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Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders Background information Patient information Key messages for this pathway Suspected hyperthyroidism Signs of thyrotoxicosis Consider differential diagnoses Investigations to confirm diagnosis of hyperthyroidism Subclinical hyperthyroidism Distinguish cause of hyperthyroidism Follow up Thyroiditis Graves' disease Toxic multinodular goitre Thyroid adenoma Drug-induced Hyperthyroidism in pregnancy suspected Start beta blocker if symptomatic Investigations Investigations Likely solitary toxic thyroid nodule Consider whether safe to stop drug treatment Repeat thyroid function after 4 weeks and reassess Initial treatment Thyrotoxic on repeat testing Euthyroid or hypothyroid Hyperemesis gravidarum Clinical features of Graves' disease Thyroid function tests (TFTs) suggestive of hyperthyroidism Refer to endocrinologist Monitoring treatment R Refer to endocrinologist Refer to endocrinologist R R Information for primary care about antithyroid treatment and block and replace regimen Initial management Antenatal management Refer to endocrinologist Treat with antithyroid agents R Go to hyperthyroidism treatment Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 Postpartum management © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 1 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders 1 Background information Quick info: Scope: • causes and clinical features of hyperthyroidism, including: • Graves' disease • toxic multinodular goitre • thyroid adenoma • medications • thyroiditis • causes and clinical features of hypothyroidism, including: • autoimmune thyroiditis • drug-induced thyroiditis • subacute thyroiditis • postpartum thyroiditis • consideration of thyroid storm • consideration of myxoedema coma • clinical assessment of hyper- and hypothyroidism • use of thyroid function tests (TFTs) for diagnosis • management of hyper- and hypothyroidism • covers adults age 18 years and older, and pregnant women, in primary and secondary care settings Out of scope: • assessment and management of thyroid disorders in children • management of thyroid nodules Definition: • hypothyroidism is caused by underactivity of the thyroid gland: • primary hypothyroidism describes thyroid hyposecretion due to primary thyroid gland disease • a fall in thyroid hormone results in increased secretion of thyroid stimulating hormone (TSH) and elevation of serum TSH concentrations • secondary hypothyroidism is caused by insufficient TSH stimulation of the thyroid gland due to pituitary dysfunction • tertiary hypothyroidism is due to diminished hypothalamic thyroid releasing hormone (TRH) release, causing decreased pituitary stimulation and reduced TSH • secondary and tertiary hypothyroidism are termed 'central hypothyroidism' • hyperthyroidism is caused by overactivity of the thyroid gland • goitre refers to enlargement of the thyroid gland which may or may not cause under or over activity of the gland Causes of hyperthyroidism: • Graves' disease • toxic multinodular goitre • toxic adenoma • painful subacute thyroiditis • silent thyroiditis including lymphocytic and post-partum variations • iodine-induced hyperthyroidism • excessive pituitary TSH • excessive ingestion of thyroid hormone Causes of hypothyroidism: • chronic autoimmune thyroiditis (Hashimoto's disease) • surgical removal of the thyroid gland • thyroid gland ablation Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 2 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders • external irradiation • medications, eg lithium and interferon Diagnosis: • thyroid function is tested by taking blood samples to test for serum TSH and free thyroxine (T4) Incidence and prevalence: • in the UK, the prevalence of spontaneous hypothyroidism is between 1% and 2% • in the UK, the reported overall prevalence of hyperthyroidism is between 0.5% and 6.3% • hypo- and hyperthyroidism is 10 times more common in women than men References: British Thyroid Association (BTA). UK guidelines for the use of thyroid function tests. Sheffield: BTA; 2006. American Association of Clinical Endocrinologists (AACE). AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Jacksonville, FL: AACE; 2006. Clinical Knowledge Summaries (CKS). Hyperthyroidism. Version 1.1. Newcastle upon Tyne: CKS; 2008. Clinical Knowledge Summaries (CKS). Hypothyroidism. Version 1.1. Newcastle upon Tyne: CKS; 2009. Royal College of Physicians (RCP). The diagnosis and management of primary hypothyroidism. London: RCP; 2009. Wall CR. Myxedema coma: diagnosis and treatment. Am Fam Physician 2000; 62: 2485-90. Bahn RS, Burch HS, Cooper D et al. The role of propylthiouracil in the management of Graves' disease in adults: report of a meeting jointly sponsored by the American Thyroid Association and the Food and Drug Administration. Thyroid 2009; 19: 673-4. National Institute for Health and Clinical Excellence (NICE). Venous thromboembolism: reducing the risk. Reducing the risk of venous thromboembolism (deep vein thrombosis and pulmonary embolism) in patients admitted to hospital. Clinical guideline 92. London: NICE; 2010. The Endocrine Society. Management of thyroid dysfunction during pregnancy and postpartum. J Clin Endocrinol Metab 2007; 92: S1-47. Nygaard B. Hypothyroidism (primary). Clin Evid (online) 2010; 01: 605. Longmore M, Wilkinson I, Rajagopalan S. Oxford Handbook of Clinical Medicine. 6th edn. Oxford: Oxford University Press; 2004. Seshadri K. Thyroiditis, subacute. eMedicine; 2004. Nygaard B. Hyperthyroidism (primary). Clin Evid (online) 2008; 03: 611 Royal College of Physicians (RCP). Radio-iodine in the management of benign thyroid disease: clinical guidelines. London: RCP; 2007. 2 Patient information Quick info: http://www.patient.co.uk/doctor/Hyperthyroidism-(Thyrotoxicosis).htm 3 Key messages for this pathway Quick info: This pathway has been locally developed for South West Hampshire. Key messages for this pathway: • in older people, there may be few symptoms. Hyperthyroidism may present with deterioration of pre-existing heart disease, depression, anorexia or weight loss (apathetic or masked thyrotoxicosis) • diagnosis of hyperthyroidism is normally made from a suppressed thyroid stimulating hormone (TSH) and raised free thyroxine (FT4). It is only necessary to measure free triiodothyronine (FT3) when the TSH is suppressed but FT4 is in the normal range • thyroiditis usually presents with a hyperthyroidism phase followed by hypothyroidism for several months, and then resolution • in Graves' disease, TSH-receptor antibodies almost always positive and diagnostic, particularly thyroid-stimulating immunoglobulins (TSIs) • carbimazole dosage depends on the FT4 level. Warn patients about risk of agranulocytosis. A repeat thyroid function should be organized after 4-6 weeks of starting carbimazole Contributors to this pathway: • Dr Emmanuel Abu, UHS Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 3 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders • Dr Alex Freeman, NHSSC • Dr Azraai Nasruddin, UHS • Dr Derek Waller, UHS 4 Suspected hyperthyroidism Quick info: Clinical features of thyrotoxicosis include: • dyspnoea, palpitation • heat intolerance and increased sweating • restlessness, emotional lability, anxiety, irritability, and insomnia • weight loss despite increase or similar appetite • exercise intolerance, fatigue, muscle weakness • infertility, oligomenorrhoea and amenorrhoea • reduced libido, impotence and gynaecomastia in men • polyuria, thirst. generalised itch • in people with diabetes: • deterioration in diabetic control • recurrent hypoglycaemic attacks In older people, there may be few symptoms. Hyperthyroidism may present with deterioration of pre-existing heart disease, depression, anorexia or weight loss (apathetic or masked thyrotoxicosis). 5 Signs of thyrotoxicosis Quick info: Signs of thyrotoxicosis include: • agitation • sinus tachycardia, atrial fibrillation, heart failure, resting tachycardia, dependent oedema • thyroid enlargement • tremor • warm, moist skin; palmar erythema • onycholysis, pruritus, urticaria, diffuse pigmentation • diffuse alopecia • muscle wasting and weakness, proximal myopathy, hyperreflexia • gynaecomastia in men • chorea (rare) • hypokalaemic periodic paralysis in Asian men often precipitated by a large carbohydrate meal or by vigorous exercise. 6 Consider differential diagnoses Quick info: Differential diagnoses include: • anxiety state • cocaine or amphetamine overdose 7 Investigations to confirm diagnosis of hyperthyroidism Quick info: Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 4 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders Diagnosis of hyperthyroidism is normally made from a suppressed thyroid stimulating hormone (TSH) and raised free thyroxine (FT4). It is only necessary to measure free triiodothyronine (FT3) when the TSH is suppressed but FT4 is in the normal range. Overt primary hyperthyroidism diagnosis based on: • symptoms of hyperthyroidism • TSH level below the normal reference range (<0.1mU/L) • elevated level of FT4 • if FT4 is not above the reference range in a person with low serum TSH, FT3 should be measured to confirm a diagnosis of "T3-toxicosis" . This is typical in : • mild toxic nodular hyperthyroidism • early Graves' diseas Subclinical primary hyperthyroidism diagnosis based on: • TSH below normal reference range (<0.30mU/L) and FT4 and FT3 within normal range Secondary hyperthyroidism, caused by TSH-secreting pituitary adenoma, diagnosis based on: • TSH levels raised • elevated thyroid hormone levels • hyperthyroid symptoms 8 Subclinical hyperthyroidism Quick info: A diagnosis of subclinical hyperthyroidism is defined as low thyroid stimulating hormone (TSH), but asymptomatic, with normal free thyroxine (FT4) and free triiodothyronine (FT3). Subclinical hyperthyroidism should not routinely require treatment, although regular tests for TSH, FT4 and FT3 levels should be performed to monitor for progression to overt hyperthyroidism. Referral to specialist management will only be required if a goitre exists or if subclinical hyperthyroidism persists. In all cases, assess for possible causes, such as non-thyroidal illnesses, relevant drug therapies (e.g. amiodarone, lithium) and diagnostic agents (radiocontrast dyes). 9 Distinguish cause of hyperthyroidism Quick info: Hyperthyroidism may be caused by: • Graves' disease − presence of thyroid peroxidase antibodies may help to diagnose this condition, if cause of thyrotoxicosis is unclear • toxic multinodular goitre: • associated with low thyroid stimulating hormone (TSH) levels with or without high free thyroxine (FT4) levels • thyroid scan is useful in diagnosis (refer to Endocrinology) • distinguished from thyroid adenoma by enlarged thyroid gland and composed of multiple nodules • thyroid adenoma: • associated with low TSH levels with or without high FT4 levels • thyroid scan is useful in diagnosis (refer to Endocrinology) • medications, eg amiodarone or lithium: • in amiodarone-induced hyperthyroidism the TSH level is suppressed, FT4 levels are high and FT3 levels are high or normal • thyroiditis: • the thyroid may be tender or painful • erythrocyte sedimentation rate (ESR) is useful in diagnosing subacute thyroiditis • low radio-iodine uptake along with poor thyroid gland imaging is characteristic (refer to Endocrinology) 10 Follow up Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 5 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders Quick info: If the serum TSH level is less than 0.4 mU/L and the person is not on levothyroxine therapy, does not have a non-thyroidal illness, and is not on drug treatment that could suppress TSH (e.g. glucocorticoids, octreotide, cytokines, dopaminergic agents): • examine the individual for evidence of hyperthyroidism: measure TSH, FT4, and FT3 within 1–2 months to exclude progression to overt hyperthyroidism and to determine whether the biochemical abnormality is persistent. Usually, the serum TSH level will have returned to within the reference range in that time • if serum TSH remains low with normal FT4 or FT3 levels, repeated testing (serum TSH, FT4, and FT3) is necessary. The frequency of testing should be based on clinical judgement: every 3–6 months if the person is well and more frequently in elderly persons or those with underlying vascular disease • check thyroid peroxidase antibodies for evidence of Graves' disease • refer for specialist management if a goitre is present or if subclinical hyperthyroidism persists after one or two repeat tests • untreated subclinical hyperthyroidism should be followed into the long term by testing thyroid function every 6-12 months 11 Thyroiditis Quick info: Thyroiditis usually presents with a hyperthyroidism phase followed by hypothyroidism for several months, and then resolution. Clinical features of thyroiditis may include: • subacute thyroiditis: • rapid onset, malaise, fever, and thyroidal pain which may extend to the jaw, ears, or down the anterior chest wall • extremely tender, enlarged, firm, and irregular thyroid gland that is palpable and diffuse • silent or postpartum thyroiditis: • usually within 6 months post-partum • may be non-specific symptoms, eg tiredness, anxiety • gland may be mildly enlarged and non-tender • thyroid peroxidase (TPO) antibody is usually positive • type 2 amiodarone thyroiditis − small goitre usually present 12 Graves' disease Quick info: Clinical features of Graves' disease include: • diffusely enlarged thyroid gland • ophthalmology • inflammatory reaction in the skin, particularly the pretibial region • acropachy of the fingernails Rare features of Graves' disease may include: • vitiligo • urticaria Thyroid eye disease occurs in about half of people with Graves' disease − symptoms may include: • gritty sensation in the eye • excessive production of tears • pain on looking up or down or to each side • feeling of pressure behind the eye • retrobulbar pain • double vision • loss of sight or reduced colour vision Signs of Graves' disease may include: Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 6 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders • oedema of the conjunctiva and eyelid • exposure keratitis • proptosis • photophobia • diplopia • eyelid retraction or lag NB: Diagnosis may be difficult when signs and symptoms are uniocular, there is no history of Graves' disease, and there is optic neuropathy but no proptosis. 13 Toxic multinodular goitre Quick info: Toxic multinodular goitre: • at least two autonomously functioning nodules (requires thyroid isotope scanning) • usually age over 50 years • in non-toxic multinodular goitre, pharmacological doses of iodine can cause hyperthyroidism (Jod-Basedow phenomenon) Clinical features of toxic multinodular goitre include: • signs and symptoms of thyrotoxicosis • dysphagia • dyspnoea • neck pressure • non-tender nodules of the thyroid 14 Thyroid adenoma Quick info: Clinical features of thyroid adenoma include: • signs and symptoms of thyrotoxicosis • unilateral non-tender thyroid mass which is easily palpable • most common finding is undetectable thyroid stimulating hormone (TSH) • free triiodothyronine (FT3) levels are often elevated while free thyroxine (FT4) may be normal • can be asymptomatic but with biochemical hyperthyroidism 15 Drug-induced Quick info: Identify whether the patient is currently, or has recently been taking any of the following medications: • levothyroxine, triiodothyronine or thyroid extract • amiodarone • lithium • interferon 16 Hyperthyroidism in pregnancy - suspected Quick info: Thyroid biochemistry in pregnancy: • normal pregnancy causes a slight rise in thyroid secretion and transient biochemical hyperthyroidism • serum human chorionic gonadotropin (hCG) concentrations peak at 10-12 weeks and then decline Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 7 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders • at peak of serum hCG, free thyroxine (FT4), and triiodothyronine (FT3) concentrations rise, but usually remain within the normal range • thyroid stimulating hormone (TSH) concentrations respond by falling appropriately • 10-20% of pregnant women have subnormal TSH levels at peak hCG concentrations • as hCG declines, FT4, FT3, and TSH concentrations return to within the normal range • throughout pregnancy the increase in thyroxine-binding globulin causes an increase in serum total T4 and T3, but this does not indicate hyperthyroidism as FT4 and FT3 are normal • biochemical hyperthyroidism is often found in women with hyperemesis gravidarum 17 Start beta blocker if symptomatic Quick info: If thyroiditis suspected: • commence on propranolol 40mg TDS if symptomatic • do not start carbimazole 18 Investigations Quick info: TSH is suppressed to <0.1mU/L in Grave' s disease, with an elevated FT4. Unless clinical diagnosis is clear (eg the patient has a large symmetrical goitre with ophthalmopathy) antibody assay should be used to confirm the diagnosis: • TSH-receptor antibodies almost always positive, particularly thyroid-stimulating immunoglobulins (TSIs) and diagnostic for Graves' disease • thyroid auto-antibodies such as anti-thyroglobulin antibodies or anti-thyroid peroxidase antibodies usually present (but not measured unless subclinical hypothyroidism) Other investigations: • haematology – may have normochromic, normocytic or microcytic anaemia • liver function tests (LFTs) may show mild abnormality and be used as baseline to assess possible drug hepatotoxicity • blood glucose • serum calcium may be elevated 19 Investigations Quick info: Radionuclide scanning should take place after referral to Endocrinology: • amount of thyroid uptake is useful in diagnosis of thyrotoxicosis • helps distinguish thyroiditis from solitary and diffuse toxic nodular goitres 123 • scans can be performed with radioactive I or 99 Tc 99 123 • Tc isotopes have a shorter half-life and lower radiation exposure compared with I , and is considerably less expensive • diagnostic feature is focal uptake with no uptake on contralateral side 20 Likely solitary toxic thyroid nodule Quick info: Solitary toxic thyroid nodule: • requires isotope thyroid scanning after referral to endocrinology • functioning solitary nodule is almost never malignant Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 8 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders • a fine needle aspiration is not indicated 21 Consider whether safe to stop drug treatment Quick info: Amiodarone should be stopped immediately and thyroid supplements should also be stopped. Consider whether stopping lithium or interferon can be safely achieved. 23 Initial treatment Quick info: Commence on anti-thyroid medication and refer to Endocrine clinic. Suggested initial carbimazole dose: • FT4 < 30pmol/L commence on carbimazole 10mg daily • FT4 30 – 40pmol/L commence on carbimazole 20mg daily • FT4 > 40pmol/L commence on carbimazole 40mg daily Patients with significant adrenergic symptoms (tachycardia, tremor) should also be commenced on propranolol at an initial dose of 40mg TDS for symptom relief. This should be discontinued once patients are biochemically euthyroid. 24 Hyperemesis gravidarum Quick info: Graves' disease is the most common cause of hyperthyroidism in pregnancy, after hyperemesis is excluded. In hyperemesis: • there is no goitre or ophthalmopathy • absent symptoms and signs of hyperthyroidism Biochemical hyperthyroidism is often found in women with hyperemesis gravidarum: • is associated with: • severe nausea and vomiting in early pregnancy leading to a greater than 5% weight loss • higher serum human chorionic gonadotropin (hCG) • twin and multiple pregnancies • TSH concentrations are often lower than pregnant control women 25 Clinical features of Graves' disease Quick info: Clinical features include: • clinical hyperthyroidism • diffuse goitre • ophthalmopathy • presence of anti-thyroid stimulating hormone (TSH) receptor antibody • family history and previous history of Graves' disease • a bruit over the thyroid gland 26 Monitoring treatment Quick info: Endocrinology aim to see patients referred with thyrotoxicosis within 4-6 weeks of referral. Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 9 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders If there is any delay in patients being seen, a repeat thyroid function should be organized after 4-6 weeks of starting carbimazole. Patients starting carbimazole should be warned that there is a 1:1000 risk of agranulocytosis. They should be advised to have an urgent full blood count if they develop significant sore throat or febrile illness while taking carbimazole. Routine FBC monitoring of patients who do not have any infective symptoms is not recommended. Thyroid ultrasound scan is not required prior to referral to the endocrine clinic. 27 Thyrotoxic on repeat testing Quick info: Post partum thyroiditis usually returns to a euthyroid state within 12 months of delivery. However, there is a 30% risk of subsequent permanent hypothyroidism. Persistent post partum thyrotoxicosis requires further investigation to differentiate from Graves' disease, which will include an isotope uptake scan. This will require temporary cessation of breast feeding. Referral for specialist opinion is recommended. 28 Euthyroid or hypothyroid Quick info: Post viral thyrotoxicosis If euthyroid, further thyroid function check at 1 month and 3 months for possible hypothyroidism. Subacute thyroiditis is usually short lived and self limiting. Hypothyroidism may follow the thyrotoxic phase in up to 50% of people and last for 4-12 weeks. Symptoms are often mild, but may become permanent in 5-10%. If symptoms require prescription of levothyroxine, seek specialist advice on duration of treatment. Post partum thyrotoxicosis Offer long term thyroid function monitoring to women with post partum thyroiditis. Monitoring is recommended annually, and also before and at 6-8 weeks after future pregnancies. 29 Thyroid function tests (TFTs) suggestive of hyperthyroidism Quick info: In hyperemesis: • serum-free thyroxine concentrations are minimally elevated • free triiodothyronine (FT3) concentrations are usually not elevated 33 Antenatal management Quick info: Thyroid stimulating hormone (TSH) receptor antibody testing in pregnancy helps determine the risk of neo-natal Graves' disease and is: • performed in the first trimester for women who have: • current thyroid overactivity and are receiving antithyroid medications • been treated successfully with surgery or radio-iodine • repeated in the third trimester for women who are positive • the consequences of untreated fetal thyrotoxicosis include: • low birth weight and head size • fetal distress in labour • neonatal heart failure and respiratory distress Administration of antithyroid medications to the mother during pregnancy can treat the neonate in this situation − close follow-up and continued treatment is required after delivery. Fetal thyrotoxicosis: Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 10 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders • clinical sign of fetal thyrotoxicosis is fetal tachycardia and, if suspected, cordocentesis should be considered • the risk of neonatal Graves' hyperthyroidism in the babies of mothers with Graves' disease (either those being currently treated 131 on an antithyroid medication and those previously treated by iodine-131 (I ) or surgery and rendered euthyroid or hypothyroid) should be: • tested antenatally or during first trimester using the TRAK kit or a bioassay which measures thyroid stimulating immunoglobulin (TSI)/thyroid stimulating hormone (TSH) binding inhibiting immunoglobulin (TBII) • communicated to the mother, attending obstetrician, and paediatrician 34 Initial management Quick info: Specific treatment of hyperemesis gravidarum with antithyroid agents is not usually warranted as specific supportive management, eg hydration and corticosteroids may be appropriate. 35 Information for primary care about antithyroid treatment and block and replace regimen Quick info: Therapy should be continued for 4-8 weeks until the patient becomes euthyroid, based on free thyroxine (FT4) level. There are 2 options: • titration regimen − gradually reduce dose to a maintenance dose: • monitor thyroid function every 4-6 weeks • optimal duration is 12-18 months • low dose titration regimen has been shown to have fewer adverse effects than a high dose block-replace regimen • block and replace regimen − levothyroxine is usually added to a fully suppressive dose of antithyroid drug: • not recommended during pregnancy • monitor thyroid function every 3 months Long-term remission rate of more than 50% unlikely to be achieved even with prolonged (more than 18 months) antithyroid treatment. People with large goitres and severe hyperthyroidism at diagnosis are less likely to enter into remission. 37 Treat with antithyroid agents Quick info: Treatment for Graves' disease: • optimal treatment is the smallest dose necessary to achieve euthyroidism • Graves' disease often improves during pregnancy: • in a minority of patients, treatment can be withdrawn in the third trimester of pregnancy • propylthiouracil is favoured during the first trimester as carbimazole has been associated (although rarely) with fetal aplasia cutis • to avoid fetal hypothyroidism, do not use block and replace regimens in pregnancy 38 Postpartum management Quick info: Postpartum management: • check thyroid function in all mothers who had positive thyroid stimulating hormone receptor antibodies in third trimester of pregnancy • breastfeeding: • mothers can continue treatment with antithyroid medications whilst breastfeeding • if higher doses of antithyroid medications are used, monitor the baby's thyroid function Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 11 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 12 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders Key Dates Published: 21-Apr-2011, by Valid until: 31-Aug-2012 Evidence summary for Hyperthyroid (thyrotoxicosis) References This is a list of all the references that have passed critical appraisal for use in the care map Thyroid disorders ID Reference 1 British Thyroid Association (BTA). UK guidelines for the use of thyroid function tests. Sheffield: BTA; 2006. http://www.british-thyroid-association.org/info-for-patients/Docs/TFT_guideline_final_version_July_2006.pdf 2 American Association of Clinical Endocrinologists (AACE). AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Jacksonville, FL: AACE; 2006. http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf 3 Clinical Knowledge Summaries (CKS). Hyperthyroidism. Version 1.1. Newcastle upon Tyne: CKS; 2008. http://www.cks.nhs.uk/hyperthyroidism#313383001 4 Clinical Knowledge Summaries (CKS). Hypothyroidism. Version 1.1. Newcastle upon Tyne: CKS; 2009. http://www.cks.nhs.uk/hypothyroidism#252738001 5 Royal College of Physicians (RCP). The diagnosis and management of primary hypothyroidism. London: RCP; 2009. http://www.rcplondon.ac.uk/specialties/Endocrinology-Diabetes/Documents/Hypothyroidism.pdf 6 Map of Medicine (MoM) Clinical Editorial team and Fellows. London: MoM; 2011. 7 Contributors representing Royal College of Physicians. 2011. 8 Wall CR. Myxedema coma: diagnosis and treatment. Am Fam Physician 2000; 62: 2485-2490. http://www.aafp.org/afp/20001201/2485.html 9 Bahn RS, Burch HS, Cooper D et al. The role of propylthiouracil in the management of Graves' disease in adults: report of a meeting jointly sponsored by the American Thyroid Association and the Food and Drug Administration. Thyroid 2009; 19: 673-674. http://www.liebertonline.com/doi/abs/10.1089/thy.2009.0169 10 Singh S, Duggal J, Molnar J et al. Impact of subclinical thyroid disorders on coronary heart disease, cardiovascular and all-cause mortality: a meta-analysis. Int J Cardiol 2008; 125: 41-48. http://www.ncbi.nlm.nih.gov/pubmed/17434631 11 Villar HC, Saconato H, Valente O et al. Thyroid hormone replacement for subclinical hypothyroidism. Cochrane Database Syst Rev 2007; CD003419. http://onlinelibrary.wiley.com/o/cochrane/clsysrev/articles/CD003419/pdf_fs.html 12 Vaidya B, Pearce SHS. Management of hypothyroidism in adults. BMJ 2008; 337: 284-289. http://www.bmj.com/content/337/7664/Clinical_Review.full.pdf 13 National Institute for Health and Clinical Excellence (NICE). Venous thromboembolism: reducing the risk. Reducing the risk of venous thromboembolism (deep vein thrombosis and pulmonary embolism) in patients admitted to hospital. Clinical guideline 92. London: NICE; 2010. http://www.nice.org.uk/nicemedia/live/12695/47195/47195.pdf 14 The Endocrine Society. Management of thyroid dysfunction during pregnancy and postpartum. J Clin Endocrinol Metab 2007; 92: S1-S47. http://www.endo-society.org/guidelines/final/upload/Clinical-Guideline-Management-of-Thyroid-Dysfunctionduring-Pregnancy-Postpartum.pdf 15 Escobar-Morreale HF, Botella-Carretero JI, del Rey FE et al. Treatment of hypothyroidism with combinations of levothyroxine plus liothyronine. J Clin Endocrinol Metab 2005; 90: 4946-4954. http://jcem.endojournals.org/cgi/reprint/90/8/4946 16 Nygaard B. Hypothyroidism (primary). Clin Evid (online) 2010; 01: 605. http://clinicalevidence.bmj.com/ceweb/conditions/end/0605/0605-get.pdf 17 Longmore M, Wilkinson I, Rajagopalan S. Oxford handbook of clinical medicine. 6th edn. Oxford: Oxford University Press; 2004. 18 Vidal-Trecan GM, Stahl JE, Durand-Zaleski I. Managing toxic thyroid adenoma: a cost-effectiveness analysis. Eur J Endocrinol 2002; 146: 283-294. http://www.eje-online.org/cgi/reprint/146/3/283 19 Vidal-Trecan GM, Stahl JE, Eckman MH. Radioiodine or surgery for toxic thyroid adenoma: dissecting an important decision. A cost-effectiveness analysis. Thyroid 2004; 14: 933-945. http://www.ncbi.nlm.nih.gov/pubmed/15671772 20 Seshadri K. Thyroiditis, subacute. eMedicine 2004; Published: 21-Apr-2011 Valid until: 31-Aug-2012 Printed on: 19-Jan-2012 © Map of Medicine Ltd This care map was published by . A printed version of this document is not controlled so may not be up-to-date with the latest clinical information. Page 13 of 14 Hyperthyroid (thyrotoxicosis) Medicine > Endocrinology > Thyroid disorders ID Reference http://emedicine.medscape.com/article/125497-overview 21 Nygaard B. Hyperthyroidism (primary). Clin Evid (online) 2008; 03: 611. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2907936/pdf/2008-0611.pdf 22 Royal College of Physicians (RCP). Radioiodine in the management of benign thyroid disease: clinical guidelines. London: RCP; 2007. http://www.rcplondon.ac.uk/pubs/contents/0621b67a-4880-4a1b-9942-57a666efee4a.pdf 23 Walter MA, Briel M, Chris-Crain M et al. Effects of antithyroid drugs on radioiodine treatment: systematic review and meta-analysis of randomised controlled trials. 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