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Thursday, 12 December 2013

Thyroid disease: Euthyroid sick syndrome as a result of Sepsis - Treatments in Herbal medicine perspective

Euthyroid sick syndrome
Euthyroid sick syndrome is defined as a condition of  low T3 low T4 syndrome. According ot the study by the Mayo Clinic, in  other word this is the abnormalities of thyroid hormone concentrations seen commonly in a wide variety of nonthyroidal illnesses, resulting in low triiodothyronine, total thyroxine, and thyroid stimulating hormone concentrations(a). Decreased triiodothyronine (T3) levels are most common. Patients with more severe or prolonged illness also have decreased thyroxine (T4) levels. Serum reverse T3 (rT3) is increased. Patients are clinically euthyroid and do not have elevated thyroid-stimulating hormone (TSH) levels(b). Causes of euthyroid sick syndrome include a number of acute and chronic conditions, including pneumonia, fasting, starvation, sepsis, trauma, cardiopulmonary bypass, malignancy, stress, heart failure, hypothermia, myocardial infarction, chronic renal failure, cirrhosis, and diabetic ketoacidosis and inflammatory bowel disease(c). Others, in the study of classified SES into 3 subgroups according to the different alterations seen in the values of T3, T4, FT3, FT4, TSH, rT3 and TBG suggested that in SES type I the diseases seen, in order of frequency, were: obstructive chronic bronchopneumopathy with acute respiratory failure, diabetic ketoacidosis, neoplasms, ischemic heart disease, cardiac failure, chronic renal failure, liver diseases, acute cerebral vasculopathies, sepsis and collagenopathies. The disease seen in the 2 cases of SES type II was obstructive chronic bronchopneumopathy with acute respiratory failure. In SES type III the diseases seen were, in order of frequency: diabetic ketoacidosis, lung diseases, ischemic heart disease, cardiac failure, peripheral arteriopathies, acute cerebral vasculopathies, neoplasms, liver diseases, acute renal failure(d).
Treatments

E.2. Treatments in herbal medicine perspective
1. Taraxacum coreanum
Taraxacum coreanum Nakaiis a dandelion native to Korea and is widely consumed as an edible and medicinal herb. Treatment of primary macrophages with Taraxacum coreanum chloroform fraction(TCC) in vitro significantly inhibited all of the inflammatory parameters measured, including LPS-induced NO and PGE2 production, iNOS and COX-2 expression, IκBα degradation, IKK phosphorylation, and MAPK and STAT1 activation. In a mouse model of LPS-induced septic shock, TCC inhibited the production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6, and increased survival by 83%.Standard compounds (gallic acid, syringic acid) of Taraxacum coreanum were qualified by HPLC analysis, according to Kyung Hee University(62).

2. Chamaecyparis obtusa
β-thujaplicin, an active constituent from Chamaecyparis obtusa, has been shown to have acaricidal and antimicrobial effects. According to the study by the Chia-Nan University of Pharmacy and Science, the potential of β-thujaplicin in treatment of inflammation and sepsis. These effects occur through an efficient blockage of TNF-alpha and iNOS production. β-thujaplicin efficacy is comparable to that of indomethacin thus it can be a substitution but bear less depletion of PGE2, making this compound very promising in clinical applications(63).

3. Angelica sinensis
A low-molecular-weight (<10 kDa) fraction of A. sinensis extract significantly attenuated endotoxin-induced HMGB1 release in part through interfering with its cytoplasmic translocation in macrophage cultures. Prophylactic administration of an aqueous extract of A. sinensis significantly attenuated systemic HMGB1 accumulation in vivo, and conferred a dose-dependent protection against lethal endotoxemia. Furthermore, delayed administration of A. sinensis extract beginning 24 h after CLP attenuated systemic HMGB1 accumulation, and significantly rescued mice from lethal sepsis. Taken together, these data suggest that A. sinensis contains water-soluble components that exert protective effects against lethal endotoxemia and experimental sepsis in part by attenuating systemic accumulation of a late proinflammatory cytokine, HMGB1, according to the New York University School of Medicine(64).

4. Green tea
Intraperitoneal administration of EGCG protected mice against lethal endotoxemia, and rescued mice from lethal sepsis even when the first dose was given 24 hours after cecal ligation and puncture. The therapeutic effects were partly attributable to: 1) attenuation of systemic accumulation of proinflammatory mediator (e.g., HMGB1) and surrogate marker (e.g., IL-6 and KC) of lethal sepsis; and 2) suppression of HMGB1-mediated inflammatory responses by preventing clustering of exogenous HMGB1 on macrophage cell surface, according to the study by the North Shore University Hospital-New York University School of Medicine(65).
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(a) http://www.ncbi.nlm.nih.gov/pubmed/9086580
(b) http://www.merckmanuals.com/professional/endocrine_and_metabolic_disorders/thyroid_disorders/euthyroid_sick_syndrome.html
(c) http://en.wikipedia.org/wiki/Euthyroid_sick_syndrome
(d) http://www.ncbi.nlm.nih.gov/pubmed/8028742
(62) http://www.ncbi.nlm.nih.gov/pubmed/23261487 
(63) http://www.ncbi.nlm.nih.gov/pubmed/22507316
(64) http://www.ncbi.nlm.nih.gov/pubmed/16424112
(65) http://www.ncbi.nlm.nih.gov/pubmed/17987129