[The biochemistry of psoriasis].

J Meynadier, J J Guilhou
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Abstract

Numerous general metabolic systems are disturbed in association with psoriasis: the frequency of diabetes mellitus and of hyperuricaemia, lipid disturbances and a decrease in folates as a result of their excessive consumption by the skin. Cutaneous metabolism is also altered. Numerous compounds are formed in excess from glucose: amino acids, fatty acids and sterols, lactic acid--the formation of which persists in the corneal layer, ribose and ribulose--synthesised as a result of glucose-6-phosphate-dehydrogenase hyperactivity (role of the increased catabolism of dehydro-epi-androsterone) and uronic acids. The accumulation of glycogen is probably due to excessive synthesis and impaired breakdown. These abnormalities may exist to a lesser extent in healthy skin. In the corneal layer there are lipid vacuoles visible under the electron microscope. Lipogenesis is increased. The same may apply to lipolysis (blood NEFA are increased). Esterification of cholesterol is decreased. The utilisation of ATP by cell membranes is probably diminished (low ATP ase activity). The absence of formation of keratohyaline is due to persistence of the repression which normally prevents it in the mucus body. Renewal of collagen appears increased. The synthesis of DNA is increased in the lesions and neighbouring areas. It is possible that these various abnormalities are dependent upon modifications in the regulator systems of cyclic AMP and GMP, variations in which are however discussed.

[牛皮癣的生化]。
与牛皮癣有关的许多一般代谢系统受到干扰:糖尿病和高尿酸血症的频率,脂质紊乱和由于皮肤过度消耗叶酸而导致的叶酸减少。皮肤代谢也发生了改变。葡萄糖过量形成了许多化合物:氨基酸、脂肪酸和甾醇、乳酸——乳酸的形成持续存在于角膜层、核糖和核酮糖——由于葡萄糖-6-磷酸脱氢酶过度活跃(脱氢表雄酮分解代谢增加的作用)和糖醛酸而合成。糖原的积累可能是由于过度的合成和受损的分解。这些异常在健康皮肤中可能存在较小程度。电镜下可见角膜层有脂质空泡。脂肪生成增加。这同样适用于脂肪分解(血液NEFA增加)。胆固醇的酯化反应降低。细胞膜对ATP的利用可能减少(ATP酶活性低)。角膜透明素的不形成是由于持续的抑制,通常阻止它在粘液体。胶原蛋白的更新似乎增加了。DNA的合成在病变和邻近区域增加。有可能这些不同的异常依赖于环AMP和GMP调节系统的修改,但是讨论了其中的变化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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