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  Scleroderma  
 
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Scleroderma is a chronic autoimmune disease that was first described in the 18th century. The term scleroderma means "hard skin," which describes thickening of the skin from increased deposits of collagen.

There are two main types of scleroderma with a subset called CREST:
1. Localized scleroderma affects the skin in limited areas and the musculoskeletal system.
2. Systemic sclerosis causes more widespread skin changes and may be associated with internal organ damage in the lungs, heart and kidneys. It can cause arthritis, slow contractions in the gastrointestinal tract, muscle inflammation, dry eyes and dry mouth. Most people with scleroderma have cold-induced spasms of small blood vessels in their hands or feet, known as Raynaudís phenomenon, which caused the fingers or toes to turn white or blue and may be painful.

Systemic sclerosis is associated with over-activation of the immune system, which normally functions to protect the body against cancers and invading infections. This causes damage to cells that line small blood vessels, which in turn leads to the over-production of scar tissue.

In most cases, the cause of scleroderma is unknown. However, in a small minority of cases, scleroderma or scleroderma-like illnesses are associated with exposure to certain toxins or as a complication of bone marrow transplants. Scleroderma is not contagious and is rarely inherited.

Scleroderma affects women more than men and adults more than children and there are 10-20 new cases are diagnosed per million people each year. The five-year survival rate is 80 to 85%. The lung, heart and kidney can become damaged, and are the most frequent causes of severe disability and death. Many people have decreased hand function because of joint disfigurement or finger ulcers.

Diagnosis of scleroderma is based on clinical history and physical findings. Diagnosis may be delayed in those without significant skin thickening. Laboratory, X-ray and pulmonary function tests determine the extent and severity of internal organ involvement.

CREST is a form of Systemic Sclerosis (scleroderma) which is characterized by:
Calcinosis (calcium deposits), usually in the fingers;
Raynaud's;
Loss of muscle control of the Esophagus, which can cause difficulty swallowing;
Sclerodactyly, a tapering deformity of the bones of the fingers; and
Telangiectasia, small red spots on the skin of the fingers, face, or inside of the mouth.

It takes only two of the five CREST symptoms for a diagnosis of CREST (either "pure" or "plus") to be made. For example, a patient with Calcinosis and Raynaud's would have CREST (which for precision may also be written as CRest, but it is CREST nonetheless.)

PureCREST is diagnosed when patients have two or more symptoms of CREST but they do not meet the criteria for either Limited or Diffuse Scleroderma. That is, they must not have tight skin above their wrists, and if there is tight skin on their fingers, they must not have either pitting digital ulcers or lung fibrosis.

Plus CREST is when CREST symptoms appear along with another form of Scleroderma. It is referred to as "Limited Scleroderma plus CREST" or "Diffuse Scleroderma plus CREST.", for example. A person may also have any other autoimmune disease "plus CREST."

Although some doctors still believe CREST is a useful subcategory, the existing research studies have been unable to predict consistently how (or whether) the disease will progress to Diffuse Systemic Scleroderma in any specific individual.

Conventional Treatment
There is no known cure for scleroderma. No treatment has been scientifically proven to alter the overall course of the disease, although d-penicillamine is commonly used for this purpose and may be of some value.

There are a number of effective organ-specific treatments for scleroderma. Raynaudís phenomenon may be helped by calcium channel blockers. Declining renal function and hypertension are often treated with drugs. Esophageal damage from reflux of stomach contents can be treated with acid-reducing drugs. Antibiotics, special diets and medication can improve absorption of nutrients in people who have abnormalities of their intestines. Musculoskeletal pain may respond to nonsteroidal anti-inflammatory agents. Lung inflammation may be treated with cyclophosphamide.

Sclero.org provides a lot of good information about this condition.
 

 
 

Signs, symptoms & indicators of Scleroderma:
 
 
Lab Values - Cells  High ESR or elevated ESR

Lab Values - Chemistries

  (Mildly/highly) elevated ANA levels
 
 

Conditions that suggest Scleroderma:
 
 
Digestion  Delayed Gastric Emptying (Gastroparesis)
 
 

Risk factors for Scleroderma:
 
 
Autoimmune  Autoimmune Tendency
 There is an increased incidence of certain types of other autoimmune diseases and cancer among scleroderma patients.

Infections

  Nanobacteria Infection
 Researchers have identified tiny bacteria, known as nanobacteria, that may play a role in the formation of calcification found in scleroderma and other disorders. Cells infected by these bacteria develop deposits of the mineral apatite on their walls.

This is a very new field of research which is highly controversial, however it has recently attracted the attention of researchers at the Mayo Clinic and NASA. Nanobacteria have been found in kidney stones, Alzheimer's disease, heart disease, prostatitis, and some cancers.

A lot of the controversy surrounding nanobacteria has to do with its very name, in that some researchers do not believe that it represents a life form and thus cannot properly be named "bacteria", because the research on its purported nucleic acid has not been completed yet. Thus, some believe that "nanoparticles" would be a better description for it.

  CMV Infection
 Viruses have long been held to be of pathogenetic importance in the evolution of autoimmune connective tissue disease. The role of tumor necrosis factor alpha blockers in scleroderma cases temporally associated with CMV infection requires further evaluation. [PubMed. Hum Pathol. 2006, Nov 2]

  Lyme Disease
 Laboratory tests showed an infection with B. burgdorferi sensu lato that was successfully treated with intravenous ceftriaxone, an antibiotic recommended for Lyme borreliosis. This case suggests that Lyme disease should be considered in atypical cases of skin sclerosis in patients predisposed to the development of systemic scleroderma. [PubMed. J Eur Acad Dermatol Venereol. 2005 Jan;19(1):93-6]

  Mycoplasma Infection
 By Alan Cantwell, Jr., M.D. © 2000

Ask most doctors what causes scleroderma and they will tell you the cause is unknown. Furthermore, they will claim that no infectious agent has ever been shown in scleroderma. However, for more than 50 years scientific evidence has been accumulating in the medical journals showing that bacteria are indeed associated with scleroderma, and with closely allied diseases, such as lupus and rheumatoid arthritis.

In the past decade many chronic diseases once believed to be non-infectious are now thought to be caused by viruses, bacteria, or by tiny mycoplasma-like organisms which have characteristics of both bacteria and viruses. Even certain forms of cancer are now considered infectious.

Stomach ulcers were definitely thought to be non-infectious for most of the last century, and physicians and microbiologists insisted bacteria could not grow in the acid environment of the stomach. The ultimate proof that certain bacteria could cause stomach ulcer disease was obtained when a physician-researcher drank a culture of the ulcer-producing bacteria and produced the disease in himself.

It is unthinkable (but true) that decades of research showing organisms in scleroderma and arthritis would be ignored by the medical establishment. Especially now that antibiotics appear to have a beneficial effect in these diseases, it is imperative for physicians to be aware of this research and to stop pretending it does not exist.

Before reviewing the case for bacteria in scleroderma and RA, it is important to acknowledge the role of mycoplasma-like organisms in these diseases. For most of the twentieth century, medical science has regarded these bacteria-like and virus-like microbes as laboratory curiosities of little import. But mycoplasmas can invade cells and even the cell nucleus, thereby promoting chronic infection difficult to eradicate.

Mycoplasma (also known as cell-wall deficient bacteria) are derived from bacteria which have shed all or part of their cell wall. Many chronic diseases may prove to be due to infectious bacteria which transform into the mycoplasma state in order to better adapt to the body. In recent years, mycoplasmas have been discovered in such diverse diseases as Gulf War Illness, AIDS, and certain forms of cancer.

Mycoplasmas may all look and act similarly when in the cell-wall deficient phase - and if a particular mycoplasma becomes stuck in this phase and does not revert back to its original "parent" bacteria, it is impossible to determine the exact bacterial origin of the mysoplasma in question.

Mycoplasma are notoriously difficult to detect and to culture. Thus, they frequently go unrecognized in disease states. Mycoplasma research is still in its infancy, and most experts in the field are microbiologists, rather than practicing medical doctors. Nevertheless, there is a wealth of research implicating mycoplasmas in human disease. The best book on this subject is Cell Wall Deficient Forms: Stealth Pathogens, by mycoplasma expert and Professor Emeritus Lida Holmes Mattman of the Department of Biology at Wayne State University in Detroit.

The Road Back Foundation advocates the use of antibiotic therapy for scleroderma and RA, based on the mycoplasma research first undertaken in the 1940s by Thomas McPherson Brown, M.D., and his microbiologist co-worker Harold W. Clark, Ph.D., currently the Director of the Mycoplasma Research Institute of Beverly Hills, Florida.

The scientific evidence linking mycoplasma to these diseases is simply explained in Dr. Brown's book, The Road Back: Rheumatoid Arthritis, Its Cause and Treatment, [now out of print] and in Clark's Why Arthritis?: Searching for the Cause and the Cure of Rheumatoid Disease. Medical writer Henry Scammell has also authored two books based on Brown's research: The New Arthritis Breakthrough, and Scleroderma: The Proven Therapy That Can Save Your Life.

The first report of "acid-fast" bacteria (similar to the kind of microbes that cause tuberculosis) in scleroderma was published by Virginia Wuerthele-Caspe Livingston, M.D. in 1947. These unusual microbes were discovered in skin scrapings from a woman with ulcerations of the fingers. In later collaboration with pathologists, dermatologists, and microbiologists, she further characterized the peculiar and multi-shaped (pleomorphic) bacteria she consistently isolated from scleroderma cases. Her scleroderma research progressed into microbiologic studies showing similar-appearing acid-fast bacteria in various forms of cancer. Until her death in 1990 at the age of 84, Livingston constantly studied and published her findings on the various aspects of the 'sclero-bacillus' she isolated from scleroderma and the 'cancer microbes' associated with cancer. Despite the furor and controversy that her papers elicited from the cancer establishment, she never wavered in her belief that microbes were at the root of 'autoimmune' and cancerous diseases.

Livingston wrote two books about her lifelong research: Cancer: A New Breakthrough (1972), and The Conquest of Cancer (1984). Her major scientific publications (including the original scleroderma papers) and confirmatory papers by other leading scientists are collected and reprinted in Livingston's The Microbiology of Cancer, available from the Livingston-Wheeler Foundation in San Diego, California.

In 1953, Livingston's finding of bacteria in scleroderma was confirmed by scientists at the Pasteur Institute in Brussels. Additional confirmation was published in 1966 in the Archives of Dermatology, when my own research (co-authored with professors of dermatology and microbiology) showed acid-fast bacteria in the skin biopsy samples from scleroderma cases. During the 1970s and 80s nine additional papers also confirmed the presence of cell-wall deficient, mycoplasma-like microbes in the skin of scleroderma, as well as in multiple diseased organs at autopsy in a fatal case of scleroderma. Like Livingston's bacteria, the organisms we cultured from various patients were pleomorphic. In some fatal cases, the organisms cultured near death were similar to acid-fast mycobacteria associated with tuberculosis, whereas in milder cases the microbes were identified as staphlococci or corynebacteria. Using a tissue stain designed by Lida Mattman to detect acid-fast bacteria and cell-wall deficient bacteria (mycoplasma), bacteria were identified in the skin biopsy material from all cases.

Following the lead of Livingston, my scleroderma research progressed to similar studies of lupus erythematosus (another autoimmune disease) and certain forms of cancer. These studies all showed that pleomorphic bacteria, most likely in a mycoplasma state of growth within the diseased tissue, could be cultured and identified from these diseases. The results of these studies performed over a quarter-century are contained in my book, The Cancer Microbe: The Hidden Killer in Cancer, AIDS, and Other Immune Diseases. In addition, abstracts of most of these Cantwell papers can be retrieved online at the PubMed website sponsored by the National Library of Medicine ( http://www.ncbi.nlm.gov/PubMed ).

The scleroderma research of Livingston and her colleagues that began in the 1940s is undoubtedly related to current research implicating mycoplasmas in human disease. Her papers published in the 1950s clearly show pleomorphic microbes consistent with what are now known s mycoplasmas or cell wall deficient bacteria.

For the first half-century Livingston's microbiology of scleroderma and cancer has been clearly outside the mainstream of medical thought. Although ignored by the medical establishment, her discoveries have never been disproven.

Despite all this, there is a wealth of research pointing to bacteria as the cause of scleroderma. Ignoring this research is indeed [unfortunate], particularly when it is again fashionable to talk about infectious agents in cancer, and at a time when antibiotics seem to be of value in treating diseases like scleroderma and RA.
 
 

Scleroderma suggests the following may be present:
 
 
Autoimmune  Autoimmune Tendency
 There is an increased incidence of certain types of other autoimmune diseases and cancer among scleroderma patients.

Infections

  Nanobacteria Infection
 Researchers have identified tiny bacteria, known as nanobacteria, that may play a role in the formation of calcification found in scleroderma and other disorders. Cells infected by these bacteria develop deposits of the mineral apatite on their walls.

This is a very new field of research which is highly controversial, however it has recently attracted the attention of researchers at the Mayo Clinic and NASA. Nanobacteria have been found in kidney stones, Alzheimer's disease, heart disease, prostatitis, and some cancers.

A lot of the controversy surrounding nanobacteria has to do with its very name, in that some researchers do not believe that it represents a life form and thus cannot properly be named "bacteria", because the research on its purported nucleic acid has not been completed yet. Thus, some believe that "nanoparticles" would be a better description for it.

  Mycoplasma Infection
 By Alan Cantwell, Jr., M.D. © 2000

Ask most doctors what causes scleroderma and they will tell you the cause is unknown. Furthermore, they will claim that no infectious agent has ever been shown in scleroderma. However, for more than 50 years scientific evidence has been accumulating in the medical journals showing that bacteria are indeed associated with scleroderma, and with closely allied diseases, such as lupus and rheumatoid arthritis.

In the past decade many chronic diseases once believed to be non-infectious are now thought to be caused by viruses, bacteria, or by tiny mycoplasma-like organisms which have characteristics of both bacteria and viruses. Even certain forms of cancer are now considered infectious.

Stomach ulcers were definitely thought to be non-infectious for most of the last century, and physicians and microbiologists insisted bacteria could not grow in the acid environment of the stomach. The ultimate proof that certain bacteria could cause stomach ulcer disease was obtained when a physician-researcher drank a culture of the ulcer-producing bacteria and produced the disease in himself.

It is unthinkable (but true) that decades of research showing organisms in scleroderma and arthritis would be ignored by the medical establishment. Especially now that antibiotics appear to have a beneficial effect in these diseases, it is imperative for physicians to be aware of this research and to stop pretending it does not exist.

Before reviewing the case for bacteria in scleroderma and RA, it is important to acknowledge the role of mycoplasma-like organisms in these diseases. For most of the twentieth century, medical science has regarded these bacteria-like and virus-like microbes as laboratory curiosities of little import. But mycoplasmas can invade cells and even the cell nucleus, thereby promoting chronic infection difficult to eradicate.

Mycoplasma (also known as cell-wall deficient bacteria) are derived from bacteria which have shed all or part of their cell wall. Many chronic diseases may prove to be due to infectious bacteria which transform into the mycoplasma state in order to better adapt to the body. In recent years, mycoplasmas have been discovered in such diverse diseases as Gulf War Illness, AIDS, and certain forms of cancer.

Mycoplasmas may all look and act similarly when in the cell-wall deficient phase - and if a particular mycoplasma becomes stuck in this phase and does not revert back to its original "parent" bacteria, it is impossible to determine the exact bacterial origin of the mysoplasma in question.

Mycoplasma are notoriously difficult to detect and to culture. Thus, they frequently go unrecognized in disease states. Mycoplasma research is still in its infancy, and most experts in the field are microbiologists, rather than practicing medical doctors. Nevertheless, there is a wealth of research implicating mycoplasmas in human disease. The best book on this subject is Cell Wall Deficient Forms: Stealth Pathogens, by mycoplasma expert and Professor Emeritus Lida Holmes Mattman of the Department of Biology at Wayne State University in Detroit.

The Road Back Foundation advocates the use of antibiotic therapy for scleroderma and RA, based on the mycoplasma research first undertaken in the 1940s by Thomas McPherson Brown, M.D., and his microbiologist co-worker Harold W. Clark, Ph.D., currently the Director of the Mycoplasma Research Institute of Beverly Hills, Florida.

The scientific evidence linking mycoplasma to these diseases is simply explained in Dr. Brown's book, The Road Back: Rheumatoid Arthritis, Its Cause and Treatment, [now out of print] and in Clark's Why Arthritis?: Searching for the Cause and the Cure of Rheumatoid Disease. Medical writer Henry Scammell has also authored two books based on Brown's research: The New Arthritis Breakthrough, and Scleroderma: The Proven Therapy That Can Save Your Life.

The first report of "acid-fast" bacteria (similar to the kind of microbes that cause tuberculosis) in scleroderma was published by Virginia Wuerthele-Caspe Livingston, M.D. in 1947. These unusual microbes were discovered in skin scrapings from a woman with ulcerations of the fingers. In later collaboration with pathologists, dermatologists, and microbiologists, she further characterized the peculiar and multi-shaped (pleomorphic) bacteria she consistently isolated from scleroderma cases. Her scleroderma research progressed into microbiologic studies showing similar-appearing acid-fast bacteria in various forms of cancer. Until her death in 1990 at the age of 84, Livingston constantly studied and published her findings on the various aspects of the 'sclero-bacillus' she isolated from scleroderma and the 'cancer microbes' associated with cancer. Despite the furor and controversy that her papers elicited from the cancer establishment, she never wavered in her belief that microbes were at the root of 'autoimmune' and cancerous diseases.

Livingston wrote two books about her lifelong research: Cancer: A New Breakthrough (1972), and The Conquest of Cancer (1984). Her major scientific publications (including the original scleroderma papers) and confirmatory papers by other leading scientists are collected and reprinted in Livingston's The Microbiology of Cancer, available from the Livingston-Wheeler Foundation in San Diego, California.

In 1953, Livingston's finding of bacteria in scleroderma was confirmed by scientists at the Pasteur Institute in Brussels. Additional confirmation was published in 1966 in the Archives of Dermatology, when my own research (co-authored with professors of dermatology and microbiology) showed acid-fast bacteria in the skin biopsy samples from scleroderma cases. During the 1970s and 80s nine additional papers also confirmed the presence of cell-wall deficient, mycoplasma-like microbes in the skin of scleroderma, as well as in multiple diseased organs at autopsy in a fatal case of scleroderma. Like Livingston's bacteria, the organisms we cultured from various patients were pleomorphic. In some fatal cases, the organisms cultured near death were similar to acid-fast mycobacteria associated with tuberculosis, whereas in milder cases the microbes were identified as staphlococci or corynebacteria. Using a tissue stain designed by Lida Mattman to detect acid-fast bacteria and cell-wall deficient bacteria (mycoplasma), bacteria were identified in the skin biopsy material from all cases.

Following the lead of Livingston, my scleroderma research progressed to similar studies of lupus erythematosus (another autoimmune disease) and certain forms of cancer. These studies all showed that pleomorphic bacteria, most likely in a mycoplasma state of growth within the diseased tissue, could be cultured and identified from these diseases. The results of these studies performed over a quarter-century are contained in my book, The Cancer Microbe: The Hidden Killer in Cancer, AIDS, and Other Immune Diseases. In addition, abstracts of most of these Cantwell papers can be retrieved online at the PubMed website sponsored by the National Library of Medicine ( http://www.ncbi.nlm.gov/PubMed ).

The scleroderma research of Livingston and her colleagues that began in the 1940s is undoubtedly related to current research implicating mycoplasmas in human disease. Her papers published in the 1950s clearly show pleomorphic microbes consistent with what are now known s mycoplasmas or cell wall deficient bacteria.

For the first half-century Livingston's microbiology of scleroderma and cancer has been clearly outside the mainstream of medical thought. Although ignored by the medical establishment, her discoveries have never been disproven.

Despite all this, there is a wealth of research pointing to bacteria as the cause of scleroderma. Ignoring this research is indeed [unfortunate], particularly when it is again fashionable to talk about infectious agents in cancer, and at a time when antibiotics seem to be of value in treating diseases like scleroderma and RA.
 
 

Scleroderma can lead to:
 
 
Digestion  Delayed Gastric Emptying (Gastroparesis)
 
 

Recommendations for Scleroderma:
 
 
Diet  Gluten-free Diet
 Gluten sensitivity and Celiac disease are a suspected cause of scleroderma and other autoimmune diseases. Even if tests for gluten sensitivity and Celiac disease are negative or inconclusive, a trial of a gluten-free and casein-free (GFCF) should be considered.

  Caffeine/Coffee Avoidance
 Caffeine, cocaine, marijuana, nicotine, novacaine and many herbs and medications restrict blood flow by constricting blood vessels. This could increase the incidence of Raynaud's. In Raynaud's with Scleroderma there may be blood vessel scarring which can make medication ineffective.

Drug

  Antibiotics
 Please see the link between Scleroderma and Mycoplasma Infection.

Skin

  DMSO Topically
 In an older study, later confirmed by others, Arthur Scherbel, MD, of the Department of Rheumatic Diseases and Pathology at the Cleveland Clinic Foundation, used DMSO on 42 scleroderma patients who had already exhausted all other possible therapies without relief. The investigators concluded that 26 of the 42 showed good or excellent improvement. Histotoxic changes were observed together with healing of ischemic ulcers on fingertips, relief from pain and stiffness, and an increase in strength. The investigators noted, "It should be emphasized that these have never been observed with any other mode of therapy." [Scherbel, A.L., McCormack, L.J., Layle, J.K. Further observations on the effect of dimethyl sulfoxide in patients with generalized scleroderma (progressive systemic sclerosis). Ann NY Acad Sci 141:613-629, 1967]

Vitamins

  Vitamin Paba

Not recommended:
  Vitamin C (Ascorbic Acid)
 Since scleroderma is a disorder of too much collagen, and since vitamin C is required for the proper production of collagen, it would seem to make sense that you wouldn't want to take in more vitamin C than needed for normal health. There is no real evidence to support this idea, but it would be wise not to go overboard with high doses of vitamin C in this condition.
 
 


KEY
Weak or unproven link
Strong or generally accepted link
Likely to help
Highly recommended
May have adverse consequences







GLOSSARY

AIDS:  Acquired Immune Deficiency Syndrome. An immune system deficiency disorder that suddenly alters the body's ability to defend itself. The AIDS virus invades the T4 helper/inducer lymphocytes and multiplies, causing a breakdown in the body's immune system, eventually leading to overwhelming infection and/or cancer, with ultimate death.

Alzheimer's Disease:  A progressive disease of the middle-aged and elderly, characterized by loss of function and death of nerve cells in several areas of the brain, leading to loss of mental functions such as memory and learning. Alzheimer's disease is the most common cause of dementia.

Anti-inflammatory:  Reducing inflammation by acting on body mechanisms, without directly acting on the cause of inflammation, e.g., glucocorticoids, aspirin.

Arthritis:  Inflammation of a joint, usually accompanied by pain, swelling, and stiffness, and resulting from infection, trauma, degenerative changes, metabolic disturbances, or other causes. It occurs in various forms, such as bacterial arthritis, osteoarthritis, or rheumatoid arthritis. Osteoarthritis, the most common form, is characterized by a gradual loss of cartilage and often an overgrowth of bone at the joints.

Autoimmune Disease:  One of a large group of diseases in which the immune system turns against the body's own cells, tissues and organs, leading to chronic and often deadly conditions. Examples include multiple sclerosis, rheumatoid arthritis, systemic lupus, Bright's disease and diabetes.

Bacteria:  Microscopic germs. Some bacteria are "harmful" and can cause disease, while other "friendly" bacteria protect the body from harmful invading organisms.

Biopsy:  Excision of tissue from a living being for diagnosis.

Calcium:  The body's most abundant mineral. Its primary function is to help build and maintain bones and teeth. Calcium is also important to heart health, nerves, muscles and skin. Calcium helps control blood acid-alkaline balance, plays a role in cell division, muscle growth and iron utilization, activates certain enzymes, and helps transport nutrients through cell membranes. Calcium also forms a cellular cement called ground substance that helps hold cells and tissues together.

Cancer:  Refers to the various types of malignant neoplasms that contain cells growing out of control and invading adjacent tissues, which may metastasize to distant tissues.

Chronic:  Usually Chronic illness: Illness extending over a long period of time.

Collagen:  The primary protein within white fibers of connective tissue and the organic substance found in tendons, ligaments, cartilage, skin, teeth and bone.

Cytomegalovirus:  (CMV): A member of the herpes virus family which may induce the immune-deficient state or cause active illness, such as pneumonia, in a patient already immune-deficient due to chronic illness, such as cancer or organ transplantation therapy.

Esophagus:  Commonly called the "food pipe", it is a narrow muscular tube, about nine and a half inches long, that begins below the tongue and ends at the stomach. It consists of an outer layer of fibrous tissue, a middle layer containing smoother muscle, and an inner membrane, which contains numerous tiny glands. It has muscular sphincters at both its upper and lower ends. The upper sphincter relaxes to allow passage of swallowed food that is then propelled down the esophagus into the stomach by the wave-like peristaltic contractions of the esophageal muscles. There is no protective mucosal layer, so problems can arise when digestive acids reflux into the esophagus from the stomach.

Gastrointestinal:  Pertaining to the stomach, small and large intestines, colon, rectum, liver, pancreas, and gallbladder.

Hypertension:  High blood pressure. Hypertension increases the risk of heart attack, stroke, and kidney failure because it adds to the workload of the heart, causing it to enlarge and, over time, to weaken; in addition, it may damage the walls of the arteries.

Immune System:  A complex that protects the body from disease organisms and other foreign bodies. The system includes the humoral immune response and the cell-mediated response. The immune system also protects the body from invasion by making local barriers and inflammation.

Kidney Stone:  A stone (concretion) in the kidney. If the stone is large enough to block the tube (ureter) and stop the flow of urine from the kidney, it must be removed by surgery or other methods. Also called Renal Calculus. Symptoms usually begin with intense waves of pain as a stone moves in the urinary tract. Typically, a person feels a sharp, cramping pain in the back and side in the area of the kidney or in the lower abdomen. Sometimes nausea and vomiting occur. Later, pain may spread to the groin. The pain may continue if the stone is too large to pass; blood may appear in the urine and there may be the need to urinate more often or a burning sensation during urination. If fever and chills accompany any of these symptoms, an infection may be present and a doctor should be seen immediately.

Mineral:  Plays a vital role in regulating many body functions. They act as catalysts in nerve response, muscle contraction and the metabolism of nutrients in foods. They regulate electrolyte balance and hormonal production, and they strengthen skeletal structures.

Necrosis:  Death of one or more cells, or of a portion of a tissue or organ.

Nucleic Acid:  A chemical compound found in all viruses and plant and animal cells. RNA and DNA are the two principal types.

pH:  A measure of an environment's acidity or alkalinity. The more acidic the solution, the lower the pH. For example, a pH of 1 is very acidic; a pH of 7 is neutral; a pH of 14 is very alkaline.

Pulmonary:  Pertaining to the lungs.

Raynaud's Phenomenon:  Raynaud's disease or syndrome is a disorder of blood circulation, mainly in the fingers and toes. It is of unknown cause and characterized by changes of the skin that are aggravated by exposure to cold: first, becoming white with numbness and pain as a result of inadequate oxygenation of the blood, then red/purple with a burning sensation. The sudden constriction of blood vessels causes decreased blood flow to the extremities and can, in extreme cases, lead to gangrene. Also called "white finger", "wax finger" or "dead finger".

Rheumatism:  General term applied to conditions of pain, or inability to articulate, various elements of the musculoskeletal system.

Rheumatoid Arthritis:  A long-term, destructive connective tissue disease that results from the body rejecting its own tissue cells (autoimmune reaction).

Scar Tissue:  Fibrous tissue replacing normal tissues destroyed by injury or disease.

Stomach:  A hollow, muscular, J-shaped pouch located in the upper part of the abdomen to the left of the midline. The upper end (fundus) is large and dome-shaped; the area just below the fundus is called the body of the stomach. The fundus and the body are often referred to as the cardiac portion of the stomach. The lower (pyloric) portion curves downward and to the right and includes the antrum and the pylorus. The function of the stomach is to begin digestion by physically breaking down food received from the esophagus. The tissues of the stomach wall are composed of three types of muscle fibers: circular, longitudinal and oblique. These fibers create structural elasticity and contractibility, both of which are needed for digestion. The stomach mucosa contains cells which secrete hydrochloric acid and this in turn activates the other gastric enzymes pepsin and rennin. To protect itself from being destroyed by its own enzymes, the stomachís mucous lining must constantly regenerate itself.

Tuberculosis:  Also known as TB, Consumption or "The White Plague", tuberculosis is an infectious disease caused by a bacterium called Mycobacterium tuberculosis, usually affecting the lungs but possibly also the brain, kidneys and bones. Patients may at first be symptom-free or experience a flu-like illness. In the secondary stage, there might be a slight fever, night sweats, weight loss, fatigue and various other symptoms, depending on the part of the body affected. Tuberculosis of the lung is usually associated with a dry cough that eventually leads to a productive cough with blood-stained sputum. There might also be chest pain and shortness of breath.

Ulcer:  Lesion on the skin or mucous membrane.

Virus:  Any of a vast group of minute structures composed of a protein coat and a core of DNA and/or RNA that reproduces in the cells of the infected host. Capable of infecting all animals and plants, causing devastating disease in immunocompromised individuals. Viruses are not affected by antibiotics, and are completely dependent upon the cells of the infected host for the ability to reproduce.