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Endometrial Hyperplasia 內膜增生 (in English and Chinese 中英文)

 

Translated into English by: Joe Hing Kwok Chu 朱興國編譯

 

Source of Chinese article: Taipei Veteran Main Hospital, Genealogy Department 中文資料來源:台北榮民總醫院婦女醫學部   

 

 

There are three forms of endometrial hyperplasia:

  1. cystic hyperplasia,

  2. adenomatous hyperplasia,

  3. atypical hyperplasia.

 

All of these can cause symptoms of abnormal uterine bleeding in women of any age, from girls who first experience menstruation to postmenopausal women. All forms of endometrial hyperplasia are caused by lack of ovulation and the resulting excess of estrogen, and the deficiency of progesterone to counteract it. This bleeding is called dysfunctional uterine bleeding. Through microscopic observation, adenomatous hyperplasia and cystic hyperplasia can be identified. In these cases, by stopping or suppressing estrogen or by using progesterone, health can be completely restored to normal. However, that is not the case with atypical hyperplasia. In atypical hyperplasia, the arrangement of the shape of the glandular epithelium and the splitting condition show that it can mutate into a carcinogenic condition if not deterred in time. The chance of its becoming adenocarcinoma can be as high as 12% to 14%, so some pathologists think of atypical hyperplasia as pre-cancer, or zero stage cancer. Because the first two categories of hyperplasia (cystic and adenomatous) may also mutate into cancer, any case of endometrial hyperplasia should be diagnosed and treated in a timely fashion to prevent future occurrence of endometrial cancer.

 

The cause of these three types of hyperplasia is long-term estrogen stimulation. Primate experiments also confirmed this fact. But there is evidence to show that with the long-term effects of estrogen and the lack of confrontation, most endometria will become hyperplasia in varying degrees, but only a small portion will mutate into cancer. The main reason for this may be related to the roles of estrogen receptors, time, and personal factors. During the reproductive years, women seem to have more resistance to endometrial cancer, while women

shortly before and after menopause are more prone to it. Some people think that endometrial cancer develops over time, up to as long as five years, so a long lasting menopause can develop into adenocarcinoma. The presence of hormone receptors are indispensable role of cell medium. Under normal circumstances, hormones get into the cytoplasm of cells and combine into a new complex, then enter into the nucleus and combine with chromosomes. Then, through the process of transcription, the RNA synthesis increases, resulting in a biologically active hormone. In endometrial cancer cells, there are higher levels of hormone synthesis because the receptors possess the greater affinity of the hormone. We do not know why there is a difference, that under the same conditions, 12% to 14% of the people with endometrial hyperplasia will develop cancer, while others do not. The reason is still unknown, so individual differences can be an important factor. Those women who are prone to develop cancer may possess abnormal chromosomes or DNA distribution in the cells of their endometria. A carcinogen, possibly estrogen, under a long period of stimulation, can agonize the cancer-causing gene of the nucleus and develop cancer.

 

 

Translator's note: some herbs like fennel and dill can help the body to increase progesterone.

 

內膜增生有三種形態:囊狀增生(cystic hyperplasia)腺形增生(adenomatous hyperplasia)、不典型增生(atypical hyperplasia),均可產生不正常的子宮出血症狀且見之於任何年齡婦女,尤其初經前少女與停經後婦女均直接源自不排卵以致雌激素過多並且缺乏黃體素(progesterone) 對抗所形成,所以這些出血均稱功能不良 性出血(dysfunctional uterine bleeding)。在顯微鏡下觀察囊狀及腺形增生的腺體在雌激素停止作用或在黃體素的抑制下可以 完全恢復正常,不典型增生則不然,腺體上皮的排列形態以及分裂情形均有相當的癌轉化現象,如不及時遏止,則變成腺癌的機會高達12%~14%,因此有些病理學家把 不典型增生判定為前期癌或零期癌,而前兩類增生也有惡化的可能性,因此在有內膜異常增生的情況下就應該及時診治以預防日後的發生內膜癌。
 
這三種增生的原因在臨床上肯定的與雌激素長期刺激有關,在靈長類動物實驗也證明此點,但由己有的種種證據顯示出,雌激素長期的作用並缺少對抗的情形下,雖然多數內 膜將會形成不同程度的增生,然而其中只有一小部份會惡轉為癌,主要的原因可能與作用的時間,雌激素受體(receptor)及個人因素等有關;在生育年齡的婦女似 乎比較有抗拒內膜癌化的本能,而停經前後的婦女則易遭不幸,有些人認為使內膜變癌時間長達五年以上,因此長期持續下的結果到停經前後才成腺癌;受體的存在是荷爾蒙 作用細胞不可或缺的介質,正常情況下激素進入細胞與胞漿中受體結合成複合體,再進入胞核內與染色體相合,通過轉錄等機轉使核糖核酸合成增加,產生激素的生物活性。 在內膜癌細胞中其胞漿雌激素結合量較高,是由於受體對激素有較大的親合力之故,但何種原因控制著兩者結合的差異,使在相同條件下有些人變癌──12%-14%的內 膜增生患者,而其他的人不會,仍然未明。因此個體的差異因素可能是一個重要的原因,易於致癌的人在其內膜細胞中可能潛伏著異常的染色體及DNA分配,使它們在致癌 物──很可能是雌激素──的長期催化下激發了核內致癌基因,終於不幸的產生了內膜癌。

 

譯者注: 有些中藥, 如小茴香, 蒔蘿能增加黃體素。

 

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