List of autoimmune diseases

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I was researching autoimmune disease and  found this list of many of them. It is eye opening to say the least. I was amazed how many there are. I actually have several on the list. So, in my attempt to educate others on autoimmune diseases, here is the list I found from the webpage “American Autoimmune Related Diseases Association”:

List of Autoimmune and Autoimmune-Related Diseases

 

  • Acute Disseminated Encephalomyelitis (ADEM)
  • Acute necrotizing hemorrhagic leukoencephalitis
  • Addison’s disease
  • Agammaglobulinemia
  • Allergic asthma
  • Allergic rhinitis
  • Alopecia areata
  • Amyloidosis
  • Ankylosing spondylitis
  • Anti-GBM/Anti-TBM nephritis
  • Antiphospholipid syndrome (APS)
  • Autoimmune aplastic anemia
  • Autoimmune dysautonomia
  • Autoimmune hepatitis
  • Autoimmune hyperlipidemia
  • Autoimmune immunodeficiency
  • Autoimmune inner ear disease (AIED)
  • Autoimmune myocarditis
  • Autoimmune pancreatitis
  • Autoimmune retinopathy
  • Autoimmune thrombocytopenic purpura (ATP)
  • Autoimmune thyroid disease
  • Axonal & neuronal neuropathies
  • Balo disease
  • Behcet’s disease
  • Bullous pemphigoid
  • Cardiomyopathy
  • Castleman disease
  • Celiac sprue
  • Chagas disease
  • Chronic fatigue syndrome
  • Chronic inflammatory demyelinating polyneuropathy (CIDP)
  • Chronic recurrent multifocal ostomyelitis (CRMO) 
  • Churg-Strauss syndrome
  • Cicatricial pemphigoid/benign mucosal pemphigoid
  • Crohn’s disease
  • Cogans syndrome
  • Cold agglutinin disease
  • Congenital heart block
  • Coxsackie myocarditis
  • CREST disease
  • Essential mixed cryoglobulinemia
  • Demyelinating neuropathies
  • Dermatitis herpetiformis 
  • Dermatomyositis
  • Devic’s disease (neuromyelitis optica)
  • Discoid lupus
  • Dressler’s syndrome
  • Endometriosis
  • Eosinophilic fasciitis
  • Erythema nodosum
  • Experimental allergic encephalomyelitis
  • Evans syndrome
  • Fibromyalgia**
  • Fibrosing alveolitis
  • Giant cell arteritis (temporal arteritis)
  • Glomerulonephritis
  • Goodpasture’s syndrome
  • Graves’ disease
  • Guillain-Barre syndrome
  • Hashimoto’s encephalitis
  • Hashimoto’s thyroiditis
  • Hemolytic anemia
  • Henoch-Schonlein purpura
  • Herpes gestationis
  • Hypogammaglobulinemia
  • Idiopathic thrombocytopenic purpura (ITP)
  • IgA nephropathy
  • IgG4-related sclerosing disease
  • Immunoregulatory lipoproteins
  • Inclusion body myositis
  • Insulin-dependent diabetes (type1)
  • Interstitial cystitis
  • Juvenile arthritis
  • Juvenile diabetes
  • Kawasaki syndrome
  • Lambert-Eaton syndrome
  • Leukocytoclastic vasculitis
  • Lichen planus
  • Lichen sclerosus
  • Ligneous conjunctivitis
  • Linear IgA disease (LAD)
  • Lupus (SLE)
  • Lyme disease, chronic 
  • Meniere’s disease
  • Microscopic polyangiitis
  • Mixed connective tissue disease (MCTD)
  • Mooren’s ulcer
  • Mucha-Habermann disease
  • Multiple sclerosis
  • Myasthenia gravis
  • Myositis
  • Narcolepsy
  • Neuromyelitis optica (Devic’s)
  • Neutropenia
  • Ocular cicatricial pemphigoid
  • Optic neuritis
  • Palindromic rheumatism
  • PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus)
  • Paraneoplastic cerebellar degeneration
  • Paroxysmal nocturnal hemoglobinuria (PNH)
  • Parry Romberg syndrome
  • Parsonnage-Turner syndrome
  • Pars planitis (peripheral uveitis)
  • Pemphigus
  • Peripheral neuropathy
  • Perivenous encephalomyelitis
  • Pernicious anemia
  • POEMS syndrome
  • Polyarteritis nodosa
  • Type I, II, & III autoimmune polyglandular syndromes
  • Polymyalgia rheumatica
  • Polymyositis
  • Postmyocardial infarction syndrome
  • Postpericardiotomy syndrome
  • Progesterone dermatitis
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis 
  • Psoriasis
  • Psoriatic arthritis
  • Idiopathic pulmonary fibrosis
  • Pyoderma gangrenosum
  • Pure red cell aplasia
  • Raynauds phenomenon
  • Reflex sympathetic dystrophy
  • Reiter’s syndrome
  • Relapsing polychondritis
  • Restless legs syndrome
  • Retroperitoneal Fibrosis
  • Rheumatic fever
  • Rheumatoid arthritis
  • Sarcoidosis
  • Schmidt syndrome
  • Scleritis
  • Scleroderma
  • Sjogren’s syndrome
  • Sperm & testicular autoimmunity
  • Stiff person syndrome
  • Subacute bacterial endocarditis (SBE)
  • Susac’s syndrome
  • Sympathetic ophthalmia
  • Takayasu’s arteritis
  • Temporal arteritis/Giant cell arteritis
  • Thrombocytopenic purpura (TTP)
  • Tolosa-Hunt syndrome
  • Transverse myelitis
  • Ulcerative colitis
  • Undifferentiated connective tissue disease (UCTD)
  • Uveitis
  • Vasculitis
  • Vesiculobullous dermatosis
  • Vitiligo
  • Wegener’s granulomatosis

**NOTE Fibromyalgia and Chronic Fatigue are listed, not because they are autoimmune, but because many persons who suffer from them have associated autoimmune disease(s)

Tremors In Lupus Patients

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To start this post, I find it is important to describe what the definition of tremor is. Here is the definition from wikipedia:

A tremor is an involuntary,[1] somewhat rhythmic, muscle contraction and relaxation involving to and fro movements (oscillations or twitching) of one or more body parts. It is the most common of all involuntary movements and can affect the hands, arms, eyes, face, head, vocal folds, trunk, and legs. Most tremors occur in the hands. In some people, tremor is a symptom of another neurological disorder. A very common kind of tremor is the chattering of teeth, usually induced by cold temperatures or by fear.

This would seem to be a complete definition but the things I experience do not necessarily fit into this tight definition. I do experience hands shaking, sometimes lip quivering, and muscle twitches at times. The shaking I get that drives me bonkers is where it feels like the whole inside of my body is shaking and it may or may not show in my hands or other body area. It is quite frustrating and scary. It makes me stop whatever I am doing and have to try to lay down and rest to relax my body. It does not seem to be anxiety related either. It cans trike me at random and is puzzling and frightening. So, as I usually do, I thought I would research this out too.

Amazingly, I found not one shred of medical information regarding this, other than others who have had this experience. I usually find things on medical boards or places like medline or webmd but not in this instance. It made me wonder if any of you have had this happen to you too.

I know I saw quite a few others asking this same question as well. I know I am not alone in this. It just may take some time until more is known in the realm of medical professionals for me to find anything online.

Periphreal Neuropathy Treatment and Drugs

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Part 8 in this series from the Mayo Clinic

Treatment and Drugs

Treatments and drugs

By Mayo Clinic staff

One goal of treatment is to manage the condition causing your neuropathy. If the underlying cause is corrected, the neuropathy often improves on its own. Another goal of treatment is to relieve the painful symptoms.

Medications
Many types of medications can be used to relieve the pain of peripheral neuropathy, including:

  • Pain relievers. Mild symptoms may be relieved by over-the-counter pain medications. For more-severe symptoms, your doctor may recommend prescription painkillers. Drugs containing opiates, such as codeine, can lead to dependence, constipation or sedation, so these drugs are generally prescribed only when other treatments fail.
  • Anti-seizure medications. Drugs such as gabapentin (Gralise, Neurontin), topiramate (Topamax), pregabalin (Lyrica), carbamazepine (Carbatrol, Tegretol) and phenytoin (Dilantin, Phenytek) were originally developed to treat epilepsy. However, doctors often also prescribe them for nerve pain. Side effects may include drowsiness and dizziness.
  • Capsaicin. A cream containing this naturally occurring substance found in hot peppers can cause modest improvements in peripheral neuropathy symptoms. Like spicy foods, it may take some time and gradual exposure to get used to because of the hot sensation this cream creates. Generally, you have to get used to the heat before you can experience pain relief. Doctors may suggest you use this cream with other treatments.
  • Lidocaine patch. This patch contains the topical anesthetic lidocaine. You apply it to the area where your pain is most severe, and you can use up to four patches a day to relieve pain. This treatment has almost no side effects except, for some people, a rash at the site of the patch.
  • Antidepressants. Tricyclic antidepressant medications, such as amitriptyline and nortriptyline (Aventyl, Pamelor), were originally developed to treat depression. However, they have been found to help relieve pain by interfering with chemical processes in your brain and spinal cord that cause you to feel pain. The serotonin and norepinephrine reuptake inhibitor duloxetine (Cymbalta) also has proved effective for peripheral neuropathy caused by diabetes. Side effects may include nausea, drowsiness, dizziness, decreased appetite and constipation.

Therapies
Transcutaneous electrical nerve stimulation (TENS) may help to relieve symptoms. In this therapy, adhesive electrodes are placed on the skin, and a gentle electric current is delivered through the electrodes at varying frequencies. TENS has to be applied regularly.

Periphreal Neuropathy Causes

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Part 3 of the series on this subject from the Mayo Clinic website.

Causes

Causes

By Mayo Clinic staff

It’s not always easy to pinpoint the cause of peripheral neuropathy, because a number of factors can cause neuropathies. These factors include:

  • Alcoholism. Many alcoholics develop peripheral neuropathy because they make poor dietary choices, leading to vitamin deficiencies.
  • Autoimmune diseases. These include lupus, rheumatoid arthritis and Guillain-Barre syndrome.
  • Diabetes. When damage occurs to several nerves, the cause frequently is diabetes. At least half of all people with diabetes develop some type of neuropathy.
  • Exposure to poisons. These may include some toxic substances, such as heavy metals, and certain medications — especially those used to treat cancer (chemotherapy).
  • Infections. Certain viral or bacterial infections can cause peripheral neuropathy, including Lyme disease, shingles (varicella-zoster), Epstein-Barr, hepatitis C and HIV/AIDS.
  • Inherited disorders. Examples include Charcot-Marie-Tooth disease and amyloid polyneuropathy.
  • Trauma or pressure on the nerve. Traumas, such as motor vehicle accidents, falls or sports injuries, can sever or damage peripheral nerves. Nerve pressure can result from using a cast or crutches, spending a long time in an unnatural position or repeating a motion many times — such as typing.
  • Tumors. Growths can form directly on the nerves themselves, or tumors can exert pressure on surrounding nerves. Both cancerous (malignant) and noncancerous (benign) tumors can contribute to peripheral neuropathy.
  • Vitamin deficiencies. B vitamins — B-1, B-6 and B-12 — are particularly important to nerve health. Vitamin E and niacin also are crucial to nerve health.
  • Other diseases. Kidney disease, liver disease and an underactive thyroid (hypothyroidism) also can cause peripheral neuropathy.

Periphreal Neuropathy Definition

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Well, in light of the progression of my neuropathy, I decided to check out more information. I went to the Mayo Clinic website and found this information. I have re-read the information in light of the new developments in my case. As with any portion of our lupus, or autoimmune journeys always talk to your doctor before starting any new treatments.

From Mayo Clinic website:

Periphreal Neuropathy

Definition

By Mayo Clinic staff

Peripheral neuropathy, a result of nerve damage, often causes numbness and pain in your hands and feet. People typically describe the pain of peripheral neuropathy as tingling or burning, while they may compare the loss of sensation to the feeling of wearing a thin stocking or glove.

Peripheral neuropathy can result from problems such as traumatic injuries, infections, metabolic problems and exposure to toxins. One of the most common causes is diabetes.

In many cases, peripheral neuropathy symptoms improve with time — especially if the condition is caused by an underlying condition that can be treated. A number of medications often are used to reduce the painful symptoms of peripheral neuropathy.

 

Guillain Barre Syndrome Overview

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Well, I looked around and found this interesting fact sheet on GBS, or Guillain Barre Syndrome. It is a serious condition and can cause death pretty quickly in some cases. This information came from the website: guillainbarresyndrome.net. For further information, please consult your own doctor or go to the webpage listed above for more detailed information.

 

Guillain Barre Syndrome is a rare and severe disease. It occurs after an acute infectious procedure. Guillain Barre Syndrome initially affects the peripheral nervous system. Normally it is acute form of paralysis in lower body area that moves towards upper limb and face. Gradually patient loses all his reflexes and goes through a complete body paralysis. Guillain Barre Syndrome is a life threatening disorder and needs timely treatment and supportive care with intravenous immunoglobulins or plasmapheresis. Unfortunately many people lose their lives without proper and prompt medical treatment. Dysautonomia and Pulmonary complications are the basic reason for death other fatal complications.

Symptoms and Signs!

guillainbarresyndrome Guillain Barre SyndromeAlthough Guillain Barre Syndrome is a fatal and complicated disorder of peripheral nervous system, however there are many symptoms and signs that enable you to suspect the disease at beginning. Guillain Barre Syndrome is a result of antigens that weakened the immune system. These infectious antigens attack the nervous system and damage the nerves. This auto-immune infection turns the peripheral nerves in inflammation of conduction block and myelin. The primary result would be minor muscle paralysis. Though autonomic disturbances or sensory occurs on acute complications. The most severe and obvious complication of Serum sickness is Guillain Barre Syndrome (GBS). Guillain Barre Syndrome is type of auto-immune disorder by low hypersensitivity reaction. Nausea, vomiting, loss of appetite, stomach pain, migraines, low grade fevers and chills are quite apparent symptoms of GBS. The regular headaches and migraines are result of Central Nervous System Disorder. Constant exhaustion, tiredness and pain in the back of head are early signs of Guillain Barre Syndrome. The disease initially appears in lower limb and affects the muscle reflexes. Paralysis in lower limb and legs are commonly called rubbery legs or tingling and numbness in legs. Afterwards this syndrome travels in upper part of the limb. Generally in short span of time facial muscles and arms get affected and become completely paralyzed. Normally the lower cranial nerves get damaged and lead to bulbar weakness. It affects the swallowing and breathing resulting in constant drooling. In acute cases of Guillain Barre Syndrome patients complains of temporary Bladder dysfunction. The obvious indication of GBS is pain; it is quite similar to the aching that you get after over exercise or jogging.

Diagnosis!

Constant severe pain in muscles and mild fever are common symptoms of Guillain Barre Syndrome. Usually there are many other signs like orthostatic hypotension, hypertension and unusual fluctuations in blood pressure. Prompt medical procedure ensures fast recovery and fewer complications. However If you start the treatment at late or at complicated stage then chances of recovery are very low. Success of any Guillain Barre Syndrome Diagnosis depend upon the medical reports and findings like fast growing muscle paralysis, absence of fever, a possible pro-active incident and areflexia. Normally CSF and ECD are most common treatments used to confirm and cure the disease. Sometime these treatments failed to detect early symptoms of Guillain Barre Syndrome. Generally after a week or two patients recognize the signs and then report the syndrome. At the moment there is no effective cure for Guillain Barre Syndrome. Though there are many possible medical procedures to diagnose, that may help in reducing the fatal aspect of this severe disease.

CSF

CSF is commonly used and quite successful for the findings and evidences of Guillain Barre Syndrome. Average CSF findings contain information and details of albumino-cytological dissociation. Compared to infectious symptoms, CSF is a high level protein 100 – 1000 mg/dL instead of the supplementary pleocytosis. Continuous usage of the pleocytosis may boost the immune system to resist the infections. Research has proven that high quantity of protein and pleocytosis in the CSF is essential for the diffusion of white blood cells in the myelin. In early stages of Guillain Barre Syndrome anti-inflammatory drugs and painkillers combined to offer instant relief in severe pain. Often doctors suggest blood thinners to control and prevent blood clotting.

Antibodies Role in Neurological Symptoms of Lupus

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A friend of mine posted this on facebook and I thought it was an interesting article so I am reposting it here as well. This information came from the web page http://www.prweb.com/releases/neurological_symptoms/lupus_sle/prweb4748694.htm

Feel free to share your thoughts on this article int he comments section below…

How Antibodies Play a Role in Triggering Neurological Symptoms of Lupus

Betty Diamond, MD, head of the Center for Autoimmune and Musculoskeletal Disorders at the Feinstein Institute, has collaborated with colleagues at the Burke Cornell Medical Research Institute to identify two distinct mechanisms that explain the how lupus autoantibodies alter brain function and led to such a wide array of neuropsychiatric complaints.

Quote startWe think we understand why some manifestations are transient and some are not.Quote end

Manhasset, NY (Vocus) November 5, 2010

Many patients with systemic lupus erythematosus (SLE) suffer from a variety of neuropsychiatric problems and scientists at the Feinstein Institute for Medical Research have been trying to understanding the mechanism that underlies these devastating problems. Now, Betty Diamond, MD, head of the Center for Autoimmune and Musculoskeletal Disorders at the Feinstein Institute, has collaborated with colleagues at the Burke Cornell Medical Research Institute to identify two distinct mechanisms that explain the how lupus autoantibodies alter brain function and led to such a wide array of neuropsychiatric complaints.

Patients with lupus, an autoimmune disease that targets many different organs of the body, including the brain, generate autoantibodies that frequently bind double-stranded DNA and cross react with specific glutamate receptors that are toxic to brain cells. The autoantibodies can mediate the cognitive and emotional problems (depression, memory problems and confusion) that are common among lupus patients.

Patricio Huerta, PhD, and Bruce T. Volpe, MD, of the Burke Research Institute have worked with the Diamond lab at the Feinstein to figure out what is going at the level of the neuron that could help explain why the symptoms are so varied. They report in the latest issue of PNAS that the anti-DNA antibody binds to open receptors and that the antibody to the glutamate NMDA receptor only targets activated neurons. At low concentrations, the antibodies augment (NMDA) excitatory post synaptic potentials and at high concentrations they alter mitochondria permeability and cause cell death. This could explain, said Dr. Diamond, why the severity of the symptoms differs from patient to patient.

“This finding helps explain why some cognitive problems are transient and some are permanent,” she said. “Low concentrations of antibody cause transient problems and high concentrations (that lead to cell death) cause life-long problems.”

While this part of the research was conducted in lab dishes, they also studied cerebrospinal fluid samples from lupus patients and found that the levels from low to high concentrations are associated with their symptoms. “We think we understand why some manifestations are transient and some are not,” said Dr. Diamond.

The scientists have worked with medicinal chemists at the Feinstein Institute on the development of drugs that block the antibody from binding to the NMDA receptor. There is now work underway in laboratory models to test whether these can prevent the devastating neuropsychiatric symptoms of lupus.

About The Feinstein Institute for Medical Research

Headquartered in Manhasset, NY, The Feinstein Institute for Medical Research is home to international scientific leaders in cancer, leukemia, lymphoma, Parkinson’s disease, Alzheimer’s disease, psychiatric disorders, substance abuse, rheumatoid arthritis, lupus, sepsis, inflammatory bowel disease, diabetes, human genetics, neuroimmunology, and medicinal chemistry. Feinstein researchers are developing new drugs and drug targets, and producing results where science meets the patient, annually enrolling some 10,000 subjects into clinical research programs.