OUTLINE Biosynthesis of Thyroid Hormones

I. Thyroid Hormone IV. Iodine Uptake of Iodide Oxidation & Iodination

II. Antithyroid Drugs V. Radioactive Iodine = Iodine ingested → reaches circulation = Transport from follicular cells →
III. Ionic Inhibitors VI. Thyroid Cancer colloid via pendrin
(in the form of Iodide ion)
Legend = Iodine in blood (0.2 – 0.4 ug/dL or 15 – = Oxidation of iodide → active form via
Verbatim Book High yield thyroid peroxidase → MIT and DIT in
30 nM)
= Thyroid actively transports Iodine via thyroglobulin → Organification
I. THYROID HORMONES NIS and ↓stores of thyroid iodine
Thyroid gland → thyroid follicle & thyroid parafollicular cells enhance iodide uptake
o Follicular cells → iodothyronine hormones T3 & T4 Synthesis & Secretion of Thyroid Formation of thyroxine and
o Parafollicular cells (C cells) → Calcitonin (useful in osteoporosis and Hormones triiodothyronine from Iodotyrosines
hypercalcemia) = Proteolysis = Coupling of 2 DIT residues → T4
Chemistry of Thyroid Hormones: = Endocytosis of colloid (apical surface) = MIT + DIT → T3
o Principal hormones → Iodine-containing amino acid derivatives of + Megalin (thyroglobulin receptor) → = Reactions are catalyzed by thyroid
thyronine intracellular colloid droplets → fuse peroxidase
o T3 → much higher affinity for nuclear TR compared with T4 with lysosomes = Intrathyroidal & secreted T3 →
= TSH enhances degradation of generated by 5-deiodination of T4
thyroglobulin via ↑thiol
endopeptidase → cleaves
thyroglobulin → liberated hormones
Conversion of T4 & T3 in peripheral tissues
= Normal production of T4: bet 80 and 100 ug
= Normal production of T3: bet 30 and 40 ug
= Metabolism of T4 by 5’ or outer ring deiodination in peripheral tissues → 80%
circulating T3

Table 43-1: FACTORS THAT ALTER BINDING OF THYROXINE TO THYROXINE-BINDING GLOBULIN

INCREASE (↑) BINDING DECREASE (↓) BINDING
Drugs
Discussion Estrogens, Tamoxifen Corticosteroids, Androgens
o All of the steps are presented by the letters Selective estrogen receptor modulators L-Asparaginase, Furosemide
o Inhibitors are also present as seen in the blue box Methadone, Heroin Salicylates
o First would be the uptake of Iodine. Iodine is very little in the soil so very little in the food. Clofibrate, 5-fluorouracil Anti-seizure medications
For Iodide to be taken up by the follicular cells, it requires the NIS → Iodine transport →
Systemic Factors
through colloid via pendrin → oxidation of Iodine to more active form (Iodide) by thyroid
peroxidase → MIT, DIT → coupling of DIT-DIT → T4 then coupling of MIT-DIT → T3 → T3 Liver disease, porphyria Acute and chronic illness
and T4 will remain the thyroglobulin until there is stimulation by TSH HIV infection Inheritance
o Upon stimulation by TSH, thyroglobulin is taken up by follicular cells → interacts with Inheritance
enzymes for hydrolysis → releasing of T3 and T4 in plasma
o Deiodination of T4 → T3

Trans # 10 | TransTeam2024: shaweefa Page 1 of 8

A. Therapeutic Uses of Thyroid Hormone ▪ On weight basis: given TID, daily dose: one-third that of L-T4
❖ Major Indications ▪ Normalization of circulating TSH results in an almost 2-fold higher serum T3
▪ Hormone Replacement Therapy: Hypothyroidism compared with levothyroxine since negative feedback on TSH relies in the local
▪ TSH suppression therapy: Thyroid cancer generation of T3 from circulating T4
❖ Drugs
▪ Levothyroxine Table 43-2: FACTORS INFLUENCING ORAL LEVOTHYROXINE THERAPY
▪ Liothyronine Drugs and other factors that may increase (↑) levothyroxine dosage requirements
Impaired levothyroxine absorption
Discussion
o If there is an increase in the hormone, there is a decrease in the stimulating hormone. So Aluminum-containing antacids, PPI, sucralfate
if thyroid hormone is given to patients with thyroid cancer, there would be suppression Bile acid sequestrants (cholestyramine, colestipol, colesevelam)
of TSH. Calcium carbonate (effect generally small), phosphate binders (lanthanum
carbonate, sevelamer)
LEVOTHYROXINE Chromium picolinate, raloxifene, iron salts
Food, soy products (effect generally very small), lactose intolerance
▪ Synthetic forms of T4 (thyroxine)
▪ Preparations: Tablets, liquid-filled capsules (oral) and lyophilized powder Increased (↑) thyroxine metabolism, CYP3A4 induction
(injection) Rifampin, carbamazepine, phenytoin, sertraline
Incomplete absorption in the stomach and small intestine (~80% tablet dose) Impaired T3 → T4 conversion
Absorption slightly increased → taken on an empty stomach with less Amiodarone
variability in TSH levels Mechanisms uncertain or multifactorial
▪ If GI problems → better absorption with liquid-filled capsules Estrogen, pregnancy, lovastatin, simvastatin, ethionamide, tyrosine kinase
▪ Serum T4: peaks 2–4 h (oral) inhibitors
▪ Plasma t1/2: about 7 days
Drugs and other factors that may decrease (↓) levothyroxine dosage requirements
Omission one day’s dose → marginal effects on the serum TSH and FT4
Consistent dosing → double dose the next day. Advancing age (>65 years), androgen therapy in women
Follow-up blood tests: about 6 weeks (after initiation of treatment) due to the Drugs that may decrease (↓) TSH without changing free T4 in Levothyroxine-treated
1-week plasma t1/2 of T4 patients
If cannot take oral medications or intestinal absorption: Metformin
= IV once daily at a dose of about 80% of the patient’s daily oral
requirement B. Clinical Uses
o Thyroid hormone Replacement o Congenital Hypothyroidism
LIOTHYRONINE Therapy in Hypothyroidism o Thyroid Cancer
▪ Salt of T3 (tablets, injectable form) o Hypothyroidism in Pregnancy o Thyroid Nodules
▪ Absorption: nearly 100% o Myxedema Coma
▪ Peak serum levels 2–4 h (oral)
Used occasionally when more rapid onset of action is desired ❖ THYROID HORMONE REPLACEMENT THERAPY IN HYPOTHYROIDISM
= Rare presentation of myxedema coma ▪ Thyroxine = hormone of choice
= If rapid termination of action (preparing a patient with thyroid cancer ▪ Relies on deiodinase enzymes D1 and D2 → T4 to T3 to maintain a steady serum
for 131I therapy) level of free T3.
Less desirable for chronic replacement therapy due to: ▪ Average daily adult full replacement dose of L-T4: 1.7 μg/kg body weight (0.8
1) More-frequent dosing (plasma t ½ = 18–24 h) μg/lb) based on lean body mass.
2) Higher cost ▪ Goal of therapy:
3) Transient elevations of above T3 above the normal range. o Normalize the serum TSH (in primary hypothyroidism)

Trans # 10 | TransTeam2024: shaweefa Page 2 of 8

 o Normalize free T4 (in secondary or tertiary hypothyroidism)
o Relieve symptoms of hypothyroidism
▪ >60 years + known or suspected cardiac disease / with areas of autonomous
thyroid function → sub replacement dose of L-T4 (12.5–50 μg/d)
▪ Dose increased by 25 μg/d every 6 weeks until the TSH is normalized.
▪ Monotherapy with levothyroxine most closely mimics normal physiology and
generally is preferred
❖ HYPOTHYROIDISM IN PREGNANCY
▪ Higher dose of levothyroxine due to the
1) ↑serum concentration of TBG induced by estrogen
2) expression of D3 by the placenta
3) small amount of transplacental passage of L-T4 from mother to fetus
▪ Overt hypothyroidism → ↑risk of miscarriage, fetal distress, preterm delivery, and
impaired psychoneural and motor development in the progeny.
▪ ↑dose by about 30% as soon as pregnancy is confirmed
▪ Serum TSH: measured in the first trimester
▪ Levothyroxine dose adjusted for maintaining the TSH in the lower portion of the
reference range.
▪ Subsequent dosage adjustments:
o based on serum TSH → measured 4–6 weeks after each adjustment.
▪ TSH monitoring periodically:
1) through to 20 weeks’ gestation
2) Dose adjustment maximal
3) Once between weeks 26 and 32 → confirmation of adequate dose
▪ Dose changed back to pre-pregnancy levels the day after delivery → follow-up
TSH 6 weeks later.
TSH = best test during pregnancy to evaluate thyroid status in pregnancy and
response to treatment.
❖ MYXEDEMA COMA
▪ Rare, extreme expression of severe, long-standing hypothyroidism.
▪ Precipitating factors: infection, congestive heart failure, and medical
noncompliance.
Cardinal features: hypothermia, respiratory depression, and decreased
consciousness.
IV thyroid hormone advised
▪ Levothyroxine: loading dose of 200–400 μg → a daily full replacement dose.
▪ Recommend adding liothyronine (10 μg IV followed by 2.5 to 10 μg every 8 h)
until the patient is stable and conscious.
▪ Ventilatory support, passive warming with blankets, correction of hyponatremia,
and treatment of the precipitating cause.
IV glucocorticoids: recommended until coexisting adrenal insufficiency is
excluded.
Trans # 10 | TransTeam2024: shaweefa
❖ CONGENITAL HYPOTHYROIDISM
▪ Success depends on the age at which therapy is started and the speed with which
hypothyroidism is corrected.
If instituted w/in the first 2 weeks of life → normal physical and mental
development can be achieved
To rapidly normalize T4 concentration:
o initial daily dose of levothyroxine of 10–15 μg/kg is recommended
▪ Goal = achieve a free T4 in the upper half of the reference range and a TSH in the
lower half
✓ Serum TSH and free T4 performed
✓ 2 and 4 weeks after treatment is initiated
✓ Every 1–2 months in the first 6 months
✓ Every 2–3 months between 6 months and 3 years of age
✓ Every 6–12 months from age 3 years until the end of growth
❖ THYROID HORMONE REPLACEMENT THERAPY IN THYROID CANCER
Papillary, Follicular type
o primary management: surgical thyroidectomy, radioiodine and
levothyroxine to maintain a low TSH
▪ Rationale for TSH suppression: TSH is a growth factor for thyroid cancer, but no
RCT that addressed the optimal TSH target range.
▪ Reasonable approach:
1) Adjust the levothyroxine dose to maintain a low-normal TSH value in
patients without persistent disease and at low risk for recurrence
2) Mildly subnormal TSH value (~0.1 mU/L) in patients at high risk for
recurrence
3) More subnormal TSH level for patients with persistent disease.
▪ Benefits of TSH suppression → need to be weighed against the risks, including
osteoporosis and atrial fibrillation.
❖ THYROID NODULES
Most common endocrinopathy, more frequent in women
▪ Usually asymptomatic, may cause discomfort, dysphagia, and choking sensation.
▪ Risk: Exposure to ionizing radiation
▪ 5% that come to medical attention → malignant.
▪ Most are euthyroid
▪ Diagnostic procedures:
o ultrasound imaging and fine-needle aspiration biopsy (FNAB).
▪ Use of levothyroxine to suppress TSH in euthyroid individuals with thyroid
nodules cannot be recommended as a general practice.
▪ If the TSH elevated:
o levothyroxine is given to bring the TSH into the lower portion of the
reference range.
Page 3 of 8
 Methimazole
C. Adverse Effects of Thyroid Hormone = 0.5 mg → ↓the organification of radioactive iodine in the thyroid gland
▪ Occur only on overtreatment and similar to the consequences of = Single dose of 10–25 mg → needed to extend the inhibition to 24 h
hyperthyroidism. = Methimazole t ½ = 4–6 h
▪ Risk *take note of the pharmacokinetics of the drugs – Doc Mau
o Atrial fibrillation (elderly)
o Osteoporosis (post- menopausal women) Table 43-4: PHARMACOKINETIC FEATURES OF ANTITHYROID DRUGS
PROPHYLTHIOURACIL METHIMAZOLE
II. ANTI-THYROID DRUGS Plasma protein binding ~75% Nil
❖ Anti-Thyroid Drugs Plasma t ½ 75 min ~4 – 6 h
❖ Therapeutic Use
Volume of distribution ~0.4 L/kg ~0.7 L/kg
❖ Response to Treatment
❖ Untoward Reactions Concentrated in thyroid Yes Yes
Metabolism of drug during
illness
ANTI-THYROID DRUGS
Severe live disease Normal Decreased (↓)
▪ Thiourelynes = family of thioamides Severe kidney disease Normal Normal
Prophylthiouracil = prototype
Dosing frequency 1 – 4x daily Once or twice daily
A. Mechanism of Action Transplacental passage Low Low
▪ inhibit the formation of thyroid Levels in breastmilk Low low
hormones by interfering with the incorporation of iodine into tyrosyl residues of
thyroglobulin C. Therapeutic Uses
▪ inhibit the coupling of these iodotyrosyl residues to form iodothyronines Definitive treatment: control the disorder in anticipation of a spontaneous
▪ Inhibit the peroxidase enzyme remission in Graves’ disease
Results in the depletion of stores of iodinated thyroglobulin as the protein is ▪ In conjunction with radioactive iodine → hasten recovery while awaiting the
hydrolyzed and the hormones are released into the circulation. effects of radiation
PTU inhibits the peripheral deiodination of T4 to T3. ▪ To control the disorder in preparation for surgical treatment
o Methimazole does not have this effect = Methimazole = drug of choice for Graves disease
o This is the rationale for the choice of PTU in the treatment of severe ▪ Effective as a single daily dose, improved adherence, less toxic
hyperthyroid states or of thyroid storm than PTU
▪ Long plasma and intra- thyroidal t ½, long duration of action.
B. ADME ▪ Starting dose = 15–40 mg per day.
▪ PTU, Methimazole = PTU starting dose = 100 mg every 8 h
▪ Drugs concentrated in the thyroid = Doses >300 mg daily → administration to every 4–6 h
▪ Drugs and metabolites appear largely in the urine ▪ Euthyroidism achieved → within 12 weeks
= dose of antithyroid drug can be reduced, but not stopped, lest an
exacerbation of Graves’ disease occur.
Carbimazole Propylthiouracil (PTU)
= carbethoxy derivative of methimazole = Absorption: w/in 20–30 min of an oral
D. Response to Treatment
= antithyroid action: conversion to dose
methimazole after absorption = 100 mg → wane in 2–3 h ▪ Thyrotoxic state improves within 3–6 weeks after therapy
= 500-mg → inhibitory for only 6–8 h. ▪ Clinical response: related to the dose of drug, size of the goiter, and pretreatment
= PTU t ½ = about 75 min serum T3 concentration.

Trans # 10 | TransTeam2024: shaweefa Page 4 of 8

 ▪ Rate of response determined by the ff:
1) quantity of stored hormone
2) rate of turnover of hormone in the thyroid
3) t1/2 of the hormone in the periphery
4) completeness of the block in synthesis imposed by the dosage given
▪ Hypothyroidism → may develop due to overtreatment.
▪ After treatment:
1) Patients should be examined
2) Thyroid function tests (serum FT4 and total or free T3 concentrations)
measured every 2–4 months.
3) Euthyroidism achieved → follow-up every 4–6 months
▪ Control of the hyperthyroidism → usually associated with a ↓goiter size and
normalization of serum TSH concentration.
= dose decreased to avoid hypothyroidism
E. Untoward Reactions
▪ incidence from PTU and methimazole → relatively low.
Agranulocytosis = absolute neutrophil count (ANC) <100 neutrophils per microlitre
of the blood
o Most serious reaction (first few weeks or months)
o Occurs rapidly
o Not associated with a gradual reduction in granulocyte count, periodic
prospective monitoring of granulocyte counts not generally helpful.
o Patients report for sore throat or fever
o Discontinue antithyroid drug
o Obtain a granulocyte count.
o Reversible on discontinuation of the offending drug
o Administration of recombinant human granulocyte colony-stimulating
factor may hasten recovery.
o Mild granulocytopenia = may be due to thyrotoxicosis or may be the first
sign of this dangerous drug reaction; frequent leukocyte counts are then
required.
▪ Most common reaction = mild urticarial papular rash
o often subsides spontaneously without interrupting treatment
o sometimes requires administration of an antihistamine and
corticosteroids and changing to another antithyroid drug
F. Clinical Uses
❖ Thyrotoxicosis in Pregnancy
❖ Adjuvant Therapy
❖ Thyroid Storm
Trans # 10 | TransTeam2024: shaweefa
❖ THYROTOXICOSIS IN PREGNANCY
▪ 0.2% occurrence → caused frequently by Graves disease
Antithyroid drugs = treatment of choice
Radioactive iodine = clearly contraindicated
▪ PTU and methimazole cross the placenta equally, and either may be used safely in
the pregnant patient.
o Methimazole
= avoided in the first trimester in favor of PTU due to methimazole-
associated embryopathy
= used for the remainder of the pregnancy due to the concern for
PTU-associated liver failure in pregnancy.
o Carbimazole
= used in the E.U. during pregnancy, rarely associated with
congenital abnormalities.
▪ Dose minimized to keep the serum FT4 index in the upper half of the normal range
or slightly elevated.
▪ As pregnancy progresses, Graves’ disease often improves.
▪ Relapse or worsening of Graves’ disease → common after delivery, and patients
should be monitored closely.
▪ In nursing mothers,
= Methimazole is given up to 20 mg daily → no effect on thyroid function
in the infant
= PTU partition into breast milk even less than methimazole.
G. Adjuvant Therapy
β-adrenergic Receptor Antagonists
▪ Propranolol (20–40 mg qid) or Atenolol (50–100 mg OD)
▪ antagonizing the sympathetic/adrenergic effects of thyrotoxicosis
▪ ↓tachycardia, ↓tremor, and ↓stare
▪ relieving palpitations, anxiety, and tension.
Ca2+-channel blockers
▪ Diltiazem (60–120 mg qid)
▪ Control tachycardia and decrease the incidence of supraventricular
tachyarrhythmias
✓ Short-term treatment (2–6 weeks) with β adrenergic receptor antagonists or Ca2+
channel blockers required → discontinued once the patient is euthyroid.
✓ Immunotherapy: used for Graves hyperthyroidism and ophthalmopathy.
✓ B-lymphocyte–depleting agent rituximab, when used with methimazole,
prolongs remission of Graves’ disease.
Page 5 of 8
❖ THYROID STORM III. IONIC INHIBITORS
▪ uncommon but life-threatening complication of thyrotoxicosis Additive in inhibiting iodine uptake
▪ occurs in untreated or partially treated thyrotoxic patients. ▪ interfere with the concentration of iodide by the thyroid gland
▪ Precipitating factors: ▪ Thiocyanate, Perchlorate, and Fluoroborate
o Infections o Diabetic ketoacidosis
o Stress o labor Thiocyanate Perchlorate
o Trauma o heart disease = differs from the rest qualitatively = 10 times as active as thiocyanate.
o thyroidal or nonthyroidal o rare: radioactive iodine = not concentrated by the thyroid gland = blocks the entrance of iodide into the
surgery treatment. but in large amounts may inhibit the thyroid by competitively inhibiting the
▪ Clinical features = exaggerated thyrotoxicosis organification of iodine. NIS, and itself can be transported by
▪ Coma and death → 20% of patient NIS into the thyroid gland.
▪ Thyroid function abnormalities similar to in uncomplicated hyperthyroidism. = used to control hyperthyroidism;
▪ Primarily a clinical diagnosis = If in excessive amounts (2–3 g daily):
fatal aplastic anemia
= 750 mg daily = treatment of Graves’
disease
= used to “discharge” inorganic iodide
from the thyroid gland in a diagnostic
test of iodide organification.
Fluoroborate (BF4-) Lithium
= As effective as perchlorate = decreases secretion of T4 and T3,
which can cause overt
= hypothyroidism in some patients
taking Li+ for the treatment of mania

IV.
▪ Treatment:
✓ Supportive measures such as IV fluids, antipyretics, cooling blankets, and
sedation.
✓ Antithyroid drugs given in large doses:
o PTU preferred over methimazole → also impairs peripheral
conversion of T4 → T3.
o Oral iodides used after the first dose of an antithyroid drug has
been administered.
✓ Treatment of the underlying precipitating illness
IODINE
▪ Oldest remedy
▪ limits its own transport and acutely and transiently inhibits the synthesis of
iodotyrosines and iodothyronines (the Wolff-Chaikoff effect)
▪ clinical effect of high [I−] plasma → inhibition of the release of thyroid hormone.
▪ Action = rapid and efficacious in severe thyrotoxicosis
▪ Effect exerted directly on the thyroid gland and can be demonstrated in the
euthyroid subject as well as in the hyperthyroid patient.
A. Response to Iodine in Hyperthyroidism
▪ Often striking and rapid
▪ Release of thyroid hormone into the circulation is rapidly blocked, and its synthesis
is mildly decreased.
▪ Thyroid gland:
✓ vascularity is reduced
✓ gland becomes much firmer
✓ cells become smaller
✓ colloid reaccumulates in the follicles as iodine concentration increases.

Trans # 10 | TransTeam2024: shaweefa Page 6 of 8

 ▪ Maximal effect = 10–15 days of continuous therapy. B. Untoward Reactions
▪ Note: Iodide therapy → does not completely control the manifestations of Angioedema: prominent symptom, and laryngeal edema may lead to suffocation.
hyperthyroidism, and the beneficial effect disappears. ▪ Multiple cutaneous hemorrhages may be present → manifestations of the serum-
▪ Uses of iodide in the treatment of sickness type of hypersensitivity
hyperthyroidism ▪ Thrombotic thrombocytopenic purpura and fatal periarteritis nodosa attributed to
1) preoperative period in hypersensitivity to iodide also have been described.
preparation for thyroidectomy ▪ Severity of symptoms of chronic intoxication with iodide (iodism) is related to the
2) in conjunction with antithyroid dose.
drugs and propranolol, in the
treatment of thyrotoxic crisis. V. RADIOACTIVE IODINE
▪ Protect the thyroid from 123
I = short-lived γ-emitter, t ½ = 13 h, used in diagnostic studies
radioactive iodine fallout following 124
a nuclear accident or military I = used with positron emission tomographic/computed
exposure. tomographic scanning for more precise dosimetry in high-risk
▪ Uptake of radioactive iodine is thyroid cancer
131
inversely proportional to the serum I = t ½ of 8 days, emits both γ rays and β particles
concentration of stable iodine = >99% of its radiation expended within 56 days.
= the administration of 30–100 = used therapeutically for thyroid destruction of an overactive
mg of iodine daily → markedly or enlarged thyroid
↓ the thyroid uptake of = in thyroid cancer for thyroid ablation and treatment of
radioisotopes. metastatic disease
= rapidly and efficiently trapped by the thyroid
❖ Strong iodine solution (Lugol solution) = incorporated into the iodoamino acids
▪ consists of 5% iodine and 10% potassium iodide, yielding a dose of about 8 mg of = deposited in the colloid of the follicles, from which it is slowly
iodine per drop. liberated.

❖ KISS (potassium iodide saturated solution)
▪ available, containing 50 mg per drop
▪ Typical doses include 16–36 mg (2–6 drops) of Lugol solution or 50–100 mg (1–2
drops) of KISS three times a day.
❖ Potassium iodide
▪ over the counter drug to take in the event of a radiation emergency and block the
uptake of radioiodine into the thyroid gland.
= adult dose is 2 mL (130 mg) every 24 h
A. Therapeutic Uses
▪ Euthyroid patients + history of a wide variety of underlying thyroid disorders
= may develop iodine-induced hypothyroidism when exposed to large
amounts of iodine present in many commonly pre-scribed drugs (Table
43–5)
= these patients do not escape from the acute Wolff-Chaikoff effect
▪ destructive β particles → originate within the follicle and act almost exclusively on
the parenchymal cells of the thyroid, with little or no damage to surrounding
tissue.
▪ γ radiation → passes through the tissue and can be quantified by external
detection.
▪ Effects of the radiation depend on the dosage.
▪ Properly selected doses: possible to destroy the thyroid gland completely without
detectable injury to adjacent tissues.
Treatment of hyperthyroidism and diagnosis of disorders of thyroid function
▪ Clearest indication hyperthyroidism in older patients and in those with heart
disease.
▪ Effective treatment
✓ when Graves disease has persisted or recurred after subtotal
thyroidectomy
✓ when prolonged treatment with antithyroid drugs has not led to
remission.

Trans # 10 | TransTeam2024: shaweefa Page 7 of 8

 ✓ toxic nodular goiter = not currently approved to prepare patients for radioiodine ablation of
▪ Sodium iodide 131I = available as a solution or in capsules containing carrier-free metastatic disease.
131I suitable for oral administration, available for scanning procedures.

Advantages Disadvantages
= Patient spared the risks and = Chief consequence → high incidence
discomfort of surgery of delayed hypothyroidism
= Low cost = Cancer death rate is not increased
= Hospitalization is not required after radioiodine therapy
= Patients can participate in their = Small but significant increase in
customary activities during the entire stomach, kidney, and breast cancer.
procedure, although there are o Since with expression of NIS -
recommendations to limit exposure in susceptible to effects of
young children radioactive iodine
= Radiation thyroiditis, with release of
preformed T4 and T3 into the
circulation (asymptomatic, or
worsening of symptoms of
hyperthyroidism)
o Pretreatment with antithyroid
drugs → reduce or eliminate this
complication.
o Main contraindication:
pregnancy.
= Use in children → controversial, data
insufficient, many clinics decline to
treat younger patients and reserve
radioactive iodine for patients older
than 25–30 years.

VI. THYROID CARCINOMA

▪ Well-differentiated thyroid carcinomas accumulate very little iodine
▪ Stimulation of iodine uptake with TSH = required to treat metastases effectively
▪ Endogenous TSH stimulation by withdrawal of thyroid hormone replacement
therapy in patients previously treated with near-total or total thyroidectomy.
▪ Ablative dose of 131I ranging from 30 to 150 mCi is administered + a repeat total
body scan is obtained several days to 1 week later.
▪ Recombinant thyrotropin alpha (recombinant human TSH)
= used instead of thyroid hormone withdrawal to prepare a patient for
radioiodine ablation of thyroid remnant tissue
= to test the capacity of thyroid tissue, both normal and malignant, to take
up radioactive iodine and to secrete thyroglobulin.

Trans # 10 | TransTeam2024: shaweefa Page 8 of 8