DEFINITION
Hypothyroidism is a morbid condition caused by a lack of thyroid hormones (T3 and T4) or a lack of their effect on target tissues (TH resistance), dependent on genetic factors or competition for RXR by different hormones (eg. glucocorticoids , 1,25(OH)2VitD etc)
The disease definition according to a specific consensus conference or to The Diseases Database based on the Unified Medical Language System (NLM)
EPIDEMIOLOGY
The hypothyroidism is commonly in the elderly. The increased frequency is observed in women. Prevalence over 60 years is the 1.5-2%.
It may already be present at birth and determine, if not promptly treated, serious problems of intellectual and physical development (cretinism sporadic), now easily preventable through the tests that are found all the babies to see if their thyroid is well developed during the pregnancy and especially function normally at birth (neonatal screening of hypothyroidism)
Thanks to improved social conditions and health, a diet richer and more balanced - even with the use of iodized salt (iodine prophylaxis) - Neonatal screening and advances in the diagnosis and treatment of thyroid diseases, today these serious forms of hypothyroidism in early childhood onset are actually missing.
Remains very frequently hypothyroidism in:
- children of school age
- adolescents
- adults
In these cases the hormonal deficiency appears in a body already more or less fully developed, particularly in the brain, and therefore does not give cretinism. Are present goiter other disorders more or less severe. If not properly treated, hypothyroidism can impair the efficiency of the whole body.
The disease is found:
- Europe
- North America
- Nepal
- New Guinea
- Zaire
In some countries, including Italy, hypothyroidism from lack of iodine in the diet is still quite common, even in children and adolescents. Over 10 million Italians are suffering because of goiter endemic iodine deficiency. One problem not yet solved, so that was recently approved by Parliament a law to encourage the consumption of iodized salt in place of common table salt. The use of salt enriched with iodine in the preparation and storage of foods is an effective form of prophylaxis of endemic goiter.
SYMPTOMS
Symptoms affect all the organs because they are all
sensitive to hormone (Symptoms)
In some ways the most serious one has the so-called facies myxedematosa, resulting in swelling of the face and is due mainly to an increase of interstitial fluid in skin tissue.
The myxedema is a hard swelling which can affect:
- mouth (swelling)
- vocal cords (deterioration of the voice becomes throaty)
- skin and appendages (hair loss, dry skin)
- yellowing of the skin (palms of the hands and soles of the feet).
- goitre may be present, if the cause is due to an altered synthesis of thyroid hormones, for example, to lack of iodine. In some patients the goitre disorders may give local compression, especially if you have retrostenal extension. In this case you can have compression and displacement of the trachea or esophagus, the patient complains of difficulty swallowing solid foods.
Myxedema coma
It’s a serious medical condition that appears rarely, is exceptionally the final stage of hypothyroidism, occurs most often after prolonged exposure to cold, infections and trauma, or following ingestion of sedative drugs.
Symptoms:
- slowed heart rate
- hypothermia (body temperature below 34 ° C)
- somnolence gradually until coma.
- cardiomegaly
- bradycardia
- abnormalities of the genital tract, with decreased libido in men and women, and abnormal menstrual cycle
- muscle fatigue
- alterations of the skeleton (hypothyroidism occurs during childhood)
DIAGNOSIS
The symptoms are not sufficient to make diagnosis, but must be used at a dose of thyroid hormones.
Laboratory tests:
- thyroid hormone dosing: FT3 and FT4 (reduced); thyrotropin, TSH (increased)
In patients where there is evidence of low FT4 and normal or low TSH, you should seek a secondary hypothyroidism with interest then of hypothalamus and pituitary. In this case the tests are made more complicated, one of which is the Test to TRH
- antithyroid antibodies: antithyreoglobulin and antiperoxidase to search for an autoimmune involvement, as in thyroiditis.
- complete blood count:hypercholesterolemy, anaemia (reduction of hemoglobin values)
PATIENT RISK FACTORS
Vascular
Genetic
Acquired
Hormonal
Genetic
Acquired
Stress dependent high serum cortisol
StressHacker: Towards Practical Stress Monitoring in the Wild with Smartwatches. 2018
Elevated thyroid stimulating hormone is associated with elevated cortisol in healthy young men and women. 2012
- BACKGROUND:
Recent attention has been given to subclinical hypothyroidism, defined as an elevation of TSH (4.5-10 uIU/L) with T4 and T3 levels still within the normal range. Controversy exists about the proper lower limit of TSH that defines patients in the subclinical hypothyroidism range and about if/when subclinical hypothyroidism should be treated. Additional data are needed to examine the relationship between markers of thyroid function in the subclinical hypothyroidism range, biomarkers of health and ultimately health outcomes.
OBJECTIVE:
We aimed to assess the relationship between serum TSH levels in the 0.5-10 uIU/L range and serum cortisol in a cohort of healthy young men and women without clinical evidence of hypothyroidism. Based on data in frank hypothyroidism, we hypothesized that serum TSH levels would be positively correlated with serum cortisol levels, suggesting derangement of the cortisol axis even in subclinical hypothyroidism.
METHODS:
We conducted a cross sectional study in 54 healthy, young (mean 20.98 +/- 0.37 yrs) men (19) and women (35). Lab sessions took place at 1300 hrs where blood was drawn via indwelling catheter for later assessment of basal serum TSH, free T3, free T4, and cortisol levels.
RESULTS:
All but 1 participant had free T3 levels within the normal reference intervals; free T4 levels for all participants were within the normal reference intervals. Linear regression modeling revealed that TSH levels in the 0.5-10 uIU/L were significantly and positively correlated with cortisol levels. This positive TSH-cortisol relationship was maintained below the accepted 4.5 uIU/L subclinical hypothyroid cutoff. Separate regression analyses conducted by systematically dropping the TSH cutoff by 0.50 uIU/L revealed that the TSH-cortisol relationship was maintained for TSH levels (uIU/L) ≤4.0, ≤3.5, ≤3.0, and ≤2.5 but not ≤2.0. Linear regression modeling did not reveal a relationship between free T3 or free T4 levels and cortisol levels.
CONCLUSIONS:
Results suggest a positive relationship between TSH and cortisol in apparently healthy young individuals. In as much as this relationship may herald a pathologic disorder, these preliminary results suggest that TSH levels > 2.0 uIU/L may be abnormal. Future research should address this hypothesis further, for instance through an intervention study.
Social stress-induced hypothyroidism is attenuated by antidepressant treatment in rats. 2012
Although serotonergic system has been classically implicated in mood modulation, there has been relatively little study on the relationship between this system and thyroid hormones (TH) economy in stress models. When TH are studied, the effects of stress on thyroid function seems to be complex and depend on the kind and time of stress which counts for the elusiveness of mechanisms underlying changes in TH economy. Herein, we hypothesized that serum TH are affected in a time-dependent fashion after repeated social stressful stimuli and serotonergic system is implicated in these changes. Therefore, we aimed to investigate the possible alterations in thyroid hormone economy and type 1 (D1) and type 2 (D2) deiodinase activity in a model of social defeat stress. Thereafter, we tested the responsiveness of these changes to fluoxetine treatment. Both short (STS) and a long-term (LTS) stress were performed. Blood samples were drawn just before and 1 (STS) or 4 and 8 weeks (LTS) after the beginning of stress to assess serum T4, T3 and corticosterone. Deiodinases activity was assessed at the end of each protocol. Stress-induced behavior studied in open field arena and hypercorticosteronemia were mainly observed in LTS (week 4). Stress-induced behavior was associated to hypothyroidism which occurred before, since week 1 in stressed group. Serum TH was restored to control levels in week 8, when behavior changes were not observed anymore, and was mainly associated with high brown adipose tissue D2 activity since thyroid and liver D1 activity were low or normal in the STS and LTS respectively in stressed rats compared to control. Antidepressant study revealed that fluoxetine treatment (10mg/kg po during four weeks) fully reversed stress-induced behavior and normalized serum T4, but not T3 levels and hypercorticosteronemia in stressed group compared to control. The current work adds new concepts concerning TH metabolism changes induced by social stress and suggests that serotonergic system impairment may take part in the key events which ultimately lead to hypothyroxinemia and behavioral changes induced by chronic social defeat. This article is part of a Special Issue entitled 'Anxiety and Depression'.
TISSUE SPECIFIC RISK FACTORS
anatomical (due its structure)
vascular (due to the local circulation)
physiopathological (due to tissue function and activity)
PATHOGENESIS
The system includes hypothalamus -> pituitary -> thyroid -> liver -> receptors
tissue (muscle, liver, heart etc) any alteration in one of these points induces different disease:
- hypothalamus and pituitary
- mutated gene for the hypothalamic receptor -> thyroid hormones act through negative feedback on hypothalamus and pituitary tying a subtype of THRB that could be mutated
- levels of thyroid hormones slightly subnormal -> increase secretion of TSH from the pituitary gland
- lesion -> hormone insufficient respectively TRH and TSH hormone, resulting in reduced incentives for the production of thyroid hormones (secondary hypothyroidism)
- thyroid
- development of congenital deficiency of thyroid gland -> at birth there is a reduced mass of thyroid tissue; during fetal life and neonatal deficiency of thyroid hormones causes a developmental delay of the central nervous system
- autoimmune processes -> body due to an infection of the thyroid (Hashimoto thyroiditis) produces antibodies against its own thyroid tissue. The thyroid gland becomes fibrotic and has a low volume, the synthesis function is impaired.
- post-treatment -> reduction of thyroid tissue due to thyroid surgery or radiation therapy with radio-iodine, used in hyperthyroidism; also use of drugs antithyroid
- iodine deficiency, or intake of high amounts of iodine in the form of drugs (it's content, for example, in the cough syrups) or dietary supplements.
- selenium deficiency
- changes in the proteins necessary for synthesis of biochemical processes of thyroid hormones
- lack of conversion of T4 to T3 in the liver, but is not documented in humans or animals. Low T3 with normal T4 values are often due to concomitant disease (euthyroid syndrome) or administration of drugs:
- amiodarone
- lithium
- propranolol
- corticosteroids
- contrast media iodates
GUIDE LINES
04. TSH normal range 0.5-4.5 ????
TREATMENT
Thyroid Hormone Replacement Therapy
Patients info
Hypothyroidism overview at endocrineweb
Laura Piredda e Marzia Pera