基于“中虚精变”的男性精液疾病与脾胃关系探讨

"中虚精变"是类比《内经》"中气不足,溲便为之变"所提出的理论,中虚指代中焦脾胃之虚衰,精变包含了精子、精浆的变化,整个理论的提出旨在分析男性精液疾病与脾胃间关系,以及从脾论治精液疾病的相关策略。首先,脾胃经筋联络阴器,构成脾胃与男性生殖器官生理联系的前提,包括脾胃生血,精血互化,血盛精充而能育;脾胃生气,固摄精关,调精关开阖则能控精液藏泄;脾胃斡旋气机,畅达精道,使精液运行有序而不受阻;脾胃运化水液,濡润精室,则精室阴阳和调而生精、藏精、泻精有道。其次,中焦脾胃虚衰原因复杂,饮食失节、情志失调、先天不足、药物及手术损伤、应激损伤、久病虚损和湿邪困遏等皆可诱发其虚而引发精液疾病。再次,中虚所致精变,包含精子数量、活力的异常,精液量、色、质的异常,精液排泄的异常,基本涵盖了所有精液疾病的内容。最后,形成虚证健脾兼益肾、实证祛邪兼护脾,虚实夹杂分轻重、疾病混杂抓病机,无证可辨用通补、方药有度不偏颇的论治原则,为从脾论治精液疾病确立了基本框架,并借助于动物实验研究和临床研究报道对上述内容进行了简要论证,表明"中虚精变"的理论是真实的,是能够作为临床参考的理论。

“中虚精变”理论与男性精液疾病辨治再谈

“中虚精变”理论的提出,分析了男性精液疾病与脾胃的关系,为从脾胃论治精液疾病确立了基本框架。脾胃作为运化精微、濡养脏腑的重要器官,脾胃异常势必影响其他脏腑功能,从而共同影响精室。据此,进行“中虚精变”理论与男性精液疾病辨治的再探讨,明确中虚致病的若干途径,确立具体治法,拓展理论内涵,对于临床实践有着莫大裨益。首先,脾居中央以溉四旁,心、肺、肝、肾四脏的生成皆与脾胃有关,这决定了中虚在引发精液疾病过程中的关键地位;其次,导致精液改变的原因众多,既包括脾胃对精室的直接影响,亦包含兼有的四脏病变,如脾虚及肾导致精气皆亏,脾虚及肝导致血乏气郁,脾虚及肺导致宣肃失职,脾虚及心导致血亏神乱,脾虚生邪导致痰湿瘀结,皆能引发精室的异常和精液的改变;再次,精液疾病的辨治除纯用健脾法外,更当肾脾同治以复先后天之资助,肝脾同治以复精血之化生,肺脾同治以复气机之宣肃,心脾同治以复心神之调控,兼祛实邪以复气血之畅通;最后,“中虚精变”指导精液疾病的治疗具有减少疾病辨治难点、拓宽疾病辨治思路的优势,但未来仍需积极纳入和拓展优势病种,进行健脾方药影响精子的分子水平论证,以及肠道菌群失调为介质的中虚与生殖关系研究,以使“中虚精变”理论的内涵更加丰富。

“中虚精变”理论构建与应用

[目的]阐发“中虚精变”理论的构建过程及应用。[方法]以《内经》经典论述为研究对象,结合《金匮要略》《辨证录》《严氏济生方》等古籍以及临床见闻,从理论构建和应用两个方面进行探究。[结果]“中虚精变”立足脾虚视角,原因在于现今诱发脾胃损伤的因素繁多,门诊脾虚患者多见,而男科病病程迁延、久治不愈,须从脾胃论治等。《内经》“中气不足,溲便为之变”的论述启发了中气不足导致精液改变的思路,尤其精液、尿液取象比类。脾胃虚衰之不运、不固、不温和失却推动,同样是引发精液疾病的重要原因。“中虚精变”虽寥寥四字,但涉及脾虚对精室的直接损害以及中虚致虚、中虚致实的间接损害。以“中虚精变”指导临床治疗,当确立健脾顾四脏、不忘祛实邪,祛邪固脾胃、清利不伤正,虚实难辨别、通补最相宜的原则,补中益气汤、四君子汤、归脾汤、桂枝加龙骨牡蛎汤、当归芍药散五首代表方以健脾为核心,治疗精液疾病效果显著,启发了临床论治的思路。[结论]“中虚精变”理论主要阐发了男性精液疾病与脾虚的关系,通过理论构建及应用阐发,为此类疾病从脾胃论治提供了理法方药的借鉴,对临床具有积极意义。

Serum leptin and soluble leptin receptor in non-alcoholic fatty liver disease

AIM: To determine the role of leptin system in non-al- coholic fatty liver disease (NAFLD) development by deli- neating the changes in serum levels of leptin and soluble leptin receptor (sOB-R). METHODS: Blood samples were collected from 30 consecutive patients with liver-biopsy-proven NAFLD and 30 patients with cholecystolithiasis (stationary phase) as controls. Serum leptin levels were determined by radio- immunoassay and concentration of sOB-R was measured by ELISA. Body mass index (BMI) was calculated for all subjects, and serum insulin, C-peptide, and lipoprotein levels were also detected. RESULTS: Mean serum leptin level and BMI in the NAFLD group were significantly higher than in the con- trols (both P < 0.001), but mean sOB-R level was lower in the NAFLD group when compared to the controls. Both men and women in the NAFLD group had higher mean serum leptin levels and lower sOB-R levels than did the men and women in the control group (all P < 0.001). The- re was a significant negative correlation between serum leptin and sOB-R levels (r = -0.725, P < 0.001). Multiva- riate analysis showed that the percentage of hepatocyte steatosis, sex, BMI, and homeostasis model assessment of insulin resistance (HOMA IR) were independently rela- ted to serum leptin levels. CONCLUSION: Elevated serum leptin seems to be afeature of steatosis, and serum leptin seems to increase as hepatocyte steatosis develops. An enhanced release of leptin is accompanied by an decrease in sOB-R con- centration, which suggests higher resistance of periphe- ral tissues towards the action of leptin.