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Tamoxifen is a drug that is used as a complementary therapy for breast cancer. It is used for a period of 5 years after the end of surgery and chemotherapy and has been shown in different studies to significantly reduce the likelihood of a recurrence of the tumor.
It is marketed in the form of 10 and 20 mg tablets. The daily dose ranges between 20 and 40 mg divided into one or two doses.
Technically, it is classified as a selective modulator of estrogen receptors. Its mechanism of action is based on its antiestrogenic effect, that is, it blocks the action of this hormone that stimulates the development of tumor cells. It is not useful in all breast cancers, but only in those whose cells have specific estrogen receptors. Breast tumors are heterogeneous at the cellular level and only 60% present hormonal receptors of this type.
Its action is not limited to the breast, because different organs have receptors for estrogen. In the uterus it has paradoxically an estrogenic agonist effect and in the bone it improves the assimilation of calcium, which is why it is beneficial in osteoporosis, in the case of menopausal women. Since in the premenopausal women it can generate the opposite effect, increasing the loss of bone mineral density.
In some patients, an increase in the thickness of the innermost part of the uterus (endometrial hyperplasia) occurs as a side effect. In less than 1% of people treated can cause the onset of uterine cancer, so annual reviews are recommended to detect this condition. Other side effects are hot flashes and vaginal dryness.
Despite the adverse effects that are sometimes serious, the benefits of the drug are far superior to its disadvantages, improving the quality of life and survival of patients.
It has been seen in several studies that tamoxifen can produce an increase in transaminases (ALAT and ASAT) in blood, which are biomarkers of liver damage, the damage in hepatocytes makes these enzymes go into the bloodstream. An increase in the size of the hepatocytes was also observed, which leads to the appearance of cholestasis and steatohepatitis and there have also been cases of cholestatic jaundice and fatty liver, which may even cause the death of the patient.
In published cases, two lesion patterns predominate: cholestasis with or without cytolysis and steatohepatitis, pattern of lesion similar to that produced by estrogen.
The conclusion we reached is that although the hepatotoxicity of tamoxifen is not very frequent, it can cause chronic liver damage with or without steatohepatitis, most of the times with little clinical symptoms, so that all patients under treatment with tamoxifen for prolonged periods they must have a periodic control of liver enzymes, as a way to prevent chronic injuries.
The mechanism by which tamoxifen exerts ocular toxicity is not exactly known, but we know that it has a structure similar to that of other drugs of known ocular toxicity such as imipramine, amiodarone and chloroquine, these having polar and apolar junctions with Lipids that are not metabolized accumulate in the intracellular complexes of lysosomes.
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