October 16, 2019

Graves' Disease
Graves’ disease is the most common autoimmune disease in the United States. It is known to affect an estimated 2 to 3 percent of the world’s population. Read on to learn more about Graves’ disease.

February 3, 2017

Stiff Person Syndrome (SPS)

Stiff Person Syndrome, also known as Stiff Man Syndrome, is a neurological condition believed to be of auto-immune origin. It is unique among neurological diagnoses due to its lack of significant similarity to any other neurological diseases. Although rare, once observed it is quite unforgettable. Because of its rarity, many neurologists and GPs are not aware of the condition. In most cases, the first symptoms are insidious and victims are often initially misdiagnosed with depression. The onset is most frequent between the third and fourth decades of life.

SPS was the name assigned to the condition when first identified in the 1950s by Moersch and Woltman in the USA. SPS is characterized by fluctuating muscle rigidity in the trunk and limbs and a heightened sensitivity to stimuli such as noise, touch, and emotional distress, which can set off muscle spasms. Abnormal postures, often hunched over and stiffened, are characteristic of the disorder. People with SPS can be too disabled to walk or move, or they are afraid to leave the house because street noises, such as the sound of a horn, can trigger spasms and falls. SPS affects twice as many women as men.   It is frequently associated with other autoimmune diseases such as diabetes, thyroiditis, vitiligo, and pernicious anemia.

The disorder is often misdiagnosed as Parkinson’s disease, multiple sclerosis, fibromyalgia, psychosomatic illness, or anxiety and phobia. A definitive diagnosis can be made with a blood test that measures the level of glutamic acid decarboxylase (GAD) antibodies in the blood. People with SPS have elevated levels of GAD, an antibody that works against an enzyme involved in the synthesis of an important neurotransmitter in the brain.

Women appear most likely to fall victim to SMS/SPS. The age range is wide, with some victims presenting in their teens. However, the majority are aged 30 and over. SMS/SPS has many variants.

Another abnormality in SPS is called co-contraction: when the person attempts to contract a muscle to move in one direction, muscles that pull in the opposite direction are involuntarily activated. Individuals with SPS may have difficulty making sudden movements and may have a stiff-legged unsteady gait (manner of walking). The muscle contractions are usually reduced with extra rest.

Eventually, persons with stiff person syndrome may develop a hunched posture (kyphosis) or a swayback (lordosis).

Causes

The cause of stiff person syndrome is unknown, however, researchers theorize that SPS may be an autoimmune disorder. An autoimmune disorder involves a malfunction of the immune system, where the body produces antibodies against its own tissues. Antibodies are proteins produced by the body as part of its defense against foreign bacteria, viruses, or other harmful substances. Other autoimmune disorders such as diabetes, pernicious anemia (a chronic, progressive blood disorder), and thyroiditis (inflammation of the thyroid gland) may occur more frequently in patients with SPS.

 

Often SPS, antibodies are produced against glutamic acid decarboxylase (GAD), an enzyme largely found in the central nervous system . However, GAD antibodies alone appear to be insufficient to cause SPS, as some persons with stiff person disease do not have the GAD antibodies, and GAD antibodies are associated with a number of diseases.

Symptoms

SPS is characterized by constant painful contractions and spasms of voluntary muscles, particularly the muscles of the back and upper legs.

In general, increased muscle tension, which is more marked proximally than distally, is present. Less frequently, lower extremities are most affected. More rarely, upper and lower extremities are affected. In people with diabetes, one limb may be affected, sparing other muscle groups. In most if not all patients, opposing muscle groups are noted to be tense, and tonic contraction with long relaxation times may be noted following percussion of the muscle. In most patients, the neurologic examination findings are otherwise normal.

Symptoms may occur gradually, spreading from the back and legs to involve the arms and neck. Symptoms may worsen when the affected individual is anxious or exposed to sudden motion or noise. Affected muscles may become twisted and contracted, resulting in bone fractures in the most severe cases.

Individuals with stiff-person syndrome may have difficulty making sudden movements and may have a stiff-legged, unsteady gait. Sleep usually suppresses frequency of contractions. Stiffness may increase and patients may develop a hunched posture (kyphosis) or a swayback (lordosis).

Treatment

Treatment with IVIg, anti-anxiety drugs, muscle relaxants, anti-convulsants, and pain relievers will improve the symptoms of SPS, but will not cure the disorder. Most individuals with SPS have frequent falls and because they lack the normal defensive reflexes; injuries can be severe. With appropriate treatment, the symptoms are usually well controlled.

SPS is clinically elusive, but potentially treatable. Traditional treatment for SPS starts with medications such as baclofen or a benzodiazepine . Commonly used benzodiazepines are diazepam (Valium) or lorazepam (Ativan). Both benzodiazepine and baclofen act increasing the activity of the central inhibitory systems. Although no studies have been performed, tizanidine (Zanaflex) may be a less sedating alternative, and prednisone is also a commonly prescribed drug for treatment of SPS.

In some patients, plasmapheresis, a process of filtering the blood to remove excess antibodies, has been demonstrated to be useful in removing anti-GAD antibodies from the bloodstream. In the hospital setting, intravenous immunoglobulin (IVIG) has also been used in the treatment of SPS.

 

Alternative Treatment

Posted in AUTOIMMUNE
February 3, 2017

Sjogren’s syndrome (pronounced Show- grins) is an auto immune disease – a disease in which the immune system turns against the body’s own cell. Sjögren’s syndrome is also known as “Mikulicz’s disease” and “Sicca syndrome”.

In Sjorgren’s Syndrome (SS) the immune system attacks the moisture producing glands and causes dryness in the mouth and eyes. In some cases, other parts of the body can be affected as well, resulting in multiple possible symptoms.It was first identified by a Swedish physician, Dr. Henrik Sjögren in 1933.

The immune system is responsible for protecting the body from various diseases by destroying harmful invaders like viruses and bacteria. In SS, the immune system attack the glands that produce tears and saliva (the lacrimal and salivary glands). Damage to these glands keeps them from working properly and causes dry eyes anddry mouth. Dry eyes are called kerato-conjunctivitissicca, or KCS, and dry mouth is called xero-stomia. This disease can affect other glands too, such as the glands in the stomach, pancreas, and intestines, and can cause dryness inother places that need moisture, such as the nose, throat, airways, and skin. Since, SS causes inflammation in joints,muscles, skin, or other body tissue, it is considered to be a rheumatic disease. Sjögren’s is also considered a disorder of connective tissue, which is the framework of the body that supports organs and tissues (joints, muscles, and skin).

Between 400,000 to 3.1 million Americans, i.e. about one to two percent of the population is affected by Sjogren’s syndrome. It generally affects people between 45 and 55 years old, although it can affect anyone regardless of age. It is also found mostly in women – women are 10 times more likely to have Sjögren’s than men.

Causes

While it’s not known exactly what causes Sjogren’s syndrome, a combination of the following may be to blame:

  • Abnormal immune response
  • Sex hormones
  • Inheritance or genetics
  • Environment (although the exact environmental factors aren’t known)

It is classified in the following :

  • Primary – The syndrome is developed by itself and not as the result of another condition. For example, certain people are born with specific genes that make them more vulnerable to a faulty immune system. Then, many years later, an environmental factor, possibly a common virus, triggers the immune system to stop working properly.
  • Secondary – The syndrome is developed in combination with another autoimmune disorder, such as lupus or rheumatoid arthritis

The causes are listed as below –

  • Autoimmune Factor – Salivary glands that produce saliva exist in “grape-like” clusters. There are no or few lymphocytes in the normal salivary gland but are present in Sjogren’s syndrome. Lymphocytes are part of the immune system that normally protect the body from infection and tumors.When they appear to attack the body’s tissue (as in Sjögren’s syndrome, systemic lupus, or in rheumatoid arthritis), the term “autoimmunity” is used. Lymphocytes originate in the bone marrow. Two types of lymphocytes, termed “T cells” and “B cells” are responsible for mediating immune reactions. The entire lymphoid system is precisely regulated, largely by messenger molecules that instruct cells to “turn on” or “turn off.” Autoimmunity, the excessive reaction against one’s own tissues, then results from a failure of the normal regulation of T cells and B cells. This may be due either to an excessive production of helper signals or a failure to respond to suppressor signals. As a consequence, lymphocytes infiltrate the tissues and attack normal cellular structures.

 

  • Virus & Infections – Studies suggest that a virus is involved. One possible candidate is the Epstein-Barr virus (EBV), which causes infectious mononucleosis, a condition characterized by swollen salivary glands, joint aches and fatigue. Virtually all adults have been infected with EBV by age 20 years. After the initial infection, this virus normally resides in the salivary glands for life but causes no problems. We and others have speculated that this virus (or a closely-related virus) may trigger an autoimmune response in genetically susceptible individuals.

It is thought that an as yet unknown infectious agent damages the salivary gland and attracts the “immune” lymphocytes into the salivary gland. These lymphocytes release specific autoantibodies such as rheumatoid factor (RF) and antinuclear antibodies; antibodies are directed against proteins termed Sjögren’s-associated antigens A and B (or SS-A and SS-B). These antibodies can enter the bloodstream and are measured in the blood tests that we obtain to confirm the diagnosis of Sjögren’s syndrome.

 

  • Hereditary Factor – Particular genes (such as human leukocyte antigen or HLA genes) are inherited in the same manner from parents as are genes for hair color or eye color; that is, one gene from each parent. The HLA genes are important in controlling the immune response and many current research studies are trying to determine exactly how they perform this task. A specific gene named HLA-DR3 is found in high frequency in Caucasian patients with primary Sjögren’s syndrome.

 

  • Evironmental Factors – These include:
    • Toxic Metal Exposure – Studies have shown that exposure to toxic metals such as mercury, cadmium, lead, arsenic, aluminum, nickel and other heavy metals can be linked to the autoimmune process: The heavy metals induce autoantibodies, which then create autoimmune diseases, including Sjogren’s syndrome. These free radicals then alter the body’s pH (which must be kept constant). An altered pH allows viruses, bacteria, candida and other pathogens to thrive, which then sets the stage for more free radicals. The free radicals damage the cells, making it impossible for the cells to communicate with each other. Autoimmunity results when the immune system attacks the damaged cells.
    • Toxic Chemical Exposure – Toxins such as pesticides, solvents, industrial chemicals, even household cleaners and hair dyes are being implicated in autoimmune diseases. These toxins are everywhere, and they greatly increase the risk of all diseases in general.
    • Smoking – Smoking increases the risk of several autoimmune diseases, primarily because of the chemicals in cigarettes.

 

  • Nutritional Deficiencies – Poor diet is an important factor in autoimmunity because poor nutrition compromises the immune system. Processed foods are loaded with chemicals, hormones, steroids, trans-fats and sugars, which promote the creation of free radicals in the body, which in turn damage the cells.

Symptoms

The main symptoms are

  • Dry eyes—Your eyes may be red and burn and itch.People say it feels like they have sand in their eyes.Also, your vision may be blurry, and bright light,especially fluorescent lighting, might bother you.
  • Dry mouth—Dry mouth feels like a mouth full ofcotton. It’s difficult to swallow, speak, and taste.Your sense of smell can change, and you may developa dry cough. Also, because you lack the protectiveeffects of saliva, dry mouth increases your chances ofdeveloping cavities and mouth infections.

Both primary and secondary Sjögren’s syndrome can affectother parts of the body as well, including the skin, joints,lungs, kidneys, blood vessels, and nervous system, and causesymptoms such as –

  • Dry skin
  • Skin rashes
  • Thyroid problems
  • Joint and muscle pain
  • Pneumonia
  • Vaginal dryness – painful sexual intercourse
  • Numbness and tingling in the extremities

When Sjögren’s affects other parts of the body, the condition is called extraglandular involvement because the problems extend beyond the tear and salivary glands. Finally, Sjögren’s can cause extreme fatigue that can seriously interfere with daily life.

Less common features of Sjögren’s syndrome are:

  • Irritation of the nerves in the arms, hands, legs, or feet (neuropathy)
  • Feeling of numbness or tingling
  • Thyroid gland abnormalities
  • Skin rashes
  • Memory loss, difficulty concentrating or confusion
  • Gastrointestinal problems, such as acid reflex, bloating, abdominal pain, or diarrhea
  • Inflammation of the lungs, kidneys (unlike lupus nephritis), liver, or pancreas
  • Cancer of the lymphatic tissue (occurs in up to 5% of patients with the disease)

Treatment

The goals of treatment are to decrease discomfort and reduce the harmful effects of dryness. Generally, physicians use medications to control symptoms (symptomatic treatment). The type of treatment will be tailored to each patient’s symptoms and needs.

  • Good oral hygiene – Good mouth/dental care may prevent or reduce dental decays, infections, or tooth loss:
    • Toothpastes (biotene type) and oral gels are available for people with dry mouth                                 symptoms. These products may also have antibacterial action to reduce the severity of dental cavities over a long period of time.
    • Chewing sugar-free gums can be helpful.
    • Taking frequent sips of water without swallowing (spitting it out) may improve dry mouth.

 

  • Increasing Eye Moisture
    • Dry eyes are mainly treated with the use of artificial tears. A wide variety of over-the-counter products is available. Artificial tears can be used regularly and more often in dry environmental conditions such as on airplanes, in air-conditioned buildings, and on windy days.
    • While artificial tears are helpful, they often do not last long enough. Thicker                 preparations (gel form) that last longer are available. These are often used at bedtime because they can sometimes cause blurry vision. Eye doctors can prescribe an eye drop called Restasis to treat more severe form of dry eyes. A small procedure called punctal plugs, to slow the disappearance of tears, is another treatment option when artificial tears are not sufficient.

 

  • Medications – Medications that tend to reduce body fluids should be avoided.
    • Mild pain-relieving medications (analgesics), includingacetaminophen, such as Tylenolor non-steroidal anti-inflammatory drugs – NSAIDs, such as Motrin and Aleve, can reduce muscle or joint pain.
    • In some patients, the anti-rheumatic drug hydroxychloroquine has been beneficial in decreasing pain and salivary gland swelling and improving fatigue, muscle pain, joint pain, or rash. This drug generally does not help with dry symptoms, however.
    • For patients with internal organ symptoms (particularly when the disease affects internal organs), steroids and immunosuppressive medications may be used. These include medicines such as prednisone (a steroid) and, rarely, chemotherapy-type medications.
    • Systemic corticosteroids and/or immunosuppressive agents like cytotoxic drugs have been used for various extra glandular symptoms of SS, such as: vasculitis, lung involvement kidney involvement. However, cytotoxic agents should be used with great care as they may increase the risk of lymphoma.
    • Water-based vaginal lubricants (K-Y Jelly, Astroglide, Replens, Luvena) can ease vaginal dryness and painful intercourse. Estrogen creams or other preparations may be helpful for women who have vaginal dryness due to reduced estrogen levels related to menopause.

It is important to know that the medications also involve numerous side effects that can prove harmful and may result in creating additional complications.

 

  • Balance of rest and exercise – Guided exercise programs can help patients overcome fatigue, maintain flexibility, and overcome joint and muscle pain. Good sleep hygiene is helpful for improving fatigue and body pain.

 

Alternative Treatment

Alternative medicine definitely has more treatment options. The model of simply fixing the gut, stabilizing the blood sugar level, balancing the hormones, taking enough essential fatty acids and anti-inflammatory protocols, and so forth, are effective. However, they are not any different than treating any type of autoimmune disorders.

  • Detoxification Therapy – Detoxification thrapy utilizes clinical procedures that safely reduce the body’s burden of toxic chemicals, including chemicals stored following occupational, accidental, and/or chronic airborne exposures. Chemicals bind to human tissues on the basis of their lipophilic properties — meaning literally “attracted to fats.”
  • Green tea and EGCG for Sjogren’s syndrome – Green tea polyphenols reduce autoimmune symptoms in a murine model for human Sjogren’s syndrome and protect human salivary acinar cells from TNF-alpha-induced cytotoxicity.Green tea contains several antioxidants that have been shown to curb inflammation, prevent cell death, and possibly even ward off cancer.EGCG reduced the severity and delayed the onset of salivary gland damage associated with Sjogren’s syndrome.
  • Fish oils, Wheat Germ oil &flax seeds – Effect of omega-3 and vitamin E supplementation on dry mouth in patients with Sjögren’s syndrome.Omega3 Fatty acid rich fish oil (FO) and vitamin E may delay the progress of certain autoimmune diseases.omega-3 (n-3) increases saliva production in patients with Sjögren’s syndrome. Wheat germ oil helps in stimulating saliva production in patients with Sjögren’s syndrome.
  • DHEA -Low serum levels of sex steroids are associated with disease characteristics in primary Sjogren’s syndrome; supplementation with dehydroepiandrosterone restores the concentrations. It also helps in stimulating saliva production.
  • Flavonoids -Plant-derived flavonoids are inhibitors of various intracellular processes, notably phosphorylation pathways, and potential inhibitors of cellular autoimmunity. This includes – apigenin and luteolin, fisitin, quercetin, morin and hesperitin. It acts as strong inhibitors for T cells.
  • Rose hip herbal remedyfor SS, Probiotic for gut
  • Vitamin D – Vitamin D inhibits pro-inflammatory processes by suppressing the enhanced activity of immune cells that take part in the autoimmune reaction. Supplementation may be therapeutically beneficial particularly for Th1 mediated autoimmune disorders. Some reports imply that vitamin D may even be helpful in multiple sclerosis and diabetes type 1.

Integrated Treatment

Integrated medical practitioners treat the whole body as a single system and work with interdependent, oscillating energies and seek to achieve balance and integration of the entire body. There are natural, non-invasive, and wholistic approaches that incline toward discovering the imbalances, and integrate to correct them through diet and nutrition, exercise, acupuncture, massage, and individual customized education.

With the variety of symptoms that encompass Sjogren’s syndrome, it is very important to have a plan and helpful practitioner who works with full oversight and a set of complimentary skills under one roof, i.e. our center.

Posted in AUTOIMMUNE
February 3, 2017

Scleroderma, also known as systematic sclerosis, is a chronic auto immune rheumatic disease. It affects skin and connective tissues of the body, which means that it is a condition where the body’s immune system acts abnormally. Hardening of the skin is one of the most visible effect of the disease. It also involves inflammation and scarring of many body parts, leading to problems in the lungs, kidneys, heart, intestinal system and other areas. Scleroderma is not contagious, infectious, cancerous or malignant.

The word “scleroderma” comes from two Greek words: “sclero” meaning hard, and “derma” meaning skin. The disease has been called “progressive systemic sclerosis,” but the use of that term has been discouraged as it has been found that scleroderma is not necessarily progressive. The disease varies from patient-to-patient.

Scleroderma is a rare disease. It is more common in women than men. Anyone can get it, even children. About 75,000 to 100,000 people in the U.S. have this disease.

Types of Scleroderma

There are two types of Sclerodera and each are sub classified.

Localized Scleroderma

The changes, which occur in localized scleroderma, are usually found in only a few places on the skin or muscles, and rarely spread elsewhere. It is relatively mild in nature. The internal organs are usually not affected, and persons with localized scleroderma rarely develop systemic scleroderma. It is classified in two types :

  • Morphea

Morphea is a form of localized scleroderma characterized by waxy patches on the skin of varying sizes, shapes and color. The skin under the patches may thicken. The patches may enlarge or shrink, and often may disappear spontaneously. It mostly occurs between the ages of 20 and 50, but is often seen in young children.

  • Linear scleroderma

It is a form of localized scleroderma which frequently starts as a streak or line of hardened, waxy skin on an arm or leg or on the forehead. Sometimes it forms a long crease on the head or neck, referred to as en coup de sabre because it resembles a saber or sword wound. This type tends to involve deeper layers of the skin as well as the surface layers, and sometimes affects the motion of the joints, which lie underneath and usually develops in childhood.

 

Systemic scleroderma (systemic sclerosis)

The changes occurring in systemic scleroderma may affect the connective tissue in many parts of the body. Systemic scleroderma can involve the skin, esophagus, gastrointestinal tract (stomach and bowels), lungs, kidneys, heart and other internal organs. It can also affect blood vessels, muscles and joints. It involve –

  • Limited Scleroderma – CREST Syndrome

Limited scleroderma means only limited areas of skin are thick; usually just the fingers and/or face. Limited scleroderma is the milder form of scleroderma. The CREST syndrome is a type of limited scleroderma. CREST stands for the following:

  • C – is for the calcium deposits under the skin and in tissues (calcinosis)
  • R – for Raynaud’s phenomenon.
  • E – esophageal dysmotility. This causes heartburn, which is often experienced by CREST patients.
  • S – is for sclerodactyly; that means thick skin on the fingers.
  • T – is for telangiectasias, which are enlarged blood vessels. These appear as red spots on the face and other areas.

Limited scleroderma causes less involvement of body organs than the more severe form. Some patients can develop lung and heart disease.

  • Diffuse Scleroderma

This type of scleroderma is called diffuse scleroderma. It means that more areas of the skin are involved and thickened, but there is a high degree of variability among patients. Skin of the arms, legs, and trunk are more likely to be involved. The tightened skin makes it difficult to bend fingers, hands, and other joints. There is sometimes inflammation of the joints, tendons and muscles. Tight skin on the face can reduce the size of a person’s mouth and make good dental care very important.

Diffuse scleroderma can have associated involvement of internal organs such as the gastrointestinal tract, heart, lungs, or kidneys. The degree of organ involvement is highly variable – some get none at all and other patients organs may be badly affected.

 

Causes

The cause of scleroderma is not known. We don’t yet know why people’s immune system becomes overactive and initiates excessive production of collagen or the reason for blood vessel abnormalities; but it is thought to be a combination of genetic and environmental factors.

 

Environmental Factors

  • Toxic Exposure – Exposure to cadmium, mercury (dental amalgam), solvents (such as paint thinners), radiation, and silica as either known or suspected causes of autoimmune diseases or scleroderma.
  • Artificial Joints and Silicon Implants – Some cases of connective tissue disease, such as scleroderma, related to artificial joints or silicone breast implants.
  • Asbestos – Asbestos is relatively harmless. However, when asbestos is become dry and brittle or is ground or broken up, the fibers become airborne and can be ingested through the mouth or inhaled through the lungs. As a result, once inhaled or ingested, asbestos fibers often remain in the body and can cause a multitude of medical problems like Scleroderma, lung cancer etc.
  • Air Pollution – Diseases such as scleroderma may be triggered by the inhalation of chemical solvents, herbicides and silica.
  • Drugs & Medications – Some medications and street drugs are known or thought to induce scleroderma or Raynaud’s, such as Bleomycin, Cocaine, Marijuana, and Paclitaxel (Taxanes).

Genetic Factors

Research has demonstrated that systemic sclerosis is a polygenic (involving more than one gene) autoimmune (involving the immune system response) disease. Several genes and gene-gene interactions have been identified as playing a role in systemic sclerosis.

Inflammatory Response and Autoimmunity

The disease cause leading to scleroderma seems to occur as an autoimmune response, in which an abnormal immune system attacks the body itself. In scleroderma, this response produces swelling (inflammation) and too much production of collagen. Collagen is the tough protein that helps build connective tissues such as tendons, bones, and ligaments. Collagen also helps scar tissue form. When normal tissue from skin, lungs, the esophagus, blood vessels, and other organs is replaced by this type of abnormal tissue, none of these body parts work as well, and many of the symptoms previously described occur.

Other Factors

  • Proteins – Increased amount of S100A8 (calcium- and zinc-binding protein) and S100A9 (Calcium Binding Protein) in patients with diffuse coetaneous systemic sclerosis. A correlation with organ involvement and immunological abnormalities. These two proteins may play important roles in the development of systemic sclerosis.
  • Oxidative Stress- Lipid Peroxidation – Oxidative Stress is an imbalance between pro-oxidants and antioxidants that can result in cellular degeneration.
  • Gluten – Studies suggest, of several rheumatological disorders , including Raynaud’s phenomenon in people with celiac disease, but this seems to be the first report of extensive microvascular damage, similar to capillary changes in scelroderma, documented by nailfold capillaroscopy in a patient with celiac disease.
  • Thyroid – It is common for people with systemic scleroderma to also have other health problems, and thyroid disease can often be associated with it. However, thyroid disease is very common in the general population, whereas systemic scleroderma is very rare, and thyroid disease is not considered to be a symptom of any type of scleroderma.
  • B and T Cells – B and T cells are white blood cells that help stimulate an immune response to infections. In the thymus gland, lympohocytes are matured into these cells. Sometimes these cells become overactive, which is suspected as being part of the process that leads to autoimmune diseases like Scleroderma.

Symptoms

Symptoms vary greatly from person to person depending on what part of the body is involved.

For some people, following symptoms are among the early signs of scleroderma:

  • Raynaud’s phenomenon – The fingers or toes turn white, then blue in the cold, and then red as blood flow returns. This is caused by narrowing of the blood vessels. It is possible to have Raynaud’s without having scleroderma, but most people with scleroderma will have symptoms of Raynaud’s at some time and it’s often one of the first symptoms to appear.
  • Thickening and hardening of the skin on the hands, arms and face
  • Stiffness and pain in the muscles and/or joints
  • Swelling of hands and feet, especially in the morning
  • Thinning of the pads at the finger tips
  • Small white chalky lumps (calcium deposits) under the skin
  • Indigestion or heartburn
  • Diarrhoea or constipation
  • Shortness of breath or reduced ability to exercise
  • Kidney problems and high blood pressure
  • Gut Problems – The gastrointestinal (GI) tract is primarily responsible for the processes of digestion and excretion, and is frequently affected by manifestations of Scleroderma.
  • Dryness – It is characterized by a decrease in secretions of the tear glands and the salivary glands, which provide lubrication for the eyes and mouth. The unusual dryness of the eyes resulting from this condition can lead to serious irritation and inflammation. Excessive dryness of the mouth may lead to difficulties in swallowing and speaking, a pronounced increase in tooth decay and cavities, and a reduced sense of taste. Dryness may also involve vagina and other areas of the body.

Related Complications

  • Digestive Systems – Digestive problems associated with scleroderma can lead to acid reflux and difficulty swallowing — some describe feeling as if food gets stuck midway down the esophagus.
  • Heart – Scarring of heart tissue increases the risk of abnormal heartbeats (arrhythmias) and congestive heart failure, and can cause inflammation of the membranous sac surrounding the heart (pericarditis). Scleroderma also can raise the pressure on the right side of the heart and cause it to wear out.
  • Teeth – Severe tightening of facial skin can cause the mouth to become smaller and narrower, which may make it hard to brush teeth or to even have them professionally cleaned.
  • Kidneys – When scleroderma affects the kidneys, it can develop an elevated blood pressure and an increased level of protein in the urine.
  • Lungs – Scarring of lung tissue (pulmonary fibrosis) can result in reduced lung function, reduced ability to breathe and reduced tolerance for exercise.
  • Sexual function – Men who have scleroderma often experience erectile dysfunction. Scleroderma may also affect the sexual function of women, by decreasing sexual lubrication and constricting the vaginal opening.
  • Gut – Evidence suggests that the involuntary muscle of the gastrointestinal tract (smooth muscle) can be affected in scleroderma. When this muscle is involved, abnormal motor function of the esophagus, stomach, small or large bowel results.

 

Treatment

  • Medications

Calcium-channel blockers are the standard drugs to open the blood vessels, and may be used for pulmonary artery hypertension and Raynaud’s phenomenon. This may involve – diltiazem (Cardizem, Dilacor), dihydropyridine medications (felodipine, amlodipine, and isradipine).

Side effects may include fluid buildup in the feet, constipation, fatigue, gingivitis, erectile dysfunction, flushing, and allergic symptoms.

  • ACE Inhibitors

Many medications are available for controlling blood pressure, but ACE inhibitors appear to be the most effective for scleroderma patients because of their protective actions in the kidney. This includes – captopril (Capoten), enalapril (Vasotec), quinapril (Accupril), benazepril, and lisinopril (Prinivil, Zestril). Side effects may include irritating cough, large drops in blood pressure, and allergic reactions.

  • Angiotensin Receptors – This involves losartan, candesartan cilexetil, and valsartan. They have positive effects on blood vessels. Small studies showing improvement in Raynaud’s phenomenon warrant further research.
  • Nitrates – Nitrates relax smooth muscles and open arteries, and are therefore sometimes used for the short-term management of Raynaud’s phenomenon. Side effects of nitrates include headaches, dizziness, nausea, blurred vision, fast heartbeat, and sweating.
  • Cyclophosphamide (Cytoxan) – Cyclophosphamide is the most important immunosuppressant currently used for scleroderma. It blocks some of the destructive actions of scleroderma in the lungs. Intravenous cyclophosphamide can be life-saving for patients with pneumonia caused by interstitial lung disease. Side effects may include – hair loss, infection, and bleeding into the urinary tract.
  • Other Drugs – D-penicillamine (which may be useful for skin symptoms), methotrexate (Rheumatrex), sirolimus (rapamycin), antithymocyte globulin (ATG), corticosteroids, cyclosporine A, and chlorambucil (Leukeran). All of these drugs have potentially severe side effects.

Surgeries

  • Sympathectomy and Hand Surgeries – This uses procedures that block or remove the nerve responsible for narrowing blood vessels in the hand. The result is increased blood flow in the hand.
  • Other Surgeries – Disabling deformity of the hand is a common feature of scleroderma. Various surgical procedures can relieve pain, prevent tissue loss, protect hand function, and improve the appearance of the hands.

Alternative Treatment

Environmental Medicine is a branch of medicine whose domain is not limited by anatomical boundaries but, rather, is concerned with the whole person and the way that a person reacts to his/her total environment. At our center we first carry out Comprehensive Approach of studying the patient’s medical history, where we are able to get hold of the root cause and treat accordingly.

  • Bio-detoxification Programme – The Center’s Bio-detoxification Program utilizes clinical procedures that safely reduce the body’s burden of toxic chemicals, including chemicals stored following occupational, accidental, and/or chronic airborne exposures.
  • Alka Vita Supplements – This has the tremendous advantage that it alkalises, therefore increases oxygenation, counteracts free radical attack and damage and therefore undermines the basis of disease. It is also directly ‘anti-septic’ against fungal infections, including Candida and possibly all harmful micro-organisms and parasites, although there is not enough information on this, we do know that all anaerobic infections (the harmful ones) are attacked by free electrons that Alka- vita supplies and are eventually destroyed or severely limited by an alkaline environment.
  • AA and DHA – The essentiality of arachidonic acid (AA) and docosahexaenoic acid (DHA), when dosed appropriately, fish oil-based lipid emulsions contain sufficient essential fatty acid (EFAs) to prevent essential fatty acid deficiency.
  • Curcumin (Tuermeric) – The varied biological properties of curcumin and lack of toxicity even when administered at higher doses makes it attractive to explore its use in various disorders like tumors of skin, colon, duodenum, pancreas, breast and other skin diseases.
  • Vitamin B – A growing body of research is drawing a link between low B12 and early cognitive decline, a condition that often leads to auto immune disease.
  • Probiotics – Yogurt may be helpful for combatting bowel involvement with systemic scleroderma, especially small bowel bacterial overgrowth. It may also be particularly helpful when taking antibiotics.
  • Lipioc acid – Dihydrolipoic acid (DHLA) not only acts as an antioxidant but also an antifibrotic since it has the ability to reverse the profibrotic phenotype of Sclerodermal fibroblasts.
  • Vitamins & Minerals – Different Vitamins are essential to aid the immune system and many biochemical processes including the utilisation of calcium and magnesium. Its deficiency is almost universal in northern climates and even more so since the introduction of sun screen. Its deficiency has been linked strongly to auto-immune diseases. Zinc has critical effect in homeostasis, immune function, oxidative stress, apoptosis, aging and in chronic diseases, including atherosclerosis, several malignancies, neurological disorders, autoimmune diseases. Vitamin D is essential for promoting calcium absorption in the gut, build and preserve bone, helps prevent osteoporosis and helps decrease fracture risk.
  • Herbs – Herbs such as Cleavers and Red Clover help to cleanse toxins from the lymphatic system and to purify the blood, allowing much needed nutrients to reach the skin and tissues.

Referneces –

www.sclero.org

www.medicinenet.com

www.hopkinsscleroderma.org

www.mayoclinic.org

www.raynauds.org.uk

www.rheumatology.oxfordjournals.org

www.arthritis-research.com

www.todaysdietitian.com

www.scleroderma.ca

www.aarda.org

www.niams.nih.gov

Posted in AUTOIMMUNE
February 3, 2017

Rheumatoid Arthritis is a chronic disease whereby various joints in the body are inflamed, leading to stiffness, pain, swelling and the possible loss of function. It usually affects the joints symmetrically i.e. on both the sides equally and may initially begin in couple of joints only and most frequently attacks knees, ankles, shoulders, wrists and hands.
Rheumatoid Arthritis is an autoimmune disease in which the body’s immune system – which generally protects its health by attacking foreign substances like viruses and bacteria – mistakenly attack the joints and other tissues causing chronic inflammation. The immune system contains complex organization of cells and anti bodies designed normally to find and destroy the invaders of our system, particularly infections. Though inflammation of the tissue around the joints and inflammatory arthritis are characteristics of rheumatoid arthritis, the disease also causes inflammation and injury to other organs of the body. As it can affect multiple other organs of the body, rheumatoid arthritis is referred to as a systemic (body-wide) illness and sometimes is also known as rheumatoid disease. Rheumatoid arthritis that affects children under 16 years of age is referred as juvenile idiopathic arthritis.

  • The process of disease leading to rheumatoid arthritis begins with synovium – the tissues that lines the inside of joints and around the joins that makes a fluid that lubricates joints making them move smoothly creating a protective sac.
  • In addition of lubrication of joints, this fluid also supplies nutrients and oxygen to cartilage, a slippery tissue that coats the ends of bones; it composes of collagen – the structural protein in the body that forms a network to give support and flexibility to joints.
  • In rheumatoid arthritis, an affected immune system produces destructive molecules that cause continuous and harmful inflammation of synovium. Gradually, the collagen is destroyed, hence narrowing the joint space and eventually damaging bone.
  • If the disease develops into a form called progressive rheumatoid arthritis, the destruction process accelerates.
  • Fluid and immune system cells gathers in synovium, producing a pannus – a growth composed of thickened synovial tissues. With the development of the disease, the pannus produces more enzymes that destroy nearby cartilage, aggravating the area and attracting more inflammatory white cells, thereby perpetuating the process.

Causes

The exact causes of Rheumatoid arthritis are still not known, but this condition is most likely triggered by a combination of factors such as abnormal autoimmune response, inflammatory process, genetic factors and at times environmental or biological factors like viral infections and/or hormonal changes.

  • Abnormal Autoimmune Response & Inflammatory Process
    The immune system helps the body to fight and respond to the foreign substance and antigens – a substance that induces the formation of antibodies, since it is recognized as a threat by our immune system – like toxins and viruses. It helps the body fight these infections and accelerates the healing of wounds and injuries. The inflammatory process is an outgrowth of the immune system. There are two main components of the immune system that are associated with rheumatoid arthritis, namely, B cells and T cells, both belonging to a group of immune cells called lymphocytes – a type of white blood cell.
    If the T cell recognizes an antigen as “non self”, it will result in producing chemicals (cytokines) which in turn causes B cell too multiply and release many antibodies (immune proteins). These antibodies spread in the bloodstream, and help identifying foreign substances and ultimately causing inflammation in order to get rid of these invaders of the body.
    For unknown reasons, these T cells and B cells become over active in patients with Rheumatoid Arthritis.
  • Genetic Factors
    Genetic Factors may play a significant role in either increasing the chances of developing RA condition or by worsening the process of the disease. The key genetic marker of RA is Human Leukocyte Antigen (HLA). HLA is not responsible is the development of Rheumatoid arthritis, but they can worsen the condition once developed. Other than that, STAT4 – a gene that plays an important role in the regulation and activation of immune system; TRAF1 and C5 – genes relevant to chronic inflammation; and PTPN22 – gene associated with both development and progression of RA, are connected to Rheumatoid Arthritis. Yet not all people with these genes develop RA and not all RA patients have these genes.
  • Environmental Factors
    These factors include infectious agents like bacteria and viruses which may trigger the development of the disease in a person who is more likely to get RA. Research shows that factors like obesity, physical or emotional stress, exposure to cigarette smoke, air pollution, harmful chemicals, occupational exposure to mineral oil, silica etc.

Symptoms

Researchers have proven that about 1.3 million Americans e affected by Rheumatoid Arthritis. Although RA can develop in any age from childhood to old
age, it normally begins between the ages of 30 – 50 years. Women are more likely to develop this condition than men.
The symptoms of Rheumatoid Arthritis are:

  • Swelling And Pain
    Te inflamed joints are usually swollen and are often warm and spongy when touched. The pain occurs on both sides of the body and may be more severe on either side.
  • Building up of certain
    Fluid may get accumulated in joints. The fluid gathered in the joint sac behind the knee forming a tumor like substance called Baker’s Cyst. This cyst sometimes extends down the back of the calf and causes severe pain.
  • Nodules
    In some cases of RA, inflammation of small blood vessels may cause nodules or lumps, under the skin. These nodules are often situated near the elbow (it can show up at other places too) and are about the size of pea or slightly larger than that. These nodules can become sore and infected, particularly if their location is where stress occurs, for e.g. Ankles.
  • Specific Joint Pain
    Although RA mostly develops in the wrists and knuckles, the balls of the foot and knees are often affected too. Joints like those in the cervical spine, shoulders, jaw, elbows and even the joints between the inner ear, gets eventually affected.
  • Flu like Symptoms
    Fatigue, loss of weight and fever are also few symptoms.

Complications Involved

  • Anemia – RA patients tend to develop anemia i.e. decrease in the number of red blood cells.
  • Eye Problems – Inflammations of the blood vessels in the eyes, like scleritis and episcliritis that can result in corneal damage. Symptoms include redness of the eye and gritty sensation.
  • Skin Problems – Skin problems are common in RA patients, usually on the fingers and under the nails.
  • Infections – RA patients are at a higher risk of being affected by infections, because of the disease itself and also due the immune suppressing drugs used in the treatment.
  • Peripheral Neuropathy – RA condition affects the nerves, most often n hands and feet.
  • Joint Deterioration and Pain – Affected joints become deformed due to the disease.
  • Osteoporosis – Loss of bone density, is more common than average in postmenopausal women with RA. The hip is particularly affected. The risk for osteoporosis also appears to be higher in men with RA who are over 60 years old.
  • Lung Diseases – Chronic lung diseases like interstitial fibrosis, pulmonary hypertension etc. are also caused in RA condition.
  • Pregnancy Complications – Women with RA are more prone to premature delivery. They are also at higher risk of developing high blood pressure than in normal cases.
  • Kidney and Liver Problems
  • Heart Problems

Treatment

The primary goal of treating RA is:

  • Stop inflammation
  • Prevent joint and organ damage
  • Relieve Symptoms
  • Improve physical functions
  • Reducing long term complications

The treatment is of different types:

Medications

Different drugs are used in the treatment of Rheumatoid Arthritis. Some are to ease the symptoms of RA, others to slower and eventually stop the different activities of RA.
Drugs used to ease the symptoms – Non-steroidal anti-inflammatory drug (NSAIDs) are used to ease the pain and inflammation involved in the condition of RA. These drugs include ibuprofen, ketoprofen and naproxen sodium. Patients with stomach ulcers are prescribed to take celecoxib, also known as COX-2 inhibitor, which is proven to be safer for stomach. These drugs can be taken by mouth or also can be applied to the skin.

Drugs that slower the RA activity– Corticosteroids medications like prednisolone, prednisone and methylprednisolone are some of the fast acting anti-inflammatory medications used in the treatment.
Disease Modifying Anti-Rheumatic Drugs (DMARDs) are the standard medical treatment for RA. Their ability is to slow down the progression of RA. These include- Methotrexate, leflunomide, hydroxychloroqune, minocycline and sulfasalazine. Unfortunately, all DMARDs tend to lose effectiveness over time and may also produce stomach and intestinal side effects.
Biological DMARDs – drugs made out of living cells are also used in the treatment. They are subsets of DMARDs. They target specific components of the immune system that contribute to the various attributes of rheumatoid arthritis. They include abatacept, adalimumab, anakinra, certolizumab pegol, etanercept, infliximab, golimumab and rituximab.

Surgery

Some people with RA are benefitted by joint surgeries. It can help in relieved joint pains and correcting deformities and at times it modestly improves joint function.

Joint Replacement

Joint replacement (arthroplasty) is usually done for people over age 50 or those whose joint damage is rapidly progressing. The joint replacement can last for 20 years or more.

Exercise

Its’ advisable for RA patients to maintain balance between rest and moderate exercise. Studies suggest that even little physical therapy can help the patients and that these benefits are sustained.

Natural Treatment

Natural Supplements

  • Boswellia Serate (Indian Frankincense) – contains anti-inflammatory and pain relieving properties.
  • Capsicum Fruitescens – reduces substance P, a pain transmitter. Research suggest that it helps in 50 percent reduction of joint pain. It’s available in the form of topical cream, gel etc.
  • Fish Oil Capsules (EPA & DHA) – Omega-3 blocks inflammatory cytokines and prostaglandins, and are converted into effective anti-inflammatory chemicals. EPA and DHA are very effective for treating RA and other inflammatory conditions. Studies prove that fish oil significantly decreases joint tenderness and stiffness in RA patients, helping in reduction or elimination of NSAIDs.
  • Gamma Linolenic Acid (GLA) – GLA is an Omega-6 fatty acid that the body converts into anti-inflammatory chemicals. Its intake shows significant improvement in joint pain, stiffness and grip strength. Studies show that a combination of fish oil and GLA reduces the need for conventional pain relievers.
  • Ginger – Ginger has the properties of anti-inflammatory components similar to ibuprofen and COX-2inhibitors, without any side effects. Its intake reduces osteoarthritis pain in the knee and other joints. It also reduces inflammatory reactions of RA.
  • Pine bark extract, rosehips, green-lipped mussel, devil’s claw, borage seed oil etc. also help in the treatment.
  • Change in Diet
Posted in AUTOIMMUNE
February 3, 2017

Definition:

Psoriasis is an autoimmune disease that causes a chronic skin condition where cells grow too quickly. The rapid growth of cells causes patches of plaque on areas of the skin. These patches appear as red raised areas on the skin, and most often occur on the elbows, knees, and scalp, however the patches can appear on any area of the body. Many individuals with psoriasis report these areas can be itchy and tender.

Symptoms:

Symptoms of Psoriasis vary from mild to severe. Mild Psoriasis can appear on the body as a small rash. Moderate Psoriasis can appear as raised red areas with loose, silvery, scaling. These areas can be small or as large as an individual’s entire back. Finger and toe nails can also be affected with pitting, color changes, and separation from the nail bed. Joint pain and inflammation can be symptom of psoriasis. This condition is called psoriatic arthritis.

Causes:

Autoimmune response is when the body’s immune system recognizes normal cells as a threat, and attacks them. In the case of psoriasis immune response is attacking the skin. Although causes of psoriasis and autoimmune is unknown, much research is connecting the body’s immune response to the health of the gut. Research has linked gut permeability with autoimmune disorders. This research has found that the gut’s natural permeability has been compromised, allowing particles that should remain in the intestine to escape into the blood stream, thus causing an immune response. These cells mimic other cells in the body, causing the immune system to attack normal cells, thus causing the autoimmune disease.

Common triggers of psoriasis are widely recognized. These triggers include cold, dry weather, stress, alcohol consumption, smoking, and certain medication. Food sensitivity and allergy may also be a culprit in triggering psoriasis, as well as common environmental allergens may trigger an episode of psoriasis. Certain fungal infections may also contribute to triggering psoriasis.

Diagnostic tools:

  • Autoimmune Panel
  • Food IgG 90/120
  • CDSA
  • ALT/ALS (CMP)

 

Treatment:

  • LDN
  • Stone Age Diet / Rotation Diet
  • Guided Imagery/Stress reduction
  • Adding Fermented foods to the diet
  • Yeast Eradication

 

Products and Services:

Nutritional Supplements:

  • Galactomunepowder or capsules
  • Probiotic:
    • Therbiotic Complete
    • Culturelle
    • LactoPrime
    • Vital 10
    • Biotagen
    • Saccharomyces Boulardii

Allergy Extracts/Signal Therapies:

  • Allergy Testing to foods
  • Allergy Extract
  • Interferon Alpha B
  • M2
  • M4
  • BCG II

Preparing for your appointment:

Prior to your appointment with a doctor at the Center for Occupational and Environmental Medicine it is important for you to review the new patient information sent to you by our new patient coordinator. This packet includes specific information about preparing for you visit as well as an in depth medical history form. Please take some time to fill out the form to the best of your ability. This form will take some time, and may require reaching out to family members for additional medical history. Please also complete all registration forms prior to arriving at the center for your appointment. If you have completed any recent blood work or laboratory tests please bring copies with you to your appointment. Your clinician and doctor will review this information as part of your medical history. Plan on being with us at the center for a full day on the first day of your appointment. Some of your recommendations may include allergy testing, and this process will take some time.

 

Sites:

National Psoriasis Foundation.org

WebMD, Psoriasis

Mayoclinic.org

Experiencing Life, when your body turns on you

Posted in AUTOIMMUNE
February 3, 2017

 Primary biliary cirrhosis (PBC) is an inflammation with chronic and slowly progressive scarring of bile ducts in the liver. If left untreated, or if a patient does not adequately respond to treatment, chronic inflammation and fibrosis can advance to cirrhosis.

The bile ducts carry a fluid called bile from the liver to the gallbladder, where it is stored. When food enters the stomach after a meal, the gallbladder contracts, and the bile ducts carry bile to the duodenum, the first part of the small intestine, for use in digestion. The liver makes bile, which is made up of bile acids, cholesterol, fats, and fluids. Bile helps the body absorb fats, cholesterol, and fat-soluble vitamins. Bile also carries cholesterol, toxins, and waste products to the intestines, where the body removes them. When chronic inflammation, or swelling, damages the bile ducts, bile and toxic wastes build up in the liver, damaging liver tissue. This damage to the liver tissue can lead to cirrhosis, a condition in which the liver slowly deteriorates and is unable to function normally. In cirrhosis, scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver.

The buildup of scar tissue that causes cirrhosis is usually a slow and gradual process. In the early stages of cirrhosis, the liver continues to function. However, as cirrhosis gets worse and scar tissue replaces more healthy tissue, the liver will begin to fail. Chronic liver failure, which is also called end-stage liver disease, progresses over months, years, or even decades. With end-stage liver disease, the liver can no longer perform important functions or effectively replace damaged cells.

Causes

Autoimmune System – Most research suggests the disease is an autoimmune condition. The immune system usually protects the body from harmful substances such as bacteria and viruses by attacking and destroying them. In autoimmune diseases, the immune system instead attacks the body’s own tissues. In primary biliary cirrhosis, the immune system attacks the bile ducts.

Genetic Factor – Genetic factors may make a person prone to develop primary biliary cirrhosis. Primary biliary cirrhosis is more common in people who have a parent or sibling-particularly an identical twin-with the disease. Genetic factors may also make some people prone to develop other autoimmune diseases. People with primary biliary cirrhosis may have other autoimmune conditions such as rheumatoid arthritis or autoimmune thyroiditis. A person who has genetic factors for primary biliary cirrhosis may be more likely to develop the disease after exposure to chemicals or infections, such as urinary tract infections.

Environmental Factors – Environmental factors may have a potential causative role – infection, chemicals, smoking. It may trigger or worsen the disease.

Risk Factors

PBC is most commonly diagnosed after the age of 40 years. Of patients with PBC, 90% are women. The prevalence is higher in northern European population groups and lower in Japan. Disease prevalence estimates have ranged from 40 to 400 cases per 1,000,000 population, with an incidence between 4 and 30 cases per 1,000,000 per year. In particular the following women are most at risk –

  • Women who are middle aged or older
  • Women who have a family history of PBC.

Symptoms

Some people with PBC will never get any symptoms of the disease. Clear symptoms of PBC are constant tiredness (for some people this can be severe) and intense itching in any part of the body. Itching, also known as pruritus, may be a result of your liver’s inability to process bile. It is thought that bile acids are not the cause of the itching but rather other chemicals that are retained in the body. As with tiredness, the severity of the itching will vary from person to person. Severity is not an indication of the amount of liver damage.

Other symptoms that may develop usually include the following –

  • Dry eyes and/or dry mouth
  • Constant or variable ache or discomfort in the upper right hand side, below your ribs
  • Indigestion, nausea or poor appetite
  • Arthritis (inflammation of the joints)
  • Pain in the bones
  • Mottled palms with red or pink blotches
  • Diarrhoea
  • Dark urine and/or stools
  • Jaundice – yellowing of the skin and whites of the eyes.

Tiredness and itching are generally the first symptoms to appear while jaundice is usually associated with the later stages of the disease.

Complications

Most complications of primary biliary cirrhosis are related to cirrhosis and start after primary biliary cirrhosis progresses to cirrhosis. In some cases, portal hypertension and esophageal varices may develop before cirrhosis.

  • Edema and Ascites
  • Portal Hypertension
  • Varices
  • Splenomegaly
  • Hepatic encephalopathy
  • Gallstones and bile duct stones
  • Metabolic bone diseases
  • Liver cancer
  • Steatorrhea

Treatment

Medications – Stuies suggest ursodiol (Actigall, Urso) to treat primary biliary cirrhosis. Ursodiol is a nontoxic bile acid that people can take orally. Ursodiol replaces the bile acids that are normally produced by the liver, which are more toxic and can harm the liver. Treatment with ursodiol can reduce levels of bilirubin and liver enzymes in the blood. Early treatment with this medication reduces the likelihood of needing a liver transplant and improves survival. Researchers continue to explore other drugs for treating primary biliary cirrhosis. Immunosuppressant drugs, in particular methotrexate (Trexall, Rheumatrex) and colchicine (Colcrys), have been widely used, but their effectiveness remains unproved.

Surgery – A health care provider may consider a liver transplant when cirrhosis leads to liver failure or treatment for complications is ineffective. Liver transplantation is surgery to remove a diseased or an injured liver and replace it with a healthy liver or part of a liver from another person, called a donor.

Lifestyle Changes – People with cirrhosis should not drink any alcohol or take any illegal substances, as both will cause more liver damage. People with cirrhosis should avoid complementary and alternative medications, such as herbs. People with cirrhosis should be careful about starting new medications and should consult a health care provider before taking prescription medications, over-the-counter medications, or vitamins. Many vitamins and prescription and over-the-counter medications can affect liver function.

Alternative Treatment

Vitamin B complex is a group of vitamins (B1, thiamine; B2, riboflavin; B3, niacin; B5, pantothenic acid; B6, pyridoxine; folic acid; betaine; inositol; and B12, cyanocobalamin) that differ from each other in structure and the effect they have on the human body. The B vitamins (thiamine, riboflavin, niacin, pantothenic acid, pyridoxine) play a vital role in numerous metabolic functions including enzyme activities.

Folic acid (vitamin B4) is an important member of the B complex family, known for reducing harmful levels of homocysteine (a sulfur-containing amino acid) known to be a major culprit in heart disease. At normal levels, homocysteine plays a vital role in the biosynthesis of cysteine, which assists glutathione in the liver to detoxify carcinogens and other toxins, but without adequate methylation, which is provided by folic acid and other B vitamins, biochemical reactions generated from beneficial byproducts of homocysteine cannot occur.

Choline is another of the B complex vitamins, essential for the use of fats in the body.

Selenium is a trace element that acts by several mechanisms, including detoxifying liver enzymes, exerting anti-inflammatory effects, and providing antioxidant defense.

Zinc is used in numerous drugs and preparations that are protective: zinc oxide in skin ointments; zinc stearate in acne and eczema preparations; and zinc permanganate to treat bladder inflammation. Zinc deficiency features weakness, decreased taste and appetite, lengthy wound healing, and risk of infection. Zinc levels that are low have also been related to the progression of cirrhosis to hepatic encephalopathy.

Coenzyme Q10 (CoQ10) is an excellent antioxidant that is protective for a liver that has been damaged by ischemia (reduced blood flow). CoQ10 is also an important component of healthy metabolism.

N-acetyl-cysteine (NAC) is a substance that acts as an antioxidant or free-radical scavenger. Most scientific articles related to liver protection with NAC emphasize this effect.

S-Adenosyl Methionine (SAMe) is a methylation agent (a methyl group donor) and is necessary for the synthesis of glutathione, necessary for liver health.

Polyenylphosphatidylcholine (PC) is one of the most important substances for liver protection and health and is a primary constituent of the cell membrane. As such, PC is necessary for integrity of liver cells.

Alpha-lipoic acid is an antioxidant that has been shown to decrease the amount of hepatic fibrosis associated with liver injury. Both of these mechanisms suggest it has promise for cirrhosis.

Acetyl-L-carnitine is the biologically active form of the amino acid L-carnitine that has been shown to protect cells throughout the body from age-related degeneration. By facilitating the youthful transport of fatty acids into the cell mitochondria, acetyl-L-carnitine facilitates conversion of dietary fats to energy and muscle.

Taurine is a conditionally essential amino acid produced from cysteine by the body. It is abundantly found in the body, particularly the central nervous system where it is thought to have a regulating influence. Taurine is a crystallized acid that comes from bile, which is produced by the liver.

L-glutamine is a nonessential amino acid that has benefits for the liver and intestines, particularly for those who use NSAIDs (nonsteroidal anti-inflammatory drugs). L-glutamine may also be useful in neutralizing the effects of alcohol and strengthening the immune system.

L-arginine is an essential amino acid. L-arginine is also a key building block for repair of damaged tissue.

Branched-Chain Amino Acids are considered to be essential amino acids because humans cannot survive unless these amino acids are present in the diet. BCAAs are needed for the maintenance of muscle tissue and appear to preserve muscle stores of glycogen (stored form of carbohydrates that can be converted into energy).

Silymarin (also known as milk thistle or Silybum marinum) is a member of the aster family (Asteraceae) that has been used as a medicinal plant since ancient times and is widely used in traditional European medicine.

 

Reference –

http://patient.info/doctor/primary-biliary-cirrhosis-pro

https://www.aasld.org/sites/default/files/guideline_documents/PrimaryBillaryCirrhosis2009.pdf

http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/cirrhosis-cholangitis-other-cholestatic-liver-disease/

https://www.interceptpharma.com/research-development/therapeutic-areas/primary-biliary-cirrhosis/

http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=GB&Expert=186

http://www.liver.ca/liver-disease/types/primary-biliary-cirrhosis.aspx

http://www.nhs.uk/conditions/Primary-biliary-cirrhosis/Pages/Introduction.aspx

http://www.mayoclinic.org/diseases-conditions/primary-biliary-cirrhosis/basics/definition/con-20029377

http://www.niddk.nih.gov/health-information/health-topics/liver-disease/primary-biliary-cirrhosis/Pages/facts.aspx

http://emedicine.medscape.com/article/171117-overview

http://www.pbcfoundation.org.uk/about-us/services

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(15)00154-3/fulltext?rss%3Dyes

http://www.surgery.ucsf.edu/conditions–procedures/primary-biliary-cirrhosis.aspx

Posted in AUTOIMMUNE
February 3, 2017

Myasthenia Gravis (MG) is a rare life-threatening auto immune neuromuscular junction disorder. The name Myasthenia Gravis is derives from Greek (myasthenia = muscle illness) and Latin (gravis = grave) words, together, meaning “grave muscular weakness”. MG is characterized by painless, fluctuating, fatigable weakness involving specific muscle group.

The prevalence of MG is estimated to be about 20/100,000 population in the United States. It occurs in all races, both genders and at any age, but the average age of onset in females is 28; in males, it’s 42. In about 10 percent of cases, MG begins in childhood (juvenile onset). In some cases, the foetus of a pregnant mother with MG may acquire immune antibodies. Congenital Myasthenia is a rare disorder where babies are born with a genetic defect in neuromuscular transmission similar to MG; however, it is not an auto-immune disorder. This is called Neonatal Myasthenia and is generally temporary, with the child’s symptoms often disappearing within few weeks after birth. Some children may develop MG indistinguishable from adults. MG is not directly inherited nor is it contagious. It does occasionally occur in more than one member of the same family.

Generally, the immune system releases antibodies to attack foreign invaders, such as bacteria. In autoimmune diseases, the antibodies mistakenly attack a person’s own tissues. In myasthenia gravis, they attack and damage muscle cells; in Lambert-Eaton myasthenic syndrome, they attack nerve cells that send messages to muscle.

MG can affect any voluntary muscle i.e. skeletal muscle muscles. Involuntary muscles such as the digestive system, heart and brain are not affected. MG tends to affect the muscles that control movement of the eyes and eyelids, causing ocular weakness, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder.

Causes

  • Muscle Functions

Generally, the brain sends an electrical signal along the motor nerves to the muscle to make movements, during this process, a chemical transmitter – acetylcholine (ACh) is released from the nerve ending. It immediately crosses to the muscle where it

locks onto the ACh receptors (AChR), causing the muscle to contract. The spare ACh

is broken down by ACh esterase, allowing the muscle to relax.

However, in myasthenia gravis the immune system produces antibodies (proteins) that block or damage the muscle acetylcholine receptors, which prevent the muscles contracting. The disruption caused due to this, weakens the muscles.

These antibodies may also block the function of a protein called a muscle-specific receptor tyrosine kinase. This protein is involved in forming the nerve-muscular junction. When antibodies block the function of this protein, it may lead to myasthenia gravis.

 

  • Thymus Gland

Studies suggest that the thymus gland – part of the immune system situated in the upper chest beneath the breastbone, may trigger or maintain the production of the antibodies that block acetylcholine. Thymomas (tumour of the thymus) tend to be noncancerous and occur in 10% of individuals with MG. In 70% of individuals with MG, the thymus contains clusters of immune cells (hyperplasia) that indicate an active immune response.

The exact nature of the relationship between the thymus and MG is still uncertain. It is believed that the abnormal thymus gland may give incorrect instructions to developing immune cells, resulting in auto-immunity and consequently, defective transmission of nerve impulses to muscles.

 

  • Toxic Metals

Heavy metals are metallic elements with a high atomic weight and a density at least five times greater than that of water. Of the 20-plus heavy metals, four– lead (Pb), cadmium (Cd), mercury (Hg), and inorganic arsenic (As)–cause toxicity in humans, even at low levels. Present in toxic waste, they enter the body through the food chain and accumulate in both hard and soft tissue. Other heavy metals, such as nickel, can cause toxicity, but people are less likely to encounter them at toxic levels.

Underlying heavy metal toxicity may contribute to muscle insufficiencies.

 

  • Auto Immune Attack

This factor is always present and is usually connected with the other causes, e.g. mercury and pesticide toxicity and Candida infection can keep the immune system in a state of imbalance, producing auto-immune reactions.

 

  • Other

Symptoms among patient who already have the disease may worsen with some medications, such as beta blockers, calcium channel blockers, quinine, and some antibiotics. Many believe some people have a genetic propensity to developing the disease. The following are known to make symptoms worse:

  • Emotional/mental stress
  • Illness
  • Some medications
  • Tiredness
  • Very high temperatures
  • Muscle relaxants used during surgery
  • Aminoglycoside and Quinolone
  • Antibiotics like – cardiac anti-arrhythmics, local anesthetics, magnesium salts (including milk of magnesia)

Symptoms

The symptoms of myasthenia gravis can come on suddenly, but it may take some time before the condition is correctly diagnosed. MG symptoms tend to progress over time, usually reaching their worst within a few years after the onset of the disease.

The symptoms of myasthenia gravis include –

  • Eye Muscle – The muscles around the eyes are most commonly affected first, as these are constantly used and can quickly tire. This causes drooping of the eyelid, and double vision. In some people, the muscles around the eyes are the only ones affected (when the level of abnormal antibody is low). If symptoms only affect the muscles around the eyes for longer than two years then the condition is unlikely to progress to other muscles. This is known as ocular myasthenia and affects 1 in 6 people with myasthenia gravis.
  • Face and Throat Muscle – Muscles around the face and throat are also often affected. Difficulty in swallowing and slurred speech may be the first signs of myasthenia gravis.
    • Altered SpeakingSpeech may become very soft or nasal, depending on the affected muscles.
    • Limited Facial Expressions
    • Problems in Chewing – The muscles used for chewing may wear out halfway through a meal, particularly if you’ve been eating something hard to chew.
    • Difficulty in Swallowing
  • Neck and Limb muscles – MG can affect the muscles of the arms, legs and neck. This can cause mobility problems, such as a waddling gait, head drop and difficulty performing physical tasks such as lifting.
  • Other Symptoms
    • Breathing
    • Seeing
    • Swallowing
    • Chewing
    • Walking
    • Using your arms or hands
    • Holding up your head

 

 

Diagnosis

The following diagnostic tests will probably be carried out by the GP –

  • Blood Test – A blood test may reveal the presence of abnormal antibodies that disrupt the receptor sites where nerve impulses signal the muscles to move.
  • Ice Pack Test – If the patient is detected with a droopy eyelid, an ice pack test may be conducted. In this test, a bag filled with ice is placed on the patient’s eyelids for 2 minutes; once the bag is removed an analysis for any signs of improvement in the movement of eyelids is carried out.
  • Edrophonium test –This test is usually carried ,out only when other tests have not yet yielded a conclusive diagnosis. Edrophonium chloride (Tensilon, Reversol) or neostigmine (Prostigmin) is injected into a vein – the drug clocks the breakdown of acetylcholine by cholinesterase (cholinesterase inhibitors) and temporarily increases the levels of acetylcholine at the neuromuscular junction – put simply, edrophonium bocks an enzyme that breaks down acetylcholine, the chemical that transmits signals from the nerve ending to the muscle receptor sites. Some patients may experience a brief period in which muscle weakness is relieved, especially those with weakness in the eye muscles.
  • Repetitive nerve stimulation – In this test, electrodes are attached to the skin over the affected muscles. Small electrical pulses are sent through the electrodes to measure how well the nerves send a signal to the muscle. The electrical pulses will be applied several times to determine whether signals get worse when the muscle is tired.
  • Pulmonary function test (spirometry) – In this test, the aim is to determine whether the patient is breathing adequately. The forced vital capacity (the maximum amount of air a person can expel from the lungs after a maximum inspiration) may be periodically measured so as not to miss a gradual worsening of muscular weakness in the lungs. MG patients with severe symptoms are at risk of respiratory failure due to exhaustion of the respiratory muscles. Respiratory failure is when there is inadequate gas exchange by the respiratory system, with the result that arterial oxygen and/or carbon dioxide levels cannot be maintained within their normal ranges.
  • Muscle Biopsy – this is only done if the diagnosis is in doubt and a muscular condition is suspected. A needle or small incision is used to remove a small sample of muscle. The patient will receive a local anesthetic.
  • Single-fiber electromyography (EMG) – Electromyography (EMG) measures the electrical activity traveling between your brain and your muscle. It involves inserting a fine wire electrode through your skin and into a muscle. In a single-fiber EMG, doctors test a single muscle fiber.
  • Imaging Scans – Doctors at times prescribe CT scan or MRI test to check if there’s a tumor or other abnormality in the thymus.

Treatment

  • Medications
    • Cholinesterase inhibitors – These inhibitors block the action of the chemical that normally makes the muscle relax after it has contracted. They improve communication between nerves and muscles. This medication is very effective for patients with mild MG symptoms. Some side effects may include nausea and/or stomach cramps.
    • Steroids or Immunosuppressant – These help in altering the body’s immune system and lower the production of antibodies that cause MG. This includes – prednisolone (a steroid drug) or azathioprine (an immunosuppressant drug)

 

  • Therapies
    • Plasmapheresis – In this therapy blood is removed from the body, the plasma (the abnormal antibodies that cause MG) is separated from the cells, the cells are then suspended in saline (or a plasma substitute or donor plasma), and the reconstituted solution is returned to the patient.
    • Intravenous immunoglobulin therapy – In this therapy, normal antibodies that alter the way the immune system acts are injected into the patient.

 

  • Removal of the thymus gland (thymectomy) – About 15 percent of the people with myasthenia gravis have a tumor in their thymus gland, a gland under the breastbone that is involved with the immune system. A thymectomy may be performed as an open surgery or as a minimally invasive surgery.

Alternative Treatment

Environmental Medicine is a branch of medicine whose domain is not limited by anatomical boundaries but, rather, is concerned with the whole person and the way that a person reacts to his/her total environment. It involves treating the cause of the disease. In MG, the treatment involves –

  • Herbs – Herbs like Liquorice and Kallawala (Polypodium leucotomos) can insignificantly turn off the auto-immune destructive reactions that maintain the disease. Also, colloidal silver (used to fight the infections) has some immune regulatory and healing effect. These herbs act as repairing agents for the immune system.
  • Thymus Treatment – Herbs like Echinacea, yarrow, thyme, barley grasslicorice, olive leafpau d’arco rosehips, wheatgrass help in keeping the thymus gland strong and enhances its immunity. Cruciferous vegetables like broccoli, cauli flower, cabbage etc. also appear to enhance thymus function, as do the essential oils of bergamot,clove, tea tree, oregano, thyme and eucalyptus, Nutrients like black current oil, organic germanium, vitamin A and beta carotene and zinc helps the thymus function.
  • Biodetoxification Program – The Center’s Bio-detoxification Program utilizes clinical procedures that safely reduce the body’s burden of toxic chemicals, including chemicals stored following occupational, accidental, and/or chronic airborne exposures.
  • Alka Vita Supplements – This has the tremendous advantage that it alkalises, therefore increases oxygenation, counteracts free radical attack and damage and therefore undermines the basis of disease. It is also directly ‘anti-septic’ against fungal infections, including Candida and possibly all harmful micro-organisms and parasites, although there is not enough information on this, we do know that all anaerobic infections (the harmful ones) are attacked by free electrons that Alka- vita supplies and are eventually destroyed or severely limited by an alkaline environment.
  • Colloidal Silver – Eliminates infections of various types, known and unknown that contribute to auto-immune disorders leading to the improper function of the immune function.
  • Vitamin Supplements -Different Vitamins are essential to aid the immune system and many biochemical processes including the utilisation of calcium and magnesium. Its deficiency is almost universal in northern climates and even more so since the introduction of sun screen. Its deficiency has been linked strongly to auto-immune diseases.
  • Omega 3 Fatty Acids – For improving the body function.
  • Exercise – Helps to –
    • Increase flexibility
    • Improve range of motion of your joints
    • Boost circulation
    • Promote better posture
    • Relieve stress

References –

www.musculardystrophyuk.org

www.medind.nic.in

www.mayoclinic.org

www.healthcommunities.com

www.myasthenia.org

www.mda.org.au

www.mga-charity.ie

www.nhs.uk

www.chealth.canoe.com

www.healthcommunities.com

www.regenerativenutrition.com

Posted in AUTOIMMUNE
February 3, 2017

Mixed connective tissue disease (MCTD) is an autoimmune disease first described in 1972 and is considered an “overlap” of three diseases, systemic lupus erythematosus (lupus), scleroderma and polymyositis. People with MCTD experience symptoms of each of these three diseases. In many cases, this mixed set of symptoms is eventually dominated by symptoms characteristic of one of the three illnesses, especially scleroderma or lupus.

Mixed connective tissue disease has features of three other connective tissue diseases –

  • Systemic lupus erythematosus (SLE) – An inflammatory disease that can affect many different organs. Symptoms include fever, fatigue, joint pains, weakness, and skin rashes on the face, neck, and upper body.
  • Scleroderma – Abnormal thickening and hardening of the skin, underlying tissue, and organs
  • Polymyositis – Muscle inflammation (swelling)

About 25% of patients with a connective tissue disease (such as dermatomyositis, rheumatoid arthritis, Sjogren’s syndrome, and the three disease listed above), develop another connective tissue disease over the course of several years. This is known as an “overlap syndrome.”

Mixed connective tissue disease occurs most often in women and is usually diagnosed in young adults in their 20s and 30s. Children have also been diagnosed with mixed connective tissue disease.

Mixed connective tissue disease is somewhat of a controversial term among arthritis specialists (rheumatologists). Some question whether mixed connective tissue disease is its own specific disease or whether it’s a precursor to another connective tissue disease.

Causes

The exact underlying cause of mixed connective tissue disease (MCTD) is currently unknown. It is an autoimmune disorder, which means the immune system mistakes normal, healthy cells for those that that body should “fight off.” There are ongoing studies exploring how immune system dysfunction may be involved in the development of this condition.

Risk Factors

Mixed connective tissue disease can occur in people of any age. However, it appears to be most common in women under the age of 30.

Symptoms

In the beginning stages, patients who have MCTD have symptoms similar to those of patients with other connective tissue disorders, including –

  • Fatigue
  • Muscle pain with no apparent cause
  • Joint pain
  • Low-grade fever
  • Raynaud phenomenon (reduced blood flow to the fingers, toes, ears, and nose). This causes sensitivity, numbness, and loss of color in these areas.

Less common early symptoms may include –

  • Severe polymyositis, often in the shoulders and upper arms
  • Acute (intense) arthritis
  • Aseptic meningitis (inflammation of the brain and spinal cord meninges, not caused by a bacteria or virus)
  • Myelitis (inflammation of the spinal cord)
  • Gangrene (death and decay) of fingers or toes
  • High fever
  • Abdominal pain
  • Neuropathy (nerve disorders) affecting the trigeminal nerve in the face
  • Hearing loss

The “classic” symptoms of MCTD are –

  • Raynaud phenomenon
  • swollen “sausage-like” fingers, sometimes temporary but at other times progressing into sclerodactyly (thin fingers with hardened skin and limited movement)
  • inflamed joints and muscles
  • pulmonary hypertension (high blood pressure in the blood vessels of the lungs)

Complications

Mixed connective tissue disease can lead to serious complications, including –

  • High blood pressure in the lungs (pulmonary hypertension) – This condition is the main cause of death in people with mixed connective tissue disease.
  • Interstitial lung disease – This large group of disorders can cause scarring in the lungs, which affects the ability to breathe.
  • Heart disease – Parts of the heart may become enlarged, or inflammation may occur around the heart. Heart disease is the cause of death in about 20 percent of people with mixed connective tissue disease.
  • Kidney damage – About one-fourth of people with mixed connective tissue disease develop kidney problems. Sometimes, that damage can lead to kidney failure.
  • Digestive tract damage – People may develop abdominal pain and problems with digesting food.
  • Anemia – About 75 percent of people with mixed connective tissue disease have iron deficiency anemia.
  • Tissue death (necrosis) – People with severe Raynaud’s phenomenon can develop gangrene in the fingers.
  • Hearing loss – Often unrecognized, hearing loss may occur in as many as half the people with mixed connective tissue disease.

Treatment

Treatment for MCTD depends on which organs are involved and the severity of the disease. Some people need continuous treatment, while others need it only during periods of heightened disease activity, called flares.

Treatment may include corticosteroids to reduce inflammation and immunosuppressive drugs to suppress the immune system and its attack on healthy tissue. Other medications may be prescribed to treat or reduce the risk of certain complications of the disease.

Treatment considerations include the following –

  • Pulmonary hypertension is the most common cause of death in people with MCTD, and must be treated with antihypertensive medications.
  • People with a mild form of MCTD may not need treatment, or only low doses of nonsteroidal anti-inflammatory drugs, antimalarials, or low-dose corticosteroids (such as prednisone) to treat inflammation.
  • Higher doses of corticosteroids are often used to manage the signs and symptoms of moderate to severe MCTD. If major organs are affected, the patient may have to take immunosuppressants (to suppress the immune system).
  • MCTD patients are also at risk of developing heart disease, including an enlarged heart or pericarditis (inflammation around the heart). Patients may need regularly scheduled electrocardiograms to monitor the heart’s condition.

Alternative Treatment

Acupuncture – An acupuncture practitioner inserts tiny needles into the skin at precise points on the body. Studies of acupuncture have found it may help relieve many types of pain. Acupuncture is safe when done by a certified practitioner.

Fish oil supplements – Fish oil supplements have shown some promise in relieving signs and symptoms of other connective tissue diseases, such as lupus and rheumatoid arthritis. Fish oil supplements may help relieve joint pain and stiffness.

Hypnosis – During a hypnotherapy session, a therapist talks in a gentle voice that helps you relax. The therapist helps you reach a state of altered consciousness that lets people focus their mind on their goals or think positively about their challenges. Hypnosis may help relieve pain and stress.

Relaxation techniques – Relaxation techniques may help people take their mind off their signs and symptoms and help people relax. Relaxation techniques include activities such as progressive muscle relaxation and guided imagery. People can learn relaxation techniques from a therapist, or they can do them on their own. Relaxation techniques are generally safe.

Flaxseed – Flaxseed contains a fatty acid called alpha-linolenic acid, which may decrease inflammation in the body. Some studies have found that kidney function may improve in lupus patients who have kidney problems, such as like lupus nephritis. Abdominal pain and bloating can be side effects of taking flaxseed.

DHEA – DHEA is a steroid molecule manufactured by the cholesterol-pregnenolone pathway, and is an intermediate to androstenediol and androstenedione, which have the potential to become either estrone or testosterone. Supplements containing this hormone have been shown to reduce the dose of steroids needed to stabilize symptoms in some people who have lupus

Herbal Medicine – Feverfew, goldenseal, and pau d’arco are just a few of the helpful herbs one can use, please consult the physician before adding any of these supplements as they may interfere with the other medications or have unwanted effects.

Chiropractic therapy – This therapy relies on the manipulation of the spine to improve the mobility of the joints and reduce pain. Chiropractic therapy practitioners have to go through training and licensing exams, and chiropractic care is often covered by insurance.

Vitamin A – Vitamin A is an antioxidant and is commonly found in whole milk, liver, and some fortified foods. Beta-carotene is a pro-vitamin found in carrots and many colorful vegetables that are then converted to vitamin A in the body. Vitamin A protects against free radicals (harmful substances in your body) which can damage DNA and lead to cancer and other diseases, and has anti-inflammatory effects.

Vitamin D – People with lupus have shown some benefits from taking Vitamin D supplements   In recent testing, high doses of vitamin D were safe and appeared to temper some of the destructive immune system responses believed to cause lupus. Research is pointing to an immune-regulating role for vitamin D.

Vitamin E – This vitamin supplement comes in several different forms. The alpha-tocopherol type of Vitamin E may help prevent heart disease by slowing the release of inflammatory substances that damage the heart.* Alpha-tocopherol also might be effective for easing lung .inflammation related to allergies. However, because studies were conducted on animals, it’s not yet clear whether the results will translate to humans.

Evening primrose oil – Used to treat inflammation, evening primrose oil is associated with alleviating rheumatoid arthritis.

 

Reference –

https://www.cedars-sinai.edu/Patients/Health-Conditions/Mixed-Connective-Tissue-Disease.aspx

http://www.cincinnatichildrens.org/health/m/mctd/

https://www.fightlikeagirlclub.com/category/fight-like-a-girl-power-stories/mixed-connective-tissue-disease-stories/

https://www.hss.edu/conditions_undifferentiated-connective-tissue-disease-overview.asp

http://lupusmctd.com/index.php?topic=1088.0;wap2

http://www.arthritisvirginia.com/mixed-connective-tissue-disease.php

http://patient.info/doctor/mixed-connective-tissue-disease

http://www.mayoclinic.org/diseases-conditions/mixed-connective-tissue-disease/basics/causes/con-20026515

http://www.sclero.org/scleroderma/support/stories/english/s/silezia/a-to-z.html

http://www.homeopathicmd.com/2011/04/psychosomatics-and-homeopathy/

Posted in AUTOIMMUNE
February 3, 2017

Lynch syndrome (LS) is a condition that can run in families. It is also known as hereditary non-polyposis colorectal cancer (HNPCC). LS doesn’t cause any symptoms itself. But people with LS have an increased risk of developing bowel cancer, cancer of the womb and some other cancers. If the family has a history of developing these cancers at a young age (under 50), it is possible that people have the altered gene that causes LS.

It is estimated that around 1 in 440 Americans possess a gene mutation associated with Lynch syndrome. The condition is most commonly associated with greater risk of colorectal cancer, accounting for around 3-5% of all cases. Women with Lynch syndrome, however, are also at 40-60% greater risk of endometrial cancer – a cancer that begins in the lining of the uterus, called the endometrium.

Some people with Lynch syndrome may also develop sebaceous adenomas, which are noncancerous tumors of an oil-producing gland in the skin.

Lynch syndrome is caused by a change in a gene that normally functions to protect a person from getting cancer. If you have a parent or sibling with Lynch syndrome, you are potentially at risk of developing Lynch syndrome. If you have been diagnosed with Lynch syndrome, your children are at risk. When a parent carries a change known as a mutation, in one of the Lynch syndrome genes, they have one working and one non-working copy of the gene. Each child will have a 50% chance of inheriting the gene mutation.

Not everyone with Lynch syndrome will develop bowel cancer. A person who inherits a Lynch syndrome mutation has around 30-50% chance of developing cancer (risks vary depending upon which gene is affected) unless preventative measures are taken. Developing bowel cancer at a young age is not uncommon.

Causes

Lynch Syndrome is caused by an abnormality in one of four mismatch repair genes (MLH1, MSH2, MSH6, and PMS2). These are the genes responsible for correcting mistakes that occur in genes when body cells divide.   More recently an error in a gene called EPCAM has been identified and this also stops the MSH2 gene working properly meaning it can’t fix up those “spelling” mistakes.

Nearly every cell in our bodies contains two copies of each gene and genes are the “instruction manuals” for building and running the body. DNA is the genetic material within each cell that contains instructions for every chemical process in the cells of the body. As cells grow and divide they make copies of their DNA and it is common for minor mistakes to occur.   Normally the mismatch repair genes recognize these mistakes and repair them, similar to the “spell check” function on your computer. However, people who inherit a fault in one of the four mismatch repair genes lack the ability to repair these minor mistakes. An accumulation of these mistakes may eventually lead to the development of a cancer.    

Inheritence

Men and women can inherit a gene mutation associated with Lynch syndrome from either their mother or father. People with one of these mutations can also pass it on to their children. If one parent has the mutation in 1 of the 2 copies of a Lynch syndrome gene, a child has a 50% chance of inheriting the gene mutation. This also means there is a 50% chance that a child will not inherit the gene mutation.

Healthcare professionals use certain criteria to determine if a Lynch syndrome gene mutation may be present in a family. These are referred to as the Amsterdam criteria.

  • At least 3 family members have colorectal cancer or another cancer related to Lynch syndrome. At least 1 of these family members is a first-degree relative (parent, sibling or child) of the other 2 family members.
  • At least 1 family member was diagnosed with cancer before age 50.
  • Cancer occurs in at least 2 generations in a row.
  • FAP has been ruled out.

Symptoms

People with Lynch syndrome may have –

  • Colon cancer that occurs at a young age, especially before age 45
  • A family history of colon cancer that occurs at a young age
  • A family history of endometrial cancer
  • A family history of other related cancers, including ovarian cancer, kidney cancer, stomach cancer, small bowel cancer, liver cancer or other cancers

Those with Lynch syndrome have a 70 percent chance of developing colon cancer by age 70. Colon cancer patients with Lynch syndrome have an estimated 40 percent risk of developing a second primary colon cancer within seven years of being diagnosed after the first tumor. Women with Lynch syndrome have a 40 percent to 60 percent estimated lifetime risk of developing endometrial cancer.

Lynch syndrome may also increase a person’s risk for cancers of the stomach, ovary, urinary tract, hepatobiliary tract, brain, small intestine, skin and pancreas.

Treatment

Surgery is recommended to remove the colon (subtotal colectomy) if colon cancer is detected in someone with a known diagnosis of Lynch syndrome due to the high risk for second primary colon cancers. Surgery to remove the uterus and ovaries before cancer develops (prophylactic) is a consideration for women who have Lynch syndrome and have completed childbearing. Individuals with Lynch syndrome should be monitored every one or two years with examinations of the colon (colonoscopy) beginning at age 20-25 or 2 to 5 years before the youngest age that a family member was diagnosed, whichever is earlier. Prophylactic removal of the colon is not usually recommended because colonoscopy is usually effective in detecting colon cancer at an early stage or at preventing colon cancer entirely.

Genetic counseling is recommended for affected individuals and their family members. Other treatment is symptomatic and supportive.

Alternative Treatment

Calcium & Vitamin D – There is evidence that higher calcium and vitamin D intake lowers the risk of developing colon cancer.

Folic Acid – In observational studies, low folate has been linked to increased risk of colon cancer. However, some data suggest that high intake of folate may have a paradoxical effect, raising the risk of developing colorectal cancer in some individuals.

Selenium – In several studies, selenium status was lower in those with adenomas and colon cancer versus controls. One study of selenium-deficient patients with a history of adenomas showed that repletion of selenium corrected both selenium status and activity of glutathione peroxidase in the colonic mucosa.

Curcumin, the collective term for the 3 curcuminoids that give Turmeric (Curcuma longa) its distinct yellow color, may be the most well-characterized chemopreventative agent from any spice. Spices are collectively composed of a myriad of chemopreventative phytochemicals, including phenolics, terpenoids, and flavonoids

Omega-3 fatty acids – Omega 3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have potent anti-inflammatory effects. There is also evidence for direct protective effects regarding proliferation, apoptosis, angiogenesis, and metastasis in colon cancer cells.

Garlic (Allium sativum) – The anticarcinogenic effects of garlic are thought to be derived primarily from organosulfur compounds, including the odiferous diallyl sulfide that gives garlic its distinct smell.106 Garlic and its constituents have been well proven to lessen CRC carcinogenesis, reduce proliferation, block angiogenesis, induce differentiation and apoptosis, inhibit cyclooxygenase-2 and squelch free radical.

Probiotics – The interplay between dietary components and the microbiota of the colon is thought to have a integral role in carcinogenic processes of the colonic epithelium, as well as overall health and disease. The short-chain fatty acid butyrate is a product of microbiota metabolism of fiber from the diet, and butyrate is involved in colonic homeostasis of colonic crypts. Many other compounds formed from microflora may influence the inflammatory environment of the colon, systemic immune function, and the presence of bioactive compounds locally that may promote or inhibit carcinogenic processes.

Green tea components such as polyphenols (eg, epigallocatechin-3-gallate, EGCG) can affect colorectal carcinogenic processes.

 

Reference –

http://www.nzfgcs.co.nz/syndromes/lynch-syndrome

http://www.cancer.ca/en/cancer-information/cancer-101/what-is-a-risk-factor/genetic-risk/lynch-syndrome/?region=on

http://www.lynch-syndrome-uk.org/

http://www.macmillan.org.uk/information-and-support/diagnosing/causes-and-risk-factors/genetic-testing-and-counselling/lynch-syndrome.html

http://www.medicalnewstoday.com/articles/296384.php

http://www.abc.net.au/news/2015-03-21/cancer-riddled-family-speaks-out-about-lynch-syndrome/6327544

http://www.webmd.com/colorectal-cancer/lynch-syndromes

http://www.hopkinsmedicine.org/gastroenterology_hepatology/diseases_conditions/small_large_intestine/hereditary_nonpolyposis_colorectal_cancer.html

Posted in AUTOIMMUNE