ase because is determined by a self-aggression of the immune system. It means that the production of antibodies and killer cells into the thyroid tissue determines the progressive destruction and the frequent development towards the HYPOTHYROIDISM, that is a reduction of the gland functional activity.
Patients with Hashimoto’s thyroiditis have very variable SYMPTOMATOLOGY correlated to the disease clinical trend, to the age of onset and to the presence of other concomitant diseases. When the disease manifests itself in a serious form (minority of cases) there is a rapid glandular destruction with a consequent release of thyroid hormones deposits in the blood. The thyroid may enlarge, gives pain and gives the typical symptoms of Hyperthyroidism (Tachycardia, Asthenia, Emaciation, Fever, Insomnia, etc. ..). In most of the cases, however, the onset is slow and often asymptomatic. For a long time thyroid maintains a normal hormone production and symptoms arise only when there is development to hypothyroidism. Indeed, Hashimoto’s thyroiditis is the most common cause of hypothyroidism. The development -often slow- to a reduced thyroid function is in fact frequently. The typical symptoms of hypothyroidism are lack of energy, depression, cold intolerance, difficulty concentrating, hair loss. Often, an enlarged and progressively harder to the touch gland (goiter) is concurrent. In women, irregular menstruation may also occur. This disease can be associated with other diseases typically linked to impaired function of the immune system such as Basedow-Graves disease, Atrophic Gastritis, Coeliac disease, Hepatitis C, Myasthenia Gravis, Xerostomia, Keratoconjunctivitis Sicca, Adrenal insufficiency, Premature Ovarian Failure (POF or early menopause), Vitiligo, Schmidt’s Syndrome (adrenal insufficiency, hypoparathyroidism, diabetes, ovarian failure).
The DIAGNOSIS is based on anamnesis (family and personal medical history of the patient), physical examination (inspection and palpation of the gland and neck) and on important laboratory and instrumental tests such as TSH (pituitary hormone that controls thyroid), FT4 and FT3 (free fractions of thyroid hormones circulating in the blood); the detection of anti-thyroperoxidase antibodies (AB) (a thyroid enzyme) is positive in 95% of cases; thyroglobulin antibody is positive in 60% of cases; it is also useful AB anti-TSH receptor search and thyroid ultrasound. The latter allows a morphological study of the glandular parenchyma, and an assessment of its size. Sometimes it may also be necessary to recourse to a cytology check-up (needle aspiration biopsy) and/or to a scintigraphy.
In the differential diagnosis it is good to keep-out drugs that can induce the formation of antibodies against the thyroid gland like amiodarone, interferon-alpha, interleukin-2. Always report to your physician or to a specialist the kind of medicines taken or you are taking.
The THERAPY is in relation to thyroid function at the moment of diagnosis. Being frequently a state of hypothyroidism, the therapy is based on levothyroxine (LT4) dosage (replacement therapy). In the rare cases when it is showing during an hyperthyroid stage, a glandular function inhibition therapy will be given to the patient.
POSTPARTUM THYROIDITIS is a special form of Thyroid autoimmune inflammation that begins very soon after childbirth with transient hyperthyroidism followed by hypothyroidism. This disease is characterized by a frequent return to a normal glandular function.
I would like to emphasize here the importance of patients clinical monitoring not only for therapy necessary changes but also for those diseases that precede or which may accompany this condition. For women, I would like to point in particular to the risk of premature ovarian failure (early menopause): it is not a frequent occurrence but it must still be considered in women who have not yet had a pregnancy.