Destrogen

Generally refers to the 17-beta-isomer of estradiol, an aromatized C18 steroid with hydroxyl group at 3-beta- and 17-beta-position. Destrogen-17-beta is the most potent form of mammalian estrogenic steroids. In humans, it is produced primarily by the cyclic ovaries and the placenta. It is also produced by the adipose tissue of men and postmenopausal women. The 17-alpha-isomer of estradiol binds weakly to estrogen receptors (receptors, estrogen) and exhibits little estrogenic activity in estrogen-responsive tissues. Various isomers can be synthesized.

Oral

Menopausal hormone replacement therapy

Adult: In menopausal women: 10-20 mcg daily in conjunction with a progestogen in women with uterus.

Oral

Female hypogonadism

Adult: 10-50 mcg daily in a cyclical regimen.

Oral

Palliative treatment of breast carcinoma

Adult: In postmenopausal women: 0.1-1 mg tid.

Oral

Palliative treatment of prostatic carcinoma

Adult: 0.15-3 mg daily.

Oral

As part of combined oral contraceptive

Adult: As the oestrogenic component of combined oral contraceptive: 20-40 mcg/day.

Oral

Menopausal hormone replacement therapy

Adult: In menopausal women: 10-20 mcg daily in conjunction with a progestogen in women with uterus.

Oral

Female hypogonadism

Adult: 10-50 mcg daily in a cyclical regimen.

Oral

Palliative treatment of breast carcinoma

Adult: In postmenopausal women: 0.1-1 mg tid.

Oral

Palliative treatment of prostatic carcinoma

Adult: 0.15-3 mg daily.

Oral

As part of combined oral contraceptive

Adult: As the oestrogenic component of combined oral contraceptive: 20-40 mcg/day.

Estrogens should not be used in individuals with any of the following conditions:

1. Undiagnosed abnormal genital bleeding.

2. Known, suspected, or history of cancer of the breast.

3. Known or suspected estrogen-dependent neoplasia

4. Active deep vein thrombosis, pulmonary embolism, or history of these conditions.

5. Active or recent (e.g., within the past year) arterial thromboembolic disease (e.g., stroke, myocardial infarction).

6. Liver dysfunction or disease.

7. EstroGel therapy should not be used in patients with known hypersensitivity to its ingredients.

8. Known or suspected pregnancy. There is no indication for EstroGel in pregnancy. There appears to be little or no increased risk of birth defects in children born to women who have used estrogens and progestins from oral contraceptives inadvertently during early pregnancy.

Concurrent use with hepatic enzyme inducers e.g. barbiturates, primidone, phenobarbitone, phenytoin, phenylbutazone, rifampicin, carbamazepine and griseofulvin may affect contraceptive efficacy. Short courses of broad-spectrum antibiotics may also reduce the efficacy of the oral contraceptive. Concurrent use with HIV protease and non-nucleoside reverse transcriptase inhibitors may affect hepatic metabolism of gestodene and/or Destrogen. May increase plasma concentrations of ciclosporin and decrease the serum levels of lamotrigine. Concurrent use with felbamate may increase the clearance of gestodene. Gestodene may increase serum levels of buprenorphine. Co-trimoxazole, miconazole and etoricoxib may increase serum levels of Destrogen. Aprepitant, modafinil and bosentan may reduce the serum levels of Destrogen. Metabolism of omeprazole may be inhibited by Destrogen. GI absorption of Destrogen may be increased by concurrent admin of paracetamol.

Food Interaction

Concurrent treatment with St John’s wort may reduce efficacy of the oral contraceptive.

Menstrual irregularities; headache, dizziness; breast discomfort; gynaecomastia; depression; disturbance of appetite; wt changes; fluid retention; oedema; changes in libido; hair loss or hirsutism; GI disturbances (nausea and vomiting); genitourinary changes; haematologic disorders; endocrine and metabolic disorders; cholestatic jaundice; local skin reactions; chorea; contact lens intolerance; steeping of corneal curvature; pulmonary thromboembolism; carbohydrate and/or glucose intolerance; depression; chloasma; BP increase, liver impairment; reduced menstrual loss, ’spotting’ in early cycles, absence of withdrawal bleeding; rarely photosensitivity; increased risk in breast cancer; elevation of plasma bound iodine, cortisol and thyroid binding, erythrocyte sedimentation may be accelerated; increases in plasma copper, iron and alkaline phosphatase; may affect serum triglyceride and lipoprotein levels; retinal vascular thrombosis.

Potentially Fatal: Hepatic tumours; increased risk of thromboembolism.