Graves’ disease is normally a non-life-threatening condition that influences the thyroid gland. Caleb Hillier Parry initially described it in 1786. However, the disease is named after the Irish doctor, Robert J. Graves, who depicted several cases in 1825 in the London Medical Journal (Yeung, 2017). Originally called ‘exophthalmic goiter,' Graves' disease is otherwise called Parry's ailment or Basedow's illness in Europe. It is a disorder that affects the immune system and causes hyperthyroidism. There are a few things that can cause hyperthyroidism; however, Graves' disease is the most common cause (Longo, 2016). The thyroid hormones impact various distinctive body parts so signs and side effects related with Graves can come in a wide range of ways that influence the body’s health. It is caused by the production of abnormal antibodies by the immune system which imitates the thyroid stimulating hormones (TSH). Usually, TSH is released by the pituitary gland in the brain, yet with Graves, it is not discharged. The antibodies send the thyroid into overdrive thus producing too much of the hormone. The reason why the thyroid goes into overdrive is not definite, but studies point to environmental causes and genetics as the trigger.
A dysfunction in the body's immune system causes Graves' disease. It affects about 0.5% of the world population and is the cause of up to 80% of all hyperthyroidism cases (Brent, 2008). The pituitary organ directs the standard thyroid function but when Graves' strikes, it triggers unique IgG antibody production to attack a particular protein on the surface of cells in the thyroid (Girgis & Champion, 2011). When these antibodies begin attacking, numerous things can go wrong including heart and sensory system functions, muscle strength, body temperature, and fluctuations in a ladies' menstrual cycle. After, there is follicular cell growth which causes increased production of thyroid hormones and thyroid enlargement. Despite the fact that anybody can develop Graves', various variables can increase the danger of the malady. The emergence of this immune system process is most likely because of a basic hereditary susceptibility with overlaid environmental factors (Girgis & Champion, 2011). Specific HLA alleles on chromosome six: HLA-DRB1-08 and DRB3-0202, are known to present an increased danger of Graves' disease (Girgis & Champion, 2011). Ecological triggers incorporate infections, stressful life occasions, recent childbirth, and exposure to high amounts of iodine.
Graves’ disease symptoms range from uncomfortable to practically insufferable and in rare cases, death. Symptoms depend on the span of the malady, the amount of abnormal antibody that the individual is producing, and the person’s age. One symptom is vocal problems if the thyroid becomes excessively enlarged. The most visible symptom of the ailment is a protruding eyeball or both eyeballs. At times, the skin on the lower legs can end up noticeably lumpy, uneven and red. Also, the heartbeat will, for the most part, be somehow irregular, and in rare and severe cases it can cause death due to a cardiovascular collapse. Patients have low heat resilience and will appear to sweat easily or have extreme sweating issues. Mild hyperthyroidism may cause serious disability in patients with an underlying heart illness. Subsequently, all patients with atrial arrhythmias or unexplained heart failure ought to be examined for thyrotoxicosis.
Diagnosis of Graves’ depends on characteristic biochemical abnormalities and clinical elements (Longo, 2016). In the event that pathognomonic elements such as dermopathy and ophthalmopathy are missing, and there is no detection of a diffuse goiter, radionuclide scanning can affirm the diagnosis. These scans and radioiodine uptake estimations can be utilized to distinguish Graves' from different causes for thyrotoxicosis. It is recommended to diagnose Graves' disease by increased twenty-four-hour radioiodine uptake (RAIU). It is not mandatory for routine measurement of thyrotropin receptor antibodies, but when such measures are performed, they have 99% specificity and sensitivity for Graves' disease. They are additionally useful in diagnosing Graves' in people with associative nodular goiter. Measuring levels of TSH receptor antibodies could eventually replace the requirement for the RAIU for diagnosis confirmation (Ginsberg, 2003). Despite the fact that there is a straightforward diagnostic testing procedure once doctors suspect Graves' disease, doctors should be aware of heterogeneous and atypical presentations of the malady, especially in elderly patients.
There are a number of treatments for Graves' disease. The objectives when treating Graves’ disease are to reduce the generation of the thyroid hormone and to hinder their impacts. Treatments include radioactive iodine treatment that is taken orally. Radioactive iodine treatment destroys the overactive thyroid cells. Through this treatment, symptoms will slowly diminish, but it is possible that due to the declined thyroid activity, patients will possibly have to go on medication later in their life to supplement for this. Another treatment method for Graves’ disease is anti-thyroid drugs. These drugs inhibit the thyroid's utilization of iodine to produce hormones. While using this technique, a relapse of the malady may happen again later on in life, and side effects could lead to liver failure. Beta blockers are another broadly utilized treatment which obstructs the impact that the hormones have on the body. They work fast to lessen the side effects of Graves’ disease; however, if a patient stops taking it all together, it could bring about heart failure. Surgery is a last resort option if medications fail to work. The surgery would totally expel one’s thyroid, and the individual would need to be on lifelong medications to provide their thyroid with normal hormones.
Graves' disease is a condition whose management poses complex difficulties. Its symptoms range from barely any to extremely discernible. Sadly, there is no cure for the malady, but there are treatments that can make patients more comfortable. It is possible to live with the disease and patients have to make their physical and mental wellbeing a priority. If patients go untreated, the disease decreases their quality of life significantly, but when patients are properly treated, they often stabilize and live a healthy medicated life. There have been advances in Graves’ disease such as “increasing characterization of extrathyroidal organ involvement, the emerging role of thyroid ultrasonography in the investigation of Graves' disease and the emergence of novel small-molecule TSH-receptor ligands as potential targets in the treatment of Graves' disease” (Girgis & Champion, 2011) which provide hope for patients.