Hyperthyroidism and thyrotoxicosis: Difference between revisions

Revision as of 15:12, 30 May 2024

Thyrotoxicosis or hyperthyroxinaemia is the state where the level of circulating free T3 and T4 is elevated, causing hypermetabolism. It is most commonly caused by hyperthyroidism, which is the state where the thyroid is overactive. However, thyrotoxicosis can also be caused by ectopic hormones or destruction of the thyroid. Because the most common cause of thyrotoxicosis is hyperthyroidism, the two terms are often used interchangeably.

Etiology

Thyrotoxicosis can be caused by many conditions:

Primary hyperthyroidism
Destruction of the thyroid gland – causes release of stored thyroid hormone in the early phase of disease
- Hashimoto thyroiditis
- De Quervain thyroiditis
- Postpartum thyroiditis
- Drug and contrast-induced thyroiditis (amiodarone, contrast material)
Secondary hyperthyroidism
- Gestational thyrotoxicosis – hCG stimulates TSH receptors due to their structural similarity
- Struma ovarii – an ovarian teratoma which produces thyroxine
- TSH-producing pituitary adenoma

In regions without iodine deficiency, Graves disease is the most common cause of thyrotoxicosis. In iodine deficient regions, toxic adenoma and toxic multinodular goitre are more common.

Clinical features

Thyrotoxicosis can cause many symptoms, most of which are related to the hypermetabolic state and to the overactivity of the sympathetic nervous system:

Weight loss despite increased appetite
Warm, moist skin
Tachycardia or arrhythmia
Heat intolerance
Palmar erythema
Nervousness
Diarrhoea
Hypertension with widened pulse pressure
Palpitations
Fine tremor
Anxiety, restlessness

Diagnosis and evaluation

The diagnosis of (primary) hyperthyroidism is based on the levels of TSH, the most sensitive biomarker. Free T4 and T3 are measured to look for subclinical hyperthyroidism.

	TSH	Free T4	Free T3
Euthyroidism	Normal	Normal	Normal
Subclinical hyperthyroidism	Decreased	Normal	Normal
Overt hyperthyroidism	Decreased	Increased	Increased

The clinical features, including the thyroid size, consistency, nodularity, as well as the presence of eye symptoms, can help narrow the differential diagnosis. The following investigations are important in determining the etiology:

Autoantibodies against thyroid peroxidase (anti-TPO), thyroglobulin (anti-Tg), and TSH receptor (anti-TSHR)
- Anti-TPO and elevated in autoimmune thyroiditis
- Anti-thyroglobulin may also be used in autoimmune thyroiditis, but is less sensitive and specific than anti-TPO, so anti-TPO is used instead
- Anti-TSHR is elevated in Graves disease
Ultrasound
Thyroid scintigraphy (nuclear imaging)

Treatment

Specific treatment depends on the underlying etiology, but supportive treatment is also available. Beta blockers can be used, of which propranolol is the first choice as it inhibits conversion of T3 to T4. Benzodiazepines may also be used in very short courses for anxiety.

Surgical treatment of hyperthyroidism

Surgery may be used for both Graves disease, toxic adenoma, and toxic multinodular goitre. The main treatment of hyperthyroidism nowadays consists of antithyroid drugs and radioactive iodine ablation. However, there remain some indications for thyroid surgery in case of hyperthyroidism:

Very large goitre (> 80 g)
Goitre causing airway or oesophageal obstruction
If malignancy cannot be ruled out
Hyperthyroidism with moderate to severe Graves ophthalmopathy
Contraindications to antithyroid drugs and radioiodine
Hyperthyroidism refractory to antithyroid drugs and radioiodine

Complications

@@ Line 1: / Line 1: @@
-'''Thyrotoxicosis''' or hyperthyroxinaemia is the state where the level of circulating free T3 and T4 is elevated, causing hypermetabolism. It is most commonly caused by '''hyperthyroidism''', which is the state where the thyroid is overactive, but it can also be caused by ectopic hormones or destruction of the thyroid. Because of this, the two terms are often used interchangeably.
+<section begin="clinical biochemistry" />'''Thyrotoxicosis''' or hyperthyroxinaemia is the state where the level of circulating free T3 and T4 is elevated, causing hypermetabolism. It is most commonly caused by '''hyperthyroidism''', which is the state where the thyroid is overactive. However, thyrotoxicosis can also be caused by ectopic hormones or destruction of the thyroid. Because the most common cause of thyrotoxicosis is hyperthyroidism, the two terms are often used interchangeably.
 == Etiology ==
@@ Line 18: / Line 18: @@
 ** TSH-producing pituitary adenoma
-In regions without [[iodine deficiency]], Graves disease is the most common cause of thyrotoxicosis. In iodine deficient regions, toxic adenoma and toxic multinodular goitre are more common.
+In regions without [[iodine deficiency]], Graves disease is the most common cause of thyrotoxicosis. In iodine deficient regions, toxic adenoma and toxic multinodular goitre are more common.<section end="clinical biochemistry" />
 == Clinical features ==
@@ Line 34: / Line 34: @@
 * Fine tremor
 * Anxiety, restlessness
+<section begin="clinical biochemistry" />
 == Diagnosis and evaluation ==
 The diagnosis of (primary) hyperthyroidism is based on the levels of [[TSH]], the most sensitive biomarker. Free T4 and T3 are measured to look for subclinical hyperthyroidism.
@@ Line 61: / Line 61: @@
 * Autoantibodies against thyroid peroxidase (anti-TPO), thyroglobulin (anti-Tg), and TSH receptor (anti-TSHR)
+** Anti-TPO and elevated in autoimmune thyroiditis
+** Anti-thyroglobulin may also be used in autoimmune thyroiditis, but is less sensitive and specific than anti-TPO, so anti-TPO is used instead
+** Anti-TSHR is elevated in Graves disease
 * [[Ultrasound]]
 * Thyroid [[scintigraphy]] (nuclear imaging)
+<section end="clinical biochemistry" />
 == Treatment ==
 Specific treatment depends on the underlying etiology, but supportive treatment is also available. [[Beta blocker|Beta blockers]] can be used, of which propranolol is the first choice as it inhibits conversion of T3 to T4. Benzodiazepines may also be used in very short courses for anxiety.