圓錐角膜(一)

西醫的認識:

        圓錐角膜是一種雙側非炎癥性角膜擴張為特征,致角膜中央部向前凸出呈圓錐形及產生高度不規則近視散光和不同視力損害的原發性角膜變性疾病。其可以是一種獨立的疾病,也可以是多種綜合征的組成部分。其多發生于青春期前后,也有部分發生于中老年更年期前后,不伴有炎癥。晚期會出現急性角膜水腫,形成瘢痕,視力嚴重受損。早期無典型臨床表現易漏診,很多患者起初都是在誤認為是近視導致的視物模糊去配鏡驗光時發現的,或因原來的鏡片佩戴不合適到醫院進行驗光配鏡時因為散光無法糾正時查出圓錐角膜的,圓錐角膜首先表現為因近視和近視散光而導致的裸眼視力下降,而且散光度數較高,并常帶有不規則散光。其發病機制是角膜中央區進行性變薄、膨隆,呈圓錐狀突出,到晚期會突然發生急性角膜水腫、混濁,使得視力在短期內更進一步下降。這時,就無法用RGP矯正。

中醫的認識:

       古代中醫醫學書籍上記載圓錐角膜(旋臚泛起)比較少見,近年來發病卻逐年增多,眾多醫學書籍都有記載,卻無有效診治方案。《證治準繩?雜病》指出該病是風輪高聳而起的疾病。本病與旋螺突起之翳色青白、累及瞳神不同。旋臚泛起證氣輪自平。水輪自明。惟風輪泛起也。或半邊泛起者。亦因半邊火盛。火郁風輪。故隨火脹起。非旋螺突起。已成證而頂尖俱凸。不可醫治之比也。《審視瑤涵》記載:火郁風輪,則旋臚泛起;血瘀火熾,則旋臚尖生。精虧血少虛損,則起坐生花;竭視酒色思慮,則昏蒙干澀。暴盲似祟,痰火思慮并頭風。赤痛如邪,肝腎虧損榮衛弱。棗花障起痰火色酒怒勞瞻。螢星滿目,辛燥火痰勞酒色。眼若蟲行因酒欲,悲思驚恐怒所傷,云翳移睛見旗旆,蠅蛇異形虛所致。淫欲多而邪氣侵,則膜入乎水輪。

簡要臨床分類:

按Duke-Elder(1946)和Eapbenb(1960)的分類為:

(1)前部形圓錐角膜。 (2)后部型圓錐角膜:又分為完全型和局限型(3)也可以分為早期、中期、晚期、水腫期

起病要點:

1.遺傳學說 較多學者認為本病為常染色體隱性遺傳。如Ammon(1830)報告6個家系均有不規律的病例。高橋報告一家同胞3人均患此病。還發現這些病例的親代往往有近親通婚史。但有些病例可連續2或3代出現,有時發生中斷現象,提示為外顯不全,這些應考慮為規律或不規律的顯性遺傳。常染色體顯性遺傳的圓錐角膜致病基因位于染色體16q22和3q23。在某些遺傳性疾病如視網膜色素變性,Downs綜合征、藍色鞏膜病和Marfan綜合征等都可能合并圓錐角膜。

2.發育障礙學說 Collins等(1925)認為本病是角膜中央部膠原纖維堅韌性降低所致。Mihalyhegy(1954)指出,本病不僅角膜中央變薄,彎曲度增加,鞏膜亦有相似改變。認為其病因與間質發育不全有關。有些病例除圓錐角膜外,尚發生晶狀體脫位或視網膜脫離,亦提示與膠原組織脆弱相關。

3.內分泌紊亂學說 Siegrist(1912)、Knapp(1929)和Stitcherska(1932)均認為甲狀腺功能減退與本病發生有重要關系。Hippel(1913)強調胸腺在本病發生中的重要作用。

4.代謝障礙學說 Myuhnk(1959)發現本病患者的基礎代謝率明顯降低。Tntapeho(1978)報告本病患者血液中鋅、鎳含量明顯降低,鈦、鉛和鋁的含量升高,而錳的含量正常,因此認為這些微量元素的變化對發生本病有一定的影響。Yukobckaa等(1979)報告,在本病患者的血液和房水中,6-磷酸葡萄糖脫氫酶的活性明顯下降致谷胱甘肽氧化作用不全,使過氧化物過多堆積,這些過氧化物就可能是促使角膜發病的重要因子。此外患者的膠原酶活性有所提高,致膠原組織的喪失大于蛋白合成,使基質層變薄。

5.變態反應學說 圓錐角膜常與春季卡他性角結膜炎等變態反應性疾病同時發病,其特點是IgA反應降低,IgE反應增高,細胞免疫也有缺陷。Boland(1963)統計,本病患者中有32.6%患過花粉癥,有33.3%患過哮喘病。Ruedeman報告本病86%的患者有過敏反應病史。

6.戴角膜接觸鏡可以誘發圓錐角膜 Hartstein(1968)報告4例戴角膜接觸鏡后發生圓錐角膜者,認為戴接觸鏡可能誘發此病。眼球及角膜硬度降低可能是戴接觸鏡后發生本病的危險因素。

7.PRK、LASIK等準分子激光角膜切除術后繼發圓錐角膜。

8.慢性眼部干燥性病變及淚液缺少時會使下方角膜變陡,并產生高度角膜散光,形成繼發性圓錐角膜。

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