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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
Diets high in fruits and vegetables tend to lower the risk of developing fibroids. Fruits, especially citrus, have a greater protective benefit than vegetables. Normal dietary levels of vitamin D is shown to reduce the risk of developing fibroids. No protective benefit has been found with the consumption of folate, whole grains, soy products, or fiber. No association between the consumption of fat, eggs, dairy products has been shown to increase the risk of fibroids.
Some risk factors associated with the development of uterine fibroids are modifiable.
Fibroids are more common in obese women. Fibroids are dependent on estrogen and progesterone to grow and therefore relevant only during the reproductive years.
Most of the risk factors for endometrial cancer involve high levels of estrogens. An estimated 40% of cases are thought to be related to obesity. In obesity, the excess of adipose tissue increases conversion of androstenedione into estrone, an estrogen. Higher levels of estrone in the blood causes less or no ovulation and exposes the endometrium to continuously high levels of estrogens. Obesity also causes less estrogen to be removed from the blood. Polycystic ovary syndrome (PCOS), which also causes irregular or no ovulation, is associated with higher rates of endometrial cancer for the same reasons as obesity. Specifically, obesity, type II diabetes, and insulin resistance are risk factors for Type I endometrial cancer. Obesity increases the risk for endometrial cancer by 300–400%.
Estrogen replacement therapy during menopause when not balanced (or "opposed") with progestin is another risk factor. Higher doses or longer periods of estrogen therapy have higher risks of endometrial cancer. Women of lower weight are at greater risk from unopposed estrogen. A longer period of fertility—either from an early first menstrual period or late menopause—is also a risk factor. Unopposed estrogen raises an individual's risk of endometrial cancer by 2–10 fold, depending on weight and length of therapy. In trans men who take testosterone and have not had a hysterectomy, the conversion of testosterone into estrogen via androstenedione may lead to a higher risk of endometrial cancer.
Some therapies for other forms of cancer increase the lifetime risk of endometrial cancer, which is a baseline 2–3%. Tamoxifen, a drug used to treat estrogen-positive breast cancers, has been associated with endometrial cancer in approximately 0.1% of users, particularly older women, but the benefits for survival from tamoxifen generally outweigh the risk of endometrial cancer. A one to two-year course of tamoxifen approximately doubles the risk of endometrial cancer, and a five-year course of therapy quadruples that risk. Raloxifene, a similar drug, did not raise the risk of endometrial cancer. Previously having ovarian cancer is a risk factor for endometrial cancer, as is having had previous radiotherapy to the pelvis. Specifically, ovarian granulosa cell tumors and thecomas are tumors associated with endometrial cancer.
Low immune function has also been implicated in endometrial cancer. High blood pressure is also a risk factor, but this may be because of its association with obesity. Sitting regularly for prolonged periods is associated with higher mortality from endometrial cancer. The risk is not negated by regular exercise, though it is lowered.
Endometrial polyps usually occur in women in their 40s and 50s. Endometrial polyps occur in up to 10% of women. It is estimated that they are present in 25% of women with abnormal vaginal bleeding.
The risk of a repeat GTD is approximately 1 in 100, compared with approximately 1 in 1000 risk in the general population. Especially women whose hCG levels remain significantly elevated are at risk of developing a repeat GTD.
Endometrial polyps are usually benign although some may be precancerous or cancerous. About 0.5% of endometrial polyps contain adenocarcinoma cells. Polyps can increase the risk of miscarriage in women undergoing IVF treatment. If they develop near the fallopian tubes, they may lead to difficulty in becoming pregnant. Although treatments such as hysteroscopy usually cure the polyp concerned, recurrence of endometrial polyps is frequent. Untreated, small polyps may regress on their own.
The cause is not entirely clear. Risk factors include having a family history of the condition.
Some factors associated with endometriosis include:
- not having had yet given birth
- prolonged exposure to estrogen - for example, in late menopause or early menarche
- obstruction of menstrual outflow - for example, in Müllerian anomalies
Several studies have investigated the potential link between exposure to dioxins and endometriosis, but the evidence is equivocal and potential mechanisms are poorly understood. A 2004 review of studies of dioxin and endometriosis concluded that "the human data supporting the dioxin-endometriosis association are scanty and conflicting", and a 2009 follow-up review also found that there was "insufficient evidence" in support of a link between dioxin exposure and women developing endometriosis. A 2008 review concluded that more work was needed, stating that "although preliminary work suggests a potential involvement of exposure to dioxins in the pathogenesis of endometriosis, much work remains to clearly define cause and effect and to understand the potential mechanism of toxicity".
Most women with GTD can become pregnant again and can have children again. The risk of a further molar pregnancy is low. More than 98% of women who become pregnant following a molar pregnancy will not have a further hydatidiform mole or be at increased risk of complications.
In the past, it was seen as important not to get pregnant straight away after a GTD. Specialists recommended a waiting period of 6 months after the hCG levels become normal. Recently, this standpoint has been questioned. New medical data suggest that a significantly shorter waiting period after the hCG levels become normal is reasonable for approximately 97% of the patients with hydatidiform mole.
Adenomyosis itself can cause infertility issues, however, fertility can be improved if the adenomyosis has resolved following hormone therapies like levonorgestrel therapy. The discontinuation of medication or removal of IUD can be timed to be coordinated with fertility treatments. There has also been one report of a successful pregnancy and healthy birth following high-frequency ultrasound ablation of adenomyosis.
Preterm labour and premature rupture of membranes both occur more frequently in women with adenomyosis.
In sub-fertile women who received in-vitro fertilization (IVF), women with adenomyosis were less likely to become pregnant and subsequently more likely to experience a miscarriage. Given this, it is encouraged to screen women for adenomyosis by TVUS or MRI before starting assisted reproduction treatments (ART).
Adenomyosis is a benign but often progressing condition. It is advocated that adenomyosis poses no increased risk for cancer development. However, both entities could coexist and the endometrial tissue within the myometrium could harbor endometrioid adenocarcinoma, with potentially deep myometrial invasion. As the condition is estrogen-dependent, menopause presents a natural cure. Ultrasound features of adenomyosis will still be present after menopause. People with adenomyosis are also more likely to have uterine fibroids or endometriosis.
Tubal cancer is thought to be a relatively rare primary cancer among women accounting for 1 to 2 percent of all gynecologic cancers, In the USA tubal cancer had an incidence of 0.41 per 100,000 women from 1998 to 2003. Demographic distribution is similar to ovarian cancer, and the highest incidence was found in white, non-Hispanic women and women aged 60–79. However, recent evidence suggests tubal cancer to be much more frequent .
Evidence is accumulating that individuals with mutations of BRCA1 and BRCA2 are at higher risks for the development of PFTC.
AS has a reported incidence of 25% of D&Cs performed 1–4 weeks post-partum, up to 30.9% of D&Cs performed for missed miscarriages and 6.4% of D&Cs performed for incomplete miscarriages. In another study, 40% of patients who underwent repeated D&C for retained products of conception after missed miscarriage or retained placenta developed AS.
In the case of missed miscarriages, the time period between fetal demise and curettage may increase the likelihood of adhesion formation due to fibroblastic activity of the remaining tissue.
The risk of AS also increases with the number of procedures: one study estimated the risk to be 16% after one D&C and 32% after 3 or more D&Cs. However, a single curettage often underlies the condition.
In an attempts to estimate the prevalence of AS in the general population, it was found in 1.5% of women undergoing hysterosalpingography HSG, and between 5 and 39% of women with recurrent miscarriage.
After miscarriage, a review estimated the prevalence of AS to be approximately 20% (95% confidence interval: 13% to 28%).
The extent of adhesion formation is critical. Mild to moderate adhesions can usually be treated with success. Extensive obliteration of the uterine cavity or fallopian tube openings (ostia) and deep endometrial or myometrial trauma may require several surgical interventions and/or hormone therapy or even be uncorrectable. If the uterine cavity is adhesion free but the ostia remain obliterated, IVF remains an option. If the uterus has been irreparably damaged, surrogacy or adoption may be the only options.
Depending on the degree of severity, AS may result in infertility, repeated miscarriages, pain from trapped blood, and future obstetric complications If left untreated, the obstruction of menstrual flow resulting from adhesions can lead to endometriosis in some cases.
Patients who carry a pregnancy even after treatment of IUA may have an increased risk of having abnormal placentation including placenta accreta where the placenta invades the uterus more deeply, leading to complications in placental separation after delivery. Premature delivery, second-trimester pregnancy loss, and uterine rupture are other reported complications. They may also develop incompetent cervix where the cervix can no longer support the growing weight of the fetus, the pressure causes the placenta to rupture and the mother goes into premature labour. Cerclage is a surgical stitch which helps support the cervix if needed.
Pregnancy and live birth rate has been reported to be related to the initial severity of the adhesions with 93, 78, and 57% pregnancies achieved after treatment of mild, moderate and severe adhesions, respectively and resulting in 81, 66, and 32% live birth rates, respectively. The overall pregnancy rate after adhesiolysis was 60% and the live birth rate was 38.9% according to one study.
Age is another factor contributing to fertility outcomes after treatment of AS. For women under 35 years of age treated for severe adhesions, pregnancy rates were 66.6% compared to 23.5% in women older than 35.
The average age at time of EIN diagnosis is approximately 52 years, compared to approximately 61 years for carcinoma. The timeframe and likelihood of EIN progression to cancer, however, is not constant amongst all women. Some cases of EIN are first detected as residual premalignant disease in women who already have carcinoma, whereas other EIN lesions disappear entirely and never lead to cancer. For this reason, treatment benefits and risks must be individualized for each patient under the guidance of an experienced physician.
Risk factors for development of EIN and the endometrioid type of endometrial carcinoma include exposure to estrogens without opposing progestins, obesity, diabetes, and rare hereditary conditions such as hereditary nonpolyposis colorectal cancer. Protective factors include use of combined oral contraceptive pills (low dose estrogen and progestin), and prior use of a contraceptive intrauterine device.
Endometrioma is the presences of endometrial tissue in and sometimes on the ovary. More broadly, endometriosis is the presence of endometrial tissue located outside the uterus. The presence of endometriosis can result in the formation of scar tissue, adhesions and an inflammatory reaction. It is a benign growth. An endometrioma is most often found in the ovary. It can also develop in the cul-de-sac (space be hind the uterus), the surface of the uterus, and between the vagina and rectum.
Endometrial hyperplasia is a condition of excessive proliferation of the cells of the endometrium, or inner lining of the uterus.
Most cases of endometrial hyperplasia result from high levels of estrogens, combined with insufficient levels of the progesterone-like hormones which ordinarily counteract estrogen's proliferative effects on this tissue. This may occur in a number of settings, including obesity, polycystic ovary syndrome, estrogen producing tumours (e.g. granulosa cell tumour) and certain formulations of estrogen replacement therapy. Endometrial hyperplasia is a significant risk factor for the development or even co-existence of endometrial cancer, so careful monitoring and treatment of women with this disorder is essential.
Prognosis depends to a large degree on the stage of the condition. In 1991 it was reported that about half of the patients with advanced stage disease survived 5 years with a surgical approach followed by cisplatinum-based chemotherapy.
Endometrial tissue is the mucous membrane that normally lines the uterus. The endometrium is richly supplied with blood and its growth is regulated by estrogen and progesterone. It consits of glandular and stroma tissue from the lining of the uterus.
In gynecology, endosalpingiosis is a condition in which fallopian tube-like epithelium is found outside the fallopian tube. It is unknown what causes this condition. It is generally accepted that the condition develops from transformation of coelomic tissue. It is often an incidental finding and is not usually associated with any pathology.
Endometrial atrophy, uterine fibroids, and endometrial cancer are common causes of postmenopausal vaginal bleeding.
The significance of endosalpingiosis is not settled; medical experts differ on whether the condition itself causes issues or whether it is an asymptomatic finding. Common symptoms include, pelvic pain, infertility, menstrual irregularities and dyspareunia. Further reports suggest chronic back pain as a common issue reported years before diagnosis. Experts are unclear as the condition itself is a rare finding and lack of knowledge presents itself as a challenge.
Like the uterine endometrium of Endometriosis, estrogen can cause salpingoitic tissues outside of the fallopian tubes to grow and potentially aggravate the surrounding areas. High levels cause the glandular tissues to proliferate and, especially important, they cause the number of and activity of ciliated epithelial cells (that would normally line the fallopian tubes) to increase.
Vaginal bleeding occurs during 15-25% of first trimester pregnancies. Of these, half go on to miscarry and half bring the fetus to term. There are a number of causes including rupture of a small vein on the outer rim of the placenta. It can also herald a miscarriage or ectopic pregnancy, which is why urgent ultrasound is required to separate the two causes. Bleeding in early pregnancy may be a sign of a threatened or incomplete miscarriage.
In the second or third trimester a placenta previa (a placenta partially or completely overlying the cervix) may bleed quite severely. Placental abruption is often associated with uterine bleeding as well as uterine pain.
Vaginal adenosis is characterised by the presence of metaplastic cervical or endometrial epithelium within the vaginal wall, considered as derived from Müllerian epithelium islets in later life. In women who were exposed to certain chemicals, vaginal adenosis may arise in up to 90%. Since these contraceptives were discontinued, incidence has dropped dramatically. Risk is however still present in subsequent generations due to recent exposure.
It is thought steroid hormones play a stimulatory growth in adenosis formation. Vaginal adenosis is also often observed in adenocarcinoma patients.