TG and hematocrit: Subsequently, there is a compensatory increase in TSH secretion that maintains the thyroid with a sufficient reserve until it is overwhelmed by massive thyroid follicle destruction and fibrosis, both by cytotoxic T cells (Th1) and by increased levels of antibodies against thyroid peroxidase (TPO) and thyroglobulin (Tg) (Th2-related IgG4), which arise after chronic immune stimulation (over a number of years), resulting in thyroid failure (HT) [224].