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Duphaston (Dydrogesterone)

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Generic Duphaston is an orally active progestogen which acts directly on the uterus, producing a complete secretory endometrium in an estrogen-primed uterus. At therapeutic levels, Generic Duphaston has no contraceptive effect as it does not inhibit or interfere with ovulation or the corpus luteum. Furthermore, Generic Duphaston is non-androgenic, non-estrogenic, non-corticoid, non-anabolic and is not excreted as pregnanediol.

Other names for this medication:

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Also known as:  Dydrogesterone.


Generic Duphaston is an orally active progestogen which acts directly on the uterus, producing a complete secretory endometrium in an estrogen-primed uterus. At therapeutic levels, Generic Duphaston has no contraceptive effect as it does not inhibit or interfere with ovulation or the corpus luteum. Furthermore, Generic Duphaston is non-androgenic, non-estrogenic, non-corticoid, non-anabolic and is not excreted as pregnanediol.

Generic name of Generic Duphaston is Dydrogesterone.

Duphaston is also known as Dydrogesterone.

Brand name of Generic Duphaston is Duphaston.


The dosage schemes below are meant as general recommendations. For optimal therapeutic effect, the dosages are to be adapted to the nature and severity of the disorder.

In irregular cycles due to endogenous progesterone deficiency

Generic Duphaston 5 to 10 mg is recommended especially in irregular cycles due to shortened luteal phase (ie pre-menopause). Treatment should be repeated for several cycles.

In secondary amenorrhoea

Administration of Generic Duphaston in combination with an estrogen is usually recommended as in these conditions endogenous progesterone deficiency is nearly always accompanied by estrogen deficiency. 0,05 mg ethinylestradiol is administered each day from the 1st to the 25th day of the cycle, and 5 mg Generic Duphaston is added twice daily from the 11th to the 25th day. Five days after the subsequent withdrawal bleeding, the same is repeated to imitate a natural cycle.

In dysfunctional uterine bleeding

The symptomatic treatment is aimed at stopping the bleeding and including a subsequent withdrawal bleeding.

To stop bleeding: Generic Duphaston 10 mg together with 0,10 mg ethinylestradiol twice daily for 5 to 7 days.

To prevent heavy bleedings: Generic Duphaston 5 mg twice daily from day 11 to day 25 of the cycle, if necessary, combined with an estrogen during the first half of the cycle.

In post-menopausal complaints

If for the symptomatic treatment of post-menopausal complaints estrogens are used (hormone replacement therapy A?A?A? HRT), Generic Duphaston 10 mg is used to counteract the effects of unopposed estrogens on the endometrium. A subsequent withdrawal bleeding is induced.

On continuous estrogen therapy: Generic Duphaston 10 mg twice daily during the first 12 to 14 days of each calendar month.

On cyclic estrogen therapy: Generic Duphaston 10 mg twice daily during the last 12 to 14 days of the treatment.

If you want to achieve most effective results do not stop taking Generic Duphaston suddenly.


If you overdose Generic Duphaston and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Duphaston overdosage: diarrhea, stomach pain, hot and dry skin, confusion, uneven heart rate, extreme thirst, increased urination, leg discomfort, and muscle weakness or limp feeling.


Store at room temperature below 25 degrees C (77 degrees F) away from moisture, light and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Duphaston are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Duphaston if you are allergic to Generic Duphaston components.

It is unknown how Generic Duphaston affects pregnant women or nursing mother.

Do not take Generic Duphaston if you have undiagnosed vaginal bleeding or a history of thromboembolic disorders.

Be careful with Generic Duphaston if you have cardiovascular, renal or hepatic impairment, diabetes mellitus, asthma, epilepsy and migraine, history of mental depression.

Drug interactions can result in unwanted side effects or prevent a medicine from doing its job. Some medicines or medical conditions may interact with this medicine. Inform your doctor or pharmacist of all prescription and over-the-counter medicine that you are taking.

Do not stop taking Generic Duphaston suddenly.

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Development of endometrial glands corresponded to an early secretory phase in five out of six cases supplemented with DG (out-phase). In contrast, five out of six cases treated with micronized progesterone showed an endometrium corresponding to a mid-luteal phase (in-phase) (P = 0.021 versus DG). There was a significant difference in the mean progesterone value [8.6 versus 0.3 microg l(-1) (P = 0.013)], the mean LH value [12.9 versus 22.5 IU l(-1) (P = 0.049)] and the mean FSH value [13.0 versus 23.9 IU l(-1) (P = 0.047)] between the progesterone and DG group, respectively, on day 21 of the cycle.

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In this pilot study, sexual desire in transsexual women improved significantly after treatment with the testosterone patch, without noticeable side effects.

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After 12 months of the transdermal HT, a decrease in both fasting (P < 0.002) and postprandial (P < 0.05) plasma glucose levels was observed. Oral HT reduced only the fasting plasma glucose level in the 12th month of treatment (P < 0.05). Regardless of the route of administration, HT reduced postprandial plasma levels of insulin (oral HT: P < 0.05; transdermal HT: P < 0.02). Fasting plasma levels of GIP were reduced after 6 and 12 months of transdermal HT (P < 0.002 and P < 0.001, respectively). Moreover, levels of postprandial GIP were reduced after 6 and 12 months of transdermal HT (P < 0.002 in both cases). Fasting and postprandial GLP-1 levels were reduced by transdermal HT after 12 months of supplementation. Oral HT also decreased these levels, but not significantly. The observed differences may, however, be related not only to the route of administration, but also to the difference in the dose of estradiol. Regardless of the route of administration, HT did not influence plasma levels of CCK.

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The only adverse endometrial outcome at the end of the study was one case of simple hyperplasia. This gives an overall incidence of 0.27% (95% CI: 0.01-1.48%) in the per protocol sample (n=395). The overall rate of amenorrhoea in the full sample (n=446) was 68% and 14% had only one or two bleeding/spotting episodes. The rate of amenorrhoea in months 10-12 (n=413) was 88%. The number of bleeding/spotting days per cycle fell during the study. The mean number of bleeding/spotting days was 5.8 and the mean number of days without bleeding was 358.2. Spotting alone was the most prevalent bleeding intensity, whilst heavy bleeding was rare.

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The women were randomised to receive continuous 17 beta-oestradiol, either orally (2 mg daily; n = 35) or transdermally (50 micrograms daily; n = 35), plus 10 mg dydrogesterone daily for 14 days of each 28-day cycle; or 2.5 mg tibolone daily (n = 35). Thirty-five untreated women acted as controls.

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Within 15 months of 17 beta-estradiol and dydrogesterone treatment no clinically relevant differences were found in the M-mode, quantitative 2-dimensional, and Doppler echocardiographic parameters measured in this study. It is suggested that 15 months of treatment probably is too short a period for detection of direct effects on the heart itself.

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We have observed different kind of hormonal reaction according to FSH, LH, estradiol and progesterone levels due to various hormonal replacement therapy. The administration of various HRT regimens presented with a decrease in the blood concentration of estradiol E2 and progesterone and a concomitant increase of FSH and LH. These findings demonstrate a shift to physiological ranges and a simultaneous improvement of symptoms associated with CI-POF.

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Combined sequential HRT with progestogen given for 12-14 days very rarely fails to protect the endometrium. Such failures can not be detected by noting the bleeding pattern. The only suspicious pattern is non-cyclic bleeding, but this will not detect every case of hyperplasia or persistent proliferative endometrium.

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Lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerosis. Serum Lp(a) concentrations increase after menopause, and postmenopausal estrogen replacement appears to decrease Lp(a) levels. In a randomized, double blind study, we examined the effects of 6-month treatment with daily 17 beta-estradiol (E2; 2 mg, orally) continuously combined with one of four dosages [2.5 mg (n = 41), 5 mg (n = 38), 10 mg (n = 38), and 15 mg (n = 20)] of dydrogesterone on fasting serum Lp(a) concentrations in 137 healthy postmenopausal women. At baseline, no significant differences were noted among the four treatment groups. During the study period of 6 months the median serum Lp(a) concentration decreased significantly from 128 mg/L (range, 5-1660) to 110 mg/L (range, 1-1530) in the total population, corresponding to a reduction of 13% (P < 0.001). The percent changes in serum Lp(a) correlated positively with the percent changes in serum E2 at 3 as well as 6 months of therapy (r = 0.38; P < 0.001 and r = 0.35; P < 0.001, respectively). A dose response of dydrogesterone on serum Lp(a) was not found. In addition, serum lipids and (apo)lipoproteins improved significantly in all four treatment groups. In conclusion, oral E2 continuously combined with dydrogesterone has beneficial effects on the lipid and lipoprotein profile and is effective in lowering Lp(a) concentrations in postmenopausal women.

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Although the minimal dose of 17beta-estradiol in hormone replacement regimens was originally considered to be 2 mg/day, it is now increasingly accepted that a lower dose of 1 mg/day is effective in protecting women from the detrimental effects of the menopause. A 1-year, multicentre, double-blind, randomised study was conducted in 214 healthy postmenopausal women in order to assess the effect of 17beta-estradiol (1 mg/day) continuously combined with dydrogesterone (5, 10 or 20 mg/day) in preventing bone loss. Bone mineral density (BMD) was evaluable in 177 women who completed the study. In all women, a statistically significant increase from baseline in lumbar vertebrae (L2-L4) BMD was seen after 6 months ( + 2.4%; p < 0.01); this increase was somewhat greater after 12 months ( + 3.6%; p < 0.01). Similar effects were seen in the hip. After 6 months, BMD in the femoral neck, Ward's triangle and trochanter had increased by 0.20% (not significant [n.s.]), 0.32% (n.s.) and 1.08% (p < 0.01), respectively, compared with baseline. Greater increases were again seen after 12 months ( + 1.16%, + 1.62% and + 2.83%, respectively), all of which were statistically significant (p < 0.01) compared with baseline. The change in BMD from baseline did not differ significantly between the three dydrogesterone dosages for either L2-L4 or hip. All dosages were well-tolerated and amenorrhoea was achieved in over 70%. In conclusion, 17beta-estradiol (1 mg/day) continuously combined with dydrogesterone (5, 10 or 20 mg/day) results in a significant increase in lumbar vertebrae and hip BMD in postmenopausal women. The lower dose of oestrogen and the avoidance of cyclical bleeding make this a particularly suitable regimen for the prevention and treatment of osteoporosis in older women.

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Fifty-nine women completed the study. After 6 months of therapy, homocysteine concentrations showed a statistically significant reduction in the treated groups versus both baseline and controls, and no further significant variations were found thereafter. The mean reduction in the homocysteine levels throughout the study was 13.6% in the oral and 8.9% in the transdermal group, respectively, without significant difference between the two routes of estradiol administration. Women with the highest baseline levels of homocysteine experienced the greatest reduction. No significant variations in homocysteine concentrations were found in the control group.

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To assess serum lipid and lipoprotein concentrations and oral glucose tolerance in postmenopausal women treated with 17 beta-oestradiol (2 mg/day) and cyclical dydrogesterone (10 mg/day for 14 days per 28 day cycle).

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Healthy postmenopausal women.

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Both the natural and surgical menopause patients were found to have more favorable lipid profiles after treatment with estrogen progesterone combined formulations and estrogen only replacement.

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The objective of this open, longitudinal, controlled study was to assess the effect of transdermal estradiol alone or combined with cyclical dydrogesterone on the markers of cardiovascular disease (CVD) risk in postmenopausal women with type 2 diabetes. The control group consisted of postmenopausal diabetic women who declined menopausal hormone replacement therapy (HRT). Twenty-eight postmenopausal women (19 on HRT and 9 controls) with type 2 diabetes were followed up for 12 months. From the active treatment group 14 women with a uterus in situ had 80 microg/24 hr transdermal estradiol (Fematrix 80; Solvay Healthcare Ltd, Southampton, UK) and oral dydrogesterone 10 mg daily for the first 12 days of the calendar month, whereas 5 women with previous hysterectomy had 80 microg/24 hr transdermal estradiol (Fematrix 80) alone. CVD risk markers were measured before and at regular intervals after starting HRT. The main outcome measures were weight, systolic and diastolic blood pressure, fasting plasma glucose, glycated hemoglobin (HbA1c), glucose/insulin ratio, total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, triglycerides, lipoprotein (a), high-sensitivity C-reactive protein (hs-CRP), fibrinogen, and endothelin-1. Transdermal estradiol with or without dydrogesterone in women with type 2 diabetes did not adversely affect any of the measured markers of cardiovascular risk. There was a significant decrease in HbA1c, total cholesterol, and LDL cholesterol at 6 months in women receiving HRT. Some of the cardiovascular disease risk markers may improve in postmenopausal women with type 2 diabetes with transdermal estradiol. This effect may have important clinical implications and it deserves further investigation in appropriately designed trials.

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Estrogen/gestagen replacement therapy prevents excess bone loss in postmenopausal women. The mode of action by which these sex steroids exert their anabolic effects on bone has not been completely clarified yet. In this study, 17 beta-estradiol (E2), as well as progestins progesterone (P), dydrogesterone (DD), 20 alpha-dihydroxydydrogesterone (DHD), medroxyprogesterone acetate (MPA), and cyproterone acetate (CPA) were able to stimulate the mitogenesis and differentiation of normal adult human osteoblast-like (HOB) cells harvested from female trabecular bone explants. The different progestins exerted a more pronounced stimulatory effect on HOB proliferation than E2 did. The combination of E2 with P, DD, or DHD did not result in a statistically significant further increase of HOB proliferation, as compared with the progestins alone. In general, E2 showed a stronger differentiation-inducing effect than the progestins, as measured by histochemical staining of the HOB cells for alkaline phosphatase activity. Combining E2 and the progestins did not result in a further increase of the number of alkaline phosphatase positive cells, compared with E2 alone. The different progestins proved to be equally potent in stimulating HOB proliferation and differentiation. In conclusion, progestins as well as E2 exerted anabolic but differential effects on normal adult human osteoblasts in vitro.

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Estraderm TTS 100 micrograms twice weekly is as effective as 200 micrograms twice weekly in reducing symptom levels in severe premenstrual syndrome but is better tolerated. Estraderm 100 micrograms suppresses ovulation and results in a mean plasma oestradiol level similar to that observed in a spontaneous cycle.

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Abstract Background Ultra-low-dose estradiol is known to improve menopausal symptoms and increase bone mineral density. However, the effect of ultra-low-dose estradiol on vascular function has not been clarified. Objectives We examined the effects of ultra-low-dose estradiol on brachial-ankle pulse wave velocity (baPWV) and circulating markers of cardiovascular risk. Patients and methods Twenty-eight postmenopausal women were enrolled in this study. Fourteen women received oral estradiol (0.5 mg) and dydrogesterone (5 mg) every day for 12 months (ultra-low-dose group) as hormone replacement therapy (HRT) and 14 women as a control group did not receive HRT. The baPWV, lipid profiles, homeostasis model assessment of insulin resistance (HOMA-IR) and vascular inflammatory markers were measured. Results The baPWV level significantly decreased in the ultra-low-dose group (p = 0.037), while the baPWV level did not significantly change in the control group. HOMA-IR tended to decrease in the ultra-low-dose group (p = 0.076). Systolic blood pressure and diastolic blood pressure did not change significantly in either group. Conclusion An HRT regimen using oral ultra-low-dose estradiol and dydrogesterone has an effect on arterial stiffness and insulin resistance.

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Congenital heart disease is the most frequent form of congenital anomaly in newborn infants and accounts for more than a quarter of all serious congenital afflictions worldwide. A genetic etiology is identified in <20 % of cases of congenital heart defects, and in most cases the etiology remains a mystery. In the context of the health burden caused by congenital heart disease, the contribution of non-inherited risk factors is important especially if it turns out to be caused by a drug which can be avoided during pregnancy. We sought to determine whether maternal dydrogesterone treatment in early pregnancy is associated with congenital heart disease in the infant. We conducted a retrospective case-control study of birth defects and associated risk factors. Data were obtained and compared between 202 children born with congenital heart disease and a control group consisting of 200 children. All children were born in the period of 2010-2013. Dydrogesterone exposure was defined as any reported use during the first trimester of pregnancy. Exclusion criteria included stillbirths, children with chromosomal abnormalities and infants of mothers with chronic medical illnesses, e.g., diabetes. Binary logistic regression analyses were used to analyze the data and attempt to identify a causal relationship between drug exposure and congenital heart disease. Mothers of children born with congenital heart disease received more dydrogesterone during first trimester of pregnancy than mothers of children in the control group [adjusted odds ratio 2.71; (95 % CI 1.54-4.24); P = 0.001]. We identified a positive association between dydrogesterone usage during early pregnancy and congenital heart disease in the offspring. Nevertheless, further studies are needed to confirm these results.

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Dydrogesterone is widely used for menstrual disorders, endometriosis, threatened and habitual abortion and postmenopausal hormone replacement therapy. Although progestins have a promiscuous nature, dydrogesterone does not have clinically relevant androgenic, estrogenic, glucocorticoid or mineralocorticoid activities. To date, systematic biochemical characterization of this progestin and its active main metabolite, 20α-dihydrodydrogesterone, has not been performed in comparison to progesterone. The objective of this study was to evaluate the selectivity and potential androgenic/antiandrogenic effects of dydrogesterone and its metabolite in comparison to progesterone and medroxyprogesterone acetate by analyzing their interference with AR signaling in vitro. We characterized dydrogesterone and its metabolite for their binding and transactivation of androgen and other steroid hormone receptors and for their potential inhibitory effects against androgen biosynthetic enzymes, 17β-hydroxysteroid dehydrogenase types 3 and 5 and 5α-reductase types 1 and 2. We found that dydrogesterone resembled progesterone mainly in its progestogenic effects and less in its androgenic, anti-androgenic, glucocorticoid and antiglucocorticoid effects; whereas, 20α-dihydrodydrogesterone showed reduced progestogenic potency with no androgenic, glucocorticoid and mineralocorticoid effects. Effects on the androgen and glucocorticoid receptor differed depending on the technology used to investigate transactivation. Progesterone, but not dydrogesterone and 20α-dihydrodydrogesterone, exerted anti-androgenic effects at the pre-receptor level by inhibiting 5α-reductase type 2. Dydrogesterone, 20α-dihydrodydrogesterone and progesterone inhibited the biosynthesis of testosterone catalyzed by 17β-hydroxysteroid dehydrogenase types 3 and 5; however, due to their micromolar K(i) values, these activities appeared to be not of relevance at therapeutic levels. Overall, our data show that the anti-androgenic potential of dydrogesterone and 20α-dihydrodydrogesterone is less pronounced compared to progesterone.

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To establish reference estimates of the effects of different hormone replacement therapy (HRT) regimens on lipid and lipoprotein levels.

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Long-term combined hormone replacement therapy with E2 and dydrogesterone in healthy women was associated with sustained improvement in some aspects of endothelial function and in clottable fibrinogen levels.

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Fibrinogen was reduced in both groups but more markedly in the DYDR group. Factor VIIc activity levels decreased in both groups with a greater change in the T-group. Factor VII antigen was increased in both groups with a greater increase in the DYDR group. Factor VIIa was increased in the DYDR group only. Plasminogen levels were also increased in both groups with a greater increase in the T-group. There were no statistically significant changes in lipid variables between the different regimens. Changes in total cholesterol and LDL cholesterol were correlated positively with changes in factor VIIc in the DYDR group and negatively with changes in factor VIIc in the T-group. Trigemestone was associated with a better bleeding pattern.

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Gestational hypertension (GH) remains one of the main causes of high maternal and perinatal morbidity and mortality worldwide with the highest incidence among primigravidae of about 10%-15%. However, it was noted that the incidence of GH in primigravidae who conceived following assisted reproductive technique (ART) or intrauterine insemination (IUI) supplemented with dydrogesterone during the first trimester was low.

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The peak of progesterone concentration was assessed in the midluteal phase (7th day) in both supplemented groups, significantly higher than in the placebo group, also in group with dydrogesterone and HCG it was higher than in group with dydrogesterone alone. Progesterone concentration decrease on the 11th day after the ovulation to the values comparable with the placebo group.

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The study enrolled 81 patients aged 18 to 50 years with stage III or IV endometriosis, as diagnosed by surgery. All patients were given GnRHa 3.6 mg by subcutaneous injection once every 28 days for a total of three times. Patients were divided into three groups: the first (n = 35; GnRHa only group) received GnRHa only without add-back therapy, the second (n = 35; 0.5 mg E(2)+P add-back group) received GnRHa plus 0.5 mg estradiol valerate and 5 mg dydrogesterone orally every day, and the third (n = 11; 1 mg E(2)+P add-back group) received GnRHa plus 1 mg estradiol valerate and 10 mg dydrogesterone orally every day for the duration of treatment. All patients were required to follow up at our hospital at 4, 8 and 12 weeks after treatment initiation to assess efficacy and levels of serum reproductive hormones.

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A randomized placebo controlled trial in which a methionine-loading test was performed, in 25 healthy postmenopausal women, before and after a 12-week oral treatment with placebo or daily 4 mg 17beta-estradiol with (HRT) or without (ERT) 10 mg dydrogesterone. Fasting and post-load homocysteine as well as Vitamins B(6), B(12) and folate were determined.

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To determine the effectiveness of both the progestagens and anti-progestagens in the treatment of painful symptoms ascribed to the diagnosis of endometriosis.

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The progestagen medroxyprogesterone acetate (100 mg daily) appeared to be more effective at reducing all symptoms up to 12 months of follow-up (MD -0.70, 95% CI -8.61 to -5.39; P < 0.00001) compared with placebo. There was evidence of significantly more cases of acne (six versus one) and oedema (11 versus one) in the medroxyprogesterone acetate group compared with placebo. There was no evidence of a difference in objective efficacy between dydrogesterone and placebo.There was no evidence of a benefit with depot administration of progestagens versus other treatments (low dose oral contraceptive or leuprolide acetate) for reduced symptoms. The depot progestagen group experienced significantly more adverse effects.There was no overall evidence of a benefit of oral progestagens over other medical treatment at six months of follow-up for self-reported efficacy. Amenorrhoea and bleeding were more frequently reported in the progestagen group compared with other treatment groups.There was no evidence of a benefit of anti-progestagens (gestrinone) compared with danazol. GnRH analogue (leuprorelin) was found to significantly improve dysmenorrhoea compared with gestrinone (MD 0.82, 95% CI 0.15 to 1.49; P = 0.02) although it was also associated with increased hot flushes (OR 0.20, 95% CI 0.06 to -0.63; P = 0.006).

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Pharmacological regulation of transcription of estrogen-converting enzymes in human endometrium cultured in nude mice may help to develop new therapeutic concepts based on local regulation of estrogen metabolism in endometriosis.

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duphaston buy usa 2015-09-23

Plasma fasting homocysteine concentrations are lowered by E2-dydrogesterone therapy in buy duphaston postmenopausal women.

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To investigate the effects of 1 mg 17beta-estradiol continuously combined with 2.5, 5, 10, or 20 mg dydrogesterone on the buy duphaston serum lipid profile of postmenopausal women.

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Healthy postmenopausal buy duphaston women.

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While phase I and phase II drug metabolites are important for drug development and toxicity studies, e.g. in the context of metabolites in safety testing (MIST), they are often not commercially available and their classical chemical synthesis can be cumbersome. Therefore, a biotechnological production of drug metabolites using microorganisms that recombinantly express human enzymes has been established in recent years. However, no whole-cell biotransformations that make use of human aldo-keto reductases (AKRs) have yet been reported. In this study, we have functionally expressed human AKR1C1 (20α-hydroxysteroid dehydrogenase) in the fission yeast Schizosaccharomyces pombe and demonstrate the ability of the resulting yeast strain to efficiently catalyze the reduction of progesterone or dydrogesterone to 20α-dihydroprogesterone (20α-DHP) and 20α-dihydrodydrogesterone (20α-DHD), respectively. The formation of any by-products or the occurrence of a back reaction were not detected. Seven other steroids with a 20-keto group (pregnenolone, 17α-hydroxyprogesterone, 11-deoxycortisol, cortisol, 11-deoxycorticosterone, corticosterone, and aldosterone) were not reduced by this system. At shaking flask scale we obtained conversion rates of 90 (±26) μM/d 20α-DHP and 244 (±93) μM/d 20α-dihydrodydrogesterone (20α-DHD), respectively. In a fed-batch fermentation under optimized reaction conditions an average 20α-DHP production rate of 300 μM/d was determined for a total biotransformation time of 72 h. We thus established an AKR-dependent whole-cell biotransformation process buy duphaston that can be used for production of human AKR metabolites on a large scale.

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No significant national differences existed in the pretreatment levels of lipids and lipoproteins. Mean cholesterol, LDL, Lp(a), and triglycerides decreased during HRT, and HDL and HDL2 increased. Individual changes in responses to HRT were strongly dependent on pretreatment values. In this regard, British buy duphaston women differed from the others: their cholesterol, HDL, HDL2, and Lp(a) responses, when related to the pretreatment levels, were smaller than those of the others.

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Hysteroscopic and histopathologic endometrial study by commune and immunohistochemical techniques on 2 groups of menopausal women on HRT-sequential (24 months) and continuous combined (12 months) compared to pretherapy or a control untreated group showed the changes of endometrial superficial microvascular net-work, with new blood vessels and ecquimosis/subepithelial haemorrhages. Endometrial neoangiogenesis varied according to progestogens/progesterone: type (less on dydrogesterone, more important on cyproterone acetate, medroxyprogesterone acetate, norethisterone), dose (large doses of medroxyprogesterone acetate induce greater changes in sequential buy duphaston HRT, and small doses induce less changes), time (minimum when progestogen is cyclic at 3 months). The vascular changes are more accentuate in the first year of HRT. The correlation between the number of new vessels and type of endometrial pathology showed that the neoangiogenesis is greater in secretory and atrophic endometrium.

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Both oestrogen-only and oestrogen-progestogen HRT may reduce ACE activity buy duphaston in blood. Oestrogen and progestogen may exhibit additive effects on blood ACE activity.

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Compared with conservative management, dydrogesterone had beneficial effects on maintaining pregnancy in women with threatened miscarriage. buy duphaston

duphaston tablet dosage 2015-05-26

Thirty-two (32) menopausal women were entered into the study (16 in each treatment group), of whom 24 completed the study. The objectives were to compare the long-term efficacy and the local and systemic tolerance of Menorest and Premarin in the control of menopausal symptoms, and the prevention of bone loss. After a 4-week treatment-free run-in period, patients were treated with continuous estrogen therapy (a twice weekly application with Menorest 50 or a daily oral administration of Premarin 0.625 mg) for one year. Patients were also given 20 mg oral Dydrogesterone per day for the last 12 days of each 28 day cycle of treatment. The main efficacy criterion was the reduction in the mean number of hot flushes per day at 12 months compared to baseline. This study was also considered as a pilot study to collect data on changes in the bone mineral density of the lumbar spine (L1-L4) assessments from baseline to week 30 and week 56. Menorest and Premarin were equally effective in the relief of menopausal symptoms over the 1-year period of treatment. The mean number of hot flushes per day decreased from 6.9 at baseline to 0.5 at 12 weeks and 0.1 at 12 months in the Menorest group, and from 7.0 to 0.3 and 0.0 in the Premarin group. Regarding the lumbar spine and hip densitometry results, Menorest prevented bone loss to the same extent as Premarin. This data confirms the positive action of estrogen, with oral in addition to transdermal administration on both trabecular and cortical BMD over 1 year of treatment. Tolerance was similar, with approximately the same number of patients with AEs, severe AEs and related to study drug AEs in both groups. There was one serious AE (breast carcinoma) diagnosed after 6-months of treatment. Chemotherapy and radiotherapy was initiated prior to surgery. According to the investigator it was not related to study drug and must have been present prior to study start. Menorest 50 and Premarin 0.625 were equally effective over the 1-year treatment period in reducing the mean number of hot flushes and the severity score of menopausal symptoms, including vasomotor, psychological and urogenital buy duphaston symptoms.

duphaston dosage 2016-12-03

To investigate the regulation buy duphaston of estrogen-converting enzymes in human ectopic endometrial tissue.

duphaston 10mg tablet 2017-11-22

Randomised or quasi-randomised controlled trials, including cluster-randomised trials, with or without full text, comparing Chinese herbal medicines (alone or buy duphaston combined with other intervention or other pharmaceuticals) with placebo, no treatment, other intervention (including bed rest and psychological support), or other pharmaceuticals as treatments for unexplained recurrent miscarriage. Cross-over studies were not eligible for inclusion in this review.

duphaston capsule 2015-06-07

Evidence is increasing suggesting that adding progestogens to estrogens can increase the risk of breast cancer. However, our experimental data as a result of scientific collaboration between university of Tuebingen, Germany, and university of Beijing, China, comparing all available progestogens used in hormone therapy and hormonal contraception present high evidence that there may be differences regarding breast cancer risk. Especially of concern may be to differentiate between primary and secondary risk i.e. between the effect of on benign and malignant breast epithelial cells suggesting differences in primary risk and risk in patients after breast cancer. Of importance also is that in contrast to natural progesterone the apocrine impact of stromal growth factors and also certain cell components of breast epithelial cells can strongly increase proliferation rates of some (but not all. synthetic progestogens which can lead to clinical cancer before (in contrast to estrogen-only therapy. carcinoprotective mechanisms can work. Regarding clinical data, epidemiological studies and especially the Women's Health Initiative, so far the only prospective placebo-controlled study, demonstrate an increased risk under combined estrogen/progestogen-, but not under estrogen-only therapy. However, up to now the clinical studies cannot discriminate between the various progestogens mostly due to too small patient numbers in the subgroups, and in most studies either medroxyprogesterone acetate or norethisterone have been used. However, there is evidence that the natural progesterone and dydrogesterone, possibly also the transdermal usage of synthetic progestogens, may have less risks buy duphaston , but this must be proven in further clinical trials.

duphaston missed dose 2016-02-18

Insulin-like growth factor I (IGF-I) has a role in the whole-body anabolism and promotes both normal and abnormal cell growth in several tissues. Although IGF-I is also synthesized locally at numerous other sites, the liver does constitute the major site of its synthesis, and circulating IGF-I is buy duphaston mainly of hepatic derivation. The production of IGF-I is stimulated by growth hormone (GH), the secretion of which is influenced by circulating IGF-I level through a negative feed-back mechanism. Oral estrogen treatment causes a significant decrease of the IGF-I serum level, probably through a hepatocellular effect due to the first hepatic passage. Treatment with transdermal estradiol (tdE2) at the currently used doses does not cause, on average, substantial variations in the IGF-I serum level. The addition of an androgenic progestin--with strong hepatocellular actions, opposite to those of estrogen--completely reverses the IGF-I decrease induced by oral estrogens, and even causes a trend to IGF-I increase when tdE2 is used. Conversely, the addition of a non androgenic progestin, like dydrogesterone, does not cause interference with the estrogen effect.

duphaston 40 mg 2015-09-04

Forty-four healthy postmenopausal women 50-60 years old participated in the study. Eighteen were treated by combined oral hormonal replacement therapy (estradiol 2 mg per Combivir Overdose day during days 1-25 and 10 mg of dydrogesterone on days 10-25) for at least 2 years, and 26 were untreated.

duphaston review 2016-11-25

The objective of the study was to evaluate the efficacy of progestogenic therapy for the prevention of spontaneous abortions in patients with subchorionic hemorrhage. One hundred pregnant women with bleeding and ultrasonographic evidence of subchorionic hematoma were treated with oral dydrogesterone 40 mg/day. Only cases in which the embryo was viable were included. The follow-up included ultrasonography and intravaginal examination. Of the 100 pregnancies, 93 had a favorable evolution with maintenance of pregnancy. The abortion rate was therefore 7 Effexor Overdose Death %. This compares with an abortion rate of 18.7% obtained in a previous study in women with subchorionic hematoma treated with micronized progesterone. The abortion rate was therefore reduced by up to 37% with dydrogesterone, as most cases had large-volume hematomas at the first visit and thus a poor prognosis. In conclusion, the marked immunomodulatory effect of dydrogesterone in maintaining a T helper-2 cytokine balance means that it is a good choice for preventing abortion in women suffering from subchorionic hemorrhage.

duphaston tab dose 2015-12-04

To formulate a position statement on the management of the menopause in obese Prograf Open Capsule women.

duphaston medicine dosage 2016-02-07

Twelve weeks of Seroquel Pill Identifier treatment with combined HRT was associated with an increase in platelet activation parameters P-selectin and glycoprotein 53 (by 17% and 14%, respectively, P = 0.04 vs. the placebo group for both comparisons), suggesting alpha granule and lysosome degranulation. E2 replacement therapy was associated with an increase in P-selectin labelling by 22% (P = 0.04 vs. the placebo group).

duphaston tab 2015-01-16

Hormone therapy significantly influences the enteroinsular axis in postmenopausal women and contributes to Tofranil 200 Mg the normalization of plasma glucose levels.

duphaston 5mg tablets 2016-06-05

Adipose tissue was obtained from 12 non-diabetic women, mean age 51 years (range 37-78) and mean body mass index 25.4 kg/m(2) (range 20.3-26.4). Adipocytes were treated with increasing doses of DYD and Lasix Water Pill NET for 48 h prior to protein extraction. Effects on lipogenesis and lipolysis were assessed using western blotting to determine the expression of key enzymes, LPL (56 kDa) and HSL (84 kDa) respectively. Measurement of glycerol release into the medium provided an assessment of lipolytic activity.

duphaston tab indication 2016-09-11

The objective of this systematic review was to assess whether the orally acting progestagen, dydrogesterone lowers the incidence of miscarriage in women with threatened miscarriage. A computerized search was performed in Medline, Embase, and Ovid Medline for original reports with the product name 'Duphaston' or 'dydrogesterone', and limited to clinical human data. Twenty-one reports of dydrogesterone treatment were identified with 1380 patients. Five randomized trials were identified, including 660 women who fulfilled the criteria for meta-analysis. The number of subsequent miscarriages or continuing pregnancies per randomized woman was compared in women receiving dydrogesterone compared to standard bed rest or placebo intervention. There was a 13% (44/335) miscarriage rate after dydrogesterone administration compared to 24% in control women [odds ratio for miscarriage 0.47, (CI = 0.31-0.7), 11% absolute reduction in the miscarriage rate]. The adverse and side effects were summarized in all 21 reports, and seemed to be minimal. Although all the predictive and confounding 5 Voltaren Gel factors could not be controlled for, the results of this systematic review show a significant reduction of 47% in the odds for miscarriage when dydrogesterone is compared to standard care indicating a real treatment effect.

duphaston generic price 2016-05-29

The progestagen medroxyprogesterone acetate (100 mg daily) appeared to be more effective at reducing all symptoms up to 12 months of follow-up (MD -0.70, 95% CI -8.61 to -5.39; P < 0.00001) compared with placebo. There was evidence of significantly more cases of acne (six versus one) and oedema (11 versus one) in the medroxyprogesterone acetate group compared with placebo. There was no evidence of a difference in objective efficacy between dydrogesterone and placebo.There was no evidence of a benefit with depot administration of progestagens versus other treatments (low dose oral contraceptive or leuprolide acetate) for reduced symptoms. The depot progestagen group experienced significantly more adverse effects.There was no overall evidence of a benefit of oral progestagens over other medical treatment at six months of follow-up for self-reported efficacy. Amenorrhoea and bleeding were more frequently reported in the progestagen Voltaren Gel 8 group compared with other treatment groups.There was no evidence of a benefit of anti-progestagens (gestrinone) compared with danazol. GnRH analogue (leuprorelin) was found to significantly improve dysmenorrhoea compared with gestrinone (MD 0.82, 95% CI 0.15 to 1.49; P = 0.02) although it was also associated with increased hot flushes (OR 0.20, 95% CI 0.06 to -0.63; P = 0.006).

duphaston medicine wikipedia 2015-07-08

A general hospital. Luvox Dosage Strengths

duphaston 10mg dosage 2016-10-09

In December, 1986, a 29 year old woman developed nephrosis due to systemic lupus erythematosus after taking oral contraceptives (OC) for 6.5 years. Hospitalized for 3 months, she received steroid treatment, which lowered albumin in urine. At the time of hospitalization, the following symptoms were noted. Edema on all her limbs, 4.5 g/dl of urine albumin per day, white blood cell count of 2600/mm, 640 time positive anti-nuclear antibodies, pseudo-positive response to syphilis via bentonite flocculation on particle (BFP). OC she had taken since 1980 were 0.5 mg of norgestrel day and 0/05 mg of ethinyl estradiol day. She had been routinely checked on her kidney function biannually and everything had been normal till then. For 2 months starting in December, 1987, at the patient's request, progesterone along (dydrogesterone 10 mg/day) was administered for contraception. No urine albumin was detected. It appears that autoimmune-type thyroid gland abnormality preceded systemic lupus erythematosus (SLE) which was triggered by the oral contraceptive use. Estrogen metabolism of SLE patients is characterized by estrogen active 16 alpha Deltasone Generic Name hydroxyestrone.

duphaston drug 2016-10-27

Dienogest was introduced as an oral progestin. Yet its strong oral potency on endometrial activity is not clearly explained. To circumvent this situation, steroid hormone receptor profiling using transactivation assay and endometrial activity test in rabbits were carried out with determination of plasma drug concentration. Agonistic/antagonistic activity on human progesterone receptor (PR), androgen receptor (AR), glucocorticoid receptor (GR), mineralocorticoid receptor (MR), estrogen receptor alpha (ERalpha), or estrogen receptor beta (ERbeta) were determined. Dienogest activate PR (EC50=3.4 or 10.5 nmol/l) with antagonistic activity on AR (EC50=420.6 or 775.0 nmol/l) but not agonistic nor antagonistic action on GR, MR (3000 nmol/l). Dienogest activate neither ERalpha nor ERbeta (3000 nmol/l). Progesterone activated PR with antagonistic activity on AR and on MR. Dydrogesterone showed a similar profile to progesterone. Norethisterone activated PR, AR, and ERalpha. Medroxyprogesterone acetate activated PR, AR, and GR. Danazol activated PR and AR. Collectively, dienogest has a good specificity to PR compared with the other drugs. By oral treatment, dienogest showed the strongest endometrial activity (ED50=0.0042 mg/kg) in McPhail test among other progestins (ED50 values for MPA, DYG, NES were 0.074, 1.9, >0.05 mg/kg, respectively). Dienogest showed higher plasma concentrations than those of the other progestins with higher doses. The estimated plasma concentration of dienogest at ED50 (3.66 nmol/l) was close to its EC50 value to activate PR. Thus, the stronger oral activity of dienogest could be explained simply by its in vitro potency on PR and its oral pharmacokinetic profile.

duphaston cost 2015-04-24

The aim of the study is to evaluate the effects of dydrogesterone in the treatment of cycle disturbances in adolescence. The study included 55 girls, aged between 12 and 17 years, with the gynecological age 1 to 5 years. The groups included patients with painful menstruation, oligomenorrhoea, dysfunctional uterine bleeding (DUB) and benign breast disease. Different regiments of treatment with dydrogesterone were applied. Dydrogesterone in low therapeutical dose is an effective and save drug in the treatment of menstrual cycle disturbances in adolescence.

duphaston online usa 2016-08-07

Serum lipoprotein and apoprotein concentrations were monitored for 24 weeks in 26 postmenopausal women treated with conjugated equine estrogens (0.625 mg/day) with the addition of dydrogesterone (10 mg/day) for the last 12 days of each 28 day cycle. The women had had no previous hormone replacement therapy. The estrogen plus dydrogesterone regimen caused significant (P less than 0.05) increases in triacylglycerol and HDL cholesterol concentrations. Both HDL2 and HDL3 cholesterol were increased. There were no other significant changes in lipoprotein concentrations. Both apoprotein AI and apoprotein AII concentrations increased significantly (P less than 0.05) over the study period. The ratios of apoprotein AI to apoprotein AII, apoprotein AI to HDL cholesterol and apoprotein AII to HDL cholesterol did not change. At the doses employed in this study, the use of dydrogesterone as a progestogen alters the effects of conjugated equine estrogens on lipoproteins and reinforces the view that the effects of a combined HRT regimen cannot be predicted from a consideration of the effects of the individual components.

duphaston 10 mg 2015-06-11

Medroxyprogesterone acetate (MPA) and dydrogesterone (DDG) are synthetic progestins widely used in human and veterinary medicine. Although aquatic organisms are exposed to them through wastewater and animal farm runoff, very little is known about their effects in the environment. Here we provide a comprehensive analysis of the responses of zebrafish (Danio rerio) to MPA, DDG, and their binary mixtures at measured concentrations between 4.5 and 1663 ng/L. DDG and both mixtures impaired reproductive capacities (egg production) of breeding pairs and led to histological alterations of ovaries and testes and increased gonadosomatic index. Transcriptional analysis of up to 28 genes belonging to different pathways demonstrated alterations in steroid hormone receptors, steroidogenesis enzymes, and specifically, the circadian rhythm genes, in different organs of adult zebrafish and eleuthero-embryos. Alterations occurred even at environmentally relevant concentrations of 4.5-4.8 ng/L MPA, DDG and the mixture in eleuthero-embryos and at 43-89 ng/L in adult zebrafish. Additionally, the mixtures displayed additive effects in most but not all parameters in adults and eleuthero-embryos, suggesting concentration addition. Our data suggest that MPA and DDG and their mixtures induce multiple transcriptional responses at environmentally relevant concentrations and adverse effects on reproduction and gonad histology at higher levels.