An Examination Of The Possible Causes And The Known Healing Method for Hidradenitis
MEDICAL INTRODUCTION
Hidradenitis suppurativa as described in medical terms is a chronic inflammatory skin condition that affects inverse areas of the body, armpits, inner thighs, buttocks, genitals, breasts in women, hairline, stomach, nape of the neck and behind the ears.[2] Hidradenitis Suppurativa is characterized by swollen, painful, pus filled lesions that at times can grow to the size of a golf ball. The skin shows a deep-seated mixed inflammatory cell infiltrate with scarring, granulation tissue, and foreign body giant cells. Lesions may open and drain pus or blood on their own, however surgical lancing may be required for draining of the debris. Foul-smelling drainage from the fistular openings has been reported. Raised lesions are often described as brown or red in color. [2]
Authors Note- (The lesions come in all shapes, sizes, and colors, and are often seen as purple in color)
Hidradenitis Suppurativa has often been described as an "orphan disease" or rare although it has been reported by some physicians as very common with no precise cause or cure known. Because of the "orphan disease" label very little research has been done. It has been reported that there may be an existing genetic" predisposition" to develop Hidradenitis Suppurativa as it often occurs in multiple members within families. [7]
A series of detailed histopathological studies in the 1980s and 1990s prove that hidradenitis is primarily an acne-like disease of follicular occlusion where apocrine glands only become involved in the context of an intense perifollicular inflammation. The initial process was found to be one of cornification of the follicular infundibulum, followed by an early inflammatory reaction and ultimately the rupture of the involved hair follicle. This leads on to the formation of abscesses that can either subside spontaneously over a matter of days or which occasionally progress into a chronic process of cutaneous or subcutaneous tunneling, which is referred to as sinus tract formation. [8]
Knowledge of this process has given a better understanding of the disease and has helped to point towards treatment attempts resembling those successfully used in acne vulgaris. Previously many Hidradenitis patients had received treatments for presumed apocrine gland infections that had virtually no benefit at all. [8]
Stages Of Hidradenitis Suppurativa: Hidradenitis Suppurativa has been grouped into three clinical stages:
Stage 1: Single or multiple lesion formation without sinus tracts and scar formation.
Stage 2: Recurrent lesions with tract formation and scar formation with single and multiple widely spread lesions.
Stage 3: Scattered or broad involvement of multiple interconnected tracts and lesions across the entire area.
Complications Of Hidradenitis Suppurativa: Restricted limb mobility from scarring,
Lymphedema due to lymphatic injury from inflammation and scarring, Squameous Cell carcinoma (may develop in indolent sinus tracts), Arthritis secondary to inflammation injury,Anemia secondary to chronic infection
Hidradenitis Suppurativa may be observed as a primary disease without any obvious cause but has been observed with auto-immune disorders and linked with the following conditions:
Crohn Disease,Irritable bowel syndrome,Down syndrome,Certain forms of arthritis,Graves disease or Hashimoto thyroiditis,Herpes simplex,Sjogren syndrome.[37]
The signs of perianal HS may be clinically identical to the cutaneous manifestations of Crohn's Disease. CD may be complicated by a variety of skin manifestations, and HS has been reported to precede or complicate CD.[2]
Other Problems To Be Considered:Granuloma inguinale,Pilonidal cysts,Tuberculous inflammation of the skin
Lymphogranuloma venereum, Bacterial folliculitis and furunculosis.[2]
Observations In Hidradenitis Suppurativa
·Recently, a subtype of neutrophil-rich CD30- positive anaplastic large cell lymphoma has been described, which may enter the differential diagnosis of cutaneous neutrophil-rich inflammatory infiltrates. A study of atypical CD30-positive lymphoid cells was done in five eosinophil-rich and 23 neutrophil-rich nonneoplastic skin infiltrates. Hidradenitis Suppurativa was included in the 9 inflammatory neutrophil-rich cases. The study concluded that Atypical CD30-positive cells were found in 8 of 9 neutrophil-rich inflammatory conditions. [1]
·Host-defense defects in patients with Hidradenitis Suppurativa have been suspected but not yet proven. Hyper-reactive Neutrophils have been proposed to be of pathophysiologic importance in many chronic inflammatory diseases involving the destruction of the surrounding tissue by the simultaneous release of reactive oxygen species and active protease. The higher sensitivity of PKC to PMA in patients with HS is unlikely to have been induced by the disease and its local lesions because the systemic effects were minor in the quiescent state. Therefore, a defect in the function of the neutrophils might be of pathogenic importance in Hidradenitis Suppurativa. [2]
·An abnormal end-organ response to normal circulating levels of androgens is proposed. On the other hand, sebum excretion is not an important factor in the development of HS. Thus hormonal influence remains controversial. [2]
·Glucose tolerance, clinical, microbiologic, and immunologic features and HLA frequencies in 27 people. The frequency of HLA-A and HLA-B antigen loci and the median values of peripheral blood T lymphocytes are similar to the control population. However, seven patients with moderate or severe clinical disease had a marked reduction in T Lymphocytes and theses patients had an increased frequency of the HLA antigens, A1 and B8. This study suggests that T lymphocytes may play a role in the pathogenesis of Hidradenitis Suppurativa and that HLA-A1 and HLA-B8 may predispose the patient to more severe disease, but further research is necessary to clarify this. [3]
·Granulomatous Hidradenitis Suppurativa and cutaneous Crohn Disease. This study showed that, although foreign body type granulomas are common findings in hidradenitis, the presence of discrete epithelioid granulomas in the dermis away from the site activate inflammation is unusual and should alert the pathologist to the possibility of systemic granulomatous disease such as crohn disease or sarcoidosis. Foreign body type granulomas were identified in 25% of the reactions adjacent to ruptured hair follicles, sinus tracts or nearby degenerate sweat glands. [4]
·The inflammatory infiltrate found in Hidradenitis Suppurativa is composed of neutrophils, lymphocytes, plasma cells, and occasionally eosinophils. Active formation around the sweat glands is less common than inflammation around the hair follicles. Apocrine gland destruction by neutrophils is occasionally observed. Abscess formation occurs, leading to the destruction of the pilosebaceous unit and eventually the other adnexal structures. Chronic lesions have a dermis with an inflammatory cell infiltrate and foreign body-type granulomas around the hair follicles and sinus tracts. The presence of epithelioid granulomas in so-called granulomatuous Hidradenitis Suppurativa should alert one to the possibility of coexisting granulomatuous disease such as Crohn Disease or Sarcoidosis. [2]
MEDICAL TREATMENTS FOR HIDRADENITIS SUPPURATIVA:
Medical therapy is of limited value once HS has progressed past its early stage. [5]
The surgical option of choice for late stage Hidradenitis Suppurativa is wide local excision with healing by secondary intention. [6] It should always be remembered that surgery, even if extensive, can never be curative, as the disease can erupt outside the operation area at a later stage. [8]
Treatment of Hidradenitis Suppurativa remains a challenge. Therapeutic options for Hidradenitis Suppurativa are the use of local disinfectants and systemic antibiotics, as well as repeated incisions and drainage, which produce only short-term benefits. Medical management is recommended in early stages, whereas surgery should be performed as early as possible after the formation of abscesses, fistulas, scars and sinus tracts. [2]
DRUG CATEGORY
Antibiotics- Some authors advocate long-term treatment with systemic antibiotics such as tetracycline, minocycline, clindamycin, and erythromycin in combination with metronidazole. Mild topical steroid creams in combination with topical antibiotics in the aminoglycoside group such as clindamycin 2% solution and erythromycin 3% gel, have been favored. No evidence suggest that the long-term use of antibiotics alters the natural course of Hidradenitis Suppurativa. [2] Retinoids- Vitamin A derivative. Encourage cellular differentiation, they are anti-proliferative, and they serve as immunomodulators. Retinoids may be useful only as an adjunct to reduce inflammation before and after surgery. [2] Sulfones- These agents have anti-inflammatory effects. Because dapsone is less teratogenic than other drugs, it may be the preferred option in young women with Hidradenitis Suppurativa. [2] Corticosteroids- These agents have anti-inflammatory properties and cause profound varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli. [2]
Hormones- Combined treatment of antiandrogen, cyproterone acetate, and oestradiol have been shown to be of benefit to women with long standing Hidradenitis Suppurativa. Treatment with antiandrogen cyproterone acetate in combination with estrogen ethinyl estradiol in combination with low-dose progestin norgestrel may significantly improve disease activity, especially in patients with mild forms of Hidradenitis Suppurativa, but many conditions fail to respond to theses treatments. [2]
DIET: Patients who are obese should be advised to lose weight. [2]
ACTIVITY: Some patients can obtain relief from their condition by making certain lifestyle changes and by engaging in activities, such as swimming, bathing, avoiding smoking, and wearing loose-fitting clothing. [2]
ALTERNATIVE INTRODUCTION:
These alternative findings and successful treatments are the results of layperson research done by a natural healer, through working with over 100 Hidradenitis Suppurativa cases. These findings and successful treatments have been documented over a 3-year period. The results and observations through alternative treatment conclude complete remission of Hidradenitis Suppurativa, which include the author, (a past sufferer of Hidradenitis Suppurativa for 7 years), and/ or extreme improvement to complete healing of Hidradenitis Suppurativa in most other participants in the program.
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HIDRADENITIS SUPPURATIVA
The term Hidradenitis comes from "hidros", meaning sweat "adeno" meaning gland. The ending- "itis" indicates an "inflammation of". The word suppurativa or suppurative defines the formation of pus within tissues or organs, result is an abscess. Pus is mostly dead neutrophils.
In Hidradenitis Suppurativa this chronic inflammation and pus formation has traditionally been classified as a disease of the apocrine gland. However, results of a heterogeneous histological picture was found that Apocrine glands were only involved in a minority of 60 specimens, 17 showed poral occlusion, 17 simple follicilitis without poral occlusion, 9 sinus tracts, 6 epithelial cysts, 5 abscess, 3 apocrinitis, 2 diffuse dermal inflammation, and 1 pyogenic granuloma and scaring. Secondary involvement of Aprocrine glands was found in only 12% of all specimens, and secondary involvement of Eccrine glands was found in 25%. The conclusion was the clinical picture of Hidradenitis Suppurativa covers a broad histological spectrum. The disease appears to be predominantly follicular, and Aprocrine glands appear to be primarily involved in only a minority of axillary lesions. [9]
Another study found that T cells predominated in the lymphocytic cell population. A high percentage of HLA-DR (HLA= Human Leukocyte antigen) positive lymphocytes were found in an inverse relationship with Leu-8 positive lymphocytes. Additionally, a sharp decline in the T-helper/suppressor ration was observed after the initiation. [10]
A study concluded that Atypical CD30-positive cells were found in 8 of 9 neutrophil-rich inflammatory conditions, Hidradenitis Suppurativa was
Hidradenitis Suppurativa was included in the 9 inflammatory neutrophil-rich cases. [11]
Again host-defense (immune) defects in patients with Hidradenitis Suppurativa have been suspected but not yet proven. Hyper-reactive Neutrophils have been proposed to be of pathophysiologic importance in many chronic inflammatory diseases, therefore, a defect in the function of the neutrophils might be of pathogenic importance in Hidradenitis Suppurativa. The inflammatory infiltrate found in Hidradenitis Suppurativa is composed of neutrophils, lymphocytes, plasma cells, and occasionally eosinophils. Chronic lesions have a dermis with an inflammatory cell infiltrate and foreign body-type granulomas around the hair follicles and sinus tracts. . The presence of epithelioid granulomas in so-called granulomatuous Hidradenitis Suppurativa should alert one to the possibility of coexisting granulomatuous disease such as Crohn Disease or Sarcoidosis. [2]
SCIENTIFIC EXPLANATION OF FINDINGS IN HIDRADENITIS SUPPURATIVA LAYPERSONS/NATURAL HEALERS FINDINGS AND EXPLANATION:
In order to give an explanation to the medical findings in Hidradenitis Suppurativa, we must go through each part of the Immune system and the Immune response and reactions to foreign antigens starting with a brief explanation of the immune system and its functions, to the final outcome of what we believe provokes Hidradenitis Suppurativa to occur explaining each process according to scientific studies of the body's function and the findings in Hidradenitis Suppurativa as explained in the first part of this report and as listed above. We will then explain the alternative treatments used that have been reported to produce complete remission of Hidradenitis Suppurativa and/or extreme improvement to complete healing of Hidradenitis Suppurativa in most other participants in the program.
The Immune System:
The human body is one of the greatest wonders of nature and the immune system is designed to defend the body against foreign antigens that invade it.
An Antigen is a substance that can elicit an immune response through association to specific T and B receptor. These antigens may be contained within or on bacteria, viruses, other microorganisms, or cancer cells. Antigens may also exist on their own- for example, as pollen or food molecules. A normal immune response consists of recognizing a foreign antigen, mobilizing forces to defend against it, and attacking it. There are many substances, which can bind with antibodies or lymphocytes. The bigger and more complex an antigen is, the more likely it is to be capable of starting the specific immune response (which makes it an immunogen). All known biochemical families of compounds- such as carbohydrates, lipids, proteins, and nucleic acids, as well as drugs, antibiotics, food additives, cosmetics and small synthetic peptides can be antigens. Proteins, being the largest and most complex, are most immunogenic. Carbohydrates (polysaccharides) are second most immunogenic. Others such as lipids, drugs, antibiotics and nucleic acids are poor immunogens, but can become immunogenic if bound to a carrier protein.
How Does The Body Recognize That The Antigen Is Foreign?
Glycoproteins in the cell membrane of the body's cells are necessary for self-recognition; if the proteins are not self, the body then assumes that they are foreign and will attack them.
Major Organs Of The Immune:
1. Thymus- Organ located in the upper chest. Immature lymphocytes leave the bone marrow and find their way to the thymus where they are "educated" to become mature T-lymphocytes.
2. Liver- Major organ responsible for synthesizing proteins of the complement system. In addition, it contains large numbers of phagocytic cells which ingest bacteria in the blood as it passes through the liver. Detoxification of chemical elements whether ingested or inhaled.
3. Bone Marrow- Is the location where all cells of the immune system begin their development from primitive stem cells.
4. Tonsils- Collections of lymphocytes in the throat.
5. Lymph Nodes- Collections of B-lymphocytes and T-lymphocytes throughout the body. Lymph nodes are one of the major sites of antibody formation.
6. Spleen- Collection of T-lymphocytes, B-lymphocytes, and monocytes located mid-stream in the blood.
7. Blood- Circulatory system that carries cells and proteins of the immune system for one part of the body to the other.
The normal immune system has two "arms" non-specific ( innate) immune response to initial infection and specific (adaptive) immune response or specific to a particular antigen or pathogen. Together, these arms work to maintain normal host function and resistance to infection. Disruption of any part of this immune response can result in an inability to control infection and subsequent illness.
Foreign invaders get into our bodies through our skin, airways and digestive system.
Immune Response: Non-Specific Immunity (Innate or Natural Immunity)
You are born with Innate immunity. It is active or capable of being activated at all times. The innate immunity is the barriers that keep harmful materials from entering the body and is the first line of defense in the immune response. Innate immunity does not require prior exposure to activate a response and does not involve memory or recognition. Examples of Non-Specific protection or barriers are: Skin and mucous membranes (traps microorganisms and small particles) cough and sneeze reflex, pH of body secretions, antimicrobial enzymes, complement proteins, and cilia in lungs to sweep out bacteria or particles. Inflammation is the result of actions taken by the Non-specific immune system- neutrophils, monocytes, mast cells, basophils, and macrophages- (macrophages are monocytes which are matured into organ specific cells fixed in one location). Some examples of macrophages are Kupffer cells in the liver, Alveolar macrophages in the lungs, and histiocytes in lymphoid tissue. If an antigen gets past the external barriers, it is attacked and destroyed by other parts of the immune system.
Specific Immune System: (Adaptive or Acquired Immune Response)
You develop specific immunity throughout life. Specific immunity is the mechanism that provides protection against specific types of bacterial or toxins and involves recognition and memory. Can tell self from non-self. The cells involved are Lymphocytes, which produce antibodies and lymphokines and requires a prior exposure to an antigen. It takes about 10 days or so before we make effective antibodies. In the secondary response, we quickly develop lots of antibodies and kill the organism without getting sick. The response developed is specific for just that antigen, and does not work against any other antigen. The specific immune system is more advanced that the non-specific system. It is made up of two major components:
Cellular (Cell-Mediated-T Cells) and Humoral (Antibody-Mediated-B-Cells)
Cell-Mediated- This response requires the T-Cells that are produced in bone marrow but mature in the Thymus. Cell-Mediated immunity defense activities are carried out by specialized T-Cells that circulate through the body. They defend against: bacteria, fungi and protozoans, own cancer cells and tissue transplant. Delayed type hypersensitivity reactions are antigen-specific, cell-mediated immune response which, depending on the antigen involved; mediate beneficial (resistance to viruses, bacteria, fungi, and tumors) or harmful (allergic dermatitis, autoimmunity) aspects of the immune function.
Humoral Immunity- The humoral immune responses require B-Cells which are also produced in bone marrow, however unlike T-Cells they under go maturity in the bone marrow. Humoral immunity results in the production of antibodies that circulate around the body in blood and lymph (humors) and defend against free bacteria and viruses. B-Cells respond to antigen by producing antibodies.
The Cells Of The Immune Network:
Immune cells circulating in the blood are called White Blood Cells this group includes: lymphocytes, neutrophils, eosinophils, basophils, and monocytes.
Example Of A Immune Response:This is a good example of the Immune Response to foreign antigen from: Stephen J. Gislason MD- The Book Of Allergy and Immunology
Imagine (but do not do) an experiment: make a small incision in the skin of your arm and place a few fibers of meat (eg. Scraping from the surface of a steak) in the incision; tape the incision closed and cover with a protective dressing; observe at daily intervals. The meat fibers include muscle cell components from an animal whose tissue is foreign to yours. Many of these cell components will act as antigens. Immune cells will swarm around the foreign cells and within 48 hours, local inflammation will set in. The small wound will swell and fester. The typical signs of inflammation, redness, swelling, pain, and heat will persist for many days, leaving a scarred lump behind as a permanent reminder of the event. This experiment would illustrate the transplant rejection reaction. Similar zones of inflammation can be set up in your tissues by meat-fiber antigens arriving via an internal route. [12]
Inflammatory Response:
The inflammatory response (inflammation) is part of the (non-specific) innate immunity. It occurs when bacteria, trauma, toxins, heat, or any other cause injures tissues. Inflammation means, "to set on fire" and is divided into acute inflammation or chronic inflammation and repair.
The cells present (inflammatory infiltrate) in an area of inflammation determines how to classify it. If the infiltrate is composed predominantly of neutrophils and some macrophages, it is called acute inflammation. If the infiltrate is composed of macrophages, lymphocytes, and or plasma cells, it is called chronic inflammation. Chronic meaning can last for weeks, months or years.
The Cells Of Inflammation:
Neutrophil- (polymorphonuclear leukocyte, poly, PMN) Usually the first cell on the scene.
Eosinophils- These cells are more durable than neutrophils. They arrive on the scene later and last longer.
Lymphocyte- (lymph's) Usually a marker of chronic inflammation. Recognized by its single nucleus and scant cytoplasmic rim.
Macrophage- (histiocyte, macs) These are large, mononuclear phagocytic cells; hence the name macrophage. Macrophages may fuse to form giant cells in response to indigestible microorganisms or foreign material.
Plasma Cells- These are terminally differentiated B-lymphocytes which are producing antibody. They are seen later in the inflammatory response (chronic inflammation) and indicate that an antigenic stimulus is present in the injury.
Endothelial Cells- Neo-vascularization (angiogenesis) of an idealized tissue defect occurs approximately 3 days into the inflammation response (repair stage).
Fibroblast- These cells manufacture collagen. Proliferating fibroblast are the other key components of granulation tissue.
The obvious signs of inflammation are: redness, swelling, heat, pain and loss of movement or function. The fourth cardinal sign (pain) is the result of increased pressure in the interstitium due to edema. Pain fibers are stimulated through pressure receptors but also may be stimulated by the direct effects of bradykinin, a plasma protease end product of the kinin system.
Chemicals including histamine (first chemical mediator) bradykinin, serotonin, and others are released by damaged tissue. These chemicals cause blood vessels to leak fluid into the tissues, resulting in localized swelling. This helps isolate the antigen from further contact with body tissue.
The chemicals also attract white blood cells that eat microorganisms and dead or damaged cells. The process where these white blood cells surround, engulf and destroy antigen is called phagocytosis, and the cells are collectively referred to as phagocytes. Phagocytes eventually die and pus (referred to as pyogenic; pyo= pus; genic= producing synonym: suppurative) a thick, yellowish fluid composed dead tissue, dead bacteria, live and dead phagocytes, and remnants of the offending organism.
Inflammatory Lesions- Inflammatory reactions result in the production of lesions, which vary according to level of severity.
Types Of Lesions:
Abscesses- Localized spherical lesions filled with pus and pyogenic bacteria (usually staphylococci). Found in many areas of the body including: skin (boils, furuncles and carbuncles), teeth, appendix, bowel, breasts, and lung.
Empyema- Pus that fills pleural cavity.
Cellulitis- Spreading diffuse infection most commonly involving streptococcal infection of subcutaneous tissues.
Ulcers- Depressed or excavated lesions on skin or mucosa that may appear anywhere in the body and may involve many types of organs.
Inflammatory Repair:The cellular response is primarily responsible for neutralizing the injury or injurious agent then cleaning up the debris. Once this is accomplished, there will be a tissue defect that needs to be reconstituted. Granulation tissue will fill the defect and is the common pathway in repair. Eventually, many of the blood vessels regress and all that left is collagen and the excess collagen or fibrosis is recognized as a scar or as scar tissue. When inflammation goes awry recruitment of inflammatory cells and secretion of growth factors may cause over-exuberant granulation tissue with subsequent scarring. The inflammatory system may also be an unwitting accessory in processes such as fistula formation (e.g. inflammatory bowel disease), atherosclerotic plaques, autoimmune diseases, and immune hypersensitivity responses.
Chronic Inflammation is also a product of Delayed Type Hypersensitivity mechanism (cell-mediated immunity).
GASTROINTESTINAL TRACT AND IMMUNITY:
The lining of the gastrointestinal tract, from the mouth to the anus, is covered by mucosal barrier, and provides the first line immune defense against pathogens and a mechanism for proper recognition and processing of food antigens. The muscosal barrier contains specific adaptive immune defenses. IgA is the predominant antibody in the mucosal immune system.
Most antigens, particularly viruses, enter the body through the mucosal epithelia where they are carried by different lymphatics to regional lymph nodes for presentation to the immune system.
The gastrointestinal tract performs the complex functions of digesting and absorbing nutrients into the body while eliminating harmful substances. When this function breaks down as a result of stresses from improper nutrition, toxins and or emotional factors or illness, a combination of inadequate absorption of nutrients and increased absorption of undesirable elements in the bowel can lead to abnormal immunologic responses that result in inflammatory conditions. [13]
When the intestinal mucosa becomes inflamed it becomes more vulnerable. When the mucosal barrier is sufficiently compromised, the integrity of the bowel itself becomes compromised resulting in increased vulnerability to foreign or gut-derived antigens, allowing them to leak through the gut into the lymphatics and the systemic circulation.
Once the antigens have entered the blood they are no longer subjected to the action of the digestive tract and must be eliminated by the immune system. Acting as foreign invaders, they can target specific organs, produce pain, and an inflammatory immune response. This process is enhanced by the deposition of immune complexes in the tissues.[14]
RELATIONSHIP OF FINDINGS TO HIDRADENITIS SUPPURATIVA
The object of this report is to compare the medical observations of Hidradenitis Suppurativa to an immune related response that we found could well be described as a Delayed Type Hypersensitivity immune response to antigens. We did this by the gathering of scientific studies, biology textbooks, and other medical scientific studies. We then processed the sources for the information we found and assessed their reliability by comparing the information provided, that found a consistency in the studies for this explanation.
What we have found in the Hidradenitis Suppurativa medical findings done on the patient, which are outlined on the first page of this report are as follows:
CD30-positive cells were found in 8 of 9 neutrophil-rich inflammatory conditions Hidradenitis Suppurativa was included in this study.
CD30 cells are well recognized as a marker expressed by a heterogeneous group of lymphomas and in several immune responses and autoimmune disorders. A soluble form of CD30 (sCD30) is released into the blood stream after activation of CD30+ T Cells. In the likely event that CD30 and its soluble counterpart prove to contribute to the pathogenesis in TH2 related diseases such as allergy. It was found that patients with allergic disease have higher numbers of circulating, activated allergen-specific T cells bearing the activation markers CD25 and CD30. [16 and 17]
Hidradenitis Suppurativa is also observed with the following conditions:
Certain Forms Of Arthritis- There are many forms of arthritis, rheumatoid arthritis results from the type III hypersensitivity reaction, where B cells in the joints produce autoantibodies against collagen that covers joint surfaces. The resulting immune complexes and complement bind mast cells then release inflammatory chemicals.
Irritable Bowel Syndrome- Described as Type IV T-cell mediated delayed type hypersensitivity resulting from food intolerance with persistent antigen stimulation activating the immune response in the intestinal mucosa. Immunology is an actively studied aspect in Irritable Bowel. Disturbance of immune reaction has been observed in the patients, such as increased numbers of immune cells in lamina propria, the demonstration of humoral and cellular immune activation, and association to other immunereiated diseases. Thus, abnormalities of the intestinal mucosal immune function has been postulated to explain the clinical nature of Irritable Bowel Syndrome. [21]
Sarcoidosis- The etiology of sarcoidois is unknown, but several immune aberrations have been noted and are thought to play a role in its pathogenesis. Reduced delayed-type hypersensitivity responses are also found in many patients with sarcoidosis. [18]
Graves Disease Or Hashimoto Thyroiditis- Graves Disease is a Type II hypersensitivity which is antibody mediated. Patients with Graves Disease
also usually have inflammation and hypertrophy of the retro-ocular soft tissue, and so this disease is not strictly limited to the thyroid. At the other end of the spectrum, Hashimoto's Thyroiditis is characterized by inflammation and enlargement of the thyroid with eventual destruction of the thyroid tissue and hypothyroidism. These patients usually have more antibody and cytotoxic T cells which destroy thyroid tissue. [19]
Crohn's Disease- Is a chronic inflammatory disorder of the gastrointestinal tract. Crohn's Disease is considered to be the consequence of delayed-type hypersensitivity reaction. [22] Immune-mediated diseases affecting the intestine can be due to either a failure to establish tolerance (to food antigens), or a breakdown in tolerance (to gut bacteria). Bacterial-sized micropatricles are potent adjuvant's in model antigen-mediated immune responses and are increasingly associated with disease. Microparticles and aluminosilicate accumulate in macrophages of human gut-associated lymphoid tissue where the earliest signs of lesions in Crohn's disease are observed. [24] Crohn's Disease is an example of disease that attributes to the breakdown in tolerance to member of gut bacterial flora. [23]
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HIDRADENITIS SUPPURATIVA FINDINGS AND NATURAL TREATMENT
What we have found in our research and studies is a pattern of cell mediated immune response or reaction in Hidradenitis Suppurativa.
In over 3 years of working with Hidradenitis Suppurativa sufferers as natural healers we have observed the following conditions that accompany this disease, that were reported to us by the sufferer: Irritable Bowel, Crohn's, MS, Lupus, Arthritis, High Blood Pressure, Type II Diabetes, Insulin Resistance, Acid Reflux Disease and Cancer- (very low only 2 cases known to us).
Other conditions reported are: Yeast infection, fungal infection, pain in joints, fatigue, Headaches, Anxiety, Less resistance to viruses and bacteria (i.e. catching everything that goes around), hormonal imbalances and loss of menses, Slower Wound Healing, Allergies, Dental problems (bad teeth) Itchy Skin, Adult Acne, Cysts, and other skin conditions. All of these conditions being reported to occur as chronic. The majority of Hidradenitis Suppurativa sufferers we work with also report being overweight and most being extremely overweight, however we have seen a few cases of being ideal weight or underweight, this figure of cases being very low.
Foods reported that cause a reaction or flare of Hidradenitis lesions included: Cow dairy products, Chocolate, Fried Foods that are fried in hydrogenated oil such as fast foods, Pork, Red Meats, Smoked Meats, Salty Foods, White flour breads and products, Refined Sugar and products containing refined sugars such as, cakes, candies (chocolate), and pies. Some reactions reported to tropical fruits. Alcohol, coffee and other drinks containing caffeine have also been reported as causing major flares in (HS). There have been some reports of known sensitivities to gluten.
Results of Hidradenitis Suppurativa patient survey at HS-USA total of 1685 respondents as to this date 10/29/04. Gender responses being 87% female (1463) and 12% male (206) with dominate age being 31-40 34% (573) and highest percent (1314) 78% being of Caucasian heritage.
Out of this survey result 794 (47%) HS patients answered yes to having allergies. Other conditions results are: Crohn's (24) 1%, Irritable bowel (311) 18%, Arthritis (234) 14%, Lupus (10) 1%, Multiple Sclerosis (12) 1%, Diabetes (134) 8%, Pilonidal Cysts (218) 13%, Fibromyalgia (72) 4%, Anemia (231) 14%, Acne/Chloracne/ Rosacea (567) 34%, Asthma or other respiratory disease (329) 20%, Exczema/Rashes/ Other skin Conditions (398) 24%.
We can well see that the results from this patient survey and the actual HS cases that we have worked with as natural healers along with the medical findings in Hidradenitis Suppurativa that the disease could well be described as an immune response hypersensitivity. We can also conclude that from the cells found in HS patients that we are definitely creating an immune response from antigen presentation. We can see from the survey results of 749 known allergies reported. This number already conclusive on its own, however if we were to include the unknown allergies and the fact that Crohn's disease and Irritable bowel disease are already classified as T-cell mediated delayed hypersensitivities that the survey results for allergies would be considerably higher.
CD-30 positive cells found in Hidradenitis Suppurativa also states that patients bearing CD25 and CD30 activation markers have higher numbers of circulating, activated allergen-specific T cells. CD30 cells are well recognized as a marker expressed by a heterogeneous group of lymphomas and in several immune responses and autoimmune disorders. We also know that Hidradenitis Suppurativa is a chronic inflammatory disease. The inflammatory infiltrate found in Hidradenitis Suppurativa is composed of neutrophils, lymphocytes, plasma cells, and occasionally eosinophils.
Neutrophils live only a few hours in the blood; some migrate to the tissues to areas of infection or injury. They are phagocytic and engulf and digest bacteria and other microorganisms or microscopic particles.
Lymphocytes are produced in the bone marrow and enter the circulation through lymphatic channels that drain into the venous system of the blood and are found in large number in the lymph nodes, tonsils, thymus, spleen and lymphoid tissue of the gastrointestinal tract. There are two major classes of lymphocytes: B Lymphocytes, which after activation differentiate into plasma cells, which secrete antibodies (immunoglobulins) and T-Cells which participate in what is called cell-mediated immune responses. Once a mature B cell encounters the appropriate antigen, the cell differentiates to form a Plasma Cell.
Eosinophils are motile and phagocytic and migrate into the tissues. They are particularly important in the defense against parasites, and they participate in hypersensitivity inflammatory (allergic) reactions.
These cells are all involved in immune response. We have presented Hidradenitis Suppurativa as a Type IV Delayed Type Hypersensitivity immune response. However, in hypersensitivity reactions, there may be more than one type involved.
TypeIV Delayed Type Hypersensitivity (DTH ) (T Cell-Mediated)
Delayed Type Hypersensitivity response arise 48-72 hours after exposure rather than minutes as Type I. Th 1 cells respond to antigen and release cytokines that activate macrophages and CTL s causing inflammation, death, and tissue damage. Chronic macrophage activation can cause Chronic Inflammation which often results in tissue lesions, scarring, and granuloma formation.
Stages Of Type IV Delayed Type Hypersensitivity
1. Sensitization Stage- Th cells are turned on by macrophages or skin dendritic cells. Memory Th1 cells against (DTH) antigens are made during the sensitization stage. These Th1 cells activate macrophages to trigger inflammatory response.
2. Effector Stage- Secondary contact yields Delayed Type Hypersensitivity. Th1 memory cells become activated and produce the following cytokines:
A) IFN- g activates macrophages
B) TNF- a and TNF b which causes tissue destruction, and inflammation.
C) IL-2 that activates T cells and CTLs.
D) Chemokines- for macrophage recruitment.
E) IL-3, GM-CSF for increased monocyte/macrophage production and phagocytic activity.
Inflamed area becomes red and fluid filled and forms lesion. From tissue damage there is activation of clotting cascades and tissue repair. Continuous exposure to antigen can cause Delayed Type Hypersensitivity inflammation and tissue from activated macrophages which will result in granuloma formation.
There are three other types of hypersensitivity reactions. Hypersensitivity refers to undesirable (damaging, discomfort producing and sometimes fatal) reactions produced by the normal immune system. Frequently, a particular clinical condition (disease) may involve more than one type of reaction. The other types are:
Type I Hypersensitivity- Also known as Immediate or Anaphylactic
Type ll Hypersensitivity- Also known as Cytotoxic that affects a variety of organs and tissues.
Type lll Hypersensitivity- Also known as Immune Complex that is general or may involve individual organs. [25]
While reactions between antigens and the immune system are important protective defenses, they also have the potential of injuring normal tissues and producing disease. Disorders that result from uncontrolled, exaggerated or misdirected immune responses are called Hypersensitivity Diseases. [26]
HIDRADENITIS SUPPURATIVA FINDINGS AND NATURAL TREATMENT CONTINUED
Dr. Gislason states: "Many of the major unsolved disease of our civilization are either degenerative and or inflammatory and may are recognized to be immune-mediated or Hypersensitivity Diseases. The stakes are high both for individual patients and for the society as a whole. None of the hypersensitivity diseases have been solved, and most appear to rage on, afflicting increasing number of patients with chronic disabling diseases" [12]
The term Food Sensitivity or Hypersensitivity can be defined as a clinical manifestation of an immune response in which foods, their proteins or their metabolic derivatives act as antigens and stimulate the production of cellular responses against them. [27]
We believe this to be true for the chronic supportive inflammatory condition Hidradenitis Suppurativa. The majority of sufferers are treated with Antibiotic Therapy, which has not proved to be beneficial leaving the sufferer in a worsened condition.
Antibiotics Linked In the Rise In Allergies: Results of an experiment concluded by: Gary B. Huffnagle, Ph. D., an associate professor of internal medicine and of microbiology and immunology in the U-M Medical school states; "Antibiotics knock out bacteria in the gut, allowing fungi to take over temporarily until the bacteria grow back after antibiotics are stopped. Our research indicates that altering intestinal microflora this way can lead to changes in the entire immune system which may produce symptoms elsewhere in the body."
For the study, the team gave laboratory mice a 5-day course of antibiotics to weaken bacteria found in their gastrointestinal tracts. The mice were then given a dose of the fungus Candida Albicans- increased growth of this fungus in the gut is a common side effect of antibiotic therapy. The researchers found that the mice given the antibiotics showed much greater lung sensitivity to the mold allergen and the mice that didn't receive the antibiotics were able to fight off the mold spores.
Huffnagle states; in ways scientists don't completely understand, the GI tract immune system modulates or dampens down the allergic T cells response to incoming allergens in the lungs. When antibiotics reduce the bacterial population in the GI tract, the number of yeast and other fungal organisms increase.
If we can determine exactly how microflora in the GI tract affect the immune system, it may be possible one day to prevent or treat allergies and inflammation diseases with diet changes or probiotics- dietary supplements of "healthy" bacteria to restore the normal balance of microbes in the gut "Huffnagle" adds. "In the medical community, probiotic therapy is becoming an area of increasing interest." Until then he emphasizes the importance of a healthy low-sugar diet, with lots of raw fruits and vegetables, after being treated with antibiotics to help restore the normal mix of microbes in the GI tract. Huffnagle adds: "The old saying, an apple a day keeps the doctor way " may be more true than we thought. "Once you are done with antibiotics you are not finished," adds Huffnagle. "You need to recover from the treatment itself". [32]
GUT FLORA, YEAST AND FUNGAL INFECTIONS AND IMMUNE RESPONSE
In addition to digestion of food and absorption of nutrients, the gastrointestinal tract acts as a secretory organ, and an immune sensing device responsible for immunization against incoming antigens and tolerance to frequently appearing antigens. The permeability of the GIT determines how much antigenic material get inside. The gastrointestinal tract is a common target organ, equipped with mast cells capable of anaphylactic responses. Immediate reactions may set in motion a series of events that promote systemic disease. Immediate hypersensitivity reactions may trigger delayed hypersensitivity processes both in the gastrointestinal tract and in the rest of the body. [28]
Dr. Gary Huffnagle- "We all have a unique microbial fingerprint, a specific mix of bacteria and fungi living in our stomach and intestines. Antibiotics knock out bacteria in the gut, allowing fungi to take over". "Our research indicates that alteration of intestinal microflora leads to changes in the entire immune system, which may produce symptoms elsewhere in the body. "When antibiotics wipe out the bacterial population in the GI tract, yeast and fungus move in and multiply" Fungi may secret compounds called oxylipins, which can control the type and intensity of immune response". " Having too many oxylipins may prevent the development of the regulatory T-cells, in turn allowing for hyperactive immune response against allergens. [32}
Dr. Loomis- "Inadequately digested food in the bowel is a source of irritation to the bowel wall. This irritation eventually overwhelms the protective action of macrophages in the aggregate lymphatic follicles such as Peyer's Patches, and allows inflammation of the mucosal lining of the GI tract. Inflammation increases the permeability of the gut wall for the passage of large food molecules into the blood. Once in the blood these particles have passed any possible normal digestive process since that are too large to enter the cells and be utilized as food, they must be attacked as foreign invaders. Once food particles and/or foreign matter evade and enter the blood, the initiate and immune response and if long continued, the increasing number of these particles eventually exhausts the blood's ability to keep them in circulation and they flocculate into the tissue producing inflammatory immune response. The immune response to foreign invaders is identical, being infectious or not." [29]
Crohn's Disease has often been associated with Hidradenitis Suppurativa in many medical reports.
Dr. David A. Holland- Some Scientist have directly implicated yeast and fungus toxins, called mycotoxins, as the cause of Crohn's. When Fungi become systemic from gut inflammation and the overuse of antibiotics, you can see how the whole body, eyes, liver, gallbladder, muscles, joints, kidneys and skin becomes involved. Dr Holland states: Chapter 13 of "Principles and Practice of Clinical Mycology" deals entirely with fungal infections in the gut. They describe how Blastomyces dermatitidis, a fungus, can produce "granulomatous" lesions in the intestines. Not surprisingly, this same type of lesion has also been in patients with Crohn's disease. Another fungus called Histoplasma produces intestinal disease symptoms. The common lesions seen in the gut with the fungal infection were "masses or ulcer mimicking inflammatory bowel disease. He then asks " Sound Familiar"? Most antibiotics are mycotoxins- fungal derivatives. He then states: Just smell the air on your way to work or look at the American standard diet and the number of antibiotics we consume from childhood on. Mycotoxins are commonly found in our grain food supply. Mycotoxins can suppress our normal immune function. Therefore anyone who has taken an antibiotic or consumes grains and sugars qualifies as a potentially immunocompromised person. You do not have to have cancer or aids or be on chemotherapy to have a weakened immune system. [30]
YEAST-YET AGAIN
In an interview with Dr. Lieberman, Concepts of Environmental Medicine, June 1997 (vol. 1, No 2)
Dr. Lieberman stated: When we talk initially about the word "dysbiosis" we define it as an imbalance of all microbiological flora of the gut. Dysbiosis produces a permeability dysfunction so that things, which should remain in the GI tract, are now getting through the wall in bigger pieces. Bigger pieces are more antigenic, meaning they are capable of producing and immunologic response, especially allergic response. That's how we think the mechanism of food sensitivity is being created. In regard to yeast, the yeast seems to mimic most closely endocrine tissue, especially the ovary and thyroid. Problems related to ovarian function and other female problems, because ovarian tissue and Candida Albicans are mimics of each other, is the body attempting to destroy the Candida, and is also destroying the ovary. It was Dr. Phyllis Saifer who introduced us to this concept of poly-endocrinopathymultiple endocrine glands dysfunction. She ultimately showed the common denominator was a micro-organism, Candida Albicans, causing the molecular mimicry. And she was absolutely right. It was incredible. When I first started working with these kinds of patients, I felt that diet was not the most important thing and to just use the drugs. What I found was that it don't work too well. If you really want to hold theses organisms down, the most important thing is to stop feeding them, and that is where the diet component comes in! [31]
HIDRADENITIS SUPPURATIVA FINDINGS AND NATURAL TREATMENT CONTINUED:
Gut Flora, Yeast And Fungal Infections and Immune Response:
LEAKY GUT:
Dr. Jeremy E. Kaslow; In Leaky Gut syndrome, the lining of the small intestine becomes inflamed and irritated allowing metabolic and microbial toxins normally kept within the small intestines for passage into the colon to enter the blood stream. In technical terms this is called increased intestinal permeability. This results in involvement of the liver, lymphatic system, and immune response, which includes the endocrine system to react in a protective response. Leaky Gut could be implicated as a primary contributor to asthma, food allergies, chronic sinusitis, eczema, urticaria, migraine, IBS, fungal disorders, fibromyalgia, and inflammatory joint disorders including rheumatoid arthritis. Leaky Gut Syndrome is a very common problem of modern society in part because of antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs).
Antibiotics damage the bowel environment in two ways. The first is by destroying beneficial bacteria. Beneficial bacteria metabolizes hormones (ex. Estrogen) discharged from the liver into the small intestines. If you lack the beneficial to break down estrogen and the intestinal permeability has been altered, the patient is now reabsorbing estrogens. The extra estrogen binds to sensitive areas.
The second way antibiotics damage the intestines is by promoting the growth of Candida and other fungi and yeast. The real damage done by Candida is to the epithelial barrier, allowing the absorption of toxins agents and chemicals, which then enter the blood affecting numerous organs. With leaky gut, nutrients can be absorbed before they are fully digested. The body's immune response through specific antigen-antibody markers will identify some of theses foods as foreign invaders. What started, as an irritation from yeast with shrinking of the cells has now been complicated with active inflammation every time a particular food is eaten. Any further load from intestinal toxins can saturate the liver's capacity to detoxify the poisons, and they are returned to the blood circulation. Because blood must preserve chemical homeostasis, toxic chemicals and physical debris is excreted into the tissue.
What started as gut barrier problem can escalate into a problem of tissue toxicity. When the tissue environment is compromised microbes grow, lymphatics swell, symptoms of inflammation or deposition occur.
As more microbes (viruses, bacteria, and fungi) multiply in an unhealthy GI environment, the immune is unable to keep the microbes in check. As a result, opportunistic infections take advantage of a weakened immune system. [14]
Candida Albicans is a saprophyte, a common yeast-like fungus that survives eating dead tissue. Normally this organism is present in the blood, gastrointestinal tract and vaginas. Candida also lives in the folds, creases, and wrinkles our skin. Normally it is a harmless symbiont, living in the gastroinestestinal tract and kept under control by the actions of beneficial bacteria and a healthy immune. Unfortunately, this internal ecology can easily be disrupted as we mentioned decreasing the number of beneficial bacteria as a result yeast cells quickly multiply out of control.
Factors that encourage yeasts to grow, colonize and spread systemically include:
Hormonal Imbalances: Elevated tissue levels of steroid hormones from oral contraceptives, corticosteroid therapy, pregnancy, and chronic stress.
Antibiotics: Broad-spectrum kill beneficial gut bacteria. Antibiotics and hormones in the feed of farm animals may stimulate yeast overgrowth in people when they eat meat and dairy products.
Diet: Refined foods provide sugar and simple carbohydrates that the yeast ferment for nourishment.
Infections: Recurrent bacterial infections compounded by immune system dysfunction lead to systemic candidiasis.
Environmental Toxins: Exposure to toxic agents in food, air and water.
Physical Contact::Candida can also be spread by direct contact during sexual activity and through such medical procedures as emergency-room treatments, intravenous feedings, dialysis and surgery. In one recent study of surgery patients, 40% developed Polysystemic Candidiasis.
Systemic Problems:Systemic candida is a great imitator. It can mimic much disease such as cystitis, Crohn's, gastritis, multiple sclerosis, endometriosis and various forms of mental illness. Candida maybe be part of the pathology in colitis, pancreatitis, hepatitis, cirrhosis, diabetes mellitus, malignancies, endocrinological pathologies, and autoimmune disorders. [33]
Immune Response To Fungus/Yeast:
As we have explained yeast and fungus infections can develop after recurrent bacterial infections. When the immune system is weakened and conditions are favorable in the host such as explained previously by use of antibiotics and or other drugs, surgery, and high refined and processed diets, this allows for the development of the infections starting in the intestines and thus becoming systemic.
The Immune System Will Recognize The Fungi And Create An Immune Response
Dr. Gerald J. Tritz infectious disease lecture (superficial mycoses): During the colonization phase the host begins to respond immunologically by undergoing sensitization to soluble fungal antigens. The first detectable immune response is cell-mediated immunity, which is characterized in colonized skin as intense inflammatory process and demonstrated at a trichophyton skin test site by a delayed or tuberculin-type reaction. The genesis and expression of the cell-mediated immunity to dermatophytic antigen in an infection occurs between the 10th and 35th days and heralds the beginning of the second distinct period in pathogenesis, the host-parasite interaction phase.
During the host-parasite interaction phase, cell-mediated immunity produces most of the pathology as an acute inflammatory type of dermatophytosis. The immune inflammation which results extends in a spectrum from erythema and edema of the dermis and epidermis (spongiosis) to the formation of vesicles and pustules. Epidermal integrity is breached; oozing and weeping of the tissue fluid occur. Invasion of hair follicles results in inflamed nodules, deep-seated pustules, and abscesses. [34]
*(The Author's ask the readers, does this sound Familiar?)We ask this as the question was asked of the fungus infection lesions that were found in Crohn's formation.
There are two basic types of infection. The acute or inflammatory type infection which is associated with cell-mediated immunity to the fungus, which generally heals spontaneously or responds nicely to treatment and the chronic or types of infection, which is associated with a failure to express cell-mediated immunity to the fungus site of infection, is relapsing and responds poorly to treatment [34]
Subcutaneous Mycoses
These organisms gain access to the subcutaneous tissue through traumatic implantation. Little is known about the mechanisms of the pathogenesis. Histopathologic evidence indicates that these organisms survive in the subcutaneous tissue layers by producing proteolytic enzymes and maintaining a facultative microaerophilic existence because of the lowered redox potential of the damaged tissue. In eumycotic mycetoma there is extensive tissue damage and production of purulent fluid, which exudes through numerous intercommunicating sinus tracts. [35]
The Yeast Connection:
Dr. Marjorie Crandall- The yeast connection to chronic disease was first described by the community based physicians in the late 1970's and early 1980's. Chronic intestinal candidiasis has been shown in controlled clinical studies to produce many different nonspecific symptoms. Most of these can be explained by well-understood pathogenic mechanisms in fungal infections. Several clinical laboratories have reported that abnormally high levels of anti-Candida antibodies indicate a prolonged intestinal yeast infection. Some of these labs have also found that circulating immune complexes containing Candida antigen and anti-Candida antibodies indicate the presence of an active intestinal yeast infection. One of these laboratories has also found that some anit-Candida antibodies cross-react with specific human tissue and food antigens; these cross-reacting antibodies may produce some of the systemic symptoms typically observed in chronic candidiasis patients.
Now that scientific proof for the existence of the candidiasis hypersensitivity syndrome has been published and specific diagnostic tests are available, physicians should not arbitrarily dismiss patients who suggest their symptoms must be yeast-related. Doctors who refuse to offer testing and treatment for yeast infections and yeast allergies may be condemning their patients to needless suffering and disability. [36]
SUMMARY:
Many Hidradenitis Suppurativa sufferers have displayed fungus infections in the finger and toenails, which can be readily seen and identified. We also have reports of those we help with recurring vaginal yeast infections. In one case of Hidradenitis Suppurativa blood tests showed high total White Blood Cell count with higher Neutrophils which is the first to respond to infection. Another case in a former sufferer of HS, the blood tests revealed High White Blood Cell count with higher expression of Eosinophils, (a type of white blood cell that is primarily involved and increased in allergic disease and in response to parasites). As reported the standard treatment for Hidradenitis is with antibiotic therapy, which has proven unsuccessful in that over a period of time the body, becomes resistant to antibiotics. This of course means they are unable to use these drugs as a treatment for other illness. Many HS sufferers have reported an increase of HS lesions and worsened condition after antibiotic treatment. This demonstrates the use of antibiotics as part of the actual cause of increased yeast by the killing of beneficial bacteria thus creating the immune response to the pathogen in the form of eruptions, or the classic HS lesions. The response to fungus is also described as delayed-type hypersensitivity. We have seen the number of those reporting allergies taken from the survey as relatively high. We have also reported the foods that the HS sufferer develops the immune reaction to, all which have been proven to feed yeast and fungus. We have those who suffer from hormone problems and have demonstrated how probiotics (beneficial bacteria) is important in maintaining hormone balance and how overgrowth of yeast and fungus disrupts the endocrine system. We have reported scientific facts of the immune response to undigested food particles and pathogens such as yeast and fungi. We have provided scientific proof of how antibiotics, certain foods, and environmental factors elicit this specific immune response as demonstrated in Hidradenitis Suppurativa. We have reported on various diseases that are associated with HS to have the same mechanism of immune response.
Anyone diagnosed and suffering with Hidradenitis Suppurativa knows the misery and pain that it causes. We also know what does not work for treatment and that merely trying to cover symptoms with antibiotics, immune suppression, pain pills, and anti-inflammatory drugs do not stop the progression or cure the underlying problem. We also know that surgery is only a crutch with temporary results until the HS spreads to other parts of the glandular tissue. Even if treated with anti-fungal medication without lifestyle changes, the results are not favorable. What we have done to have to stop the disease and remain free from this disease is to treat the actual problem-causing agent. As Dr. Lieberman suggested: treating with drugs alone does not work, you must stop feeding it as well. Lifestyle changes such as removing the offending foods from the diet along with replacing beneficial bacteria belonging in the gut has brought our body back into balance. Along with bringing the body back in balance by reducing or eliminating the antigens and pathogens that the HS patient is obviously creating an immune response too, we have also reduced the allergic response by re-colonizing microflora in the gut. As the body heals and pathogens are greatly reduced and stay where they belong in the body instead of getting back into the blood and lodging into tissue, other conditions such as hormone problems will be corrected as well, as demonstrated in many HS sufferers that have successfully followed the program leading to their healing.
Some people seem to have a genetic "predisposition" toward fungal infections. They may contact infections more easily than others exposed to the same conditions. Whether it is due to differences in immune response, skin chemistry, or other factors is not known. As Dr. Crandall stated: "Doctors who refuse to offer testing and treatment for yeast infections and yeast allergies may be condemning their patients to needless suffering and disability". This leaves the HS suffer to find their own treatment to rid of the condition. In our own research we have found the problem and have been able to cure from HS. We did this through natural treatment which is less harmful than using pharmaceutical drugs. Not only have we successfully treated HS in our self, we have also seen many others either completely heal from HS or experience a major reduction in lesions. Each case is different to how much a person puts into their healing and whether they are willing to change their lifestyle and stay with the changes to maintain good health and remain HS free.
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