Introduction
According to Minako et al., (2012), Myasthenia Gravis is an autoimmune neuromuscular disease, categorized as chronic in nature. Additionally, the disease is known to result in weak skeletal muscles that are vital for breathing and movement of body parts. The name was gotten from Latin and Greek, whereby Myasthenia Gravis connotes grave. This particular condition worsens in the instances of continued activity and improves after continued rest. What is more about the disease is the fact that it has no cure; however, there are a couple of therapies that assist control symptoms, making it possible to lead a normal life expectancy.
Myasthenia gravis is particularly because of a mistake in the transmission of nerve impulses, in specificty to the muscles. In simpler terms, it is a condition that takes place when no signals are passed between nerve and muscles due to interruptions that happen within the neuromuscular junction. Neuromuscular junction is defined as a location whereby nerve cells interconnect to the muscles which they control. It happens that when electrical signals move down the motor nerve, then the nerve endings release acetylcholine, which is a neurotransmitter. Often, in most cases where individuals have myasthenia gravis, this happens as a result of antibodies to the acetylcholine receptor (Minako, et al., 2012).
Myasthenia gravis, just like any other diseases, has symptoms through which a patient can be determined to be suffering from it. These symptoms involve blurry vision, having difficulties in swallowing, having shortness in breath, ptosis, speech, and general weakness in parts such as the arms, hands, fingers, legs, and neck.
According to a research that was conducted by Jeffrey, et al. (2016) there are various effects on therapeutic plasma exchange on immunoglobulins, which is one of the ways of the way of symptoms control and treatment. The other therapies mentioned in the research is intravenous immunoglobulin (IVIg). TPE was chosen for this particular research because it is common in the MG for treatment of exacerbations, preparations of patients undergoing surgery, and before starting treatment that involves corticosteroids. So, ideally, the study was developed so as to examine the effects of TPE on Ig, as well as autoantibody levels, and proactive antibodies.
The study engaged 10 MG patients who were administered with TPE as a base for care in two hospitals. To start with, all of the patients were treated using TPE because of the exacerbations the disease in them. During the TPE treatment and colloid replacement, it is estimated that one plasma volume was exchanged at 5% albumin in 490% of procedures. Additionally, it emerged out that the biggest percentage of patients would come at first receive 5-6 TPE procedures for each standard practice for each institution. In other cases, the physicians offer additional TPE sections to their patients if they do not get the best outcome from the initial therapy sessions (Jeffrey, et al., 2016).
Data Analysis in this study was conducted based on demographic data, with statistical computations such as median, range of continuous variables, counts, and percentages for categorical parameters. One of the primary patients in this research had a new disease at the onset stage and was determined to have a thymoma. All in all, there was an expectation that the patient would respond to TPE as regards to reducing in IgG, AChR autoantibody titers as well as clinical response.
References
Jeffrey, G. et al., 2016. Effect of therapeutic plasma exchange on immunoglobulins in myasthenia gravis. Autoimmunity, 49(7), p. 472-479.
Minako, O. et al., 2012. T-cell recognition of acetylcholine receptor provides a reliable means for monitoring autoimmunity to acetylcholine receptor in antibody-negative myasthenia gravis patients. Autoimmunity, 45(2), p. 153-160.
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