на 37г. сам,много ми е хъбаво 4е ми пи6е6...само се 4ъдя за6то веднага ми напражиха биопсия и абразио....после кжо селджа,6те ме оперират ли ,6те ме гори ли ,кои,кам кого да се обарна,искам специалист....ох,изжини ме 4е толкова хаоти4но ти пи6а,но сам пред нервна криза.....много ти благодаря 4е ми обарна внимание на писмото.......
- Публикувана: 30 март 2007, 02:46 ч.
- Последно мнение: 2 септ. 2008, 11:30 ч.
Не пропускайте година без цитонамазка! Това може да Ви коства живота! ПАП и HPV
И аз пак да си кажа, че също съм така. Цапа ми по няколко дни преди да тръгне. Обсъждали сме го неведнъж и пак се шашкам всеки месец и влизам да си припомня, че и при други е така 
ми аз също съм така, без да съ се подлагала на конизация.
Липса на добри нива на прогестерон е.
два -три дни забърсвам кафеникаво течение.януари цитонамазката показа втора група.гинеколожката пък ме парира с думите
-ти си на 35,а искаш цикъл като на 20 годишна
Bobi1,на мен също веднага ми направиха биопсия и абразио.Точно като на теб.Резултатът беше не особено хубав-дисплазия трета степен.След това ми направиха конизация-лека операцийка на шийката на матката.И сега да чукна на дърво съм ОК.Описвам ти всичко това,за да знаеш какво те чака в най-лошия случай.Не си мисли глупости!!!Успех!Пиши пак като излезе резултата от биопсията.
...каза , че ми е запушен цервикалният канал...
Сигурна ли си, че точно това е казала??? Че ти е запушен цервикалния канал???
Обади й се и я питай отново, съмнявам се да е казала това...
blagodarq na vsi4ki ,okito mi pisaha,malko po spokoina sam ve4e...ama pak si me e strah....sigorno 6te jiveq....ama tr. da stana po dobra ve4e...4e sam lo6a i po tozi na4in mai poly4avam nakazanie...............dano vsi4ki ozdrraveem i samo da se zasi4ame tyk po priqtni povodi.......как да си намеря наи-добрият доктор ,които да ми направи операцията ,ако се стигне до такажв..?помогнете ми
blagodarq na vsi4ki ,okito mi pisaha,malko po spokoina sam ve4e...ama pak si me e strah....sigorno 6te jiveq....ama tr. da stana po dobra ve4e...4e sam lo6a i po tozi na4in mai poly4avam nakazanie...............dano vsi4ki ozdrraveem i samo da se zasi4ame tyk po priqtni povodi.......как да си намеря наи-добрият доктор ,които да ми направи операцията ,ако се стигне до такажв..?помогнете ми
Хей, какви са тия приказки за наказание и прочие?
Всичко ще се оправи, щом си започнала да търсиш начин! Трябва да си упорита и постоянна в лечението. На лична ти разказах за моя път. И другите момичета назад в темата са споменали своите лекари. Опитай трезво да вземеш решение и давай напред- ние стискаме палци! 
blagodarq na vsi4ki ,okito mi pisaha,malko po spokoina sam ve4e...ama pak si me e strah....sigorno 6te jiveq....ama tr. da stana po dobra ve4e...4e sam lo6a i po tozi na4in mai poly4avam nakazanie...............dano vsi4ki ozdrraveem i samo da se zasi4ame tyk po priqtni povodi.......как да си намеря наи-добрият доктор ,които да ми направи операцията ,ако се стигне до такажв..?помогнете ми
вси4ки са толкова мили,оба4е аз не мога да сам спокоина ,сами знаете как се 4ъвствам....сигорна сам 4е не6то не е както тр.,за6тото костова ми каза 4е при прегледа е видяла малак ъ4астак,които навлиза в канала......а на ситонамазката ми пи6е пап3д,но няма атипи4ни клетки...има едини4ни дискератоцити...ни6то не разбирам....наи-мн. ме притеснява това 4е сам пап3д,което е преди рака............а тя ме успокоява 4е нямам рак,можело да с еналожи само горене....аз сам на 37 год. и сам раждала....искам конизация ,според мен 6т ее по сигорно.........как мислите
Радвам се,че елементи взаимствани от моя публикация в този сайт са толкова широко дискутирани.В крайна сметка-това беше и моята цел.
Оригиналната ми публикация може да прочетете на адрес:
http://www.bg-mamma.com/site/content/view/655/37/
Успех!
Д-р Иван Трифонов д.м.
Оригиналната ми публикация може да прочетете на адрес:
http://www.bg-mamma.com/site/content/view/655/37/
Успех!
Д-р Иван Трифонов д.м.
Прилагам статия от изключително реномиран източник
ваксините се сриват постепенно
Human Papillomavirus Vaccination — Reasons for Caution
Charlotte J. Haug, M.D., Ph.D.
The NEJM 21.08.2008
Despite great expectations and promising results of clinical trials, we still lack sufficient evidence of an effective vaccine against cervical cancer. Several strains of human papillomavirus (HPV) can cause cervical cancer, and two vaccines directed against the currently most important oncogenic strains (i.e., the HPV-16 and HPV-18 serotypes) have been developed. That is the good news. The bad news is that the overall effect of the vaccines on cervical cancer remains unknown. As Kim and Goldie1 point out in this issue of the Journal, the real impact of HPV vaccination on cervical cancer will not be observable for decades.
Although it was licensed for use in the United States in June 2006, the first phase 3 trials of the HPV vaccine with clinically relevant end points — cervical intraepithelial neoplasia grades 2 and 3 (CIN 2/3) — were not reported until May 2007, first in the Journal2 and 1 month later in the Lancet.3,4 The vaccine was highly successful in reducing the incidence of precancerous cervical lesions caused by HPV-16 and HPV-18, but a number of critical questions remained unanswered.5,6 For instance, will the vaccine ultimately prevent not only cervical lesions, but also cervical cancer and death? How long will protection conferred by the vaccine last? Since most HPV infections are easily cleared by the immune system, how will vaccination affect natural immunity against HPV, and with what implications? How will the vaccine affect preadolescent girls, given that the only trials conducted in this cohort have been on the immune response? The studies with clinical end points (i.e., CIN 2/3) involved 16- to 24-year-old women. How will vaccination affect screening practices? Since the vaccines protect against only two of the oncogenic strains of HPV, women must continue to be screened for cervical lesions. Vaccinated women may feel protected from cervical cancer and may be less likely than unvaccinated women to pursue screening. How will the vaccine affect other oncogenic strains of HPV? If HPV-16 and HPV-18 are effectively suppressed, will there be selective pressure on the remaining strains of HPV? Other strains may emerge as significant oncogenic serotypes.
Resolving the first essential questions will require decades of observation of large numbers of women. The last question may be answered sooner. Published reports of trials show an increasing trend of precancerous cervical lesions caused by HPV serotypes other than HPV-16 and HPV-18.2,4,6 The results were not statistically significant, however, possibly because there were too few clinically relevant end points in the observation periods reported. If randomized, controlled trials involving vaccinated and unvaccinated women continue for a few more years, we will most likely be able to tell whether this is a true trend. If so, there is reason for serious concern.
By the summer of 2007, there were definitely promising results with regard to the effectiveness of the HPV vaccine in the prevention of precancerous lesions (i.e., CIN 2/3) caused by the HPV-16 and HPV-18 serotypes. However, serious questions regarding the overall effectiveness of the vaccine in the protection against cervical cancer remained to be answered, and more long-term studies were called for before large-scale vaccination programs could be recommended.5,6 Unfortunately, no longer-term results from such studies have been published since then.
In the meantime, there has been pressure on policymakers worldwide to introduce the HPV vaccine in national or statewide vaccination programs. How can policymakers make rational choices about the introduction of medical interventions that might do good in the future, but for which evidence is insufficient, especially since we will not know for many years whether the intervention will work or — in the worst case — do harm? One way to provide decision support is to develop mathematical models of the natural history of the disease in question, introduce various intervention strategies, and use cost-effectiveness analysis to estimate the costs and health benefits associated with each clinical intervention. The results are typically expressed in terms of the amount we will have to pay for the extra health benefit of the treatment — that is, in dollars per life-year or quality-adjusted life-year (QALY) saved. Cost-effectiveness analyses are tools for decision making under conditions of uncertainty. These analyses do not in themselves provide evidence that medical interventions are effective. In this issue of the Journal, Kim and Goldie present a model of HPV vaccination, and they use a cost-effectiveness analysis to make projections of the possible health and economic implications of the use of the vaccine.1
To evaluate the quality of a cost-effectiveness analysis, it is essential to appraise the model's input variables, the uncertainties, and the choices the researchers have made. To set up such an analysis of a preventive medical intervention — in this case, a vaccine given to healthy 12-year-old girls — that might have an effect on the incidence of cervical cancer decades from now is extremely complex. The analysis has to model the natural history of HPV infection in this cohort of girls over their lifetime, the effect of the vaccine over all those years (whether it is the same effect or one that is waning), the effect on other HPV strains, the effect of the vaccine on the natural immunity against HPV infections, the sexual behavior of the girls and women and their partners, and finally, women's cervical-cancer screening practices.
The model presented by Kim and Goldie is well done and ambitious, and it includes most of these factors. They conclude that under certain assumptions, vaccinating 12-year-old girls is associated with an incremental cost-effectiveness ratio of $43,600 per QALY gained, whereas adding a catch-up program for older girls and women is not cost-effective. However, their base-case assumptions are quite optimistic. They presume lifelong protection of the vaccine (i.e., no need for a booster dose), that the vaccine has the same effect on preadolescent girls as on older women, that no replacement with other oncogenic strains of HPV takes place, that vaccinated women continue to attend screening programs, and that natural immunity against HPV is unaffected. Whether these assumptions are reasonable is exactly what needs to be tested in trials and follow-up studies. If the authors' baseline assumptions are not correct, vaccination becomes less favorable and even less effective than screening alone. For example, as shown in the article, if the protection of the vaccine wanes after 10 years, vaccination is much less cost-effective and screening is more effective than catch-up programs.
With so many essential questions still unanswered, there is good reason to be cautious about introducing large-scale vaccination programs. Instead, we should concentrate on finding more solid answers through research rather than base consequential and costly decisions on yet unproven assumptions.
ваксините се сриват постепенно
Human Papillomavirus Vaccination — Reasons for Caution
Charlotte J. Haug, M.D., Ph.D.
The NEJM 21.08.2008
Despite great expectations and promising results of clinical trials, we still lack sufficient evidence of an effective vaccine against cervical cancer. Several strains of human papillomavirus (HPV) can cause cervical cancer, and two vaccines directed against the currently most important oncogenic strains (i.e., the HPV-16 and HPV-18 serotypes) have been developed. That is the good news. The bad news is that the overall effect of the vaccines on cervical cancer remains unknown. As Kim and Goldie1 point out in this issue of the Journal, the real impact of HPV vaccination on cervical cancer will not be observable for decades.
Although it was licensed for use in the United States in June 2006, the first phase 3 trials of the HPV vaccine with clinically relevant end points — cervical intraepithelial neoplasia grades 2 and 3 (CIN 2/3) — were not reported until May 2007, first in the Journal2 and 1 month later in the Lancet.3,4 The vaccine was highly successful in reducing the incidence of precancerous cervical lesions caused by HPV-16 and HPV-18, but a number of critical questions remained unanswered.5,6 For instance, will the vaccine ultimately prevent not only cervical lesions, but also cervical cancer and death? How long will protection conferred by the vaccine last? Since most HPV infections are easily cleared by the immune system, how will vaccination affect natural immunity against HPV, and with what implications? How will the vaccine affect preadolescent girls, given that the only trials conducted in this cohort have been on the immune response? The studies with clinical end points (i.e., CIN 2/3) involved 16- to 24-year-old women. How will vaccination affect screening practices? Since the vaccines protect against only two of the oncogenic strains of HPV, women must continue to be screened for cervical lesions. Vaccinated women may feel protected from cervical cancer and may be less likely than unvaccinated women to pursue screening. How will the vaccine affect other oncogenic strains of HPV? If HPV-16 and HPV-18 are effectively suppressed, will there be selective pressure on the remaining strains of HPV? Other strains may emerge as significant oncogenic serotypes.
Resolving the first essential questions will require decades of observation of large numbers of women. The last question may be answered sooner. Published reports of trials show an increasing trend of precancerous cervical lesions caused by HPV serotypes other than HPV-16 and HPV-18.2,4,6 The results were not statistically significant, however, possibly because there were too few clinically relevant end points in the observation periods reported. If randomized, controlled trials involving vaccinated and unvaccinated women continue for a few more years, we will most likely be able to tell whether this is a true trend. If so, there is reason for serious concern.
By the summer of 2007, there were definitely promising results with regard to the effectiveness of the HPV vaccine in the prevention of precancerous lesions (i.e., CIN 2/3) caused by the HPV-16 and HPV-18 serotypes. However, serious questions regarding the overall effectiveness of the vaccine in the protection against cervical cancer remained to be answered, and more long-term studies were called for before large-scale vaccination programs could be recommended.5,6 Unfortunately, no longer-term results from such studies have been published since then.
In the meantime, there has been pressure on policymakers worldwide to introduce the HPV vaccine in national or statewide vaccination programs. How can policymakers make rational choices about the introduction of medical interventions that might do good in the future, but for which evidence is insufficient, especially since we will not know for many years whether the intervention will work or — in the worst case — do harm? One way to provide decision support is to develop mathematical models of the natural history of the disease in question, introduce various intervention strategies, and use cost-effectiveness analysis to estimate the costs and health benefits associated with each clinical intervention. The results are typically expressed in terms of the amount we will have to pay for the extra health benefit of the treatment — that is, in dollars per life-year or quality-adjusted life-year (QALY) saved. Cost-effectiveness analyses are tools for decision making under conditions of uncertainty. These analyses do not in themselves provide evidence that medical interventions are effective. In this issue of the Journal, Kim and Goldie present a model of HPV vaccination, and they use a cost-effectiveness analysis to make projections of the possible health and economic implications of the use of the vaccine.1
To evaluate the quality of a cost-effectiveness analysis, it is essential to appraise the model's input variables, the uncertainties, and the choices the researchers have made. To set up such an analysis of a preventive medical intervention — in this case, a vaccine given to healthy 12-year-old girls — that might have an effect on the incidence of cervical cancer decades from now is extremely complex. The analysis has to model the natural history of HPV infection in this cohort of girls over their lifetime, the effect of the vaccine over all those years (whether it is the same effect or one that is waning), the effect on other HPV strains, the effect of the vaccine on the natural immunity against HPV infections, the sexual behavior of the girls and women and their partners, and finally, women's cervical-cancer screening practices.
The model presented by Kim and Goldie is well done and ambitious, and it includes most of these factors. They conclude that under certain assumptions, vaccinating 12-year-old girls is associated with an incremental cost-effectiveness ratio of $43,600 per QALY gained, whereas adding a catch-up program for older girls and women is not cost-effective. However, their base-case assumptions are quite optimistic. They presume lifelong protection of the vaccine (i.e., no need for a booster dose), that the vaccine has the same effect on preadolescent girls as on older women, that no replacement with other oncogenic strains of HPV takes place, that vaccinated women continue to attend screening programs, and that natural immunity against HPV is unaffected. Whether these assumptions are reasonable is exactly what needs to be tested in trials and follow-up studies. If the authors' baseline assumptions are not correct, vaccination becomes less favorable and even less effective than screening alone. For example, as shown in the article, if the protection of the vaccine wanes after 10 years, vaccination is much less cost-effective and screening is more effective than catch-up programs.
With so many essential questions still unanswered, there is good reason to be cautious about introducing large-scale vaccination programs. Instead, we should concentrate on finding more solid answers through research rather than base consequential and costly decisions on yet unproven assumptions.
Радвам се,че елементи взаимствани от моя публикация в този сайт са толкова широко дискутирани.В крайна сметка-това беше и моята цел.
Оригиналната ми публикация може да прочетете на адрес:
http://www.bg-mamma.com/site/content/view/655/37/
Успех!
Д-р Иван Трифонов д.м.
Оригиналната ми публикация може да прочетете на адрес:
http://www.bg-mamma.com/site/content/view/655/37/
Успех!
Д-р Иван Трифонов д.м.
Д-р Трифонов, не се заблуждавайте. Повечето момичета, пишещи тук, дори не знаят за въпросната статия. Не дискутираме елементи от нея, а елементи от ежедневието и проблемите си - проблемни цитонамазки, конизации, хистеректомии, ваксини.
Ако се върнете по-назад в темата, което очевидно не сте направил, ще разберете, че вашите 3 реда по въпроса за цитонамазка, нямат никакъв пронос относно колко информирани сме.