The liver also plays an important role in vitamin and mineral ( iron & copper ) storage. About 80% of the body's vitamin A stores are concentrated in fat droplets within the stellate cells of the liver. In pathological conditions like hepatic fibrosis or liver cirrhosis the stellate cells lose vitamin A, transform into fibroblasts or myofibroblasts and begin producing large amounts of collagen and adhesive glycoproteins. * Normal vitamin A reserves are enough to prevent a deficiency for about 10 months. The liver also contains about a year supply of B12. Vitamin D stores equal about 3-4 months. Small amounts of Vitamins E and K and Vitamin C are stored in the liver to facilitate liver functions.
An alternative cause of “atrophic” hypothyroidism is the development of thyroid stimulation blocking antibodies (TSBAb), which, as the name implies, prevent TSH binding to TSH-R, but do not stimulate thyroid cells and produce hypothyroidism. It has been proposed that TSBAb bind to epitopes near the carboxyl end of the TSH-R extracellular domain, in contrast to thyroid stimulating antibodies (TSAb), which bind to epitopes near aa 40 at the amino terminus(20). This syndrome occurs in neonates, children and adults. The prevalence of TSBAb in adult hypothyroid patients has been reported to be 10%(21). However, in contrast to the usual progressive and irreversible thyroid damage occurring in the usual setting, these blocking antibodies tend to follow the course of TSAb–that is, they decrease or disappear over time, and the patient may become euthyroid again(22). A change from a predominant TSAb response to a predominant TSBAb response can cause patients to have sequential episodes of hyper- and hypothyroid function(23). HLA antigens of hypothyroid patients with TSBAb were found to be different from patients with idiopathic myxedema or Hashimoto’s thyroiditis, and rather similar to patients with Graves’ disease(24).
All individuals, whether male or female, possess both female hormones (estrogens) and male hormones (androgens). During puberty, levels of these hormones may fluctuate and rise at different levels, resulting in a temporary state in which estrogen concentration is relatively high. Studies regarding the prevalence of gynecomastia in normal adolescents have yielded widely varying results, with prevalence estimates as low as 4% and as high as 69% of adolescent boys. These differences probably result from variations in what is perceived to be normal and the different ages of boys examined in the studies.