Hypothyroidism and anti‐endothelial cell antibodies

Wangel, A. G.; Kontiainen, Sirkka; Melamies, L.; Weber, T.

doi:10.1111/j.1699-0463.1993.tb00086.x

Cited by 10 publications

(7 citation statements)

References 15 publications

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“…The autoantibody-mediated endothelial cell stimulatory activity in two of two additional newly-diagnosed Graves' disease sera tested was also substantially or completely blocked by specific anti-insulin-like growth factor antibodies suggesting that fibroblast growth factor-like autoantibodies are not likely to play a significant role in early, active Graves' disease patients lacking comorbid diabetic nephropathy. Endothelial cell inhibitory autoantibody activity was largely absent in the protein-A eluates in seventeen of eighteen active Graves' disease patients (Fig 1) consistent with a prior report of a low prevalence of anti-endothelial cell autoantibodies in thyroid autoimmunity patients having suppressed TSH [19]. Antiendothelial cell autoantibodies were reported to occur at a (four-fold) significantly higher prevalence in thyroid autoimmunity patients having elevated TSH [19].…”

Section: Discussionsupporting

confidence: 88%

Endothelial Cell Growth Promoting Activity in Graves’ Disease Sera is Neutralized by Anti-Basic Fibroblast Growth Factor Antibodies in Patients with Fat Expansive but Not Infiltrative Orbitopathy

2019

Endocrinol Diabetes Metab J

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To report a case of orbital fat expansion leading to globe prolapse in a Graves' disease patient undergoing high-dose glucocorticoid therapy. To evaluate the growth factor receptor specificities of plasma autoantibodies in Graves' disease patients who exhibited contrasting subtypes of thyroidassociated ophthalmopathy, i.e. orbital fat expansion-type vs. infiltrative. Methods: Sera from Graves' orbitopathy and control patients with or without Graves' disease were subjected to protein-A affinity chromatography to obtain immunoglobulin G. A (1/50 th to 1/1600 th) range in dilutions of the protein-A eluate fraction was incubated for four days at 37 degrees C with bovine pulmonary artery endothelial cells to test for endothelial cell inhibition or stimulation. Growth stimulatory autoantibodies were co-incubated with specific neutralizing anti-insulin like growth factor 1 receptor antibodies or anti-basic fibroblast growth factor antibodies to assess autoantibody specificity in contrasting Graves' orbitopathy subtypes. Results: We observed increased mean endothelial cell growth promoting activity in the protein-A eluates of serum from eighteen patients with active Graves' disease (117 ± 28%, n = 18) compared to mean endothelial cell activity (89 ± 10%, n = 13, P = 0.003) in thirteen adults without Graves' disease. The protein-A eluate fraction in acute infiltrative-type Graves' orbitopathy contained a high titer (> 1: 1000) of endothelial cell stimulatory activity which was significantly neutralized by specific monoclonal anti-human insulin-like growth factor 1 receptor antibodies. The protein-A eluate fraction in fat expansion-type Graves' orbitopathy contained endothelial cell inhibitory activity (at low titers) and stimulatory activity (at high titers), and the latter stimulatory activity was completely neutralized by specific anti-basic fibroblast growth factor antibodies. Conclusion: Graves' disease suffering globe prolapse secondary to marked orbital fat-expansion had coexisting plasma fibroblast growth factorinhibitory and-stimulatory autoantibodies. The latter was completely neutralized by anti-basic fibroblast growth factor antibodies.

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Section: Discussionsupporting

confidence: 88%

Endothelial Cell Growth Promoting Activity in Graves’ Disease Sera is Neutralized by Anti-Basic Fibroblast Growth Factor Antibodies in Patients with Fat Expansive but Not Infiltrative Orbitopathy

2019

Endocrinol Diabetes Metab J

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“…Isoforms of the thyroid hormone receptor have been identified in human aortic vascular smooth muscle cells, suggesting that thyroid hormone may act directly on the vascular bed and influence vasomotion. Other studies have correlated hypothyroidism with the presence of anti–endothelial cell antibodies, which may be related to its autoimmune etiology in many patients. Endothelial dysfunction has also been linked to elevated local coronary and systemic levels of biomarkers such as lipoprotein‐lipase A2 as well as the local presence of macrophages and microchannels, features consistent with inflammation .…”

Section: Discussionmentioning

confidence: 99%

Hypothyroidism Is Associated With Coronary Endothelial Dysfunction in Women

Sara

Zhang

Gharib

et al. 2015

JAHA

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BackgroundHypothyroidism is associated with an increased risk of coronary artery disease, beyond that which can be explained by its association with conventional cardiovascular risk factors. Coronary endothelial dysfunction precedes atherosclerosis, has been linked to adverse cardiovascular events, and may account for some of the increased risk in patients with hypothyroidism. The aim of this study was to determine whether there is an association between epicardial and microvascular coronary endothelial dysfunction and hypothyroidism.Methods and ResultsIn 1388 patients (mean age 50.5 [12.3] years, 34% male) presenting with stable chest pain to Mayo Clinic, Rochester, MN for diagnostic coronary angiography, and who were found to have nonobstructive coronary artery disease (<40% stenosis), we invasively assessed coronary artery endothelial-dependent microvascular and epicardial function by evaluating changes in coronary blood flow (% Δ CBF Ach) and diameter (% Δ CAD Ach), respectively, in response to intracoronary infusions of acetylcholine. Patients were divided into 2 groups: hypothyroidism, defined as a documented history of hypothyroidism or a thyroid-stimulating hormone (TSH) >10.0 mU/mL, n=188, and euthyroidism, defined as an absence of a history of hypothyroidism in the clinical record and/or 0.3

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“…This observation may indicate direct action of thyroid hormones on the vascular bed through mechanisms that are still unknown. Other investigators correlated hypothyroid status with increased evidence of anti-endothelial cell antibodies [37] a factor that could offer an explanation for endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%