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Graves’ Disease, Its Pathogenesis and Treatment Research Paper

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Updated: Aug 12th, 2020

Graves’ disease is a term commonly used to describe a particular problem that affects the thyroid gland, skin, and eyes. It causes the gland to create an excess of thyroid hormone, which in turn causes hyperthyroidism (Toft, 2014). The disease is known by many different names. It is called Graves’ disease after being first described by Robert J. Graves – an Irish doctor who described it in a patient (Toft, 2014). This discovery happened in 1835 (Toft, 2014). However, several other physicians have made notes of the disease prior to that, and the first mentions of it could be traced to the Thesaurus of Shah of Khwarazm – a 12th-century medical tractate. It is also known as Basedow disease or Perry disease, named that way after other doctors who contributed to its discovery (Toft, 2014). This paper is dedicated to analyzing the disease based on its epidemiology, etiology, pathogenesis, clinical manifestations, and treatment.


In the United States, Graves’ disease is considered the most common reason for hyperthyroidism (Yeung, 2016). According to a study conducted in Minnesota, the yearly commonality of the disease is around three per 10,000 (Yeung, 2016). When it comes to maternal thyrotoxicosis, the incidence is one per 500 people (Yeung, 2016). Maternal Graves’ disease is the most common cause of that (Yeung, 2016). As a rule, patients tend to have a genetic predisposition towards autoimmune thyroid diseases. These include the Hashimoto thyroiditis and Graves’ disease (Yeung, 2016).

On the international scale, Graves’ disease remains the most common reason for the appearance of hyperthyroidism (Yeung, 2016). It is responsible for 60 to 90 percent of all reported cases around the world, the percentage fluctuations depending on the region (Yeung, 2016). Studies performed in the United Kingdom report that the yearly incidence of Graves’ disease is around 20 cases per 10,000, with 8 out of 20 being women (Yeung, 2016).

If untreated, it can cause life-threatening thyrotoxicosis, also known as thyroid storm. Without proper medical attention, the disease could cause abnormal weight loss, along with bone and muscle catabolism (Yeung, 2016). In addition, Graves’ disease is known to cause such complications as ophthalmopathy, acropathy, dermopathy, which could be the reason for severe morbidity (Yeung, 2016).

Graves’ disease is known for plaguing young women. However, it is possible to get it at any age. It is a disease that predominantly targets women, as the male-to-female ratio among the afflicted persons is around 1:8 (Yeung, 2016). The age of a typical patient varies from 20 to 40 years (Yeung, 2016).


As it stands, the exact reasons for the development of Graves’ disease remain unknown (Graves’ disease, 2012). Since the disease is an autoimmune disorder, it causes the organism’s immune system suddenly go haywire and attack the body, rather than the hostile microorganisms (Graves’ disease, 2012). There are researches conducted on the subject. Medical science has yet to make significant progress. What is known at the moment is that the people afflicted with Graves’ disease likely have a genetic predisposition towards it (Graves’ disease, 2012). If a person has a relative or a family member that had contracted the disease in the past – it is likely that that person would have it too. Gender affects the chances of having the disease as well – females are more likely to get afflicted by it than males (Graves’ disease, 2012). This is the case for the majority of autoimmune diseases (Graves’ disease, 2012). Other factors that may affect the organism’s predisposition towards Graves’ disease are those that could cause damage to the thyroid cell. These are:

  • Environmental toxins – certain cancerogenic chemicals and toxins can affect the thyroid and cause Graves’ disease (Graves’ disease, 2012).
  • Viruses and bacteria – the number of viruses and bacteria that could cause Graves’ disease is limited only to those who possess the antigen protein in their membrane similar to the thyroid-stimulating hormone. Yersinia enterocolitica is one such bacteria (Graves’ disease, 2012).
  • Stress – while never a sole cause for Graves’ disease, prolonged periods of mental and physical pressure make the organism more susceptible to ailments (Graves’ disease, 2012).
  • Humoral factors – a natural excess of thyroid hormones can cause the disease to appear (Graves’ disease, 2012).
  • Excessive iodine uptake – iodine is the key component in creating most thyroid hormones (Graves’ disease, 2012). An excess of iodine can cause an excess of hormones produced, which could lead to the appearance of the Graves disease.


Although no conclusive data is available for what causes the disease, there is more data pertaining to its working mechanisms. Under normal circumstances, the immune system creates thyroid-stimulating immunoglobulins, commonly known as antibodies or antigens (Prabhakar, Bahn, & Smith, 2011). They attach themselves to the thyroid cell receptors, and in so doing, affect the production rate of the thyroid-stimulating hormone. TSH is responsible for making the thyroid gland produce thyroid hormones (Prabhakar, Bahn, & Smith, 2011). There are 2 thyroid hormones – T3 (triiodothyronine) and T4 (thyroxine) (Prabhakar, Bahn, & Smith, 2011).

The former is a more active hormone when compared to the latter. It affects muscles and tissues. Thyroxine, on the other hand, affects the entire body and all of its cells. These hormones affect many processes within the body: muscle and brain activity, heart beating rate, metabolism, skin dryness, weight loss, and nervous system functions (Prabhakar, Bahn, & Smith, 2011). Graves’ disease causes the over-production of the thyroid-stimulating immunoglobulins, which in turn affects the amount of TSH. When the thyroid gland produces too much thyroid hormones, it is called hyperthyroidism (Prabhakar, Bahn, & Smith, 2011).

The inflammatory process within the thyroid gland is caused largely by the activated T lymphocytes. Many of them contain Interferon-gamma (IFN-γ), which is a strong inflammatory agent (Prabhakar, Bahn, & Smith, 2011). Some antibodies, like antithyroglobulin and antithyroid peroxidase, serve as markers for Graves’ disease against the thyroid (Prabhakar, Bahn, & Smith, 2011).

Clinical Manifestations

The symptoms of Graves’ disease are directly tied to the areas and bodily functions affected by triiodothyronine and thyroxine hormones (Menconi, Marcocci, & Marino, 2012). Since these are present throughout the entire body and affect most of its functions, the symptoms vary greatly. These include nervousness, anxiety, insomnia, and other detrimental behavioral changes. Other common symptoms are excessive weight loss, weakness in muscles, tremors, sweating, irregular heartbeat, and general fatigue (Menconi, Marcocci, & Marino, 2012). A rare symptom of Graves’ disease is dermopathy or myxedema, which usually develops in front of shins or on feet. These pathologies appear in the form of thickened reddish skin around the afflicted areas. Sometimes, soft-tissue swellings appear on hands. This is known as acropathy, although it is very rarely caused by Graves’ disease or hypothyroidism associated with it. The disease affects the menstrual cycle in females. Males may suffer a lack of erection (Menconi, Marcocci, & Marino, 2012).

Graves’ disease is often followed by ophthalmopathy – an abnormality that affects the eyes. It is very common in the majority of the people suffering from the disease. However, it is commonly manifested in a mild form. Still, around 10% of the afflicted population requires special therapy due to significant eye movement caused by ophthalmopathy (Menconi, Marcocci, & Marino, 2012). The excess of T3 and T4 hormones causes the eye sockets to swell and push the eyes forward, making them bulge. When partially emerged from the protective socket, the eyes are thus exposed, which causes redness and irritation. The pressure also causes incidents of blurred vision, light sensitivity, or temporary sight dysfunctions (Menconi, Marcocci, & Marino, 2012).


Three methods are commonly used when treating Graves’ disease. The choice usually depends on the age and gender of the patient, degree of illness, and a plethora of other factors unique to the person. The methods are:

  • Prescription of antithyroid drugs, also known as thionamides (Graves’ disease, 2016).
  • Radioactive iodine therapy (Graves’ disease, 2016).
  • Surgery (Graves’ disease, 2016).

The use of antithyroid drugs is considered the optimum way of dealing with the disease, as it is the least invasive procedure. These drugs affect the thyroid and reduce the release of the T3 and T4 thyroid hormones. They are usually prescribed to individuals with mild cases of the disease, children, and women during pregnancy (Graves’ disease, 2016).

Radioactive iodine therapy is a definitive kind of treatment. Its mechanisms destroy the thyroid in order to reduce its size. While reasonably effective, this therapy often causes hypothyroidism. The use of radioactive iodine is very popular in the United States, serving as a go-to solution for Graves’ disease (Graves’ disease, 2016). The mechanism is simple – iodine is an element required to produce thyroid hormones and thus is actively absorbed by the thyroid issue. It uses practically all of the iodine found in a person’s body. Radioactive iodine is absorbed by the thyroid and destroys the tissues from within (Graves’ disease, 2016). This, in turn, causes the production of thyroid hormones to decrease and return to normal. Sometimes, the damage to the thyroid is too great, leading to decreased levels of thyroid hormones. Additional therapy is required to deal with the aftermath (Graves’ disease, 2016).

The third and most radical way of dealing with Graves’ disease is to remove the thyroid gland partially or entirely, through surgical means. This is commonly used as a last resort, and only for individuals for whom other methods of treatment have proven ineffective. This is the quickest solution to the problem. The common aftereffect of the surgery is hypothyroidism (Graves’ disease, 2016).

Other ways of dealing with Graves’ disease include the use of beta-blockers. These are drugs that affect the thyroid hormones already released into the bloodstream (Graves’ disease, 2016). They are often prescribed as a supplement to primary therapy. Once the hormone levels return to normal, using beta-blockers is no longer required.

Biblical Perspective

From a scientific perspective, biblical advice towards dealing with Graves’ disease helps little in fighting it. The generic advice we receive from the Bible is illustrated in this quote: “Bless the Lord, O my soul, and forget none of His benefits; who pardons all your inequities; who heals all your diseases” (1 Psalm 103:2 New International Version). This passage promises that God will heal the faithful of any disease, including Graves’ disease. The effect of exercising one’s faith through prayer may have a placebo effect on the organism and assist in recovery, but is unlikely to be enough to deal with the disease on its own.


Graves’ disease is the most common cause of hyperthyroidism around the world (Yeung, 2016). The affliction targets mainly women, although it is possible for men to contract it too (Yeung, 2016). The etiology of the disease includes genetic predisposition and other factors that affect the thyroid, such as toxins, certain bacteria and viruses, and stress (Graves’ disease, 2012). The disease affects the production of T3 and T4 hormones, causing over-saturation. The inflammation of the thyroid gland is caused by the activated lymphocytes attacking it (Prabhakar, Bahn, & Smith, 2011). Common symptoms include excessive weight loss, weakness in muscles, tremors, sweating, irregular heartbeat, myxedema, ophthalmopathy, and general fatigue (Menconi, Marcocci, & Marino, 2012). There are three ways of dealing with Graves’ disease, which are antithyroid drugs, radioactive iodine, and surgical intervention (Graves’ disease, 2016). Beta-blockers are prescribed to deal with the hormones already in the system (Graves’ disease, 2016). From the biblical perspective, the best way of curing Graves’ disease, is through praying and putting one’s faith in God.


(2012). Web.

(2016). Web.

Menconi, F., Marcocci, C., & Marino, M. (2012). Diagnosis and classification of Graves’ disease. Autoimmunity reviews, 13(4), 398-402.

Prabhakar, B.S., Bahn, R.S., & Smith, T.J. (2011). Current perspective on the pathogenesis of graves’ disease and ophthalmopathy. Endocrine Society, 24(6), 802-835.

Toft, D.J. (2014). Web.

Yeung, S.C.J. (2016). Web.

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