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Thyroid. 2007 Nov;17(11):1137-42.
Thyroid disease in patients with idiopathic thrombocytopenia: a cohort study.
www.ncbi.nlm.nih.gov/pubmed/17887931
Abstract
OBJECTIVES:
To estimate the prevalence of the association between thyroid disease and idiopathic thrombocytopenia (ITP), and to examine the effect of treatment of the thyroid condition on platelet count.
DESIGN:
Retrospective cohort study performed in a tertiary care center setting. All patients who were diagnosed with ITP by a single provider at the Cleveland Clinic Hematology/Oncology Department between 1988 and 2005 were included.
MAIN OUTCOME:
Among the 98 patients, thyroid function tests were available in 80 patients. Of these, 16 (20%) had abnormal thyroid function: 6 had hyperthyroidism and 10 had hypothyroidism. The median interval from the onset of the thyroid or hematological condition (whichever came first) was 84 months (range: 25-612). The autoimmune nature of the thyroid disease was proven in 12 cases (75%). Three patients showed a transient increase in the platelet count after restoring the euthyroid state; however, durable improvement of thrombocytopenia was not encountered.
CONCLUSIONS:
The prevalence of hypothyroidism in patients with ITP is higher than in the general population. Based on this observation, routine assessment of thyroid function should be done in patients with ITP. The long-term course of ITP was not influenced by the treatment of the thyroid condition.
This was especially interesting in light of this article I found:www.nature.com/nature/journal/v496/n7446/full/nature11868.html
Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells
There has been a marked increase in the incidence of autoimmune diseases in the past half-century. Although the underlying genetic basis of this class of diseases has recently been elucidated, implicating predominantly immune-response genes, changes in environmental factors must ultimately be driving this increase. The newly identified population of interleukin (IL)-17-producing CD4+ helper T cells (TH17 cells) has a pivotal role in autoimmune diseases. Pathogenic IL-23-dependent TH17 cells have been shown to be critical for the development of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, and genetic risk factors associated with multiple sclerosis are related to the IL-23–TH17 pathway. However, little is known about the environmental factors that directly influence TH17 cells. Here we show that increased salt (sodium chloride, NaCl) concentrations found locally under physiological conditions in vivo markedly boost the induction of murine and human TH17 cells. High-salt conditions activate the p38/MAPK pathway involving nuclear factor of activated T cells 5 (NFAT5; also called TONEBP) and serum/glucocorticoid-regulated kinase 1 (SGK1) during cytokine-induced TH17 polarization. Gene silencing or chemical inhibition of p38/MAPK, NFAT5 or SGK1 abrogates the high-salt-induced TH17 cell development. The TH17 cells generated under high-salt conditions display a highly pathogenic and stable phenotype characterized by the upregulation of the pro-inflammatory cytokines GM-CSF, TNF-α and IL-2. Moreover, mice fed with a high-salt diet develop a more severe form of EAE, in line with augmented central nervous system infiltrating and peripherally induced antigen-specific TH17 cells. Thus, increased dietary salt intake might represent an environmental risk factor for the development of autoimmune diseases through the induction of pathogenic TH17 cells.
www.ncbi.nlm.nih.gov/pmc/articles/PMC2738732/
Elevated profile of Th17, Th1 and Tc1 cells in patients with immune thrombocytopenic purpura
In summary, our study demonstrates Th17 may be an important determinant in the evolution of ITP along with Th1 and Tc1, suggesting that blocking the abnormality of Th17 cells is likely to be a promising therapeutic concept for ITP.
In short, the author states that excessive iodine can cause excessive thyroid levels in certain individuals who are predisposed by an existing thyroid defect. (In most of the population, there is a very high tolerance for excessive iodine)www.thyroidmanager.org/chapter/thyrotoxicosis-of-other-etiologies/#toc-iodine-induced-hyperthyroidism [/b]
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