出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2013/11/28 12:05:39」(JST)
バセドウ病またはバセドー病(-びょう、 独: Basedow-Krankheit)[1]とは、甲状腺自己抗体によって甲状腺が瀰漫(びまん)性に腫大する自己免疫疾患(II型アレルギー)。英語圏ではグレーブス病(グレーブスびょう、 英: Graves' disease)と呼ばれる。ロバート・ジェームス・グレーブス(英語版)(1835年)とカール・アドルフ・フォン・バセドウ(1840年)によって発見、報告された。
甲状腺の表面には、下垂体によって産生される甲状腺刺激ホルモン(TSH)の受容体(甲状腺刺激ホルモン受容体、TSHレセプター)が存在する。バセドウ病では、この受容体に対する自己抗体(抗TSHレセプター抗体、TRAb)が生じ、それがTSHの代わりにTSHレセプターを過剰に刺激するために、甲状腺ホルモンが必要以上に産生されている。甲状腺ホルモンは全身の新陳代謝を高めるホルモンであるため、このホルモンの異常高値によって代謝が異常に活発になることで、心身に様々な影響を及ぼす。
この自己抗体産生が引き起こされる原因は、2007年現在不詳である。過度なストレス・過労が発症・再発に関与しているという説もある。また遺伝の影響もある程度あると考えられている。
なお、ヨウ素の摂取量が少ない地域(西ヨーロッパなど)では、ヨウ素を大量摂取することで、潜在的なバセドウ病が発症することがある。これをヨードバセドウ病と呼ぶ。
バセドウ病は、甲状腺ホルモンが過剰に作られる病気、すなわち甲状腺機能亢進症を起こす代表的な病気である。中年以上の女性がバセドウ病に罹患した場合、更年期障害と勘違いする事が多い。
ほかの甲状腺の病気と同じように女性に多い病気だが、その比率は男性1人に対して女性4人ほど。甲状腺の病気全体の男女比は男性1対女性9の割合であるから、甲状腺の病気のなかでは比較的男性の比率が高い病気である。
発病年齢は、20歳代と30歳代で全体の過半数を占め、次いで40歳代、50歳代となっており、青年から壮年に多い病気といえる。何らかのアレルギーを持っている人が多い。
上記症状のすべてが出るわけでなく、患者により差異がある。潜在的甲状腺機能亢進症で症状がない患者もいる。
甲状腺腫大、眼球突出、頻脈、体重減少、手指振戦、発汗増加等の甲状腺中毒症所見などからバセドウ病が疑われる場合、血中の甲状腺ホルモン測定などにより判断する。
これについては、日本甲状腺学会より「甲状腺疾患診断ガイドライン2010」として 「バセドウ病の診断ガイドライン」が提示されている。[4]
甲状腺ホルモンの合成を抑える薬(抗甲状腺薬:メチマゾール(チアマゾール、メルカゾール)、チウラジール(プロバジール)を、規則的に服用する方法。定期的に甲状腺ホルモンの量を測定しながら、適切な量の薬を服用することで、血液中の甲状腺ホルモンの濃度を正常にする。薬で甲状腺刺激ホルモンの量を調整することで普通の人と変わらない生活を営むことができるが、甲状腺刺激抗体が消えるまで薬を飲みつづける必要がある為、完治には長い期間を要する。副作用としては、5%に皮膚の炎症、0.05%に白血球の減少や無顆粒球症が生じることがある。これらの副作用は服用開始から3ヶ月以内に現れることが多い。無顆粒球症が生じたら直ちに服薬を中止し、他の治療法に切り替える必要がある。(好中球数 1000個/μLを下回れば中止とする。)
ヨードの放射性同位元素(ラジオアイソトープ; radio isotope; RI)を服用し、甲状腺の細胞の数を減らす方法。甲状腺細胞の数が減少すれば、分泌される甲状腺ホルモンの量が減少する。およそ2 - 6ヶ月で甲状腺ホルモンの量が減少すると言われ、手術よりは手軽で、薬より早く治るのが、この方法の長所である。但し、時間経過とともに細胞が減りすぎて、逆に甲状腺の機能低下が発生することもある。なお、放射性物質を用いるので被曝の影響が全くないとはいえず、妊娠中や授乳中の女性およびすぐに妊娠を希望する女性などには行わない。放射線の影響は約4ヶ月でなくなるとされることから、4ヶ月で妊娠を許可している施設もあるが、甲状腺機能の変動があるため1年は待つべきとされる。
甲状腺の一部を残して、切除する方法。甲状腺を切除することで甲状腺ホルモンの量を調整する。他の治療法より早く完治し、再発も少ないが、入院を要する。また、傷跡が目立つことがある。手術による合併症も起こりうるので、高齢者や心臓の病気がある人などには行わない。術後に甲状腺機能低下症に陥ることが多いが、その場合の治療は通常の甲状腺機能低下症と同じである。なお、再発した場合は再手術は行わず、ヨード治療などに切り替える。
バセドウ病は適切な治療を行えば予後良好である。しかし、治療を怠ると死亡の原因にもなる。頻脈ひいては心房細動に至ると、脳塞栓を起こすこともありうる。甲状腺クリーゼは早急に専門医に紹介されるべき病態のひとつである。
周期性四肢麻痺は、そのものは生命には関与しないが、てんかん発作と同様に車の運転中などに発作を起こすと事故に至ることも懸念される症状のひとつである。
適切な治療が行われていないとき、妊娠中、へその緒を通しての胎児への栄養がうまく送れなくなり、胎児が発育遅延になる場合がある。母体のTRAbやTSAbが多い場合、これらの抗体が胎盤を通して胎児に送られるため、新生児に一時的にバセドウ病の症状が現れることがあるが、これらの抗体は新生児が産生しているものではないため、やがて症状は消える。
甲状腺の治療薬は長い間、胎児の奇形に寄与すると信じられていたが、現在では否定されている。
アイルランドの医師グレーブス(1835年)によって初めて報告された。その後バセドウ伯(1840年)が独自に発見・報告し[6]、ゲオルグ・ヒルシュによりこの名が付けられた。症状の「メルゼブルクの三徴」は、バセドウの出身地、メルゼブルク(ドイツ語版)の地名に因む[2]。本症の発見前後、日本の医学は主にドイツからの情報に依っていたため、グレーブス病(Graves' disease)ではなくバセドウ病と言う事が多い。ちなみに欧州圏においてはバセドウ病と呼ばれることが多いようである。
未治療のバセドウ病患者や抗甲状腺薬内服後にANCA陽性となる症例が方向されている。そのほとんどはMPO-ANCAである。抗甲状腺薬内服後にANCA陽性となった場合は無症状で低抗体価ならば内服変更はせずに経過観察でもよいという報告はある。しかし、血管炎症状合併時や高抗体価の場合は内服薬の変更が好ましいとされている。
この項目は、医学に関連した書きかけの項目です。この項目を加筆・訂正などしてくださる協力者を求めています(プロジェクト:医学/Portal:医学と医療)。 |
Graves' disease | |
---|---|
Classification and external resources | |
ICD-10 | E05.0 |
ICD-9 | 242.0 |
OMIM | 275000 |
MedlinePlus | 000358 |
eMedicine | med/929 ped/899 |
MeSH | D006111 |
Graves' disease (or Basedow-Graves disease) is an autoimmune disease. It most commonly affects the thyroid, frequently causing it to enlarge to twice its size or more (goiter), become overactive, with related hyperthyroid symptoms such as increased heartbeat, muscle weakness, disturbed sleep, and irritability. It can also affect the eyes, causing bulging eyes (exophthalmos). It affects other systems of the body, including the skin, heart, circulation and nervous system.
It affects up to 2% of the female population, sometimes appears after childbirth, and has a female:male incidence of 5:1 to 10:1.[citation needed] Hereditary factors are the major risk factor for the development of Graves disease, with "79% of the liability to the development of GD ... attributable to genetic factors".[1] Smoking and exposure to second-hand smoke is associated with the eye manifestations but not the thyroid manifestations.
Diagnosis is usually made on the basis of symptoms, although thyroid hormone tests may be useful, particularly to monitor treatment.[2]
Medical eponyms are often styled nonpossessively; thus Graves' disease and Graves disease are variant stylings for the same term.
The signs and symptoms of Graves' disease virtually all result from the direct and indirect effects of hyperthyroidism, with main exceptions being Graves' ophthalmopathy, goitre, and pretibial myxedema (which are caused by the autoimmune processes of the disease). Symptoms of the resultant hyperthyroidism are mainly insomnia, hand tremor, hyperactivity, hair loss, excessive sweating, shaking hands, itching, heat intolerance, weight loss despite increased appetite, diarrhea, frequent defecation, palpitations, muscle weakness, and skin warmth and moistness.[3] Further signs that may be seen on physical examination are most commonly a diffusely enlarged (usually symmetric), nontender thyroid, lid lag, excessive lacrimation due to Graves' ophthalmopathy, arrhythmias of the heart, such as sinus tachycardia, atrial fibrillation and premature ventricular contractions, and hypertension.[3] People with hyperthyroidism may experience behavioral and personality changes including: psychosis, mania, anxiety, agitation, and depression.[4]
The Immunoglobulin G antibody recognizes and binds to the thyrotropin receptor (TSH receptor). It mimics the TSH to that receptor and activates the secretion of thyroxine (T4) and triiodothyronine (T3), and the actual TSH level will decrease in the blood plasma. The TSH levels fall because the hypothalamus-pituitary-thyroid negative feedback loop is working. The result is very high levels of circulating thyroid hormones and the negative feedback regulation will not work for the thyroid gland.[citation needed]
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.[5]
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).[citation needed]
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.[5] 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.[6] 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.[7] More recently the role for Y. enterocolitica has been disputed.[8]
Emotional stress has been posited as a possible cause of Graves' disease as well, based largely on anecdotal evidence. While there are theoretical mechanisms by which stress could cause an aggravation of the autoimmune response that leads to Graves' disease, more robust clinical data are needed for a firm conclusion.[9]
Graves' disease may present clinically with one of the following characteristic signs:
The two signs that are truly 'diagnostic' of Graves' disease (i.e., not seen in other hyperthyroid conditions) are exophthalmos and non-pitting edema (pretibial myxedema). Goitre is an enlarged thyroid gland and is of the diffuse type (i.e., spread throughout the gland). Diffuse goitre may be seen with other causes of hyperthyroidism, although Graves' disease is the most common cause of diffuse goitre. A large goitre will be visible to the naked eye, but a small goitre (mild enlargement of the gland) may be detectable only by physical exam. Occasionally, goitre is not clinically detectable but may be seen only with CT or ultrasound examination of the thyroid.
Another sign of Graves' disease is hyperthyroidism, i.e., overproduction of the thyroid hormones T3 and T4. Normothyroidism is also seen, and occasionally also hypothyroidism, which may assist in causing goitre (though it is not the cause of the Graves' disease). Hyperthyroidism in Graves' disease is confirmed, as with any other cause of hyperthyroidism, by measuring elevated blood levels of free (unbound) T3 and T4.
Other useful laboratory measurements in Graves' disease include thyroid-stimulating hormone (TSH, usually 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.
Biopsy to obtain histiological testing is not normally required but may be obtained if thyroidectomy is performed.
Differentiating two common forms of hyperthyroidism such as Graves' disease and Toxic multinodular goiter is important to determine proper treatment. Measuring TSH-receptor antibodies with the h-TBII assay has been proven efficient and was the most practical approach found in one study.[10]
Thyroid-associated ophthalmopathy is one of the most typical symptoms of Graves' disease. It is known by a variety of terms, the most common being 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 but may rarely be seen in Hashimoto's thyroiditis, primary hypothyroidism, or thyroid cancer.
The ocular manifestations that are relatively specific to Graves' disease include soft tissue inflammation, proptosis (protrusion of one or both globes of the eyes), corneal exposure, and optic nerve compression. Also seen, if the patient is hyperthyroid, (i.e., has too much thryoid hormone) are more general manifestations, which are due to hyperthyroidism itself and which may be seen in any conditions that cause hyperthyroidism (such as toxic multinodular goitre or even thyroid poisoning). These more general symptoms include lid retraction, lid lag, and a delay in the downward excursion of the upper eyelid, during downward gaze.
It is believed that fibroblasts in the orbital tissues may express the Thyroid Stimulating Hormone receptor (TSHr). This may explain why one autoantibody to the TSHr can cause disease in both the thyroid and the eyes.[11]
Mnemonic: "NO SPECS":[12]
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.)
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:
Another effect of hyperthyroidism is bone loss from osteoporosis, caused by an increased excretion of calcium and phosphorus in the urine and stool. The effects can be minimized if the hyperthyroidism is treated early. Thyrotoxicosis can also augment calcium levels in the blood by as much as 25%. This can cause stomach upset, excessive urination, and impaired kidney function.[13]
Treatment of Graves' disease includes antithyroid drugs which reduce the production of thyroid hormone; radioiodine (radioactive iodine I-131); and thyroidectomy (surgical excision of the gland). As operating on a frankly hyperthyroid patient is dangerous, prior to thyroidectomy preoperative treatment with antithyroid drugs is given to render the patient "euthyroid" (i.e. normothyroid).
Treatment with antithyroid medications must be given for six months to two years 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. Therapy with radioiodine is the most common treatment in the United States, while antithyroid drugs and/or thyroidectomy are used more often in Europe, Japan, and most of the rest of the world.
β-blockers (such as propranolol) may be used to inhibit the sympathetic nervous system symptoms of tachycardia and nausea until such time as antithyroid treatments start to take effect. Pure beta blockers do not inhibit lid-retraction in the eyes, which is mediated by alpha adrenergic receptors.
The main antithyroid drugs are carbimazole (in the UK), methimazole (in the US), 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). 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. Lygole is used to block hormone synthesis before surgery.
A randomized control trial testing single dose treatment for Graves' found methimazole achieved euthyroid state more effectively after 12 weeks than did propylthyouracil (77.1% on methimazole 15 mg vs 19.4% in the propylthiouracil 150 mg groups).[14]
A study has shown no difference in outcome for adding thyroxine to antithyroid medication and continuing thyroxine versus placebo after antithyroid medication withdrawal. However two markers were found that can help predict the risk of recurrence. These two markers are a positive Thyroid Stimulating Hormone receptor antibody (TSHR-Ab) and smoking. A positive TSHR-Ab at the end of antithyroid drug treatment increases the risk of recurrence to 90% (sensitivity 39%, specificity 98%), a negative TSHR-Ab at the end of antithyroid drug treatment is associated with a 78% chance of remaining in remission. Smoking was shown to have an impact independent to a positive TSHR-Ab.[15]
Radioiodine (radioactive iodine-131) was developed in the early 1940s at the Mallinckrodt General Clinical Research Center. 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. Hypothyroidism may be a complication of this therapy, but may be treated with thyroid hormones if it appears. The rationale for radioactive iodine is that it accumulates in the thyroid and irradiates the gland with its beta and gamma radiations, about 90% of the total radiation being emitted by the beta (electron) particles. The most common method of iodine-131 treatment is to administer a specified amount in microcuries per gram of thyroid gland based on palpation or radiodiagnostic imaging of the gland over 24 hours.[16] Patients who receive the therapy must be monitored regularly with thyroid blood tests to ensure that they are treated with thyroid hormone before they become symptomatically hypothyroid. For some patients, finding the correct thyroid replacement hormone and the correct dosage may take many years and may be in itself a much more difficult task than is commonly understood.[citation needed]
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 eventual thyroid hormone supplementation in the form of a daily pill(s). The radio-iodine treatment acts slowly (over months to years) to destroy the thyroid gland, and Graves' disease-associated hyperthyroidism is not cured in all persons by radioiodine, but has a relapse rate that depends on the dose of radioiodine which is administered.
This modality is suitable for young patients and pregnant patients. Indications are: a large goitre (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 one 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. Removal of the gland enables complete biopsy to be performed to have definite evidence of cancer anywhere in the thyroid. (Needle biopsies are not so accurate at predicting a benign state of the thyroid). No further treatment of the thyroid is required, unless cancer is detected. Radioiodine uptake study may be done after surgery, to ensure that all remaining (potentially cancerous) thyroid cells (i.e., near the nerves to the vocal chords) are destroyed. Besides this, the only remaining treatment will be Synthroid, or thyroid replacement pills to be taken for the rest of the patient's life.
Disadvantages are as follows. A scar is created across the neck just above the collar bone line. However, the scar is very thin, and can eventually recede and appear as nothing more than a crease in the neck. The patient may spend a night in hospital after the surgery, and endure the effects of total anesthesia (i.e., vomiting), as well as sore throat, raspy voice, cough from having a breathing tube stuck down the windpipe during surgery.[citation needed]
Mild cases are treated with lubricant eye drops or non steroidal antiinflammatory drops. Severe cases threatening vision (Corneal exposure or Optic Nerve compression) are treated with steroids or orbital decompression. In all cases cessation of smoking is essential. Double vision can be corrected with prism glasses and surgery (the latter only when the process has been stable for a while).
Difficulty closing eyes can be treated with lubricant gel at night, or with tape on the eyes to enable full, deep sleep.
Orbital decompression can be performed to enable bulging eyes to retreat back into the head. Bone is removed from the skull behind the eyes, and space is made for the muscles and fatty tissue to fall back into the skull.
Eyelid surgery can be performed on upper and/or lower eyelids to reverse the effects of Graves' on the eyelids. Eyelid muscles can become tight with Graves, making it impossible to close eyes all the way. Eyelid surgery involves an incision along the natural crease of the eyelid, and a scraping away of the muscle that holds the eyelid open. This makes the muscle weaker, which allows the eyelid to extend over the eyeball more effectively. Eyelid surgery helps reduce or eliminate dry eye symptoms.
If left untreated, more serious complications could result, including birth defects in pregnancy, increased risk of a miscarriage, and in extreme cases, death. Graves disease is often accompanied by an increase in heart rate, which may lead to further heart complications including loss of the normal heart rhythm (atrial fibrillation), which may lead to stroke. If the eyes are proptotic (bulging) enough that the lids do not close completely at night, dryness will occur with a 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.
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, during menopause, or 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.
Graves' disease owes its name to the Irish doctor Robert James Graves,[17] who described a case of goitre with exophthalmos in 1835.[18] The German Karl Adolph von Basedow independently reported the same constellation of symptoms in 1840.[19][20] As a result, on the European Continent, the terms Basedow's syndrome,[21] Basedow's disease, or Morbus Basedow[22] are more common than Graves' disease.[21][23]
Graves' disease[21][22] has also been called exophthalmic goitre.[22]
Less commonly, it has been known as Parry's disease,[21][22] Begbie's disease, Flajani's disease, Flajani-Basedow syndrome, and Marsh's disease.[21] These names for the disease were derived from Caleb Hillier Parry, James Begbie, Giuseppe Flajani, and Henry Marsh.[21] Early reports, not widely circulated, of cases of goitre with exophthalmos were published by the Italians Giuseppe Flajina[24] and Antonio Giuseppe Testa,[25] in 1802 and 1810, respectively.[26] Prior to these, Caleb Hillier Parry,[27] a notable provincial physician in England of the late 18th century (and a friend of Edward Miller-Gallus),[28] described a case in 1786. This case was not published until 1825, but still 10 years ahead of Graves.[29]
However, fair credit for the first description of Graves' disease goes to the 12th century Persian physician Sayyid Ismail al-Jurjani,[30] who noted the association of goitre and exophthalmos in his "Thesaurus of the Shah of Khwarazm", the major medical dictionary of its time.[21][31][32]
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リンク元 | 「グレーブス病」「バセドウ病」 |
関連記事 | 「disease」 |
(Basedow病の診断ガイドライン(日本甲状腺学会 第7次案))
3) Basedow病の疑い
Graves’diseaseまたはeuthyroidophthalmopathyといわれる.
の二種類である。薬効の高さや作用持続時間の長さの利点からMMIを第一選択とするが、胎盤移行や乳汁移行、副作用の出現頻度を考慮しPTUを用いることもある。治療中止の時期は甲状腺機能の正常化はもちろんのこと、抗TSH受容体抗体が陰性であることも必要である。
放射性ヨード療法 131療法 |
外科的治療法 | 抗甲状腺薬 | |
長所 | 治療法が簡単 | どの年代の患者でも可能(妊娠・妊娠中も可能) | |
成人合併例でも治療可能 | 通院での治療可能 | ||
比較的短期間で寛解 | 短期間に治癒 | ||
永続寛解率が高い | 高い寛解率 | ||
侵襲が少ない | 不可逆的な甲状腺機能低下は稀 | ||
短所 | 特別な施設が必要 | 手術侵襲 | 副作用(無顆粒球症・肝障害) |
永続的甲状腺機能低下症が年ごとに増加 | 永続的甲状腺機能低下症 | ||
妊娠、授乳期では禁忌 | 瘢痕 | 治療期間が長い | |
術後合併症(反回神経麻痺、テタニー) | 永続寛解率が低い | ||
術後再発 | |||
回避・禁忌 | 30歳以下は避ける | ||
妊娠予定、妊娠中、授乳中は禁忌 | |||
適応 | 欧米の第一選択 | 日本の第一選択 | |
老人で早期治療を望む場合 | 早期治癒を望む場合(社会的・妊娠希望) | 小児、妊婦 | |
抗甲状腺薬で副作用の例 | 抗甲状腺薬で副作用の例 | 外科的療法、放射性ヨード療法の明らかな適応外 | |
抗甲状腺薬で永続治癒の可能性低 | 抗甲状腺薬で永続治癒の可能性低 | FT4軽度上昇例 | |
服薬・治療コンプライアンス低 | 服薬・治療コンプライアンス低 | ||
手術適応だが合併症、患者の意志により回避される場合 | 通院が困難 | ||
手術後再発例 | 甲状腺腫が大 | 甲状腺腫が小 |
破壊性甲状腺炎 | グレーブス病 | 備考 | ||
無痛性甲状腺炎 | 亜急性甲状腺炎 | |||
病態 | 橋本病 (慢性甲状腺炎)の 経過中に濾胞の 崩壊を示す |
甲状腺の炎症による 濾胞破壊 |
TSHRの過剰刺激 | |
炎症 | mild | severe | [-] | |
末梢fT3 | ↑ | ↑ | ↑ | 甲状腺機能亢進もしくは濾胞の破壊で上昇 |
123I uptake | ↓ | ↓ | ↑ | 健全な甲状腺濾胞が存在し、甲状腺ホルモン合成能が高い |
血清TSH | ↓ | ↓ | ↓ | fT3上昇のため |
血清サイログロブリン | ↑ | ↑ | ↑ | 甲状腺機能亢進もしくは濾胞の破壊で上昇 |
TSH受容体抗体 | [-] | [-] | [+] | |
抗TPO抗体 | [+] | [-]/トキニ[+] | [+] | |
抗サイログロブリン抗体 | [+] | [-]/トキニ[+] | [+] |
[★] グレーブス病。Basedow disease Basedow's disease
.