobacillus acidophilus and bifidus as well as FOS (fructooligosaccharides) derived from Jerusalem artichoke, chicory, the dahlia plant or burdock root.

Beneficial Supplements for Leaky Gut Syndrome

Natural digestive enzymes - from plant (e,g, bromelain, papain) or pancreatic animal tissues (porcine, bovine, lamb) and aloe vera juice with a high MPS concentration (good brands are International Aloe, Earthnet and Royal) stomach acidity enhancing supplements - betaine and pepsin, glutamic acid, stomach bitters, apple cider vinegar amino acids - L-glutamine, N-acetyl-glucosamine (NAG) essential fatty acids - milled flax, flax seed oil, evening primrose oil, borage oil, olive oil, fish oils, black currant seed oil soluble fiber - psyllium seed husks and powder, apple or citrus pectin, the rice derived gamma oryzanol, antioxidants - carotenoids, B complex, vitamin C, E, zinc, selenium, germanium, Coenzyme Q10, bioflavonoids, especially quercetin, catechin, hesperidin, rutin and proanthocyanidins (pycnogenols, grape seed extract, pine bark extract, bilberry) herbs and plant extracts - kudzu, various high chlorophyll containing green drinks like spirulina, chlorella and blue green algae, burdock, slippery elm, Turkish rhubarb, sheep sorrel, licorice root, ginger root, goldenseal, bismuth and bentonite. Combination Green Foods - two excellent products are Green Life (Bioquest) and Greens Plus (Supplements Plus)”

The website quoted above is provided by the American Fitness Professionals & Associates. For more information about AFPA, they can be contacted at:

P O Box 214

Ship Bottom, NJ 08008

(609) 978-7583

afpa@afpafitness.com

I personally feel this is a site that can be trusted, but it is up to each individual to evaluate the validity of the information they provide. Their mission statement is:

“To provide Excellence in Education that is both practical and scientifically up to date for today's Health & Fitness Professionals, & Enthusiasts. AFPA's certification training programs & correspondence courses are based on the most current principals in Exercise Science, Sports Medicine , and Applied Human Nutrition.

Our primary goal is to provide an affordable educational experience that is both practical and functional for the fitness professional and the general public. The foundation of AFPA is over 35 years of combined experience in the fitness and sports medicine field. With over 65 faculty members and representatives throughout the United States, and internationally.”

I did not find commercial advertising on this site other than for the educational services they offer. They do not seem to be a non-profit organization.

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.

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. The following information shows these similarities, as well as some possible differences:

Celiac Disease

(Source: http://www.csaceliacs.org/)

“What is Celiac Disease?

Celiac disease (CD) is a genetic disorder. In people with CD, eating certain types of protein, called gluten, sets off an autoimmune response that causes damage to the small intestine. This, in turn, causes the small intestine to lose its ability to absorb the nutrients found in food, leading to malnutrition and a variety of other complications.

The offending protein, gluten, is found in wheat, barley, rye, and to a lesser extent, oats (WBRO). Related proteins are found in triticale, spelt, kamut. Refer to grains and flours for a more extensive list of both safe and offending grains.

Celiac Disease is:

* a genetic, inheritable disease.
* linked to genetically transmitted histocompatibility cell antigens (HLA DR3-DQ2, DR5/7 DQ2, and DR4-DQ8).
* COMMON. Approximately 1 in 133 people have CD, however, only about 3% of these have been diagnosed. This means that there are over 2.1 million undiagnosed people with celiac disease in the United States.
* characterized by damage to the mucosal lining of the small intestine which is known as villous atrophy.
* responsible for the malabsorption of nutrients resulting in malnutrition.
* linked to skin blisters known as dermatitis herpetiformis (DH).
* not age-dependent. It may become active at any age.

Celiac Disease is NOT:

* simply a food allergy.
* an idiosyncratic reaction to food proteins (mediated by IgE).
* typified by a rapid histamine-type reaction (such as bronchospasm, urticaria, etc.).

The Damaging Proteins

The term "gluten" is, in a sense, a generic term for the storage proteins that are found in grains. In reality, each type of protein - gliadin in wheat, secalin in rye, hordein in barley, avenin in oats, zein in corn and oryzenin in rice - is slightly different from the others. The "gluten" in wheat, rye, barley, and in a much lower amount, oats, contains particular amino acid sequences that are harmful to persons with celiac disease. The damaging proteins are particularly rich in proline and glutamine (especially the amino acid sequences which are in the following orders: Pro-Ser-Gln-Gln and Gln-Gln-Gln-Pro). As peptides, some such as 33-MER, cannot be broken down any further. In people with celiac disease, 33-MER stimulates T-cells to produce antibodies. The antibodies, in turn, attack the villi in the small intestine, reducing their ability to absorb nutrients. It is important to note that these sequences are NOT found in the proteins of corn and rice.

The Nature of the Injury

The damage to the small intestine (the jejunum) caused by this disease is very slow to develop and is insidious. It is:

* almost certainly mediated by the immune system.
* associated with ANTIBODIES to gliadin, reticulin and/or endomysial (smooth muscle) proteins.
* probably not directly caused by the antibodies, though they may be signals for cell-mediated immunity.
* probably produced by the cellular immune system (T cells) - but only when gluten-type prolamins are present.
* reversible, in most cases, to completely normal bowel function, if the injurious protein is excluded from the diet.

How Does One "Catch" Celiac Disease?

Celiac disease cannot be "caught," but rather the potential for CD may be in the body from birth. Its onset is not confined to a particular age range or gender, although more women are diagnosed than men. It is not known exactly what activates the disease, however three things are required for a person to develop CD:

* A genetic disposition: being born with the necessary genes. The Human Leukocyte Antigen (HLA) genes specifically linked to celiac disease are DR3, DQ2 and DQ8.
* A trigger: some environmental, emotional or physical event in one’s life. While triggering factors are not fully understood, possibilities include, but are not limited to adding solids to a baby’s diet, going through puberty, enduring a surgery or pregnancy, experiencing a stressful situation, catching a virus, increasing WBRO products in the diet, or developing a bacterial infection to which the immune system responds inappropriately.
* A diet: containing WBRO, or any of their derivatives.

Summary

Celiac disease is life-long and currently incurable. The only known treatment at this time is strict adherence to a gluten-free lifestyle, free of WBRO.”

(From another page on the same website:)

“What are the Symptoms of Celiac Disease?

The symptoms of celiac disease (CD) vary so widely among patients that there is no such thing as a "typical celiac." The amount of intestinal damage that has occurred and the length of time nutrient absorption has been abnormal seem to be the factors that determine the type and severity of symptoms experienced. It is interesting to note that some people with CD report no symptoms at all.

Celiac disease is one of the great mimics in gastroenterology in particular and medicine in general. Of 100 patients with CD, just over 10 percent present with classical overt symptoms of malabsorption such as weight loss, diarrhea and nutritional deficiencies. About 10 percent are incorrectly diagnosed for some length of time, in some cases years. Forty percent present in an atypical manner, which leads to lengthy delay in diagnosis. About 33 percent of patients have clinically silent disease and 7 percent have latent CD (no symptoms or small bowel lesion but will develop CD later, or had disease at an early age and resolved).

C. Robert Dahl, MD, "Celiac Disease: The Great Mimic Presentation," CSA Annual Conference, September 2000,

A. The Patient's Physical State

What are the symptoms? How long have they been present? How often do they occur?

* Abdominal cramping/bloating
* Abdominal distention
* Acidosis
* Appetite (Increased to the point of craving)
* Back pain (Such as a result of collapsed lumbar vertebrae)
* Constipation
* Decreased ability to clot blood
* Dehydration
* Diarrhea (See Stools below)
* Edema
* Electrolyte depletion
* Energy loss
* Fatigue
* Feet (Reduced fat padding)
* Flatus (Passing gas)
* Gluten ataxia
* Mouth sores or cracks in the corners
* Muscle cramping (Especially in the hands and legs)
* Night blindness
* Skin (Very dry)
* Stools (Loose? Hard? Small? Large? Foul smelling? Floating? Clay, Light tan or Gray-colored? Highly rancid? Frothy?)
* Tongue (Smooth or geographic - looks like different continents)
* Tooth enamel defects
* Weakness
* Weight loss

B. The Patient's Emotional State

What is the patient's emotional state? Is it consistent throughout the day? When and for how long do the symptoms occur?

* Depression
* Disinterested in normal activities
* Irritable
* Mood changes
* Unable to concentrate

C. Additional Conditions

What else is involved? Other diseases? Other organs?

* Amenorrhea
* Iron-deficiency anemia
* Bone disease
* Hyperparathyroidism

D. Symptoms in Children

How is the child developing?

* Slowly
* Not gaining weight
* Losing weight

Under age three:

* Growth failure
* Diarrhea
* Projectile vomiting
* Abdominal bloating/distention

Older children:

* Crankiness
* Difficulty concentrating
* Irritability
* Personality changes
* Poor memory”

This website does not appear to be commercial, and the recommended treatment is a lifelong change in diet.

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.

Candidiasis

There is an overwhelming overlap in the symptoms and diseases often associated with both Candida and HS. As such, I was sure at one point that Candida was entirely responsible for HS, but common symptoms do not prove a definite relationship. This was further stressed by the avalanche of responses I got when I proposed this idea in HS forums. Upon further investigation, I came to find out that I was not the first to put forth that idea, so I deserved a good thrashing for suggesting that Candida is THE cause of HS. I would now like to state for the record that I do NOT necessarily believe Candida to be THE cause of HS. At the current time, I consider it (most likely) to be a possible contributing factor only for some HS sufferers.

Here is some information regarding Candida:

(Source: http://www.candida-society.org.uk/)

“Candida is controversial. The medical profession denies its existence, except in very limited cases, making it very difficult to get a medical diagnosis of candida. Candida is the popular term for candidiasis (yeast overgrowth) - a condition first identified by American physicians in the 1970s.

Moderate amounts of candida (and other yeast) live in every one of us without causing any harm, but when given free rein to grow unchecked, e.g. by wiping out the surrounding bacteria with broad-spectrum antibiotics, candida can change into its fungal form and spore through the intestinal wall into the rest of the body. Once through, it rampages around the body producing a multitude of symptoms.

Common symptoms of Candida

A minority of suffers have numerous symptoms; the vast majority have thrush + a few others; not every sufferer has thrush.

Group 1: The damage to the intestinal wall allows undesirable toxins to permeate into the bloodstream. This condition called ‘leaky gut syndrome’ often leads to:

* food allergies and intolerances
* migraines
* foggy brain
* muscle aches

Group 2: Once through to the rest of the body, candida has the ability to disrupt the endocrine system causing symptoms such as:
* thrush
* cystitis
* PMS
* menstrual irregularities
* joint pains
* asthma
* hayfever
* sinusitis
* fungal infections of the nails/skin e.g. athlete’s foot
* weight gain or weight loss
* ear infections
* chronic tiredness
* allergies
* sensitivity to perfume, tobacco smoke and petrol

Group 3: Symptoms in the intestines include:
* bloatedness
* flatulence
* diarrhoea and/or constipation
* itchy anus

In addition, candida involvement has been implicated in some cases of other illnesses e.g. ME/CFS, Endometriosis.

Contributory factors

The popular perception is that candida is the consequence of antibiotics usage.The medical profession dismisses this as fantasy, saying that antibiotics could not have that effect in a healthy individual. But it may be that antibiotics act as the ‘final straw’ where health has already been compromised, most probably by one or more of the following:

* use of the contraceptive pill or HRT
* use of natural progesterone cream
* use of other steroids (hydrocortisone, prednisolone etc.)
* use of immuno-suppressive drugs
* repeated use of broad-spectrum antibiotics e.g. for acne
* dental mercury amalgam poisoning
* other heavy metal poisoning e.g. lead, cadmium
* chemical poisoning from the home, garden, workplace etc.
* hormonal changes e.g. puberty, pregnancy, menopause
* stress”

And from another site:

(Source: http://www.dermnetnz.org/fungal/candida.html) - this site is somewhat commercial.

“Candida is the name for a group of yeasts (a type of fungus) that commonly infect the skin. The name ‘candida’ refers to the white colour of the organisms in culture. Candidal infection is known as ‘candidiasis’, ‘candidosis’ or ‘moniliasis’.
Candida depends on a living host for survival. It is a normal inhabitant of the human digestive tract from early infancy, where it lives without causing any disease most of the time. However, if the host's defences are lowered, the organism can cause infection of the mucosa (the lining of the mouth, anus and genitals), the skin, and rarely, deep-seated infection.

The most common Candida (C) species to result in candidiasis is C. albicans. Other species are:
* C. tropicalis
* C. parapsilosis
* C. glabrata
* C. guilliermondii

Candidal skin infections include
* Oral candidiasis (oral thrush)
* Vulvovaginal candidiasis (genital infection in women) including cyclic vulvovaginitis
* Balanitis (penile infection)
* Intertrigo (skin fold infections)
* Napkin dermatitis (nappy or diaper rash)
* Chronic paronychia (nail fold infection)
* Onychomycosis (nail plate infection)
* Chronic mucocutaneous candidiasis

Predisposing factors for candida infection
* Infancy or old age
* Warm climate
* Occlusion e.g. plastic pants (babies), nylon pantyhose (women), dental plates
* Immune deficiencies e.g. low levels of immunoglobulins, infection with human immunodeficiency virus (HIV)
* Broad spectrum antibiotic treatment
* Contraceptive pill or injection, or pregnancy
* Chemotherapy or immunosuppressive medications such as systemic steroids
* Diabetes mellitus, Cushing's syndrome and other endocrine conditions
* Iron deficiency
* General debility e.g. from cancer or malnutrition
* Underlying skin disease e.g. psoriasis, lichen planus

Diagnosis

Microscopy and culture of skin swabs and scrapings aid in the diagnosis of candidal infections. However, candida can live on a mucosal surface quite harmlessly. It may also secondarily infect an underlying skin disorder such as psoriasis.

If you have a candida infection, consult your doctor or dermatologist for an examination and advice.”

And also, from this site:

(Source: http://www.cdc.gov/ncidod/dbmd/diseaseinfo/candidiasis_t.htm)

“Clinical Features

Oropharyngeal infection (OPC): white mucosal patches. Vulvovaginal infection (VVC): pruritus, vulval erythema, with or without discharge. Systemic infection usually presents as fever and chills unresponsive to antibacterial therapy. May manifest as renal or hepatosplenic infection, meningitis, endophthalmitis, endocarditis, osteomyelitis and/or arthritis.

Etiologic Agent

Candida albicans and C. glabrata. Less commonly, C.tropicalis, C. parapsilosis, and C. krusei. Rarely, other Candida species.

Reservoir

Forms part of the normal microbial flora of the mouth and gastrointestinal tract.

Incidence

Fourth most common cause of nosocomial bloodstream infections. Incidence is 8 cases per 100,000 in the general population. Higher incidence among neonates and African-Americans. OPC used to be a common opportunistic infection in HIV-infected persons (prior to the introduction of highly active antiretroviral therapy [HAART]). Sequelae None with appropriate antifungal therapy. Mortality rate is almost 50% with bloodstream and disseminated infection.

Transmission

Most infections are endogenous in origin, but organisms can be transmitted on the hands of care givers.

Risk Groups

Invasive disease occurs in critically ill patients in intensive-care units, in persons with severe granulocytopenia, and in hematopoietic stem cell and organ transplant recipients. OPC can be associated with HIV infection. VVC is often associated with pregnancy, diabetes mellitus, and antibiotic therapy.

Surveillance

Nosocomial disease surveillance is conducted by NNIS in selected hospitals. Active population-based surveillance for candidemia is being conducted in selected U.S. sites.

Challenges

Identifying modifiable risk factors for disease in immunocompromised and debilitated persons. Developing sensitive and specific methods for earlier diagnosis.

Opportunities

Development of rapid antigenemia and antigenuria tests and molecular probes may facilitate earlier clinical diagnosis. Availability of molecular typing methods may assist in epidemiologic studies.

December 2003”

(Source: http://www.cdc.gov/ncidod/dbmd/diseaseinfo/candidiasis_inv_g.htm)

“What is invasive candidiasis?

Invasive candidiasis is a fungal infection that occurs when Candida species enter the blood, causing bloodstream infection and then spreading throughout the body.

How common is invasive candidiasis and who can get it?

One form of invasive candidiasis, candidemia, is the fourth most common bloodstream infection among hospitalized patients in the United States.. A survey conducted at CDC found that candidemia occurs in 8 of every 100,000 persons per year. Persons at high risk for candidemia include low-birth-weight babies, surgical patients, and those whose immune systems are deficient.

What are the symptoms of invasive candidiasis?

The symptoms of invasive candidiasis are not specific. Fever and chills that do not improve after antibiotic therapy are the most common symptoms. If the infection spreads to deep organs such as kidneys, liver, bones, muscles, joints, spleen, or eyes, additional specific symptoms may develop, which vary depending on the site of infection. If the infection does not respond to treatment, the patient’s organs may fail and cause death.

How is invasive candidiasis transmitted?

Invasive candidiasis may result when a person’s own Candida organisms, normally found in the digestive tract, enter the bloodstream. On rare occasions, it can also occur when medical equipment or devices become contaminated with Candida. In either case, the infection may spread throughout the body.

How is invasive candidiasis diagnosed?

Invasive candidiasis is usually diagnosed by either culture of blood or tissue or by examining samples of infected tissue under the microscope.

How is invasive candidiasis treated?

Invasive candidiasis is usually treated with Amphotericin B given intravenously(IV) (in the vein) or with azole drugs taken by mouth or IV.”

And on the scientific side:

(Source: http://botit.botany.wisc.edu/toms_fungi/jan99.html)

“In the strictest sense of the word there are no inherently pathogenic yeasts-- those associated with human or animal disease are incapable of producing infection in the normal healthy individual. Some alteration of the host's cellular defenses, physiology, or normal flora must take place before colonization, infection, and disease production can take place. Pathogenicity among yeasts is extremely variable-- the most virulent is Candida albicans. There are also other pathogenic Candida species, as well as pathogenic species of Cryptococcus (especially C. neoformans), Torulopsis, Trichosporon, and Rhodotorula. Most of these have airborne spores or conidia and can be isolated as contaminants from skin, sputum, feces or other clinical specimens. This can lead to confusion about which organism is actually the pathogen. Only a few species in a few genera have regularly been associated with production of disease in humans or animals. In compromised host there are many others that can be opportunists.”

Overall, Candida can be intimidating. It’s just such a diverse microorganism and is so ever-present that it would be practically impossible to avoid. However, the things to concern ourselves with here are the cause of an overgrowth and possible treatments for an overgrowth. There are prescription medical treatments available, as well as dietary changes and supplements that might be effective depending on the severity of the problem. A medical diagnosis should be sought before beginning a rigorous treatment for Candida overgrowth.

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.]

Image Source: http://www.pg.com/science/skincare/Skin_tws_35.htm

However, on another website (http://health.howstuffworks.com/sweat1.htm) the following description of apocrine sweat glands is given:

“Apocrine - mostly confined to the armpits (axilla) and the anal-genital area. They typically end in hair follicles rather than pores.”

So there might be cause for additional research into the exact location of inflammation, but it is largely accepted that HS occurs in the apocrine sweat glands.

In terms of what is contained inside the inflammations, there is little information available. Some have been cultured and found to be “sterile” while others have been found to contain various bacteria. Since a single type of bacteria is not common to all cultures tested, and sometimes there is no evidence of any bacteria, bacteria is most likely not the source or cause of the fluids being present in most HS sufferers. There is very little evidence to suggest that bacteria is the cause of HS, due to the fact that (according to anecdotal accounts given in HS forums and medical information found online) antibiotics alone do not seem to cure HS. However, a few cases of HS have been claimed to have been “cured” with the use of antibiotics, but again, this information is from forum posts and there is not enough background information to prove these claims. Therefore, I do not feel that bacteria is the cause in most (certainly not all) cases of HS.

There is very little information as to whether or not cultures of HS inflammations have been tested for the presence of other pathogens, such as yeast, funguses, viruses or other microorganisms.

Therefore, we still have no information as to what the fluid in an HS inflammation contains. Could it be antibodies of some sort? I do not know what the fluid is. It is sometimes considered to contain “pus”. As the following definitions show, that could be many things.

Definition of Pus:

(Source: http://dictionary.reference.com/search?q=pus)

“1. A generally viscous, yellowish-white fluid formed in infected tissue, consisting of white blood cells, cellular debris, and necrotic tissue.

2. thick opaque usually yellowish white fluid matter formed by suppuration and composed of exudate containing leukocytes, tissue debris, and microorganisms.”

So that term doesn’t help much. The definitions are too broad and vague to really gain any insight into what the material in an HS inflammation consists of. As such, I am unable to come to any conclusions on this matter.

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.”

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.”

Given that information, it seems to be very possible that at least a small percentage of people may have been misdiagnosed. The only significant differences between HS and Fox-Fordyce disease might be that Fox-Fordyce disease tends to produce Papules, which are defined as follows:

(Source: http://dictionary.reference.com/search?q=PAPULE)

“A small, solid, usually inflammatory elevation of the skin that does not contain pus.”

“a small solid usually conical elevation of the skin caused by inflammation, accumulated secretion, or hypertrophy (a nontumorous enlargement of an organ or a tissue as a result of an increase in the size rather than the number of constituent cells) of tissue elements”

“a small inflamed elevation of skin that is nonsuppurative (as in chicken pox)”

and the lack of infection found in (presumably non-ruptured) Fox-Fordyce inflammations. 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.”

On another site:

(Source: http://www.whonamedit.com/synd.cfm/1512.html)

“A rare, chronic disease similar to prickly heat in which itchy follicular papules are present in the axillae, areola of the breast, umbilicus, pubic area, and labia majora. Pruritus is intense and sometimes almost intolerable. Almost exclusively in women, usually manifests in puberty.

Not to be confused with Fordyce’s disease, which consists of hypertrophic sebaceous glands or mucous membranes.”

I needed pictures, so here are two I found at:

Image Source: http://dermatlas.med.jhmi.edu/derm/result.cfm?Diagnosis=271470151

So the confusion goes on and on. But enough about Fox-Fordyce disease. 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.

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.

Another cause of sweat gland blockage, as it pertains to “miliaria rubrav” (not to be confused with “malaria”), or “prickly heat” was suggested on this site:

(Source: http://www.ivillage.co.uk/health/hlive/prevent/articles/0,,181165_588144-1,00.html)

“It is thought to occur when unevaporated sweat builds up on the skin in hot humid conditions so the skin becomes soggy and sweat glands are blocked. Sweat is thought to leak from the glands into surrounding tissues to trigger inflammation.

In some cases, heat rash is complicated by fungal skin infections, in which case applying an antifungal cream (e.g. one per cent clotrimazole) will help the irritation settle.”

Also, another possible cause, as it pertains to prickly heat is explored here:

(Source: http://en.wikipedia.org/wiki/Heat_rash)

“Miliaria (Prickly Heat) occurs when the sweat glands get plugged with dead skin cells and bacteria such as Staphylococcus epidermidis which are normally occuring bacteria on the skin also associated with acne. The trapped sweat leads to irritation (prickling), itching and to a rash of very small blisters, usually in a localised area of the skin.”

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.”

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.

Final note: I hope that this information is helpful and that by viewing HS and the related symptoms and diseases as a “complex” of interconnected ailments, many will find treatments for at least some of their symptoms and experience a significant improvement in their quality of life.

Sincerely,
~Jason Cameron

The information contained throughout this website is intended for educational purposes only. It is not meant to either directly or indirectly give medical advice or prescribe treatment. The information has not been scientifically validated or approved by any government or regulatory agency. Please consult with your physician or other licensed health care professional for medical diagnosis, prescription, and treatment.