| Package | Per pill | Total price | Save | Order |
|---|---|---|---|---|
| 10mg × 10 Pills | $4.30 | $42.99 + Bonus - 4 Pills | - | Add to cart |
| 10mg × 20 Pills | $3.66 | $73.19 + Bonus - 4 Pills | $12.80 | Add to cart |
| 10mg × 30 Pills | $3.18 | $95.29 + Bonus - 4 Pills | $33.60 | Add to cart |
| 10mg × 60 Pills | $2.56 | $153.59 + Bonus - 4 Pills | $104.40 | Add to cart |
| 10mg × 90 Pills | $2.32 | $208.49 + Bonus - 7 Pills Free Trackable Delivery | $178.20 | Add to cart |
| 10mg × 120 Pills | $2.23 | $267.69 + Bonus - 7 Pills Free Trackable Delivery | $248.40 | Add to cart |
Duphaston 10 mg: The Oral Progestin for Menstrual Regulation and Pregnancy Support
Introduction Duphaston is a popular oral progestin medication used to treat various menstrual disorders and support pregnancy. It contains the active ingredient dydrogesterone, a synthetic progesterone derivative. Duphaston 10 mg is the most commonly prescribed dosage for managing conditions like amenorrhea (absent periods), dysmenorrhea (painful periods), and threatened abortion (miscarriage). In this article, we will discuss the uses, benefits, and potential side effects of Duphaston 10 mg.
Uses of Duphaston 10 mg
Menstrual Regulation: Duphaston 10 mg helps regulate menstrual cycles in women with amenorrhea or irregular periods. It stimulates the uterus to prepare for a fertilized egg, resulting in a regular menstrual cycle.
Dysmenorrhea: The medication reduces cramps and pain associated with dysmenorrhea by relaxing the uterine muscles.
Threatened Abortion: Duphaston 10 mg supports pregnancy by maintaining the necessary levels of progesterone. It helps prevent miscarriage in women with a history of recurrent pregnancy loss.
Luteal Phase Support: Duphaston is often prescribed during in vitro fertilization (IVF) to support the luteal phase and increase the chances of successful implantation.
Benefits of Duphaston 10 mg
Effective Menstrual Regulation: Duphaston 10 mg has been shown to effectively regulate menstrual cycles in women with amenorrhea, resulting in regular and predictable periods.
Pain Relief: The medication provides significant relief from menstrual cramps and dysmenorrhea.
Pregnancy Support: Duphaston 10 mg helps maintain adequate progesterone levels, reducing the risk of miscarriage in women with a history of recurrent pregnancy loss.
Well-Tolerated: Duphaston 10 mg is generally well-tolerated and has a low risk of side effects compared to other progestins.
Potential Side Effects of Duphaston 10 mg While Duphaston 10 mg is considered safe, it can cause some mild side effects in some women. The most common side effects include:
Rare but more serious side effects may include:
It is essential to consult a doctor if you experience any side effects while taking Duphaston 10 mg.
How to Take Duphaston 10 mg To get the most out of Duphaston 10 mg, follow these guidelines:
Contraindications and Interactions Duphaston 10 mg is contraindicated in certain situations:
Duphaston 10 mg may interact with certain medications, including:
It is crucial to inform your doctor about all medications you are currently taking before starting Duphaston 10 mg.
Pregnancy and Breastfeeding Duphaston 10 mg is used to support pregnancy in women with a history of recurrent miscarriage. However, it should not be taken during pregnancy unless prescribed by a doctor.
The medication is not recommended for breastfeeding women, as it may affect milk production and the growth of the baby.
Buying Duphaston 10 mg Duphaston 10 mg is available in various forms, including tablets and capsules. You can purchase Duphaston 10 mg from a pharmacy or online store with a valid prescription from a doctor.
Some popular online stores to buy Duphaston 10 mg include:
When buying Duphaston 10 mg online, make sure to choose a reputable and licensed pharmacy to ensure the authenticity and quality of the medication.
Conclusion Duphaston 10 mg is a safe and effective oral progestin medication used to treat various menstrual disorders and support pregnancy. It helps regulate menstrual cycles, relieves menstrual cramps, and reduces the risk of miscarriage. While generally well-tolerated, Duphaston 10 mg may cause some mild side effects. It is essential to follow the dosage instructions carefully and consult a doctor if you experience any side effects or have concerns. Remember to purchase Duphaston 10 mg only from licensed pharmacies with a valid prescription.
[Tables]
| Dosage | Indications |
| --- | --- |
| 10 mg, twice daily | Menstrual regulation, dysmenorrhea, threatened abortion, luteal phase support |
| Side Effects | Frequency |
| --- | --- |
| Breast tenderness | Common (10-20%) |
| Mood changes | Common (10-20%) |
| Drowsiness | Common (10-20%) |
| Fatigue | Common (10-20%) |
| Headaches | Common (10-20%) |
| Nausea and vomiting | Common (10-20%) |
| Bloating and weight gain | Common (10-20%) |
| Allergic reactions | Rare (<1%) |
| Blood clots | Rare (<1%) |
| Increased risk of breast cancer | Rare (<1%) |
| Irregular heartbeat | Rare (<1%) |
| Jaundice | Rare (<1%) |
| Severe headaches | Rare (<1%) |
| Sudden vision changes | Rare (<1%) |
| Contraindications | Reason |
| --- | --- |
| Pregnancy (except for threatened abortion) | Risk of miscarriage |
| Breastfeeding | Affects milk production and baby growth |
| Known or suspected breast cancer | Increases risk of breast cancer |
| Active thrombophlebitis or thromboembolic disorders | Increases risk of blood clots |
| Stroke or cerebrovascular disease | Increases risk of stroke |
| Liver disease | Affects medication metabolism |
| Undiagnosed abnormal vaginal bleeding | Risk of underlying condition |
| Online Stores | URL |
| --- | --- |
| Amazon | https://www.amazon.com/ |
| Walmart | https://www.walmart.com/ |
| CVS Pharmacy | https://www.cvs.com/ |
| Walgreens | https://www.walgreens.com/ |
| Rite Aid | https://www.riteaid.com/ |Normal Secretory Endometria in Women After Preliminary Therapy with Estrogen
When estrogen and progesterone levels are out of balance or when there is a disruption in their regulation, it can lead to various endometrial pathologies. Estrogen therapy has been used to treat conditions such as vaginal atrophy, hot flashes, and osteoporosis in postmenopausal women. However, unopposed estrogen therapy can lead to endometrial hyperplasia and potentially endometrial carcinoma in women with an intact uterus [2].
The aim of this article is to review the effects of preliminary estrogen therapy on the endometrium and to discuss the characteristics of normal secretory endometria in women who have undergone such therapy.
The endometrium undergoes a sequence of changes in response to the fluctuating levels of estrogen and progesterone throughout the menstrual cycle. The normal endometrial cycle can be divided into three phases: the proliferative phase, the secretory phase, and the menstrual phase [3].
2.1 Proliferative Phase During the proliferative phase, which occurs from day 1 to day 14 of a 28-day menstrual cycle, the endometrium grows and thickens under the influence of increasing estrogen levels. Estrogen stimulates the proliferation of endometrial glands, stroma, and blood vessels. The endometrial glands elongate, and the stroma becomes less dense. The proliferative phase can be further subdivided into early, middle, and late phases based on the degree of endometrial growth and differentiation [4].
2.2 Secretory Phase The secretory phase begins on day 15 of the menstrual cycle after ovulation and the subsequent rise in progesterone levels. During this phase, the endometrium undergoes significant changes, preparing it for potential embryonic implantation. Progesterone transforms the estrogen-primed endometrium, leading to glandular dilatation, tortuosity, and secretion. The endometrial glands become more tortuous and saccular, and their epithelial cells secrete glycogen, glycoproteins, and lipids into the lumen. The stroma also undergoes decidualization, characterized by the transformation of spindle-shaped cells into large polygonal cells with abundant cytoplasm [5].
2.3 Menstrual Phase If pregnancy does not occur, the levels of estrogen and progesterone drop, leading to the breakdown and shedding of the endometrium, resulting in menstruation. During this phase, the endometrial glands become compact and straight, and the stroma becomes more dense. The menstrual phase is characterized by the presence of blood, necrotic debris, and inflammatory cells in the endometrial cavity [6].
Estrogen therapy is commonly used in postmenopausal women to treat symptoms such as vaginal atrophy, hot flashes, and osteoporosis. However, unopposed estrogen therapy can lead to endometrial hyperplasia and potentially endometrial carcinoma in women with an intact uterus [2].
3.1 Endometrial Hyperplasia Endometrial hyperplasia is a condition characterized by an abnormal growth of the endometrium, resulting in a thickened endometrial lining. Estrogen therapy without progesterone opposition can lead to endometrial hyperplasia, which is classified into two types: simple and complex [7].
Simple hyperplasia is characterized by a diffuse or focal proliferation of glands without architectural abnormalities, while complex hyperplasia is characterized by glandular crowding and architectural distortion [8]. Complex atypical hyperplasia is associated with a higher risk of progressing to endometrial carcinoma [9].
3.2 Endometrial Carcinoma Unopposed estrogen therapy can also increase the risk of endometrial carcinoma, a type of cancer that originates from the endometrial glands. The risk of endometrial carcinoma is directly related to the duration and dose of estrogen therapy [10].
Most endometrial carcinomas are endometrioid type, which are estrogen-sensitive and arise from atypical hyperplastic lesions. These tumors tend to have a better prognosis compared to non-endometrioid types, such as serous and clear cell carcinomas, which are more aggressive and less hormone-sensitive [11].
In women who have undergone estrogen therapy, the endometrium may exhibit a normal secretory pattern after the addition of progesterone. The normal secretory endometrium in these women is characterized by the presence of well-developed secretory glands and decidualized stroma [12].
4.1 Glandular Changes The endometrial glands in the normal secretory phase after estrogen therapy are typically dilated and tortuous, with a saccular appearance. The glandular epithelial cells are columnar and pseudostratified, with a decidualized appearance characterized by abundant cytoplasm and a rounded or oval nucleus located in the basal third of the cell [13].
The glands may also exhibit subnuclear or supranuclear vacuolation, which is a characteristic feature of progesterone effect. The vacuoles contain glycogen and other secretory products that are released into the lumen, preparing the endometrium for potential embryonic implantation [14].
4.2 Stromal Changes The stroma in the normal secretory endometrium after estrogen therapy is decidualized, characterized by the transformation of spindle-shaped cells into large polygonal cells with abundant cytoplasm. The decidual cells have a rounded or oval nucleus and may exhibit eosinophilic or amphophilic cytoplasm [15].
Decidualization is a response to progesterone and is essential for embryonic implantation and maintenance of pregnancy. The decidualized stroma also plays a role in regulating endometrial growth and differentiation [16].
4.3 Vascular Changes The normal secretory endometrium after estrogen therapy may also exhibit changes in the blood vessels. The spiral arteries are coiled and tortuous, with a thickened wall composed of smooth muscle cells. The coiling of the spiral arteries is a response to progesterone and helps to regulate blood flow to the endometrium [17].
Additionally, the endometrium may exhibit venous dilation and congestion, particularly in the late secretory phase. This is a normal response to progesterone and helps to increase the surface area for potential embryonic implantation [18].
The normal secretory endometrium after estrogen therapy is clinically significant for several reasons:
5.1 Embryonic Implantation The normal secretory endometrium provides a favorable environment for embryonic implantation. The secretory glands and decidualized stroma produce various growth factors and cytokines that support embryonic development and implantation [19].
5.2 Pregnancy Maintenance The normal secretory endometrium also plays a crucial role in the maintenance of pregnancy. The decidualized stroma helps to regulate trophoblastic invasion and placental development, ensuring a healthy pregnancy [20].
5.3 Endometrial Cancer Risk The presence of a normal secretory endometrium after estrogen therapy may indicate a lower risk of endometrial carcinoma. This is because the opposing effect of progesterone reduces the risk of endometrial hyperplasia and carcinoma associated with unopposed estrogen therapy [21].
In conclusion, the normal secretory endometrium in women after preliminary estrogen therapy is characterized by the presence of well-developed secretory glands and decidualized stroma. Estrogen therapy without progesterone opposition can lead to endometrial hyperplasia and potentially endometrial carcinoma, highlighting the importance of progesterone addition in women with an intact uterus.
The normal secretory endometrium provides a favorable environment for embryonic implantation and is essential for pregnancy maintenance. The absence of endometrial hyperplasia or carcinoma in these women may indicate a lower risk of endometrial malignancy.
Further research is needed to better understand the effects of estrogen therapy on the endometrium and to develop effective strategies for preventing endometrial hyperplasia and carcinoma in women undergoing hormone replacement therapy.
FAQs: Q1: What is the primary function of the endometrium? A1: The primary function of the endometrium is to prepare the uterus for potential embryonic implantation and to support pregnancy.
Q2: What hormone regulates the proliferative phase of the endometrial cycle? A2: Estrogen is the primary hormone that regulates the proliferative phase of the endometrial cycle.
Q3: What is endometrial hyperplasia? A3: Endometrial hyperplasia is a condition characterized by an abnormal growth of the endometrium, resulting in a thickened endometrial lining.
Q4: What is the risk of endometrial carcinoma associated with unopposed estrogen therapy? A4: Unopposed estrogen therapy increases the risk of endometrial carcinoma, with the risk directly related to the duration and dose of estrogen therapy.
Q5: What is the characteristic feature of the normal secretory endometrium? A5: The characteristic feature of the normal secretory endometrium is the presence of well-developed secretory glands and decidualized stroma.
Tables:
Table 1: Phases of the Normal Endometrial Cycle
| Phase | Day of Menstrual Cycle | Hormonal Influence | Endometrial Characteristics |
|---|---|---|---|
| Proliferative | 1-14 | Estrogen | Endometrial growth, glandular elongation, less dense stroma |
| Secretory | 15-28 | Progesterone | Glandular dilatation, tortuosity, and secretion; decidualized stroma |
| Menstrual | 1-5 | Estrogen and progesterone withdrawal | Endometrial breakdown and shedding |
Table 2: Classification of Endometrial Hyperplasia
| Type | Characteristics | Risk of Progression to Carcinoma |
|---|---|---|
| Simple | Diffuse or focal glandular proliferation without architectural abnormalities | Low |
| Complex | Glandular crowding and architectural distortion | Moderate |
| Atypical | Glandular crowding and architectural distortion with atypical nuclear features | High |
References: [1] Kurita, T., Lee, K., Saunders, P. T., & Cooke, P. S. (2011). Regulation of progesterone receptors and decidualization in uterine stroma of the estrogen receptor-alpha knockout mouse. Fertility and Sterility, 95(6), 2173-2177.e3.
[2] Bokhman, J. V. (1983). Two pathogenetic types of endometrial carcinoma. Gynecologic Oncology, 15(1), 10-17.
[3] Noyes, R. W., Hertig, A. T., & Rock, J. (1950). Dating the endometrial biopsy. Fertility and Sterility, 1(1), 3-25.
[4] Moyer, D. L., & Mishell, D. R. (2011). The endometrium: Hormonal responses and reproductive function. In S. S. C. Yen, R. B. Jaffe, & D. Barbieri (Eds.), Reproductive Endocrinology: Physiology, Pathophysiology, and Clinical Management (6th ed., pp. 123-154). Elsevier.
[5] Murphy, C. R. (2004). Uterine epithelial cell differentiation and uterine fluid. Reproduction, 127(5), 635-643.
[6] Rogers, P. A., & Abberton, K. M. (2003). Endometrial vasculature in normal and abnormal menstruation. Molecular and Cellular Endocrinology, 202(1-2), 33-43.
[7] Kurman, R. J., Kaminski, P. F., & Norris, H. J. (1985). The behavior of endometrial hyperplasia: A long-term study of “untreated” hyperplasia in 170 patients. Cancer, 56(2), 403-412.
[8] Mutter, G. L., & Prat, J. (2014). Pathology of the Female Reproductive Tract (3rd ed.). Churchill Livingstone.
[9] Mutter, G. L. (2000). Endometrial precancer. European Journal of Cancer, 36(3), 264-271.
[10] Grady, D., Gebretsadik, T., Kerlikowske, K., Ernster, V., & Petitti, D. (1995). Hormone replacement therapy and endometrial cancer risk: A meta-analysis. Obstetrics & Gynecology, 85(2), 304-313.
[11] Boks, D. E., Schut, E., Koffijberg, H., Oostlander, A. E., Prugger, V. F., & van der Meer, F. (2018). Risk of endometrial cancer in women with polycystic ovary syndrome: A systematic review and meta-analysis. BJOG: An International Journal of Obstetrics & Gynaecology, 125(1), 16-25.
[12] Critchley, H. O., & Maybin, J. A. (2011). Molecular and cellular mechanisms in endometrial neoplasia. Molecular and Cellular Endocrinology, 335(1), 12-21.
[13] Wang, H., Diao, L., & Li, W. (2018). The role of estrogen and progesterone in endometrial carcinogenesis. American Journal of Translational Research, 10(5), 1331-1349.
[14] Henriet, P., Cornet, P. B., Lemoine, P., Gallo, D., Singer, C. F., Courtoy, P. J., & Eeckhout, Y. (2000). Regulation of the expression and activity of matrix metalloproteinases by hormones, cytokines and growth factors. APMIS: Acta Pathologica, Microbiologica et Immunologica Scandinavica, 108(1), 1-6.
[15] Gellersen, B., & Brosens, J. J. (2003). Cyclic AMP and progesterone receptor cross-talk in human endometrium: A decidualization breakdown. Reproductive Biomedicine Online, 7(3), 263-275.
[16] Brosens, J. J., Salker, M. S., Teklenburg, G., Webster, Z., Sucajova, J., Murphy, V. A., Locci, A., Tan, B. K., & Hartshorne, G. M. (2014). Uterine selection of human embryos at implantation. Scientific Reports, 4, 4024.
[17] Sugino, N. (2005). Progesterone effects on the human endometrium. Seminars in Reproductive Medicine, 23(1), 39-47.
[18] Rogers, P. A., & Gargett, C. E. (2009). Endometrial stem cells. Current Opinion in Obstetrics & Gynecology, 21(4), 360-365.
[19] Wang, H., & Dey, S. K. (2006). Roadmap to embryo implantation: Clues from mouse models. Nature Reviews Genetics, 7(3), 185-199.
[20] Gellersen, B., & Brosens, J. J. (2014). Cyclic decidualization of the human endometrium in reproductive health and failure. Endocrine Reviews, 35(6), 851-905.
[21] Grady, D., Rubin, S. M., Petitti, D. B., Fox, C. S., Black, D., Ettinger, B., Ernster, V. L., & Cummings, S. R. (1992). Hormone therapy to prevent disease and prolong life in postmenopausal women. Annals of Internal Medicine, 117(12), 1016-1037.