The main laboratory pictures of the disease are represented by hyperthyroidism and hypothyroidism; both can present in different clinical forms, and the diagnosis is based on laboratory findings. Hypothyroidism has a prevalence of 4.6–8.9%, while hyperthyroidism has a prevalence of 0.9–2.0%. Hyper-/ hypothyroidisms can be classified into primary, secondary, and tertiary based on the location of the lesion (thyroid, pituitary, or hypothalamic, respectively). The diagnosis of secondary hyperthyroidism is suggested by elevated fT3 and fT4 values together with increased TSH concentrations; tertiary forms of hyperthyroidism, as well as secondary and tertiary forms of hypothyroidism, are very rare.

The finding of suppressed serum TSH (<0.1 mU/L) raises the diagnostic suspicion of primary hyperthyroidism, and the finding of elevated fT4 levels is sufficient to confirm the diagnosis of frank hyperthyroidism. Evidence of normal fT4 levels associated with low TSH concentration are indicative of subclinical hyperthyroidism; the determination of fT3 must confirm it. In 2–5% of cases of primary hyperthyroidism, in addition to the decrease in serum TSH levels, there is only an increase in fT3 and not in fT4; this condition, termed T3-thyrotoxicosis, most likely represents an early phase of hyperthyroidism, i.e., moderate hyperthyroidism. On the contrary, a very high TSH value (>10 mU/L) suggests primary hypothyroidism, and its association with low fT4 levels indicates overt primary hypothyroidism. In the presence of elevated TSH concentrations and normal fT4 levels, the diagnosis of subclinical hypothyroidism can be made without resorting to the determination of fT3, which, in more than 25% of cases of hypothyroidism, does not show any alteration; therefore, the measurement of fT3 in hypothyroidism is not appropriate (Fig.1). The anti-TPO anti body assay allows for the differential diagnosis between Hashimoto’s thyroiditis (autoimmune-based hypothyroid ism) and other forms of hypothyroidism.

Fig1. TSH reflex: diagnostic algorithm of the main alterations of the glandular function. (Copyright EDISES 2021. Reproduced with permission)

Primary Hyperthyroidism

The most common clinical form is Basedow–Graves disease, a multisystem pathology on an autoimmune basis, characterized by pathognomonic clinical signs such as exophthalmos and pretibial myxedema. In most cases, Basedow’s disease is accompanied by goiter, an enlargement of the gland which, in this case, is non-nodular or diffuse. The hyperthyroid subject is clinically thin, tachylalic, tachypsychic, and insomniac. Less common forms of hyperthyroidism are toxic multinodular goiter (TMG) and solitary hypersecreting nod ule or toxic adenoma. As mentioned above, in the presence of a clinical blur or non-nodular glandular enlargement, the determination of TRAb allows the etiologic diagnosis. The conditions of TMG and toxic adenoma are distinguished by the character of functional autonomy of the nodular lesions; on a laboratory level, this gives rise to the peculiar picture of a disproportionate increase in fT3 compared to fT4.

These forms of hyperthyroidism are accompanied by thyrotoxicosis, a clinical syndrome resulting from an excess of thyroid hormones; hyperthyroid patients always present with thyrotoxicosis, but thyrotoxicosis may not result from hyperthyroidism.

Treatment of hyperthyroidism can be ablative, radiation, or pharmacological, depending on the nature of the lesion that caused it.

Primary Hypothyroidism

 The most common cause of hypothyroidism is Hashimoto’s thyroiditis, an autoimmune disorder common in countries with adequate iodine intake. Other causes of hypothyroidism are iatrogenic and iodine deficiency. Clinically, the hypothyroid patient is asthenic, overweight, bradylalic, and bradypsychic. Determination of serum TSH and fT4 is usually sufficient to diagnose. It is helpful to determine the presence of TPOAb to confirm the autoimmune etiology; the detection of these antibodies is frequent in hyperthyroid subjects, and their use in clinical practice also extends to Basedow–Graves disease. In the early stages, Hashimoto’s thyroiditis may present with thyrotoxicosis, defined as hashitoxicosis, due to massive cell lesions with the conspicuous release of already synthesized thyroid hormones. From a biochemical-clinical point of view, it is characterized by hyperthyroidism and the presence of anti-TPO antibodies. It is short-lived and usually evolves toward spontaneous remission and, with time, toward hypothyroidism.

Laboratory alterations of the hypothyroidism may affect the lipid profile, up to frank dyslipidemia.

Treatment of hypothyroidism is always replacement therapy.

Thyroiditis

 Thyroiditis is an autoimmune, inflammatory, or infectious disease, which can be divided into acute, subacute, and chronic diseases. Riedel’s chronic fibrous thyroiditis is rare, as are acute suppurative forms due to pyogenes. Subacute forms, which are relatively frequent, include Hashimoto’s disease and De Quervain’s thyroiditis, which has a viral etiology. De Quervain’s thyroiditis, also called giant cell or granulomatous thyroiditis, is characterized, from the point of view of glandular secretion, by a succession of three phases, which correspond to as many laboratory pictures. The first phase is thyrotoxic, with low TSH levels and high fT4 and fT3 concentrations, and may be followed by a hypothyroid phase, with a slightly increased or normal TSH concentration and low fT4 levels and, finally, the recovery phase, characterized by normal TSH, fT3, and fT4. The presence of fever and pain and increased indices of acute inflammation suggest an infection as the cause of the disease.

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مواضيع ذات صلة

Laboratory Investigations of Thyroid Hormones

total blood volume (TBV, Red blood cell [RBC] volume)

TORCH test

thyroxine-binding globulin (TBG, Thyroid-binding globulin)

Diagnosis and Therapy of neurohypophysis

Laboratory Investigations of neurohypophysis

thyroxine, total and free (T4 , Thyroxine screen, FT4 )

thyroid-stimulating immunoglobulins

thyroid-stimulating hormone stimulation test (TSH stimulation test)

Disorders of ADH secretion and action

Antidiuretic Hormone

Prolactin