Adverse effects
It is important to monitor any symptoms of fever or sore throat while taking thiamazole; this could indicate the development of agranulocytosis, an uncommon but severe side effect resulting from a drop in the white blood cell count (to be specific, neutropenia, a deficiency of neutrophils). A complete blood count (CBC) with differential is performed to confirm the suspicion, in which case the drug is discontinued. Administration of recombinant human granulocyte colony-stimulating factor (rhG-CSF) may increase recovery. Other known side effects include:

skin rash
itching
abnormal hair loss
upset stomach
vomiting
loss of taste
abnormal sensations (tingling, prickling, burning, tightness, and pulling)
swelling
joint and muscle pain
drowsiness
dizziness
decreased platelet count (thrombocytopenia)
aplasia cutis congenita (prenatal exposure)
thyroid gland enlargement (prenatal exposure)
choanal atresia (prenatal exposure during the first trimester of pregnancy)
acute pancreatitis

Interactions
Adverse effects may occur for individuals who:

Take anticoagulants (blood thinners) such as warfarin (Coumadin), diabetes medications, digoxin (Lanoxin), theophylline (Theobid, Theo-Dur), and vitamins
Have ever had any blood disease, such as decreased white blood cells (leukopenia), decreased platelets (thrombocytopenia) or aplastic anemia, or liver disease (hepatitis, jaundice)

Mechanism of action
Thiamazole inhibits the enzyme thyroperoxidase, which normally acts in thyroid hormone synthesis by oxidizing the anion iodide (I−) to iodine (I2), hypoiodous acid (HOI), and enzyme linked hypoiodate (EOI), facilitating iodines addition to tyrosine residues on the hormone precursor thyroglobulin, a necessary step in the synthesis of triiodothyronine (T3) and thyroxine (T4). It does not inhibit the action of the sodium-dependent iodide transporter located on follicular cells basolateral membranes. Inhibition of this step requires competitive inhibitors such as perchlorate and thiocyanate.
Features include a thickening of the nerve fiber layer, a serrated appearance to the surface of the retina just beneath a thickened layer of glial tissue at the retinal-vitreous interface. Prevention
There is no good evidence for any preventive actions, since it appears this is a natural response to aging changes in the vitreous. It has been estimated that Posterior vitreous detachment (PVD) occurs in over 75 percent of the population over age 65, that PVD is essentially a harmless condition (although with some disturbing symptoms), and that it does not normally threaten sight. However, since epiretinal membrane appears to be a protective response to PVD, where inflammation, exudative fluid, and scar tissue is formed, it is possible that NSAIDs may reduce the inflammation response. Usually there are flashing light experiences and the emergence of floaters in the eye that herald changes in the vitreous before the epiretinal membrane forms. Treatment
Surgeons can remove or peel the membrane through the sclera and improve vision by 2 or more Snellen lines. Usually the vitreous is replaced at the same time with clear (BSS) fluid, in a vitrectomy. Surgery is not usually recommended unless the distortions are severe enough to interfere with daily living, since there are the usual hazards of surgery, infections, and a possibility of retinal detachment. More common complications are high intraocular pressure, bleeding in the eye, and cataracts, which are the most frequent complication of vitrectomy surgery. Many patients will develop a cataract within the first few years after surgery.