In some cases, excessive iodine contributes to a risk of autoimmune thyroid diseases (Hashimotos thyroiditis and Graves disease). Different experts in nutrition advise different amounts of iodine supplementation. Supplementation is typically in a product which contains roughly half iodine and half iodide (a popular product used and sold for decades is “Iodoral®” which contains 5 mg of Iodine and 7.5 mg of Iodide). On low side there is Kara Fitzgerald recommending less than 1,100 mcg per day (except when treating some medical conditions), she considers long term dosage of 40,000 mcg per day “excessive”. In the middle we have Dr. Alan Gaby who considers a “moderately high dose” to be 3,000 to 6,000 mcg per day. On the higher end we have Dr. David Brownstein, Dr. Jorge Flechas, Dr. Guy Abraham, Dr. Alan Roby and Dr. Jonathan Wright who recommend 6,000 mcg to 50,000 mcg per day. Prognosis
With iodine supplementation, goiters caused by iodine deficiency decrease in size in very young children and pregnant women. Generally, however, long-standing goiters caused by iodine deficiency respond with only small amounts of shrinkage after iodine supplementation, and patients are at risk for developing hyperthyroidism.Being pregnant while iodine-deficient additionally carries the risk of causing congenital iodine deficiency syndrome in the newborn. This disease can only be managed by lifelong administration of thyroxine (T4). Epidemiology
Iodine deficiency resulting in goiter occurs in 187 million people globally as of 2010 (2.7% of the population).
they exhibit circulating malignant pDC, anemia, thrombocytopenia, and/or leukopenia due to extensive malignant pDC infiltrations in the bone marrow. A leukemic phase of the disease is a common feature of end stage and post-therapy relapsing BPDCN. Pathophysiology
There are three types of dendritic cells, plasmacytic dendritic cells (pDC) and two types of conventional dendritic cells (cDC), myeloid cDC1 and myeloid cDC2. pDC circulate in the blood, representing <0.4% of all nucleated blood cells, and are present in various hematological tissues such as lymph nodes and spleen. Their major function is to detect and then initiate immune responses  to intracellular pathogens, particularly viruses such as the cold sore-causing Herpes simplex viruses, HIV, and hepatitis viruses but also bacteria such as the tuberculosis-causing Mycobacterium tuberculosis, fungi such as the aspergillosis-causing Aspergillus fumigatus and parasites such as malaria-causing Plasmodium falciparum. Following detection of these intracellular pathogens, pCD initiate immune responses by producing massive amounts of type I and type III interferons as well as by differentiating (i.e. maturing) into conventional dendritic cells that further promote immune responses by, e.g. functioning as antigen-presenting cells. The malignant pDC in BPDCN have the appearance of immature plasmacytoid dendritic cells. They are distinguished from other dendritic, myeloid, lymphoid and NK cell types by exhibiting at least several of the following properties: 1) plasmacytoid morphology; 2) production of large amounts of type I interferons when properly stimulated; 3) ability to differentiate into conventional dendritic cells when properly stimulated; 4) the expression of key marker proteins such as granzyme B, TCF4,  interleukin-3 receptor (i.e.