| Autoimmune thyroiditis |
| Classification and external resources |
| ICD-10 |
E06.3 |
| MeSH |
D013967 |
Autoimmune thyroiditis, or Chronic Autoimmune thyroiditis, is a disease in which the body interprets the thyroid glands and its hormone products T3, T4 and TSH as threats, therefore producing special antibodies that target the thyroid’s cells, thereby destroying it. It presents with hypothyroidism or hyperthyroidism and the presence or absence of goiters.[1] Specialists clinically separate autoimmune thyroiditis into two categories. If goiters are present, it is understood as Hashimoto’s Thyroiditis. On the other hand, if the thyroid is atrophic, but does not present goiters, it is denominated Atrophic Thyroiditis.[1] If the symptoms of thyroiditis appear in women after giving birth, it is attributed to such and therefore called Postpartum Thyroiditis.[1] The effects of this disease are not permanent but transient. Symptoms may come and go depending on whether the patient receives treatment, and whether the treatment is effective.[1]
Contents
- 1 Signs and symptoms
- 1.1 Hyperthyroidism
- 1.2 Hypothyroidism
- 1.3 Genetics
- 1.4 High iodine consumption
- 1.5 Age
- 2 Mechanism
- 3 Diagnosis
- 4 References
Signs and symptoms
The symptoms for autoimmune thyroiditis may vary depending on whether it causes hyperthyroidism or hypothyroidism.
Hyperthyroidism
Hyperthyroidism can cause sweating, rapid heart rate, anxiety, tremors, fatigue, difficulty sleeping, sudden weight loss, and protruding eyes.[2]
Hypothyroidism
Hypothyroidism can cause weight gain, fatigue, dry skin, hair loss, intolerance to cold, and constipation.[2]
Genetics
“Thyroid autoimmunity is familial.” [1] The disease is said to be inherited as a dominant trait since it has been reported that as many as fifty percent of the first degree relatives of patients with some type of autoimmune thyroiditis present thyroid antibodies in serum.[1] Some studies have even related it to chromosome 21 because of its high correlation with patients with Down’s syndrome and familial Alzheimer’s disease. Still, this theory is doubted, since patients with Turner’s syndrome also present a high prevalence of autoimmune thyroiditis (up to fifty percent).[1]
High iodine consumption
Autoimmune thyroiditis has a higher prevalence in societies that have a higher intake of iodine in their diet, such as the United States and Japan. Also, the rate of lymphocytic infiltration increased in areas where the iodine intake was once low, but had been given iodine supplementation. “The prevalence of positive serum tests in such areas rises to over forty percent within 0.5 to 5 years.” [1] When in the presence of excess iodine, the gland is unable to avoid its inhibitory effect on the biosynthesis of thyroid hormones. This is why when a person has excess iodine in his or her diet or is administered with additional supplementation in areas where sufficient iodine has been noted, it can induce reversible hypothyroidism.[1]
Age
It has been shown that “the prevalence of positive tests for thyroid antibodies increases with age, with a frequency as high as 33 percent in women 70 years old or older.” [1] The mean age of prevalence in women is higher than in men by one year, 58 and 59 years old respectively. Autoimmune thyroiditis can also affect children. Although it is very rare for children under the age of five, it can occur, and it accounts for around 40 percent of the cases in adolescents with goiters. In the case of hypothyroidism, patients over the age of 45 have more chances of developing autoimmune thyroiditis.[1]
Mechanism
Thyroid autoantibodies appear mostly with the presence of lymphocytes in the targeted organ.[1][3] Lymphocytes produce antibodies targeting three different thyroid proteins: Thyroid peroxidase Antibodies (TPOAb), Thyroglobulin Antibodies (TgAb), and Thyroid stimulating hormone receptor Antibodies (TRAb).[1][2] Some patients who are healthy may be positive for more than one of these antibodies. Doctors who attend to such patients will most likely do routine follow-ups on the patient’s health since, even though it is highly unlikely that they will present any thyroid problems, there is still a chance that they will develop some type of dysfunction with time.[2]
Diagnosis
There are various tests that can be made depending on the symptoms the patient presents. Doctors may search for TPOAb when the patient has symptoms that suggest hypothyroidism or when said patient will be started on a drug therapy associated with risks of developing hypothyroidism,[2] such as lithium or Interferon alfa.[1] This antibody is related to Hashimoto's thyroiditis and Grave’s disease. They may look for TgAb whenever a thyroglobulin test is performed to see if the antibody is present and likely to interfere. It can also be ordered in regular intervals after the patient has been diagnosed with thyroid cancer, and just like TPOAb, it can be associated with Hashimoto’s thyroiditis.[2] In the case that the patient presents symptoms for hyperthyroidism, the doctors are more likely to test for TRAb, as well as monitoring the effects of anti- thyroid therapy, also associated with Grave’s disease.[1]
Types
It can refer to:
- Hashimoto's thyroiditis
- Graves' disease
- Postpartum thyroiditis
References
- ^ a b c d e f g h i j k l m n o Dayan, Dayan, Colin M; Dayan, Colin M., and Gilbert H. Daniels. (1996). "Chronic Autoimmune Thyroiditis". The New England Journal of Medicine 335 (2): 99–107. doi:10.1056/nejm199607113350206.
- ^ a b c d e f "Thyroid Antibodies". Retrieved 4 April 2012.
- ^ Weetman, A. P.; A. M. McGregor, JPublications. 48. (1982): 196-200. H. Lazarus & R. Hall (1982). "Thyroid Antibodies are Produced by Thyroid- Derived Lymphocytes.". Blackwell Scientific Publications. 48. (1982): 196-200 48: 196–200.
|
Endocrine pathology: endocrine diseases (E00–E35, 240–259)
|
|
Pancreas/
glucose
metabolism |
| Hypofunction |
- types:
- type 1
- type 2
- MODY 1 2 3 4 5 6
- complications
- coma
- angiopathy
- ketoacidosis
- nephropathy
- neuropathy
- retinopathy
- cardiomyopathy
- insulin receptor (Rabson–Mendenhall syndrome)
- Insulin resistance
|
|
| Hyperfunction |
- Hypoglycemia
- beta cell (Hyperinsulinism)
- G cell (Zollinger–Ellison syndrome)
|
|
|
Hypothalamic/
pituitary axes |
| Hypothalamus |
- gonadotropin
- Kallmann syndrome
- Adiposogenital dystrophy
- CRH (Tertiary adrenal insufficiency)
- vasopressin (Neurogenic diabetes insipidus)
- general (Hypothalamic hamartoma)
|
|
| Pituitary |
| Hyperpituitarism |
- anterior
- Acromegaly
- Hyperprolactinaemia
- Pituitary ACTH hypersecretion
- posterior (SIADH)
- general (Nelson's syndrome)
|
|
| Hypopituitarism |
- anterior
- Kallmann syndrome
- Growth hormone deficiency
- ACTH deficiency/Secondary adrenal insufficiency
- GnRH insensitivity
- FSH insensitivity
- LH/hCG insensitivity
- posterior (Neurogenic diabetes insipidus)
- general
- Empty sella syndrome
- Pituitary apoplexy
- Sheehan's syndrome
- Lymphocytic hypophysitis
|
|
|
| Thyroid |
| Hypothyroidism |
- Iodine deficiency
- Cretinism
- Congenital hypothyroidism
- Myxedema
- Euthyroid sick syndrome
|
|
| Hyperthyroidism |
- Hyperthyroxinemia
- Thyroid hormone resistance
- Familial dysalbuminemic hyperthyroxinemia
- Hashitoxicosis
- Thyrotoxicosis factitia
- Graves' disease
|
|
| Thyroiditis |
- Acute infectious
- Subacute
- De Quervain's
- Subacute lymphocytic
- Autoimmune/chronic
- Hashimoto's
- Postpartum
- Riedel's
|
|
| Goitre |
- Endemic goitre
- Toxic nodular goitre
- Toxic multinodular goiter
|
|
|
| Parathyroid |
| Hypoparathyroidism |
- Hypoparathyroidism
- Pseudohypoparathyroidism
- Pseudopseudohypoparathyroidism
|
|
| Hyperparathyroidism |
- Primary
- Secondary
- Tertiary
- Osteitis fibrosa cystica
|
|
|
| Adrenal |
| Hyperfunction |
- aldosterone: Hyperaldosteronism/Primary aldosteronism
- Conn syndrome
- Bartter syndrome
- Glucocorticoid remediable aldosteronism
- AME
- Liddle's syndrome
- 17α CAH
- cortisol: Cushing's syndrome (Pseudo-Cushing's syndrome)
- sex hormones: 21α CAH
- 11β CAH
|
|
Hypofunction/
Adrenal insufficiency
(Addison's, WF) |
- aldosterone: Hypoaldosteronism
|
|
|
| Gonads |
- ovarian: Polycystic ovary syndrome
- Premature ovarian failure
- testicular: enzymatic
- 5α-reductase deficiency
- 17β-hydroxysteroid dehydrogenase deficiency
- aromatase excess syndrome)
- Androgen receptor (Androgen insensitivity syndrome
- general: Hypogonadism (Delayed puberty)
- Hypergonadism
- Hypoandrogenism
- Hypoestrogenism
- Hyperandrogenism
- Hyperestrogenism
|
|
|
| Height |
- Dwarfism/Short stature
- Midget
- Laron syndrome
- Psychosocial
- Ateliosis
- Gigantism
|
|
| Multiple |
- Autoimmune polyendocrine syndrome multiple
- Carcinoid syndrome
- Multiple endocrine neoplasia
- Progeria
- Werner syndrome
- Acrogeria
- Metageria
- Woodhouse-Sakati syndrome
|
|
|
|
|
noco (d)/cong/tumr, sysi/epon
|
proc, drug (A10/H1/H2/H3/H5)
|
|
|
|
