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Anterior Neck Mass Sabalvaro Dyan, Salac Carmina, Salazar Janelle, Salazar Riccel, Salcedo Von, Saldana Emmanuel, Sales Stephanie, Salonga Cryscel

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65 year old female with anterior neck mass

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History of Present Illness 5 years PTC Noted presence of 2x2 cm anterior neck mass No accompanying symptoms 4 years PTC Progressive increase in size and felt a lump in the throat which prompted consult Prescribed L thyroxine 100 ug/tab 1 tab TID which she took for one month until she noted easy fatigability, palpitations, and weight loss. She consulted again and the physician requested for serum T3,T4, and TSH after which she was advised to discontinue taking the medication. Consult Due to persistence of the mass, she sought consult at your clinic.

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Physical Examination Neck: 8 X 6 cm firm anterior neck mass with well defined borders and moves with deglutition No palpable cervical adenopathies BP=120/80 PR=85/min RR=28/min Heart/Chest/Abdomen unremarkable Pink palpebral conjunctive, anicteric sclerae

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Salient Features 65 y/o Female 2 X 2 cm anterior neck mass Progressive increase in size lump in throat Prescribed L thyroxine 100 ug/tab 1 tab TID took for one month until she noted easy fatigability, palpitations, and weight loss Discontinued medication as advised by physician Physical Examination VS: BP=120/80 PR=85/min RR=28/min Pink palpebral conjunctive, anicteric sclerae Neck: 8 X 6 cm firm anterior neck mass with well defined borders and moves with deglutition; no palpable cervical adenopathies Heart/Chest/Abdomen unremarkable

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1. If you were the physician who initially saw the patient one year ago, what would you have done?

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2. What do you think were the serum T3,T4, and TSH levels in the previous consult? What do you call this condition?

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Low circulating levels of T 4 and T 3 Primary Thyroid Failure Raised TSH levels Secondary Hypothyroidism Low TSH levels that do not increase following TRH stimulation

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HYPOTHYROIDISM Deficiency in the circulating levels of thyroid hormone leads to hypothyroidism, and, in neonates, to cretinism, which is characterized by neurologic impairment and mental retardation. Hypothyroidism may also be associated with deafness (Pendred's syndrome)4 and Turner's syndrome.

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In adults, symptoms in general are nonspecific: Tiredness, weight gain, cold intolerance, constipation, and menorrhagia Patients with severe hypothyroidism or myxedema Facial and periorbital puffiness Characteristic facial features as a consequence of the deposition of glycosaminoglycans in the subcutaneous tissues The skin becomes rough and dry and often develops a yellowish hue from reduced conversion of carotene to vitamin A. Hair becomes dry and brittle, and severe hair loss may occur Loss of the outer two-thirds of the eyebrows.

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An enlarged tongue may impair speech, which is already slowed, in keeping with the impairment of mental processes. Myxedema madness Untreated dementia Nonspecific abdominal pain accompanied by distention and constipation. Libido and fertility are impaired in both sexes. Cardiovascular changes in hypothyroidism include: Bradycardia, cardiomegaly, pericardial effusion, reduced cardiac output, and pulmonary effusions Cardiac failure is uncommon When hypothyroidism occurs as a result of pituitary failure, features of hypopituitarism such as pale, waxy skin, loss of body hair, and atrophic genitalia may be present

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LABORATORY FINDINGS Hypothyroidism is characterized by low circulating levels of T 4 and T 3. Raised TSH levels are found in primary thyroid failure, whereas secondary hypothyroidism is characterized by low TSH levels that do not increase following TRH stimulation. Thyroid autoantibodies are present and are highest in patients with autoimmune disease (Hashimoto's thyroiditis, Graves' disease), although they are also elevated in patients with nodular goiter and thyroid neoplasms. Other findings include anemia, hypercholesterolemia, and decreased voltage with flattening or inversion of T waves on electrocardiogram. Comatose patients with myxedema also have hyponatremia and CO 2 retention.

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TREATMENT THYROXINE Treatment of choice 50 to 200 mcg per day, depending upon patient's size and condition. Starting doses of 100 mcg of thyroxine daily are well tolerated Elderly patients and those with coexisting heart disease and profound hypothyroidism should be started on a considerably lower dose such as 25 to 50 mcg daily because of associated hypercholesterolemia and atherosclerosis. The dose can be slowly increased over weeks to months to attain a euthyroid state.

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A baseline ECG should always be obtained in patients with severe hypothyroidism prior to treatment. Patients are instructed to take tablets in the morning, usually without other medications, or at mealtime to assure good absorption. Thyroxine dosage is titrated against clinical response and TSH levels, which should return to normal. Patients who present with myxedema coma, in contrast to the patients with mild to moderate hypothyroidism, require an initial emergency treatment with large doses of intravenous thyroxine (300 to 400 g), and careful monitoring in an ICU setting.

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3. What is your diagnosis? Other considerations? Explain.

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Diagnosis Hyperthyroidism secondary to over dosage to L thyroxine

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Other Considerations

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Differential Diagnoses Nodular Non-toxic Goiter Graves Disease Toxic Multinodular Goiter Toxic Adenoma Solitary Thyroid Nodule

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Nodular Non-toxic Goiter FAMILIAL GOITER ENDEMIC GOITER SPORADIC GOITER Inherited enzyme defect Impaired iodine metabolism Usually associated with hypothyroidism Due to iodine- deficient diet Mountainous regions intake of substances (goitrogens) that inhibit production of thyroid hormone common goitrogens include foods such as cabbage, turnips, brussel sprouts, seaweed, and millet Tx: iodized salt No definite cause can be established

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Enlargement of the thyroid gland No toxicity; no cancer The following factors increase your chance of developing nontoxic goiter: Sex: female (nontoxic goiter is more common in women than men) Age: over 40 years Reference: http://www.mbmc.org/healthgate/GetHGContent.aspx

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SYMPTOMS Nontoxic goiters usually do not have noticeable symptoms. Swelling on the neck Breathing difficulties, coughing, or wheezing with large goiter Difficulty swallowing with large goiter Feeling of pressure on the neck Hoarseness

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MANAGEMENT A goiter only needs to be treated if it is causing symptoms. Treatments for an enlarged thyroid include: Radioactive iodine to shrink the gland, particularly if the thyroid is producing too much thyroid hormone Surgery (thyroidectomy) to remove all or part of the glandthyroidectomy Small doses of Lugol's iodine or potassium iodine solution if the goiter is due to iodine deficiency Treatment with thyroid hormone supplements if the goiter is due to underactive thyroid Reference: http://www.nlm.nih.gov/medlineplus/ency/article/001178.htm

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INDICATIONS FOR SURGERY Huge goiter which is cosmetically unacceptable Compression symptoms Suspicion of malignancy

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GRAVES DISEASE A type of hyperthyroidism, is caused by a generalized overactivity of the entire thyroid gland. An autoimmune disease; thyroid-stimulating antibodies directed at TSH receptors on follicular cells. It is named for Robert Graves, an Irish physician, who was the first to describe this form of hyperthyroidism about 150 years ago.

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ETIOLOGY The trigger for auto-antibody production is not known. Genetic predisposition HLA DR3 Since Graves' disease is an autoimmune disease which appears suddenly, often quite late in life, it is thought that a viral or 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). Yersinia enterocolitica Reference: http://en.wikipedia.org/wiki/Graves%27_disease

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CLINICAL FEATURES Triad: Goiter including the pyramidal lobe Thyrotoxicosis Exophthalmos Symptoms: Heat intolerance Thirst Sweating Weight loss despite adequate caloric intake Amenorrhea Tachycardia or atrial fibrillation Congestive heart failure

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PE: Weight loss Flushing Warm and moist skin Inappropriate sweating Tachycardia Widening of pulse pressure Fine tremor Muscle wasting Hyperactive tendon reflexes Pretibial myexedema Gynecomastia Audible bruit over the gland Laboratory Findings: Decreased TSH Increased circulating T3/T4 levels Increased circulating thyroid autoantibodies Thyroid stimulating immunoglobulins (TSI) Tyhroid stimulating antibodies (TSAb) Radioactive iodine scan shows diffuse uptake through the gland of 45-90 percent.

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GRAVES OPHTHALMOPATHY Thyroid-associated ophthalmopathy is one of the most typical symptoms of Graves' disease. Thyroid eye disease is an inflammatory condition, which affects the orbital contents including the extraocular muscles and orbital fat. Iextraocular muscles t is almost always associated with Graves' disease but may rarely be seen in Hashimoto's thyroiditis, primary hypothyroidism, or thyroid cancer. Hashimoto's thyroiditishypothyroidismthyroid cancer The ocular manifestations that are relatively specific to Grave's disease include soft tissue inflammation, proptosis (protrusion of one or both globes of the eyes), corneal exposure, and optic nerve compression.cornealoptic nerve There are 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. Reference: http://en.wikipedia.org/wiki/Graves%27_disease

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Classification of Graves Eye Disease Mnemonic: "NO SPECS Class 0: No signs or symptoms Class 1: Only signs (limited to upper lid retraction and stare, with or without lid lag) Class 2: Soft tissue involvement (oedema of conjunctivae and lids, conjunctival injection, etc) Class 3: Proptosis Class 4: Extraocular muscle involvement (usually with diplopia) Class 5: Corneal involvement (primarily due to lagophthalmos) Class 6: Sight loss (due to optic nerve involvement) Reference: http://en.wikipedia.org/wiki/Graves%27_disease

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MANAGEMENT Medical: Propylthiouracil (PTU) Methimazole (Tapazole) Carbimazole Beta-blockers (Propanolol)

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Relapse rate in 12-18 months Risk for fetal goiter, hypothyroidism No morbidity related after surgery Treatment of choice for small goiters and pregnant patients (PTU) Euthyroid state is achieved in 4-6 weeks

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Radioactive Iodine Ease of treatment Highly effective especially in diffuse goiters No morbidity related to surgery Treatment of choice for failed surgical management The effect is seen in 1.5-4 months Standard dose = 10 mCl = 8500 cGy

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Surgery Complete and permanent control of toxicity Rapid control of symptoms Removal of mass Treatment of choice for huge goiters Needs pre-operative preparation Overall morbidity of 1-2%

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Toxic Multinodular Goiter Usually occur in individuals older than 50 years of age who often have a prior history of a nontoxic multinodular goiter Over several years, enough thyroid nodules become autonomous to cause hyperthyroidism. Similar to Graves disease, but symptoms and signs of hyperthyroidism are less severe and extrathyroidal manifestations are absent. May present with atrial fibrillation or palpitations, tachycardia, nervousness, tremor or weight loss. Low TSH, normal or minimally increased T4, elevated T3, T3>T4.

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Toxic Multinodular Goiter Thyroid scan heterogenous uptake with multiple regions of increased and decreased uptake. 24hr uptake of radioiodine may not be increased. Management Antithyroid drugs + beta blockers normalize thyroid function and address the clinical features of thyrotoxicosis, but often stimulates the growth of the goiter; spontaneous remission does not occur. Radioiodine treat areas of autonomy, decrease the mass of the goiter A trial of radioiodine should be considered before subjecting patients to surgery.

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Toxic Multinodular Goiter Surgery Definitive treatment of underlying thyrotoxicosis and goiter. Subtotal thyroidectomy is the standard procedure. Patients should be rendered euthyroid using antithyroid drugs before operation.

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Toxic Adenoma A solitary, autonomously functioning thyroid nodule Typically occurs in younger patients (+) thyroid nodule with symptoms of hyperthyroidism Size is at least 3cm before hyperthyroidism occurs. Absent clinical features suggestive of Graves disease or other causes of thyrotoxicosis

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Toxic Adenoma Thyroid scan definitive diagnostic test Focal uptake in the hyperfunctioning nodules Diminished uptake in the remained of the gland Suppression of the activity of the normal thyroid

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Toxic Adenoma Radioiodine ablation treatment of choice 131I is concentrated in the hyperfunctioning nodule with minimal uptake and damage to normal thyroid tissue. Relatively large doses correct thyrotoxicosis in about 75% of patients within 3 months. Hypothyroidism occurs in

Toxic Adenoma Medical therapy using antithyroid drugs and beta blockers normalize thyroid function but is not an optimal long term treatment Ethanol injection under ultrasound guidance Repeated injections often >5 sessions Reduce nodule size

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Solitary Thyroid Nodule Present in approximately 4 percent of the population Pain is unusual. When present, it should raise suspicion for intrathyroidal hemorrhage in a benign nodule, thyroiditis, or malignancy. History of hoarseness - may be secondary to malignant involvement of the recurrent laryngeal nerves Risk factors for malignancy exposure to ionizing radiation and family history of thyroid and other malignancies associated with thyroid cancer.

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Solitary Thyroid Nodule Mass moves with swallowing. Hard, gritty of fixed nodules are more likely to be malignant. Most are euthyroid. If a patient with a nodule is found to be hyperthyroid, the risk of malignancy is approximately 1 percent. FNAB most important diagnostic test Benign 65% (includes cysts and colloid nodules) Suspicious 20% Malignant 5% Nondiagnostic 10%

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Solitary Thyroid Nodule Ultrasound For detecting nonpalpable thyroid nodules For differentiating solid from cystic nodules For diagnosing suspicious nodules with microcalcifications For identifying adjacent lymphadenopathy CT and MRI unnecessary in except for large, fixed, or substernal lesions. 123I or 99mTc rarely necessary, unless evaluating patients for hot or autonomous thyroid nodules

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Solitary Thyroid Nodule Malignant tumors generally treated by total or near- total thyroidectomy Simple thyroid cysts - resolve with aspiration in approximately 75 percent of cases Unilateral thyroid lobectomy - if the cyst persists after three attempts at aspiration Lobectomy For cysts >4 cm in diameter For complex cysts with solid and cystic components

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Solitary Thyroid Nodule Colloid nodule should be observed with serial ultrasound and Tg measurements Repeat FNAB if nodule enlarges L-thyroxine in doses sufficient to maintain a serum TSH level between 0.1 and 1.0 U/mL. 50% decrease in size Thyroidectomy if a nodule enlarges on TSH suppression, causes compressive symptoms, or for cosmetic reasons Exceptions: Patient who has had previous irradiation of the thyroid gland or who has a family history of thyroid cancer. In these patients total or near-total thyroidectomy is recommended. High incidence of thyroid cancer ( 40%) Decreased reliability of FNA biopsy

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4. How would you manage this patient now?

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Goal: restoration of clinical and biochemical euthyroid state by omitting or reducing the dosage of medications and other measures as needed depending on clinical status. ECG Blood test: TSH, T3, T4 levels, monitored regularly SYMPTOMATIC TREATMENT: To control tachycardia, hypertension and atrial fibrillation: 20 - 40 mg doses of propranolo Q 6hours; d If beta blockers are contraindicated: Diazepam and/or chlorpromazine

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RADIOACTIVE IODINE ingestion of a radioactive iodine tablet (6-12 wks) which is then taken up by thyroid cells. These overactive cells are destroyed so that the thyroid can shrink in size and produce hormone at normal levels. In patients with underlying heart disease and in elderly patients, it is desirable to treat with antithyroid drugs (methimazole) until the patient is euthyroid. The medication is then stopped for 5-7days before the appropriate dosage of 131 I. Although it is a safe treatment, most people become hypothyroid after radioactive iodine therapy and therefore require lifelong thyroid hormone replacement therapy.

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THYROIDECTOMY Now uncommonly performed; the surgeon removes most or all of the gland Candidates for surgery: include pregnant hyperthyroid patients intolerant of anti-thyroid drugs, patients desiring definitive therapy without the use of radioactive iodine, children, and patients with very large or multinodular goiters. Patients are treated with antithyroid drugs until euthyroid (about 6wks). In addition, 10-14 days prior to surgery, they receive saturated solution of potassium iodide 5 drops BID, to diminish vascularity of the gland and simplify surgery However, in cases of total removal of the thyroid gland, patient must take thyroid replacement pills for the rest of his or her life

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NON-PHARMACOLOGICAL High calorie diet in order to replace all the energy burned by the body in hyperthyroid state Drink plenty of water and juices to replace all the fluid losses. Avoid or limit caffeinated drinks for such could produce anxiety.

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Journals on Diagnosis and Treatment of Drug Induced Hyperthyroidism

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Diagnosis Newly diagnosed thyrotoxicosis in hospitalized patients: clinical characteristics Rotman-Pikielny P et. Al

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Background: Thyrotoxicosis is often diagnosed in an outpatient setting. Most common symptoms include irritablility, heat intolerance,palpitations and weakness The prevalent symptoms in hospitalized patients with newly diagnosed thyrotoxicosis have not been fully characterized

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Objective To determine the clinical characteristics of patients with thyrotoxicosis newly diagnosed during hospitalization.

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Design Retrospective computer-based search was undertaken to detect patients that were hospitalized in our medical centre during 1999-2006, and discharged with thyrotoxicosis or thyroiditis primary diagnosis.

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Results Fifty-eight patients (36F/22M; mean age 52.1 +/- 17.5 years) were identified. Weakness, weight loss and palpitations were the most common manifestations (50, 40 and 35%, respectively) and were predominantly present in patients with hyperthyroidism. Sore throat was present in 41% of patients with thyroiditis.

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Sinus tachycardia and atrial fibrillation occurred in 65.5 and 15.5% of the patients, more common in those with hyperthyroidism. The diagnoses on discharge were Graves' disease, subacute thyroiditis and multinodular goiter in 39.7, 34.5 and 8.9%, respectively.

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Conclusion Weakness, weight loss and palpitations were the main symptoms in patients diagnosed with thyrotoxicosis during hospitalization. Thyrotoxicosis should be included in the differential diagnosis when patients are admitted to the hospital with those symptoms.

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Treatment Drug induced thyrotoxicosis: the surgical option Lorberboym M., Schacter P. Background: Drug induced thyrotoxicosis is not uncommon, It may worsen life threatening arrythmias and become refractory to medical treatment

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Summary The Article talks about a near total thyroidectomy as valid alternative to medical therapy The article pursues to promote near total thyroidectomy as an early management of the disease

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Methods The study included 12 patients 7 men and 5 women aged 63-82 years of age with drug induced fulminant thyrotoxicosis Drugs such as Iodine containing Amiodarone or IFN a treatment Patients has adjunct medical therapy of an anti thyroid Propylthiouracil 1200 mg and a Beta receptor antagonist

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Thyroid scan was performed in all patients using Tc-99m pertechnate

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Results 4 patients did not respond to 3 months of medical therapy required surgical thyroidectomy due to unremitting thyrotoxicosis. Near total thyroidectomy resulted into rapid correction of thyrotoxicosis enabling continuation of anti-arrythmic drugs All patients recovered rapidly and remained well and euthyroid on thyroxine replacement therapy