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Nonautoimmune thyroid disease
Published in Philip E. Harris, Pierre-Marc G. Bouloux, Endocrinology in Clinical Practice, 2014
Arie Berghout, Alex F. Muller, Philip E. Harris
Although antithyroid drugs may be considered for patients with features of thyrotoxicosis, they may be associated with a further rise in TSH levels, overriding their effects, with an increase in the size of a goiter. Thyroid hormone analogues such as TRIAC (3,3,5-triiodothyroacetic acid) may be used. TRIAC has has predominantly pituitary and hepatic thyromimetic effects—tissues that are relatively refractory to thyroid hormones in RTH, and it has a preferential affinity for TRβ in vitro86 The Food and Drug Administration (FDA) has issued several health warnings referring to the use of TRIAC for nonmedical reasons, such as weight loss and reduction in body fat in body builders. Patients who cannot be controlled with TRIAC alone may respond to combined therapy with an antithyroid drugs such as carbimazole/methimazole.87 An alternative therapy that may be considered is with dextrothyroxine (D-T4).
Roles of macrophage migration inhibitory factor in Guillain-Barré syndrome and experimental autoimmune neuritis: beneficial or harmful?
Published in Expert Opinion on Therapeutic Targets, 2018
Donghui Shen, Yue Lang, Fengna Chu, Xiujuan Wu, Ying Wang, Xiangyu Zheng, Hong-Liang Zhang, Jie Zhu, Kangding Liu
High serum or body fluid levels of MIF and the increased predisposition to severity of MS, RA, sarcoidosis, and ulcerative colitis have been evidenced to be associated with the presence of MIF-173C allele [89]. To date, the relationship between GBS severity and MIF gene promoter polymorphisms remains unclear. The deletion of MIF gene in mice demonstrated that MIF deficiency attenuates the interactions between leukocytes and endothelial cells, as well as the expression of inflammatory cytokines, such as IL-1 and TNF. Short interference RNA (siRNA) is used to silence the expression of homologous messenger RNA. Seiichi et al. reported a decrease in MIF expression after the introduction of siRNA [90]. MIF-deficient macrophages are hyporesponsive to LPS and gram-negative bacteria, exhibiting a considerable decrease in both TNF production and NF-κB activity [38]. Therefore, MIF mutations likely alter the susceptibility to or severity of GBS. The concentrations of plasma thyroxine (T4) correlate inversely with the plasma MIF levels in the patients with severe sepsis. Dextrothyroxine (D-T4) improves the survival rate of mice with severe sepsis significantly, showing that T4 and D-T4 can inhibit the activity of MIF in a dose-dependent manner [91].