Euthyroid sick syndrome pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
[[T3]] ([[triiodothyronine]]) is the biologically active form of [[thyroid hormone]]. Normally most of the [[T3]] ([[triiodothyronine]]) is produced by peripheral deiodination of circulating [[T4]] ([[thyroxine]]) by the enzyme 5’-monodeiodinase (type I). In [[euthyroid]] sick syndrome there occurs [[inhibition]] of the [[enzyme]] 5΄-deiodinase (type I) which leads to decrease conversion of [[T4]] to [[T3]] and an increase in [[reverse T3]] from decreased metabolism. [[Euthyroid]] sick syndrome is seen in [[conditions]] of [[starvation]] and [[critical illness]] such as [[sepsis]], [[surgery]], severe [[trauma]], [[burns]], [[metabolic disorders]], [[bone marrow transplantation]], and [[malignancy]]. During these [[Stress (medicine)|stress]] conditions, there occurs [[hypermetabolism]], increased [[energy]] expenditure, [[hyperglycemia]], and [[muscle]] loss. It is speculated, that the body in order to contain this [[hypermetabolism]] induces some degree of [[hypothyroidism]] by inhibiting deiodination of [[T4]] to [[T3]] by the [[enzyme]] 5’-monodeiodinase. This is an [[adaptive]] process by which the [[Human body|body]] prevents further [[muscle]] and [[calorie]] loss. [[Euthyroid]] sick syndrome presents with low serum [[T3]]. Depending upon the severity and duration of the [[Stress (medicine)|stress]] inducing [[condition]], the [[thyroid-stimulating hormone]]([[TSH]]), [[thyroxine]] ([[T4]]), and [[free T4]] ([[FT4]]) are affected in variable proportions. The drop in levels of [[T3]] and [[T4]] are more with more severe illnesses. [[Mortality rate]] is high when there is a marked decrease in serum [[T3]] and [[T4]].<ref name="GRASBERGERGOLCHER2002">{{cite journal|last1=GRASBERGER|first1=Helmut|last2=GOLCHER|first2=Henriette M.B.|last3=FINGERHUT|first3=Anja|last4=JANSSEN|first4=Onno E.|title=Loop variants of the serpin thyroxine-binding globulin: implications for hormone release upon limited proteolysis|journal=Biochemical Journal|volume=365|issue=1|year=2002|pages=311–316|issn=0264-6021|doi=10.1042/bj20020014}}</ref><ref name="pmid10554534">{{cite journal |vauthors=Schilling JU, Zimmermann T, Albrecht S, Zwipp H, Saeger HD |title=[Low T3 syndrome in multiple trauma patients--a phenomenon or important pathogenetic factor?] |language=German |journal=Med. Klin. (Munich) |volume=94 Suppl 3 |issue= |pages=66–9 |year=1999 |pmid=10554534 |doi= |url=}}</ref><ref name="WongHershman1992">{{cite journal|last1=Wong|first1=Timothy K.|last2=Hershman|first2=Jerome M.|title=Changes in thyroid function in nonthyroid illness|journal=Trends in Endocrinology & Metabolism|volume=3|issue=1|year=1992|pages=8–12|issn=10432760|doi=10.1016/1043-2760(92)90085-F}}</ref> | [[T3]] ([[triiodothyronine]]) is the biologically active form of [[thyroid hormone]]. Normally most of the [[T3]] ([[triiodothyronine]]) is produced by peripheral deiodination of circulating [[T4]] ([[thyroxine]]) by the enzyme 5’-monodeiodinase (type I). In [[euthyroid]] sick syndrome there occurs [[inhibition]] of the [[enzyme]] 5΄-deiodinase (type I) which leads to decrease conversion of [[T4]] to [[T3]] and an increase in [[reverse T3]] from decreased metabolism. [[Euthyroid]] sick syndrome is seen in [[conditions]] of [[starvation]] and [[critical illness]] such as [[sepsis]], [[surgery]], severe [[trauma]], [[burns]], [[metabolic disorders]], [[bone marrow transplantation]], and [[malignancy]]. During these [[Stress (medicine)|stress]] conditions, there occurs [[hypermetabolism]], increased [[energy]] expenditure, [[hyperglycemia]], and [[muscle]] loss. It is speculated, that the body in order to contain this [[hypermetabolism]] induces some degree of [[hypothyroidism]] by inhibiting deiodination of [[T4]] to [[T3]] by the [[enzyme]] 5’-monodeiodinase. This is an [[adaptive]] process by which the [[Human body|body]] prevents further [[muscle]] and [[calorie]] loss. During illness there is also downregulation of TRH and TSH release from the hypothalamus and pituitary gland respectively. In vitro studies have shown that high concentrations of cytokines severely affect genes involved in the production and release of T4 and T3. [[Euthyroid]] sick syndrome presents with low serum [[T3]]. Depending upon the severity and duration of the [[Stress (medicine)|stress]] inducing [[condition]], the [[thyroid-stimulating hormone]]([[TSH]]), [[thyroxine]] ([[T4]]), and [[free T4]] ([[FT4]]) are affected in variable proportions. The drop in levels of [[T3]] and [[T4]] are more with more severe illnesses. [[Mortality rate]] is high when there is a marked decrease in serum [[T3]] and [[T4]].<ref name="GRASBERGERGOLCHER2002">{{cite journal|last1=GRASBERGER|first1=Helmut|last2=GOLCHER|first2=Henriette M.B.|last3=FINGERHUT|first3=Anja|last4=JANSSEN|first4=Onno E.|title=Loop variants of the serpin thyroxine-binding globulin: implications for hormone release upon limited proteolysis|journal=Biochemical Journal|volume=365|issue=1|year=2002|pages=311–316|issn=0264-6021|doi=10.1042/bj20020014}}</ref><ref name="pmid10554534">{{cite journal |vauthors=Schilling JU, Zimmermann T, Albrecht S, Zwipp H, Saeger HD |title=[Low T3 syndrome in multiple trauma patients--a phenomenon or important pathogenetic factor?] |language=German |journal=Med. Klin. (Munich) |volume=94 Suppl 3 |issue= |pages=66–9 |year=1999 |pmid=10554534 |doi= |url=}}</ref><ref name="WongHershman1992">{{cite journal|last1=Wong|first1=Timothy K.|last2=Hershman|first2=Jerome M.|title=Changes in thyroid function in nonthyroid illness|journal=Trends in Endocrinology & Metabolism|volume=3|issue=1|year=1992|pages=8–12|issn=10432760|doi=10.1016/1043-2760(92)90085-F}}</ref><ref name="DocterKrenning1993">{{cite journal|last1=Docter|first1=R.|last2=Krenning|first2=E. P.|last3=Jong|first3=M.|last4=Hennemann|first4=G.|title=The sick euthyroid syndrome: changes in thyroid hormone serum parameters and hormone metabolism|journal=Clinical Endocrinology|volume=39|issue=5|year=1993|pages=499–518|issn=0300-0664|doi=10.1111/j.1365-2265.1993.tb02401.x}}</ref> | ||
==Genetics== | ==Genetics== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
- The exact pathogenesis of [disease name] is not fully understood.
OR
- It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
T3 (triiodothyronine) is the biologically active form of thyroid hormone. Normally most of the T3 (triiodothyronine) is produced by peripheral deiodination of circulating T4 (thyroxine) by the enzyme 5’-monodeiodinase (type I). In euthyroid sick syndrome there occurs inhibition of the enzyme 5΄-deiodinase (type I) which leads to decrease conversion of T4 to T3 and an increase in reverse T3 from decreased metabolism. Euthyroid sick syndrome is seen in conditions of starvation and critical illness such as sepsis, surgery, severe trauma, burns, metabolic disorders, bone marrow transplantation, and malignancy. During these stress conditions, there occurs hypermetabolism, increased energy expenditure, hyperglycemia, and muscle loss. It is speculated, that the body in order to contain this hypermetabolism induces some degree of hypothyroidism by inhibiting deiodination of T4 to T3 by the enzyme 5’-monodeiodinase. This is an adaptive process by which the body prevents further muscle and calorie loss. During illness there is also downregulation of TRH and TSH release from the hypothalamus and pituitary gland respectively. In vitro studies have shown that high concentrations of cytokines severely affect genes involved in the production and release of T4 and T3. Euthyroid sick syndrome presents with low serum T3. Depending upon the severity and duration of the stress inducing condition, the thyroid-stimulating hormone(TSH), thyroxine (T4), and free T4 (FT4) are affected in variable proportions. The drop in levels of T3 and T4 are more with more severe illnesses. Mortality rate is high when there is a marked decrease in serum T3 and T4.[1][2][3][4]
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ GRASBERGER, Helmut; GOLCHER, Henriette M.B.; FINGERHUT, Anja; JANSSEN, Onno E. (2002). "Loop variants of the serpin thyroxine-binding globulin: implications for hormone release upon limited proteolysis". Biochemical Journal. 365 (1): 311–316. doi:10.1042/bj20020014. ISSN 0264-6021.
- ↑ Schilling JU, Zimmermann T, Albrecht S, Zwipp H, Saeger HD (1999). "[Low T3 syndrome in multiple trauma patients--a phenomenon or important pathogenetic factor?]". Med. Klin. (Munich) (in German). 94 Suppl 3: 66–9. PMID 10554534.
- ↑ Wong, Timothy K.; Hershman, Jerome M. (1992). "Changes in thyroid function in nonthyroid illness". Trends in Endocrinology & Metabolism. 3 (1): 8–12. doi:10.1016/1043-2760(92)90085-F. ISSN 1043-2760.
- ↑ Docter, R.; Krenning, E. P.; Jong, M.; Hennemann, G. (1993). "The sick euthyroid syndrome: changes in thyroid hormone serum parameters and hormone metabolism". Clinical Endocrinology. 39 (5): 499–518. doi:10.1111/j.1365-2265.1993.tb02401.x. ISSN 0300-0664.