- What Causes Graves’ Disease?
- Graves’ Disease
- What Is It?
- Atypical Complications of Graves’ Disease: A Case Report and Literature Review
- Graves’ Disease Causes
- Graves’ Disease
- Graves’ Disease Causes and Risk Factors
- Symptoms of Graves’ Disease
- Treating Graves’ Disease
- Graves’ Disease Symptoms
What Causes Graves’ Disease?
Hormones secreted by the thyroid gland control metabolism, or the speed at which the body converts food into energy. Metabolism is directly linked to the amount of hormones that circulate in the bloodstream. If, for some reason, the thyroid gland secretes an overabundance of these hormones, the body’s metabolism goes into high gear, producing the pounding heart, sweating, trembling, and weight loss typically experienced by hyperthyroid people. Normally, the thyroid gets its production orders through another chemical called thyroid-stimulating hormone (TSH), released by the pituitary gland in the brain. But in Graves’ disease, a malfunction in the body’s immune system releases abnormal antibodies that mimic TSH. Spurred by these false signals to produce, the thyroid’s hormone factories work overtime and exceed their normal quota.
Exactly why the immune system begins to produce these aberrant antibodies is unclear. Heredity and other characteristics seem to play a role in determining susceptibility. Studies show, for example, that if one identical twin contracts Graves’ disease, there is a 20% likelihood that the other twin will get it, too. Also, women are more likely than men to develop the disease. And smokers who develop Graves’ disease are more prone to eye problems than nonsmokers with the disease. No single gene causes Graves’ disease. It is thought to be triggered by both genetics and environmental factors.
Eye trouble — usually in the form of inflamed and swollen eye muscles and tissues that can cause the eyeballs to protrude from their sockets — is a distinguishing complication of Graves’ disease. However, only a small percentage of all Graves’ patients will experience this condition, known as exophthalmos. Even among those who do, the severity of their bout with Graves’ has no bearing on the seriousness of the eye problem or how far the eyeballs protrude. In fact, it isn’t clear whether such eye complications stem from Graves’ disease itself or from a totally separate, yet closely linked, disorder. If you have developed exophthalmos, your eyes may ache and feel dry and irritated. Protruding eyeballs are prone to excessive tearing and redness, partly because the eyelids can no longer shelter them effectively from injury.
What Is It?
Published: July, 2019
Graves’ disease is a disorder of the immune system that causes the thyroid gland to become overactive. It is an autoimmune disorder, which means the body’s immune system mistakenly attacks the body’s own cells instead of protecting them from outside invaders. In Graves’ disease, the body’s immune system makes abnormal chemicals called immunoglobulins that stimulate the thyroid gland to make too much thyroid hormone. This overactive thyroid state is called hyperthyroidism.
Doctors don’t know what causes Graves’ disease, but the fact that it tends to run in families indicates that the disease may have a genetic (inherited) component. It is possible that the abnormal production of immunoglobulins is triggered by some unknown factor in the environment, and the immune system fails to stop this overproduction because of an inherited defect.
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Atypical Complications of Graves’ Disease: A Case Report and Literature Review
Graves’ disease (GD) may display uncommon manifestations. We report a patient with rare complications of GD and present a comprehensive literature review. A 35-year-old woman presented with a two-week history of dyspnea, palpitations, and edema. She had a raised jugular venous pressure, goiter, and exophthalmos. Laboratory tests showed pancytopenia, a raised alkaline phosphatase level, hyperbilirubinemia (mainly direct bilirubin), and hyperthyroidism . Her thyroid uptake scan indicated GD. Echocardiography showed a high right ventricular systolic pressure: 60.16 mmHg. Lugol’s iodine, propranolol, cholestyramine, and dexamethasone were initiated. Hematologic investigations uncovered no reason for the pancytopenia; therefore, carbimazole was started. Workup for hepatic impairment and pulmonary hypertension (PH) was negative. The patient became euthyroid after 3 months. Leukocyte and platelet counts and bilirubin levels normalized, and her hemoglobin and alkaline phosphatase levels and right ventricular systolic pressure (52.64 mmHg) improved. This is the first reported single case of GD with the following three rare manifestations: pancytopenia, cholestatic liver injury, and PH with right-sided heart failure. With antithyroid drugs treatment, pancytopenia should resolve with euthyroidism, but PH and liver injury may take several months to resolve.
Graves’ disease (GD) is an autoimmune thyroid disease first described by Robert Graves in 1835 . Patients with GD usually present with common manifestations such as palpitations, tremors, heat intolerance, and weight loss. However, some patients may present with unusual gastrointestinal, hematologic, neurologic, and cardiopulmonary complications . We report a patient who presented to our institution with pancytopenia and pulmonary hypertension (PH) with right-sided heart failure and raised liver enzymes. She was found to have GD. Further, there was no other explanation for her manifestations as the workup failed to reveal any other pathologic conditions. The pathogenesis of these complications in patients with GD is not completely understood. However, the prognosis is good if the underlying hyperthyroidism is treated with antithyroid drugs (ATDs). In this review, we discuss the prevalence of each complication, possible mechanisms of their development in the context of GD, and the clinical course during treatment of the underlying hyperthyroidism.
2. Case Presentation
A 35-year-old woman presented to our emergency department with a two-week history of breathlessness, palpitations, and generalized edema. She had a history of having lost approximately 10 kg of weight over a 3-month period but had regained weight in the month before presentation. She had no chronic illness and was not on any medication(s). On examination, she looked tired, was afebrile, and had a blood pressure of 103/58 mmHg, pulse rate of 92/min, and a respiratory rate of 20/min. She had exophthalmos, a raised jugular venous pressure, a diffuse goiter with a positive bruit, and bilateral pedal edema extending to the thighs. She had a third heart sound and bilateral fine basal lung crepitations. Her abdominal examination was unremarkable with no tenderness or organomegaly. An electrocardiogram showed a sinus rhythm with right bundle branch block and right ventricular strain.
Table 1 Laboratory investigations at presentation and in the 3 months following carbimazole treatment.
Echocardiography showed an ejection fraction of 50–55%, a right ventricular systolic pressure (RVSP) of 60.16 mmHg measured by Doppler, and severe tricuspid regurgitation. Therefore, a computed tomography pulmonary angiogram was performed; it was negative for pulmonary embolism. A thyroid uptake scan showed diffusely increased uptake, indicating GD, and ultrasound examination showed a diffuse goiter with no nodules. She was initially started on Lugol’s iodine, 7 drops (8 mg/drop) every 8 hours, propranolol, 40 mg every 8 hours, dexamethasone, 1 mg every 8 hours, and cholestyramine, 4 grams every 6 hours, to control thyrotoxicosis and to prevent further worsening of the patient’s complications which were suspected to be related to GD. Also, 2 doses of intravenous furosemide 40 mg were given on the first hospital day then it was discontinued and the basal lungs crepitations disappeared on the following day.
Workup did not reveal any specific reason other than GD for her pancytopenia, PH, and raised alkaline phosphatase (ALP) and bilirubin. Regarding the pancytopenia, a peripheral blood smear showed a moderate normocytic anemia with mild hypochromia; a few ovalocytes, burr cells, and schistocytes; and increased rouleaux formation. There was leukopenia with neutropenia, some toxic features, a few reactive lymphocytes, and minor platelet clumps. The reticulocyte count was 3.2% (reference values: 0.5–2.5%), erythrocyte sedimentation rate was 3 mm/h (reference values: 2–37), C-reactive protein was 9 mg/L (reference values: 0–5), and hemoglobin electrophoresis was normal. The levels of all the following parameters were normal: lactate dehydrogenase, 184 U/L (reference values: 135–214); haptoglobin, 95 mg/dL (reference values: 35–250); folate, 34.5 nmol/L (reference values: 4.0–45.3); and vitamin B12, 617 pmol/L (reference values: 133–675). Iron studies showed the following: iron, 5 μmol/L (reference values: 5.83–34.5); total iron binding capacity, 32 μmol/L (reference values: 45–80); iron saturation, 15% (reference values: 15–45); transferrin, 1.29 g/L (reference values: 2–3.6); and ferritin, 38 μg/L (reference values: 11–304). Coombs test and HIV serology were negative. Additional workup for cholestatic liver impairment, viral hepatitis serology, and antimitochondrial antibodies (AMA) was negative. The patient’s abdominal ultrasound was unremarkable, with no hepatic or splenic enlargement. Further investigations for PH, rheumatoid factor, and antinuclear (ANA), anti-neutrophil cytoplasmic, anti-RO, anti-LA, anti-JO, anti-scleroderma 70, anti-RNP, and anti-smith antibodies were negative. Complements 3 (C3) and 4 (C4) were 110 mg/dL (reference values: 90–180) and 18.4 mg/dL (reference values: 10–40), respectively.
Bone marrow examination was not performed as the reticulocyte count was high and in the following two days of the initial treatment patient’s white blood cells and platelets improved; at that point carbimazole 60 mg/day was started. After six days, she was ready for discharge from hospital on the same dose of carbimazole and propranolol, and furosemide was added for the lower limbs edema.
Follow-up investigations nine days later showed improvement in white blood cell and platelet counts. In addition, the gamma-glutamyl transferase (GGT) level was high (128 U/L ).
Two months after her initial presentation, the lower limb edema had improved but had not resolved completely. A month later (3 months after presentation), the lower limb edema disappeared. Moreover, the clinical and laboratory features of hyperthyroidism resolved with carbimazole therapy, and her bilirubin level and white blood cell and platelet counts normalized; and her hemoglobin, ALP, and GGT levels improved. ALP isoenzymes were checked; the raised ALP level was mainly of hepatic origin. Repeat echocardiography showed improvement of RVSP (52.64 mmHg) measured by Doppler, with moderate tricuspid regurgitation.
GD is caused by autoantibodies that stimulate TSH receptors in the thyroid gland; it is the most common cause of hyperthyroidism . Our patient is the first reported case to have these three rare complications of GD: pancytopenia, cholestatic hepatic injury, and PH with right-sided heart failure.
It is rare for patients with GD to have pancytopenia; there are only a few documented reports in the literature . However, single lineage abnormalities (anemia, leukopenia, or thrombocytopenia) are more common in patients with hyperthyroidism (34%, 5.8%, and 3.3%, resp.) . Leukopenia with a relative lymphocytosis is not an uncommon blood abnormality in GD, named “Kocher’s blood picture.” . There was no identifiable cause for this patient’s anemia and it was similar to an anemia of chronic disease, commonly called “GD anemia,” that affects 22% of patients with GD . Bone marrow examination in patients with GD, although was not performed in our case, could show hypercellular , normocellular , or, very rarely, hypoplastic changes.
Initially, thionamides were not used. We chose a more conservative approach to treatment in this patient with multiple complications, using alternatives such as Lugol’s solution and cholestyramine, as we did not want to aggravate her pancytopenia. The use of radioactive iodine at the time of presentation might have precipitated a thyroid storm ; thus, it was not considered. However, once the workup for pancytopenia showed no other causes and the neutrophil and platelet counts were improving, we initiated treatment with carbimazole. Generally, the use of thionamides is contraindicated in patients with a baseline neutrophil count <0.5 × 109/L and should be stopped if the neutrophil count drops after their initiation below 1.0 × 109/L . Thus, although ATDs can be used in patients with hyperthyroidism-associated pancytopenia, their use is recommended only after a full hematologic assessment has been performed, as ATDs carry a minimal risk of pancytopenia . Dexamethasone was added to the initial management because of the severe thyrotoxic state of the patient with pancytopenia. However, the evidence for its use in this situation was weak, being derived from a previous case report .
The duration of hyperthyroidism related pancytopenia is variable, from 2 weeks to several months ; it resolves only when the patient is euthyroid. Pancytopenia should resolve by the time euthyroidism is reestablished; if it does not, hematologic evaluation should be revisited. It was reported that a patient with GD-related pancytopenia started on methimazole showed no improvement despite becoming euthyroid; investigations revealed methimazole-associated aplastic anemia .
The pathogenesis of GD-related pancytopenia is not fully understood and different theories exist , including the following: (i) high level of circulating thyroid hormones, resulting in ineffective hematopoiesis; (ii) shortened blood cell lifespan, either by immune destruction or by sequestration; (iii) autoimmune mechanisms, given the presence of antineutrophil and antiplatelet antibodies; and (iv) direct bone marrow toxicity, as excessive thyroid hormones may adversely affect the pluripotent stem cells.
The mechanism of pancytopenia is most likely multifactorial as no single theory could explain it completely. The association between GD and other autoimmune hematologic disorders that respond to ATDs (e.g., autoimmune hemolytic anemia, immune thrombocytopenic purpura, and Evan’s syndrome ) supports the autoimmune theory. However, pancytopenia has also been reported with other forms of hyperthyroidism that are not immunologically mediated, such as toxic multinodular goiter , toxic adenoma , and even levothyroxine overtreatment in a patient previously treated for GD .
3.2. Cholestatic Hepatic Injury
The hepatic derangement in patients with GD ranges from mild laboratory abnormalities without clinical features to overt hepatitis , with either hepatitic or cholestatic injury . Our patient had a cholestatic pattern of liver impairment with raised bilirubin (predominantly direct bilirubin), ALP, and GGT. After 3 months of carbimazole treatment with resolution of hyperthyroidism, ALP and GGT levels were better, and bilirubin normalized. Moreover, ANA and AMA were negative, thereby excluding concomitant autoimmune liver disease such as primary biliary cirrhosis. The patient had no clinical or ultrasonographic manifestations of hepatic congestion (i.e., hepatic tenderness and hepatomegaly); thus, this was excluded as a reason for cholestatic hepatic injury.
ALP is the commonest liver enzyme to be increased in hyperthyroid patients at diagnosis (25–64%) . In a study of 30 patients with GD , the reported increase in different liver enzymes was as follows: ALP (33%), ALT (26%), GGT (24%), AST (17%), and total bilirubin (8%). The initial increase in ALP may originate from the liver, bone, or both, so it is important to check for GGT and bilirubin levels to diagnose cholestasis . With treatment of hyperthyroidism, improvement of GGT has been reported while the ALP level was increasing, mainly from the bone . The ALP level can take several months to normalize after euthyroidism is reestablished; this is because of increased osteoblast activity . However, our patient’s ALP after three months of treatment was mainly of liver origin.
The possible mechanisms of liver injury in hyperthyroidism are as follows : (i) relative hypoxia due to increased oxygen demand while the splanchnic blood supply is unchanged, leading to liver impairment and cholestasis in the centrilobular hepatocytes; (ii) congestive heart failure; (iii) direct toxicity by high thyroid hormones, although this has not been confirmed; and (iv) associated autoimmune liver disease.
Treatment of hyperthyroidism in patients with raised liver enzymes is challenging, as ATDs are hepatotoxic (0.5%) . Carbimazole and methimazole usually cause cholestasis while propylthiouracil usually causes hepatocyte damage by an idiosyncratic mechanism unrelated to the dose . Thus, it is advised to investigate for a concomitant liver disease; if the workup is negative, thionamides can be used with careful monitoring; otherwise it is better to use an alternative, such as radioactive iodine ablation or thyroidectomy .
3.3. Pulmonary Hypertension
The association between hyperthyroidism and PH was first described in 1950 . PH can be found in patients with GD or nodular goiter with hyperthyroidism . In one study, PH was the most common cardiac complication detected by echocardiography in hyperthyroid patients , with a reported prevalence of 36–65% . However, most cases are mild and asymptomatic and are not identified in daily practice .
At presentation, the patient had bilateral basal lung crepitations indicative of left ventricular compromise; this can occur with hyperthyroidism. However, the left ventricular dysfunction was mild; the crepitations disappeared on the second day of hospitalization and the ejection fraction was 50–55% on initial echocardiographic examination. On the other hand, the lower limb edema secondary to right-sided heart failure took 3 months to resolve, indicating that this was the main impairment of cardiac function.
Our patient demonstrated an improvement of her RVSP, from 60.16 mmHg at presentation to 52.64 mmHg after 3 months of carbimazole with the resolution of hyperthyroid state. The weight changes that the patient experienced were interesting, as she initially lost weight secondary to hyperthyroidism but then regained some weight because of the right-sided heart failure with resultant edema. Subsequently, once treatment for GD had been initiated, unlike other patients who often gain weight, our patient lost weight as her right heart failure and edema improved. Most cases of PH recover by the time euthyroidism is reestablished. In one report, 79.2% of patients had normal pulmonary artery pressures after 11–21 weeks of ATD treatment . However, in other reports, 3–14 months were needed until normalization of PH occurred .
Theories to explain the relationship between hyperthyroidism and PH include the following: (i) autoimmune-mediated endothelial remodeling; (ii) mechanical endothelial damage caused by the high cardiac output; (iii) accelerated metabolism of pulmonary vasodilators (nitric oxide and prostacyclin); (iv) inhibited metabolism of pulmonary vasoconstrictors (endothelin-1, serotonin, and thromboxane); and (v) enhanced pulmonary vascular response to catecholamines. It has been found that pulmonary artery systolic pressure has a significant linear correlation with thyroid-stimulating hormone receptor antibody, pulmonary vascular resistance, and cardiac output .
In a study by Marvisi et al. the group of patients who received methimazole showed a more rapid improvement in PH than those who received partial thyroidectomy without pretreatment with methimazole or β-blockers; the difference in the pulmonary pressure drop was significant after 15 days, but not after 90 days, of treatment. The methimazole effect may be due to its ability to suppress Ng-nitro-l-arginine methyl ester production, which acutely inhibits nitric oxide synthesis, resulting in increased levels of nitric oxide . In addition, methimazole might cause direct vasodilatation of the pulmonary vasculature . The possibility of thyroid dysfunction should be considered in patients with unexplained PH, as long-standing untreated hyperthyroidism may lead to refractory PH .
Patients with GD may present with rare manifestations that have partially understood mechanisms. With ATDs treatment, pancytopenia should resolve as euthyroidism is reestablished. Liver enzyme levels and PH may normalize, or at least show some improvement, once normal thyroid function is established, with full recovery several months later.
When treating patients with GD, it is generally recommended that liver function tests and a complete blood count be performed before initiating ATDs . Having this baseline information gives insight about the abnormal laboratory findings primarily related to the hyperthyroid state, which is reversible with ATD treatment, and eliminates doubt around whether subsequent abnormal test results are secondary to the use of ATDs.
It is crucial to test the thyroid function of a patient presenting with any of the complications described in our patient where no clear explanation is found. Lack of awareness of such associations with GD may lead to misdiagnosis or delayed diagnosis, with a redundant workup being performed .
The authors declare that they have no competing interests.
Graves’ Disease Causes
As with most autoimmune disorders, it’s hard to pinpoint the exact cause of Graves’ disease—the most common cause of hyperthyroidism.
When you have an autoimmune disorder, such as Graves’ disease, your immune system mistakenly turns against your body.
Although researchers know very little about autoimmune diseases, here’s what we do know about what happens to your immune system when you have Graves’ disease: Your immune system creates antibodies called thyroid-stimulating immunoglobulins (TSIs). These antibodies cause your thyroid gland to produce more thyroid hormone than your body needs.
TSIs attach to thyroid cell receptors—“docking stations” for thyroid-stimulating hormone (TSH). TSH is a key thyroid hormone. It’s responsible for telling the thyroid to create thyroid hormones. But when you have Graves’ disease, the TSIs “trick” the thyroid gland into over-producing thyroid hormone, which causes hyperthyroidism.
Other Graves’ Disease Causes
Although researchers are still investigating what triggers this autoimmune response, some researchers think that the cause of Graves’ disease may be tied to your family history.
Because Graves’ disease may have a genetic link, that means if you have a family member with Graves’ disease, then you’re more likely to develop it, too.
Another risk factor that makes you more prone to developing Graves’ disease is your gender. As with other autoimmune conditions, Graves’ disease is more likely to affect women than men.
Graves’ is most common in women older than 20 years old. However, people of any age—including men—can have Graves’ disease.1
Research On Other Possible Causes of Graves’ Disease
As for other causes of Graves’ disease, researchers are working hard to determine other possible causes of this condition. For example, researchers are looking to identify the specific genes involved in triggering Graves’ disease.
If you think you could have Graves’ disease or you have questions about Graves’ disease causes, have a conversation with your doctor immediately. The more quickly you are treated for Graves’ disease, the easier it is to manage Graves’ disease symptoms.
Updated on: 02/27/18 Continue Reading Graves’ Disease Diagnosis View Sources
Graves’ Disease Causes and Risk Factors
We don’t yet know for certain the precise cause of Graves’ disease. As with any autoimmune disorder, it occurs when your immune system mistakenly attacks your body instead of an outside “invader” such as infection.
When you have Graves’ disease, your immune system creates antibodies that trick your thyroid gland into producing more thyroid hormone than your body needs, causing hyperthyroidism.
Risk factors for Graves’ disease include:
- Family history: If you have a family member with Graves’ disease, you are more likely to develop it. Scientists are working to identify the specific gene(s) that trigger(s) this disorder.
- Gender: As with many other autoimmune conditions, women are much more likely than men to develop Graves’ disease
- Age: Graves’ disease most often develops in people under age 40
- Having other autoimmune disorders: People with other immune system diseases such as rheumatoid arthritis or lupus have an increased risk of developing Graves’ disease
- Pregnancy: Being pregnant or recently giving birth may increase the risk of Grave’s disease, especially in women with a family history of this disorder
- Stress: Emotional or physical stress may trigger the onset of Graves’ disease in people who are genetically susceptible
- Smoking: Because smoking affects the immune system, it increases the risk of Graves’ disease as well as Graves’ ophthalmopathy
Symptoms of Graves’ Disease
The signs and symptoms of Graves’ disease are extremely varied and can include:
- Anxiety and irritability
- Bulging eyes (Graves’ ophthalmopathy)
- Chest pain
- Difficulty sleeping/insomnia
- Erectile dysfunction or reduced libido
- Eye problems (blurred vision, light sensitivity, grittiness sensation, eye pain)
- Frequent bowel movements or diarrhea
- Hand tremors
- Heart palpitations (fast or irregular heartbeat)
- Heat sensitivity and increased perspiration
- Increased blood pressure
- Menstrual irregularities
- Muscle weakness
- Shortness of breath and/or breathing difficulty
- Thick, red skin, usually on the shins or tops of the feet (Graves’ dermopathy)
- Thyroid gland enlargement (goiter)
- Weight loss, despite normal or increased appetite
Treating Graves’ Disease
The goals in treating Graves’ disease are to lower the production of thyroid hormones and block their effect on the body. Treatment options include:
- Radioactive iodine (RAI) therapy: This is given in a pill or water-based solution that you swallow. It works by destroying thyroid tissue cells, which reduces your thyroid hormone levels and symptoms over weeks or months. Usually only one dose is needed. Many patients eventually develop hypothyroidism (too little thyroid hormone), so you will be given synthetic thyroid pills to achieve the right balance. RAI cannot be used if you are pregnant or breastfeeding.
- Anti-thyroid medications: These prescription oral medications help prevent the thyroid from producing hormones by interfering with the gland’s use of iodine (which it needs for hormone production). These drugs may also be used before or after RAI as a supplemental treatment.
- Surgery: Surgery to remove a portion or all of your thyroid gland is also an option for treating Graves’ disease. You will probably have to take synthetic thyroid hormone pills to supply your body with the appropriate level of hormones after surgery.
- Beta blockers: While these medications don’t block production of thyroid hormones, they can block the effects of hormones on your body, providing relief for such symptoms as heart palpitations, tremors, anxiety, heat intolerance and sweating, muscle weakness and diarrhea.
If you have Graves’ ophthalmopathy, you may be able to manage mild symptoms with over-the-counter lubricating drops and gels. If your symptoms are more severe, your doctor may recommend:
- Corticosteroids to reduce swelling behind the eyeballs
- Prisms in your eyeglasses, which may correct double vision
- Orbital decompression surgery to address bulging eyes; this procedure gives your eyes room to return to their normal position. It’s usually performed if you risk vision loss due to pressure on the optic nerve.
Make an Appointment with a Graves’ Disease Expert at Cooper
To learn more about the resources available for treating Graves’ disease at Cooper or to request an appointment, please call 800.8.COOPER (800.826.6737).
Graves’ Disease Symptoms
There are numerous symptoms of Graves’ disease—an autoimmune disorder that causes the thyroid gland to over-produce thyroid hormone, which is known as hyperthyroidism.
Graves’ disease is the most common cause of hyperthyroidism, so some Graves’ disease symptoms are the same as hyperthyroidism symptoms. However, people with Graves’ disease may also have other symptoms not related to hyperthyroidism.
It can be a challenge to detect Graves’ disease early on. In fact, Graves’ disease is sometimes confused with other conditions, which can make it very difficult to diagnose. That’s why it’s important to pay attention to your symptoms to help your doctor make an accurate diagnosis.
Common Graves’ disease symptoms are:
- bulging eyes
- chest pain
- difficulty sleeping and/or insomnia
- elevated blood pressure
- hand tremors
- increased sweating
- irregular menstrual periods
- irritability or nervousness
- more frequent stools and/or diarrhea
- muscle weakness
- rapid or irregular heartbeat
- sensitivity to heat
- shortness of breath and/or difficulty breathing
- unexplained weight loss (typically despite an increase in appetite)
- vision problems or changes
In addition to these symptoms, if Graves’ disease isn’t treated, other symptoms can develop.
Eye problems: Graves’ disease is the only type of hyperthyroidism that involves inflammation of the eyes and bulging eyes. The specific eye disease associated with Graves’ disease is known as Graves’ orbitopathy or Graves’ ophthalmopathy.
Eye problems that are sometimes related to Graves’ disease can be anywhere from mild to extremely severe. In more mild cases, your eyes may become red and inflamed. Or they may tear or be very sensitive to light.
In severe cases, Graves’ disease can cause inflammation of the eye muscles. The muscles and tissues of the eyes may become swollen and may cause your eyes to protrude from their sockets. This is called exophthalmos.
Goiter: A goiter is an enlarged thyroid gland that can cause the front of the neck to look swollen. Goiters related to Graves’ disease are called diffuse thyrotoxic goiters. These goiters can be small lumps or they can be large. A goiter can make swallowing difficult. If it’s big enough, it can also cause you to cough and may make it more difficult for you to sleep.
Skin problems: In rare cases, Graves’ disease can cause you to develop lumpy reddish patches and thickening of the skin of the shin. This skin condition is called pretibial myxedema. Although it may look severe, it’s usually painless and is not serious.
It’s important to note that although some people with Grave’s disease will have many of these symptoms, not everyone with Graves’ disease will experience symptoms—at least in the early stages of the condition.
If you think you could have Graves’ disease and you have many of the Graves’ disease symptoms in this article, talk to your doctor as soon as possible. Be sure to watch your symptoms closely so that your doctor can make an accurate diagnosis.
Updated on: 04/24/17 Continue Reading Graves’ Disease Causes View Sources