CIDPUSA.ORG Autoimmune

Myasthenia diet guide,

God Our Guide

Main Links

Home page

Autoimmune Diseases Guide

Diet anti-inflammatory


Help page

Diagnosis page

Service contact Page

Welcome to CIDPUSA.ORG

Information on Myasthenia

November 2, 2021


 alternatives treatment of autoimmune disease read our e-book


Long-term treatment may include removal of the thymus gland. About 15% of patients with MG are found to have a tumor of the thymus gland, known as a thymoma. Most thymomas are benign. Thymectomy has become a common treatment modality for patients without thymoma. If most of the thymus is removed, symptoms usually lessen and, in some individuals, disappear completely. However, the thymus gland is the master gland of immunity, and removing this gland severely weakens the body's ability to fight infections and cancer.

Another long-term treatment approach is the use of immunosuppressive drugs. This group of drugs is used to suppress the body's immune system, although it is not known how they work in MG. Prednisone, azathioprine, cyclophosphamide, and cyclosporine are all immunosuppressive drugs. While patients may show significant improvement or drug-dependent remission of symptoms, they must be monitored closely for undesirable or serious side effects.


As previously mentioned, MG has been shown to be an autoimmune disease. This means that the immune system attacks some of its own body proteins. Specifically, the transmission of signals from the nerve endings to the muscle receptors is partly blocked by antibodies. The messenger chemical or neurotransmitter released as a signal from nerve endings to muscles is acetylcholine. Acetylcholine molecules travel the short distance in the gap between nerve ending and muscle to find a receptor on the motor end plate. When a sufficient number of acetylcholine molecules are attached to muscle receptors, there is an electric discharge of the normal membrane potential and the muscle fiber can contract.

In MG most of the receptors are already occupied by antibodies; therefore, not enough acetylcholine molecules find receptors to trigger this discharge and subsequent muscle contraction. Normally, the acetylcholine is split by an enzyme (cholinesterase) and, with this, is removed from the receptor in a fraction of a second. Using anticholinesterases, drugs that hinder this enzyme, acetylcholine molecules have more time to find receptors with an increased chance of leading to a discharge. However, if too much of this enzyme antagonist is present, the cells remain discharged for too long and the muscles become paralyzed. This is a "cholinergic crisis" in which heart and breathing may stop.


Celiac D Story
Celiac Neurology
Celiac Mystery
Celiac Secrets
Autoimmune diseases
Women Heart attack
Bras & Breast Cancer
Breast Cancer Chemic
Mammogram cancer
Breast Cancer Herbs
Bible Diet
Breast nutrients
Circadian Rhythm
Cancer Book
Immune deficiency
Vaccine info
Toxic Pesticide