graves disease?

graves disease? Topic: graves disease?
May 20, 2019 / By Bysshe
Question: my brother was recently diagnosed with graves disease. he is 21 years old. i need to know if there is any foods he shouldn't have if so what are they. we want him on the least medications as possible because we believe in natural remedies.
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Best Answers: graves disease?

Aldwen Aldwen | 10 days ago
Graves disease is a thyroid disorder characterized by goiter, exophthalmos, "orange-peel" skin, and hyperthyroidism. It is caused by an antibody-mediated auto-immune reaction, but the trigger for this reaction is still unknown. It is the most common cause of hyperthyroidism in the world, and the most common cause of general thyroid enlargement in developed countries. In some parts of Europe the term Basedow’s disease or Graves-Basedow disease is preferred to Graves' disease. History Graves disease owes its name to the Irish doctor Robert James Graves, who described a case of goiter with exophthalmos in 1835. However, the German Karl Adolph von Basedow independently reported the same constellation of symptoms in 1840. As a result, on the European Continent the term Basedow's disease is more common than Graves' disease.[1][2][3] Several earlier reports exist but were not widely circulated. For example, cases of goiter with exophthalmos were published by the Italians Giuseppe Flajani and Antonio Giuseppe Testa, in 1802 and 1810 respectively.[4] Prior to these, Caleb Hillier Parry, a notable provincial physician in England of the late 18th-century (and a friend of Edward Jenner),[5] described a case in 1786. This case was not published until 1825, but still ten years ahead of Graves[6] However, fair credit for the first description of Graves disease goes to the 12th-century Persian physician Sayyid Ismail Al-Jurjani, who noted the association of goiter and exophthalmos in his Thesaurus of the Shah of Khwarazm, the major medical dictionary of its time.[7] [edit] Diagnosis Graves' disease may present clinically with one of the following characteristic signs: * goiter (an enlarged thyroid gland, sometimes detectable as a swelling in the neck) * exophthalmos (protuberance of one or both eyes) * a non-pitting edema with thickening of the skin, described as "peau d'orange" or "orange peel", usually found on the lower extremities * fatigue, weight loss with increased appetite, and other symptoms of hyperthyroidism The two signs that are truly diagnostic of Graves' disease (i.e. not seen in other hyperthyroid conditions) are exophthalmos and nonpitting edema. Goiter, which is caused by an enlarged thyroid gland, can be present with other forms of hyperthyroidism, although Graves' disease is the most common cause. A large goiter is visible to the naked eye, but a smaller goiter may not be clinically detectable, though X-rays or ultrasound can assist in detecting it. Another sign of Graves' disease is hyperthyroidism, i.e. over-production of the thyroid hormones T3 and T4. Although, hypothyroidism has also been associated and may be the causating factor in some patients. Hyperthyroidism can be confirmed by measuring elevated blood levels levels of free (unbound) T3 and T4. Other useful laboratory measurements include thyroid-stimulating hormone (TSH, low in Graves' disease due to negative feedback from the elevated T3 and T4), and protein-bound iodine (elevated). Thyroid-stimulating antibodies may also be detected serologically. Definitive diagnosis requires a biopsy. [edit] Other Graves' Disease Symptoms Some of the most typical symptoms of Graves' Disease are the following: * Palpitations * Tachycardia (rapid heart rate: 100-120 beats per minute, or higher) * Arrhythmia (irregular heart beat) * Raised blood pressure (Hypertension) * Tremor (usually fine shaking eg. hands) * Excessive sweating * Heat intolerance * Increased appetite * Unexplained weight loss despite increased appetite * Shortness of breath * Muscle weakness (especially in the large muscles of the arms and legs) and degeneration * Diminished/Changed sex drive * Insomnia (inability to get enough sleep) * Increased energy * Fatigue * Mental impairment, memory lapses, diminished attention span * Decreased concentration * Nervousness, agitation * Irritability * Restlessness * Erratic behavior * Emotional lability * Brittle nails * Abnormal breast enlargement (men) * Goiter (enlarged thyroid gland) * Protruding eyeballs (Graves' disease only * Double vision * Eye pain, irritation, or the feeling of grit or sand in the eyes * Swelling or redness of eyes or eyelids/eyelid retraction * Sensitivity to light * Decrease in menstrual periods (oligomenorrhea), Irregular and scant menstrual flow (Amenorrhea) * Difficulty conceiving/infertility/recurrent miscarriage * Hair loss * Itchy skin, hives * Chronic sinus infections * Lumpy, reddish skin of the lower legs (pretibial myxedema) * Smooth, velvety skin * Increased bowel movements or Diarrhea [edit] Incidence and epidemiology The disease occurs most frequently in women (7:1 compared to men). It occurs most often in middle age (most commonly in the third to fifth decades of life), but is not uncommon in adolescents, during pregnancy, at the time of menopause and in people over age 50. There is a marked family preponderance, which has led to speculation that there may be a genetic component. To date, no clear genetic defect has been found that would point at a monogenic cause. Tissue behind the eye can become swollen or fibrous, causing the characteristic symptom of bulging eyes. [edit] Pathophysiology Graves' disease is an autoimmune disorder, in which the body produces antibodies to the receptor for Thyroid-stimulating hormone (TSH). (Antibodies to thyroglobulin and to the thyroid hormones T3 and T4 may also be produced.) This is an example of a type II hypersensitivity. These antibodies cause hyperthyroidism because they bind to the TSH receptor and chronically stimulate it. The TSH receptor is expressed on the follicular cells of the thyroid gland (the cells that produce thyroid hormone), and the result of chronic stimulation is an abnormally high production of T3 and T4. This in turn causes the clinical symptoms of hyperthyroidism, and the enlargement of the thyroid gland visible as goiter. The infiltrative exophthalmos that is frequently encountered has been explained by postulating that the thyroid gland and the extraocular muscles share a common antigen which is recognized by the antibodies. Antibodies binding to the extraocular muscles would cause swelling behind the eyeball. The "orange peel" skin has been explained by the infiltration of antibodies under the skin, causing an inflammatory reaction and subsequent fibrous plaques. There are 3 types of autoantibodies to the TSH receptor currently recognized: * TSI, Thyroid stimulating immunoglobulins: these antibodies (mainly IgG) act as LATS (Long Acting Thyroid Stimulants), activating the cells in a longer and slower way than TSH, leading to an elevated production of thyroid hormone. * TGI, Thyroid growth immunoglobulins: these antibodies bind directly to the TSH receptor and have been implicated in the growth of thyroid follicles. * TBII, Thyroid Bind Inhibiting Inmunoglobulins: these antibodies inhibit the normal union of TSH with its receptor. By doing this, several other antibodies that normally would inhibit TSH function will actually act as if TSH itself was binding to its receptor, thus inducing thyroid function. [edit] Etiology The trigger for auto-antibody production is not known. There appears to be a genetic predisposition for Graves' disease, suggesting that some people are more prone than others to develop TSH receptor activating antibodies due to a genetic cause. HLA DR (especially DR3) appears to play a significant role.[8] Since Graves' disease is an autoimmune disease which appears suddenly, often quite late in life, it is thought that a viral or bacterial infection may trigger antibodies which cross-react with the human TSH receptor (a phenomenon known as antigenic mimicry, also seen in some cases of type I diabetes). One possible culprit is the bacterium Yersinia enterocolitica (a cousin of Yersinia pestis, the agent of bubonic plague). However, although there is indirect evidence for the structural similarity between the bacteria and the human thyrotropin receptor, direct causative evidence is limited.[8] Yersinia seems not to be a major cause of this disease, although it may contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals.[9] It has also been suggested that Y. enterocolitica infection is not the cause of auto-immune thyroid disease, but rather is only an associated condition; with both having a shared inherited susceptibility.[10] More recently the role for Y. enterocolitica has been disputed.[11] The ocular manifestations of Graves disease are more common in smokers and tend to worsen (or develop for the first time) following radioiodine treatment of the thyroid condition. Thus, they are not caused by hyperthyroidism per se; this common misperception may result from the fact that hyperthyroidism from other causes may cause eyelid retraction or eyelid lag (so-called hyperthyroid stare) which can be confused with the general appearance of proptosis/exophthalmos, despite the fact that the globes do not actually protrude in other causes of hyperthyroidism. Also, both conditions (globe protrusion and hyperthyroid lid retraction) may exist at the same time in the hyperthyroid patient with Graves disease. [edit] Treatment Medical treatment of Graves' disease includes antithyroid drugs, radioactive iodine and thyroidectomy (surgical excision of the gland). Treatment of the hyperthyroidism of Graves-Basedow disease may be with medications such as methimazole or propylthiouracil (PTU), which reduce the production of thyroid hormone, or with radioactive iodine. Surgical removal of the thyroid is another option, but still requires preoperative treatment with methimazole or PTU. This is done to render the patient "euthyroid" (i.e. normothyroid) before the surgery since operating on a frankly hyperthyroid patient is dangerous. Therapy with radioactive iodine (I-131) is the most common treatment in the United States and in many other parts of the world. Thyroid blocking drugs and/or surgical thyroid removal is used more often than radioactive iodine as definitive treatment in Japan, perhaps because of general fear of radioactivity among many Japanese. The development of radioactive iodine (I-131) in the early 1940s at the Mallinckrodt General Clinical Research Center and its widespread adoption as treatment for Graves' Disease has led to a progressive reduction in the use of surgical thyroidectomy for this problem. In general, RAI therapy is effective, less expensive, and avoids the small but definite risks of surgery. Treatment with antithyroid medications must be given for six months to two years, in order to be effective. Even then, upon cessation of the drugs, the hyperthyroid state may recur. Side effects of the antithyroid medications include a potentially fatal reduction in the level of white blood cells. [edit] Antithyroid drugs The main antithyroid drugs are methimazole (US), carbimazole (UK) and propylthiouracil (PTU). These drugs block the binding of iodine and coupling of iodotyrosines. The most dangerous side-effect is agranulocytosis (1/250, more in PTU); this is an idiosyncratic reaction which does not stop on cessation of drug). Others include granulocytopenia (dose dependent, which improves on cessation of the drug) and aplastic anemia. Patients on these medications should see a doctor if they develop sore throat or fever. The most common side effects are rash and peripheral neuritis. These drugs also cross the placenta and are secreted in breast milk. [edit] Radioiodine This modality is suitable for most patients, although some prefer to use it mainly for older patients. Indications for radioiodine are: failed medical therapy or surgery and where medical or surgical therapy are contraindicated. Contraindications to RAI are pregnancy (absolute), ophthalmopathy (relative- it can aggravate thyroid eye disease), solitary nodules. Disadvantages of this treatment are a high incidence of hypothyroidism (up to 80%) requiring hormone supplementation. It acts slowly and has a relapse rate that depends on the dose administered. [edit] Surgery This modality is suitable for young patients and pregnant patients. Indications are: a large goiter (especially when compressing the trachea), suspicious nodules or suspected cancer (to pathologically examine the thyroid) and patients with ophthalmopathy. Both bilateral subtotal thyroidectomy and the Hartley-Dunhill procedure (hemithyroidectomy on 1 side and partial lobectomy on other side) are possible. Advantages are: immediate cure and potential removal of carcinoma. Its risks are injury of the recurrent laryngeal nerve, hypoparathyroidism (due to removal of the parathyroid glands), hematoma (which can be life-threatening if it compresses the trachea) and scarring. [edit] Eye disease Thyroid Eye Disease (TED) is one of the most typical symptom of Graves' Disease- also called "Graves' ophthalmopathy". Thyroid eye disease is an inflammatory condition which affects the orbital contents including the extraocular muscles and orbital fat. It is almost always associated with Graves' disease (GD) but may rarely be seen in Hashimoto's thyroiditis, primary hypothyroidism, or thyroid cancer. The ocular manifestations of TED include soft tissue inflammation, eyelid retraction, proptosis, corneal exposure, and optic nerve compression. The signs and symptoms of the disease are characteristic. These include lid retraction, lid lag, and a delay in the downward excursion of the upper eyelid in down gaze that is specific to TED. * For mild disease - artificial tears, steroid eyedrops, oral steroids (to reduce chemosis) * For moderate disease - lateral tarsorrhaphy * For severe disease - orbital decompression or retro-orbital radiation [edit] No treatment If left untreated, more serious complications could result, including birth defects in pregnancy, increased risk of a miscarriage, and in extreme cases, death. Graves-Basedow disease is often accompanied by an increase in heart rate, which may lead to further heart complications. If the eyes are proptotic (bulging) severely enough that the lids do not close completely at night, severe dryness will occur with a very high risk of a secondary corneal infection which could lead to blindness. Pressure on the optic nerve behind the globe can lead to visual field defects and vision loss as well.
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Aldwen Originally Answered: Anyone know anything about the disease Scleroderma?
Systemic sclerosis is commonly called "scleroderma" because the most obvious symptom is "hard skin." Being a systemic disease, however, it's more than skin deep. The fibrosis, or scarring, it causes can occur anywhere there's connective tissue in the body, and that's almost everywhere. Add to that the malfunction in and damage to blood vessels it can cause, and it seems like a sure recipe for disaster. Even though most systemic scleroderma patients will not die from complications of their disease, most of us struggle to live with the affects. Profound fatigue is quite common, and you can imagine how that impacts someone's life. We frequently have the joint and muscle pain of secondary fibromyalgia, and almost all have some gastrointestinal involvement - at the very least, GI reflux. Raynaud's phenomenon is constant in about 97% of us - cold and stress cause blood vessels to spasm shut, cutting blood flow to hands, feet, nose, ears, and tongue. And these are the "minor" symptoms. When it gets dangerous, scleroderma can cause fibrosis in the lungs and heart, further into the GI tract where it can cause malabsorption of nutrients, in the kidneys and it can affect the pulmonary artery. Treatment is getting better - kidney complications used to be the number one killer in scleroderma and are now very treatable with ACE inhibitors. But not all treatments work for everyone, and some just have limited usefulness. The best help you can be for your mom is to be there, whether it's going to appointments with her, cleaning house, making dinner, or just to listen when she needs to talk about her pain and fears. Scleroderma becomes like a predator to us patients, lying in wait for the time it can strike in another area or in another way. Again, though it doesn't happen to most of us, we live knowing that it can kill us. It's not an easy way to live - help your mom concentrate on positive things and to ride the ups and downs by looking forward with hope. You can find extensive information about all the forms of scleroderma at the Scleroderma Foundation website - http://www.scleroderma.org. I'd also recommend calling them at 1-800-722-HOPE for their free booklet, "Understanding and Managing Scleroderma," written in part by Dr Maureen Mayes, author of "The Scleroderma Book," another good source of info. The Scleroderma Foundation has numerous live support groups in the US where you and your mom could meet and talk to other patients and families about coping. They also directly or through their chapters sponsor local and regional educational meetings to not only benefit patients, but to spread information to health care providers on the latest research and treatments. Also, the SF funds over $1 million each year in peer-reviewed scleroderma research. Your mom may also be interested in one of the many places to get support online. Search "scleroderma" on Yahoo and you'll find tons. Just remember to take care online, as with any other "unofficial" contact.
Aldwen Originally Answered: Anyone know anything about the disease Scleroderma?
All I know is that it is thickening of the skin. It is a horrible debilitating chronic disease that effects your daily living. They say it is not cancer. It can wreak havock on your organs and intestines and such. I am very sorry to hear that your mom suffers with this disease... and the toll it is most likely having on your family.

Tallulah Tallulah
I know exactly what you are going through. I was diagnosed with Graves about 3 months ago, and I would rather suffer with an overactive thyroid than have the iodine treatment and end up with an underactive one. Start out on the medication, I am taking Neo-Mercazole twice a day at the moment. It will take at least a few months for them to find the right dose for you to take long term. If you can get it under control with medication, do it. It's a much better option in the long run. My doctors are predicting 18 months of medication then I should be able to manage it myself. The problem with Graves is that your body is producing thyroid antibodies. In half of all Graves patients, these antibodies attack your thyroid and end up damaging it anyway. There is no way to stop this happening, no matter when you get treatment. You have a 50% chance of having an underactive thyroid once the Graves burns itself out. Good luck, I hope you get it under control soon.
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Reilly Reilly
This Site Might Help You. RE: graves disease? my brother was recently diagnosed with graves disease. he is 21 years old. i need to know if there is any foods he shouldn't have if so what are they. we want him on the least medications as possible because we believe in natural remedies.
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Reilly Originally Answered: what exactly is lupus disease ?
Lupus is an autoimmune disease, which means that instead of just attacking foreign substances, such as bacteria and viruses, your immune system also turns against healthy tissue,including your joints, skin, kidneys, blood cells, heart and lungs. Her treatment will depend on what symptoms she may have. I'm sure you'll be there for her emotional support. Maybe find Lupus support groups close where your niece lives. Hope this helps. More infor check out www.lupus.org

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