多囊性卵巢
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相關網頁:
PCOS association多囊性卵巢協會
http://pcos.freeservers.com/general.html
一般的 PCOS(多囊性卵巢徵候群)的知識
PCOS是什麼? | 什麼正在我的身體在進行? | 什麼引起它?
PCOS它如何被診斷? | 與 PCOS有關的問題和危險
PCOS(多囊性卵巢徵候群)是什麼?
PCOS與不孕症(PCOD and assisted fertility)
Introduction|DiagnosisPCOD and assisted fertility)
Introduction|DiagnosisIntroduction|Diagnosis|PCOS patients present |Diagnosis |Aetiology |
Prevalence|Response of the PCO to stimulation for IVF|
Preconception counselling|Various thearpies for hyperandrogenic syndromes(1. ovarian wedge resection 2. Laser laparoscopic wedge resection 3. Medical treatment)|
Implications of the PCOS in relation to fertility
一般的 PCOS(多囊性卵巢徵候群)的知識:
多囊性卵巢徵候群 (Stein-Leventhal徵候群, 或 高男性荷爾蒙慢性不排卵症) 在 5%-10% 女人發生，是一種內分泌的混亂的疾病。
它能引起出現很多在表面上是不相關的症狀,包括:
不規則月經或月經不來
不排卵
重量增加 (特別地在腰部呈典型 "蘋果" 型的女人)
多毛症 (過度身體頭髮) 隨時間期而更嚴重
insulin resistance(胰島素抵抗力) (現在想是因素勝於症狀, 更在這之上比較更遲的) 當胰島素抵抗力連同高血壓一起被發現的時候, 高 triclyceride 水平, 減少 HDL (好的膽固醇) 和肥胖, 它有時被稱 "徵候群 X"。
痤瘡(青春痘)
男人型禿頭
卵巢上的多發性的小水囊腫
黑棘皮症 (在腋下和乳房下面和在後頸部的皮膚變黑)
我的身體怎麼了?
在 PCOS﹐月經周期是在一個對胰島素有抵抗力的環境中開始, 人體償還性的分泌越來越多的胰島素的。 這情況叫做 高胰島素血症(hyperinsulinemia)。 PCOS 女人的卵巢對胰島素的血中濃度特別敏感,同時因此過度地生產雄激素 (例如睪固酮)。 這破壞卵巢和(pituitary gland)之間的"回饋環"(feedback loop), 而使腦下垂體 腺產生過多的 LH (黃體刺激素),因而導致生產更多的雄激素。 那些卵巢裡的不成熟的卵泡因無法轉換過多雄激素成雌激素, 而抑制卵泡的發育。 因為卵不能夠適當地發育, 所以無法排卵, 而且不成熟的卵, 因無法從卵巢釋出, 變成小小的水泡,進而開始供給自己的雄激素。 到下一次月經週期時,這些自我供應雄激素的多發性小水泡妨礙這一週期卵泡的發育。
什麼引起它?
在過去﹐一般想以致 PCOS 完全地被過度雄激素製造引起﹐但是最近的研究已經顯示引起問題的因素是胰島素抵抗力和 hyperinsulinemia, 依次引起雄激素的生產過剩。 以前治療著重在控制雄激素不平衡, 但是常常不是很有效。 比較新的治療把重心集中在胰島素問題, 並且可能有很好的療效, 針對" Polycystic 卵巢徵候群裡的胰島素抵抗力"是一個新治療的方向。
它如何被診斷?
多囊性卵巢症候群通常被診斷透過各種不同的血液試驗和超音波檢查。 但是, 它不應該獨自靠超音波來診斷, 因為大約 20% 個女人有 polycystic - 出現卵巢 - 它是慢性的不排卵的一個症狀, 能被其他的事物引起。 血液試驗能測試到的許多的不同荷爾蒙濃度 : 高的男性激素濃度 (特別是自由基的睪固酮)，高濃度的 LH 或提高的 LH /FSH (黃體刺激素/卵泡刺激荷爾蒙) 比 時常是作為多囊性卵巢症候群診斷的基礎。
與多囊性卵巢症候群有關的問題和危險
有多囊性卵巢症候群的女人有發展許多的其他健康情況的被增加的危險, 包括:
第2型 (成年發作型)糖尿病。 藉由控制胰島素的製造而且與日常飲食的變化﹐這危險能被減少。 如果不治療, 在 40歲時有40%的人發展成糖尿病
高的膽固醇和 triglyceride 濃度
心臟血管的疾病。 再一次, 藉由控制胰島素的製造, 這危險能也很被降低。 如果藉由控制胰島素的製造,控制膽固醇到正常值時,則心臟血管的疾病的危險也就降低了。
子宮內膜癌。 這危險來自月經的缺乏 - 如果你還沒有到達更年期而且也沒有你自己的半規則月經, 你需要被治療，不然你可能有子宮內膜癌的危險。
PCOS與不孕症(PCOD and assisted fertility)
introduction
1. IVF is not the first-line treatment for polycystic ovaries . But many patients with PCO may end up being referred for
IVF. Either because of another reasion or faulure to conceive despite ovulating for more than 6 months.
2.PCOS and PCO
3.PCOS described by Stein and Leventhal .: enlarged, sclerocystic ov with amenorrhoea, infertility and hirsutism
4.PCO with non-hirsute and regular menstrual cycle.: Symptomless PCO
Diagnosis
no on the clinical presentation, but rather on the ovarian morphologyl
ovaries are described as polycystic if there are 10 or more cysts, 2-8 mm in diameter, arranged around a dense stroma or scattered thoughout an increased amouunt of stroma..
# they should be distinguished form mylticystic ovaires., which occur nmormally during puberty and are associated with recovering weight loss-related amenorrhea. These ovaries do not contain increased stroma and the size of the cysts is usually larger than in PCO.
PCOS and PCO :
PCO : morphological appearance of the ovary
PCOS : PCO with menstrual disturbance, most commonly oligomenorrhoea, the complications of hyperandrogenization ( seborrhoea, acne and hirsutism) and obesity.
40% (only , lower than predicted) of cases: LH increased. With increased LH/FSH
27% prevalence of raised prolactin: some with moderate hyperprolactinaemia : 600-6000 mu/l is present.
Hyperprolactinaemia may be caused hyp stimulation production rather than by a primary pituitary defect.
E2 (Estradiol) level: similar to those found in normal women during the early folicular phase of the cycle.
E1( Estrone) level : raised, mostly because of extra-ovarian conversion of androstenedione, , which takes place in adipose tissue.
Finially the PCO tends to produce an excess of androgens.
Most important : the changes are variable in PCO: PCOS may have noraml endocrine concentrations. Thus endocrine measurement is not as helpful as ultrasound in making the diagnosis.
PCOS patients present
A.
1.levated LH levels and hyperandrogenism
2.increased ovarian follicle atresia
3.oligomenorrhea and anovulation
4.reduced fertility
5.elevated miscarriage rates
B. Deranged LH secretion may contrubute to these disorders through:
1.anddrogen-induced follicle stresia
2.disruption of late follicular phase granulosa cell coommuication in the cumulus oophorus causeing:
1.accelerated oocyte meiotic maturation
2.reduced embryo quality
Diagnosis of PCOD
Disordered or absent menstrual cycles and failure of ovulation
High level of plasma androstenedione and testosterone or free testosterone
High plasma LH:FSH ratios of > 3:1
Higher levers of bioactive LH
Masculinization of facial and pubic hari and body characteristics
Obesity in some patients
Many small follicles on ultrasound or in ovarian biopsies
Obese and hirsute patients may have exaggerated insulin responses in oral glucose tolerance tests.
Aetiology
1. Etiology :: clear unknown
inherited
2.some patients : unilateral polycystic ovary
3.primary hypothalamic disturbance of gonadotrophin regulation with seconadary in the ovary
Prevalence
50% prevalence in patients with oligo- or amenorrhoea
87 % of patients with oligomenorrhoea have PCO
26% of patients with amenorrhoea have PCO
22% in “ normal “ population
50% of IVF case have PCO
First line treatment of PCO is not IVF
1f no other causes for infertility: first line treatment : ovulation induction
If with other combined causes for infertility : may be IVF for the second cause
If failed to conceive despite at least 6 ovulatory cycles : IVF
Response of the PCO to stimulation for IVF
poor responder ( small part ) : + GH
high responder :
:thecal hyperplasia (some with raised LH or Insulin) provide large amounts of androstenedione and testosterone which act as
substrates for oestrogen production. Normal amount of FSH act on large amounts of testosterone and androstenedione to
produce large amounts of intra-ovarian estrogen. Ov follicle , of which there ar too many, are increasingly senstive to
FSH( receptors of which are stimmulated by high local concentrations osestrogen) and result multiple follicular development
with high levels of circulating estrogen.
Preconception counselling
down regulation
hyperandrogenism
insulin resistance : obesity : hypertension, pre-eclampsia, GDM.
: before ap : most effective management is dietary control and weight loss
Various thearpies for hyperandrogenic syndromes:
ovarian wedge resection : the classical method for treating PCOD. : suprisingly effective
The reduction in ovarian mass can have dramatic effects, with a decrement in ovarian androgen secretion interrupting the vicious cycle that results in exaggerated LH and reduced FSH release.
Laser laparoscopic wedge resection : creating multiple pockets 1 cm deep throughout the
surface of the ovary.
All surgical methods are contraindicated in patiens desiring pregnnancy< because of the
risks of producing potentially severe periovarian adhesions. The advantage of surgery is only
lasts for 6 months.
Medical treatment: Dexamethasone or other compounds, and espiecially LH-RHa
Dexamethasone ( synthetic sex steroids):
suppress the adrenal glands and reduce the output of estradiol but not of progesterone by granulosa cells. Thus reduce the plasma cortisol ( detectable reduced in plasma and follicular fluid).
# Poor responder may be hyper-androgenic and may benefit form concurrent adrenal suppression using 0.5mg oral dexamethasone each night, particular if they produce >250 ug/dl dehydroepiandrosterone sulfate.
Ketoconazole : blocks cytochrome P450 dependnt enzymes in ovarian and adrenal steroid biosysthesis. Thereby reducing plasma levels of testosterone. I improves hair growth and normalizes menses. But careful monitoring and birth control methods are essential during this procedure.
LH-Rha ( GnRHa): effectively suppresses ovarian hyperandrogenism, even if severe, as in the hyperinsulinemia, hyperthecosis,and hirsutism. Androgen levels decline rapidly to those typical of women after oophorectomy. Gonadotrophs are desensitized and LH and E2 decline for up to 550 days. Abnormal ov responses are alleviated.
PCOD p’t may be given LH-Rha for 4 days, before FSH oar HMG for ovarian stimulation. Responses are better than with FSH oar HMG alone.
Clomiphene triggers follicle growth in some p’t but others witll have clomiphene resistance.
內科治療方式:
Dexamethasone:效抑腎上腺及減少 卵巢顆粒細胞分泌雌性素 但不影響其黃體素的分泌. 進而減少血漿 及濾泡中的 腎上腺皮質素雅(cortisol) 含量.
Ketoconazole : 降低體內男性荷爾蒙 ,減少多毛症,並使月經正常. 但此治療方式須暫時避孕.
LH-Rha ( GnRHa): 有效抑制高男性荷爾蒙症, 即使在嚴重高胰島素血症, hyperthecosis,及多毛症都有效.性腺刺激素(Gonadotrophs) 被去敏感化且LH及E2 可降低達550天, 如此異常卵巢功能可以恢復.
Clomiphene: 可誘發排卵, 但常有些人對 其有抗藥性(clomiphene resistance).
手術治療方式:
手術治療 :
卵巢楔狀切除術: 減少卵巢現有男性荷爾蒙含量,進而有效的抑制男性荷爾蒙的產生,進而打斷不正排卵及不正常荷爾蒙的惡性循環.
腹腔鏡卵巢鑽洞手術:在卵巢表面&燒灼多個深1公分的洞.
但是如果想要懷孕的人,手術治療並不合適.因為可能引起嚴重的卵巢周邊沾粘. 另外手術治療的缺點是療效大約是有維持6 個月.
Implications of the PCOS in relation to fertility
anovulation is the main cause of infertility
LH increased -> decreased fertility
->increased miscarriage
# Inappropriate LH increase : egg can’t be fertilized
reduced rate of fertilization and cleavage
and miscarriage increased
Clinical recurrent miscarriage : 82% had PCOD
LH -> androgen increased-> pg secretion at the time of preovulatory surge
RTS diagnosed PCO : 44% LH > 10
Data “ mid-follicular phase : if LH> 10 , 67% conception rate decreased
65% miscarriage rate increased.
IVF : If “premature” LH surge -> fertilized poorly-> NO AP occurred in this situation at Hallam medical Center
