trochemiluminescence immunoassay (ECLIA). These latter immunoassays provide greater precision, accuracy and a wider range of measurement [5].A high level of TSH generally indicates hypothyroidism. However, we should consider the cases of TSH-producing tumor, resistance to thyroid hormone (RTH: Refetoff syndrome), and false elevation of TSH due to heterophile antibodies specific to the reagents [6]. Autoimmunity against TSH is rare and has not been evaluated in sufficient detail, although several reviews have been published on heterophile antibodies.We examined a case with extremely high TSH levels. We decided to perform the polyethylene glycol (PEG) precipitation test. Furthermore, the TSH value was shown to be markedly low by PEG precipitation test. We eventually found macro-TSH, a unique anti-TSH autoimmune complex which may have caused the unexpectedly high elevation of TSH. Abstract. We encountered a 60-year-old woman with remarkably elevated thyroid-stimulating hormone (TSH) level as measured by electrochemiluminescent immunoassay (ECLIA), but with no specific symptoms, and with normal levels of free T3 and free T4. We performed the following investigations: polyethylene glycol (PEG) precipitation test, human antimouse IgG antibody (HAMA) interference test, and 3 additional TSH measurements by chemiluminescent immunoassay (CLIA). We then performed 2 gel filtration chromatography (GFC) procedures; one was at pH 7.2, and the other was at pH 3.0. Although the recovery of TSH shown by the PEG precipitation test was 4% which was extremely low, no HAMA interference was observed. Moreover, 3 CLIA instruments also showed various high values. The first GFC showed that the main peak of TSH immunoreactivity by ECLIA was located at a slightly larger molecular weight position than that of IgG. By the second GFC, the sample from the peak fraction of the first GFC showed that the TSH peak disappeared completely at the previous retention time but newly appeared at the same retention time as the TSH monomer. Protein G-Agarose gel removed the majority of the TSH complex. In conclusion, the majority of TSH in her serum was macro-TSH; TSH and anti-TSH IgG autoantibody complex. We should keep the possibility of macro-TSH in mind in cases with unexpectedly high TSH values, especially in autoimmune thyroidal disorders.
These results indicate that diabetes-induced vascular hypertrophy and remodeling is associated with reexpression of embryonic forms of FN and myosin heavy chain. Such changes are ET-dependent and may be mediated via TGF-beta1 and angiotensin.
Endothelin (ET) peptides perform several physiological, vascular,
and nonvascular functions and are widely distributed in a number
of tissues. They are altered in several disease processes including
diabetes. Alteration of ETs have been demonstrated in organs
of chronic diabetic complications in both experimental and clinical
studies. The majority of the effects of ET alteration in diabetes
are due to altered vascular function. Furthermore, ET antagonists
have been shown to prevent structural and functional changes induced
by diabetes in animal models. This review discusses the contribution
of ETs in the pathogenesis and the potential role of ET
antagonism in the treatment of chronic diabetic complications.
The aim of this study was to investigate the changes in mRNA level of embryonic form of myosin heavy chain (SMemb), endothelin-1 (ET-1) and plasminogen activator inhibitor-1 (PAI-1), which are considered to be involved in the angiogenesis and atherosclerosis in diabetic blood vessels, in human umbilical vein endothelial cells
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