|
|
Discussion on the pathogenesis of rectal prolapse from “middle qi collapse” |
ZHOU Jiaojiao1 CHEN Qin1 LI Yufei1 WANG Xiaofeng1 CUI Guoce2▲ LI Huashan1▲ |
1.Department of Anorectal, Guang′anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China;
2.Department of Anorectal, Southern Branch of Guang′anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 102618, China |
|
|
Abstract In order to deepen the understanding of the pathogenesis of rectal prolapse in “middle qi collapse”, this paper expounds the two aspects of traditional Chinese medicine and modern medicine, in order to better guide the clinical practice, and also to point out the direction for the modeling of rectal prolapse in scientific research. In traditional Chinese medicine, “middle qi collapse” usually refers to a kind of disease, which is caused by qi deficiency, such as tissue relaxation and organ prolapse, indicating that “middle qi collapse” is directly related to the incidence of rectal prolapse. In modern medicine, the pathogenesis of rectal prolapse is the relaxation of rectal mucosa or the relaxation and separation of the rectum and its surrounding supporting tissue, and the rectum loses its support and slides down, which is basically consistent with the cognition of traditional Chinese medicine; as well as the experimental research on the establishment of artificial rectal prolapse model, the modeling method of chronic diarrhea coincides with the cognition of traditional Chinese medicine; in addition, rectal prolapse is common in fibulin-5 the weak mice, such as gene deficient mice, transgenic mice with low immune function or colitis mice, are also in line with the description of “qi deficiency can not be fixed, but it also falls off”, which indirectly indicates that the pathogenesis of rectal prolapse is related to the theory of “middle qi collapse”.
|
|
|
|
|
[1] van der Schans EM,Paulides TJC,Wijffels NA,et al. Management of patients with rectal prolapse:the 2017 Dutch guidelines [J]. Tech Coloproctol,2018,22(8):589-596.
[2] Ram E,Hoffman A,Goldes Y,et al. Perineal stapled rectal prolapse resection in elderly patients:long-term follow-up [J]. Dis Colon Rectum,2018,61(11):1316-1319.
[3] Dilke SM,Becker C,Tozer PJ,et al. Which operation is most effective for complete rectal prolapse? [J]. BMJ,2019,366:l4723.
[4] Iida Y,Honda K,Saitou H,et al. Modified Gant-Miwa-Thiersch procedure (mucosal plication with anal encircling) for rectal prolapse [J]. Colorectal Dis,2019,21(5):588-594.
[5] Cannon JA. Evaluation,diagnosis,and medical management of rectal prolapse [J]. Clin Colon Rectal Surg,2017,30(1):16-21.
[6] Gleditsch D,Wexels WA,Nesbakken A. Surgical options and trends in treating rectal prolapse:long-term results in a 19-year follow-up study [J]. Langenbecks Arch Surg,2018,403(8):991-998.
[7] Gallo G,Martellucci J,Pellino G,et al. Consensus Statement of the Italian Society of Colorectal Surgery (SICCR):management and treatment of complete rectal prolapse [J]. Tech Coloproctol,2018,22(12):919-931.
[8] Emile SH,Elfeki H,Shalaby M,et al. Perineal resectional procedures for the treatment of complete rectal prolapse:a systematic review of the literature [J]. Int J Surg,2017, 46:146-154.
[9] Handtrack C,Brunner M,Matzel KE. External rectal prolapse:etiology,pathogenesis and diagnosis [J]. Coloproctology,2018,40(3):166-174.
[10] Patcharatrakul T,Rao SSC. Update on the pathophysiology and management of anorectal disorders [J]. Gut and Liver,2017,12(4):375-384.
[11] Attaallah W. Update on the pathophysiology of rectal prolapse [J]. Turk J Gastroenterol,2019,30(12):1074-1075.
[12] Behdin N,Selleck M,Raskin E. Rectal prolapse in the setting of ascites:a case report [J]. ANZ J Surg,2019,89(3):269-270.
[13] Li J,Chen X,Ling K,et al. Evaluation of the bioactivity about anti-sca-1/basic fibroblast growth factor-urinary bladder matrix scaffold for pelvic reconstruction [J]. J Biomater Appl,2019,33(6):808-818.
[14] Moschvowitz AV. The pathogenesis,anatomy and cure of prolapse of the rectum [J]. Surg Gynecol Obstet,1912, 15:7.
[15] Devadhar DS. A new concept of mechanism and treatment of rectal procidentia [J]. Dis Colon Rectum,1965, 8:75-78.
[16] Brodén B,Snellman B. Procidentia of the rectum studied with cineradiography. A contribution to the discussion of causative mechanism [J]. Dis Colon Rectum,1968,11(5):330-347.
[17] Shafik A. A new concept of the anatomy of the anal sphincter mechanism and the physiology of defecation. ⅩⅢ. Rectal prolapse:a new concept of pathogenesis [J]. Am J Proctol Gastroenterol Colon Rectal Surg,1981,32(9):6-8.
[18] 黄乃健,史学文.直肠脱垂动物标本的采集和动物模型的建立——探索发病机理和最佳治疗方法[C]//第十八届中国中西医结合学会大肠肛门病专业委员会学术会议暨甘肃省第五届结直肠肛门外科学术年会论文汇编,2015:366-374.
[19] 柯敏辉,叶玲,陈立武,等.兔直肠黏膜内脱垂模型的建立[J].世界中医药,2013,8(12):1458-1464.
[20] Akintunde A,Robison KM,Capone D,et al. Effects of elastase digestion on the murine vaginal wall biaxial mechanical response [J]. J Biomech Eng,2018. [Epub ahead of print].
[21] Emmerson S,Young N,Rosamilia A,et al. Ovine multiparity is associated with diminished vaginal muscularis,increased elastic fibres and vaginal wall weakness:implication for pelvic organ prolapse [J]. Sci Rep,2017,7:45709.
[22] Cao LL,Yu J,Yang ZL,et al. MMP-1/TIMP-1 expressions in rectal submucosa of females with obstructed defecation syndrome associated with internal rectal prolapse [J]. Histol Histopathol,2019,34(3):265-274.
[23] 陈志雷,王振军.细胞外基质弹性纤维与普外科疾病[J].临床外科杂志,2018,26(6):472-473.
[24] Chin K,Wieslander C,Shi H,et al. Pelvic organ support in animals with partial loss of fibulin-5 in the vaginal wall [J]. PLoS One,2016,11(4):e0152793.
[25] Khadzhieva MB,Kamoeva SV,Chumachenko AG,et al. Fibulin-5 (FBLN5) gene polymorphism is associated with pelvic organ prolapse [J]. Maturitas,2014,78(4):287-292.
[26] Joshi HM,Gosselink MP,Smyth EA,et al. Expression of fibulin-5 in the skin of patients with rectal prolapse [J]. Colorectal Dis,2015,17(11):996-1001.
[27] Casey KM,Johnson AL,Hunrath MN,et al. Proliferative typhlocolitis with multinucleated giant cells:a nonspecific enteropathy in immunodeficient sentinel mice [J]. Vet Pathol,2019,56(1):157-168.
[28] Stagaard R,Ley CD,Almholt K,et al. Absence of functional compensation between coagulation factor Ⅷ and plasminogen in double-knockout mice [J]. Blood Adv,2018,2(22):3126-3136.
[29] Dong S,Harrington BK,Hu EY,et al. PI3K p110δ inactivation antagonizes chronic lymphocytic leukemia and reverses T cell immune suppression [J]. J Clin Invest,2019,129(1):122-136.
[30] Bhatt B,Zeng P,Zhu H,et al. Gpr109a limits microbiota-induced IL-23 production to constrain ILC3-mediated colonic inflammation [J]. J Immunol,2018,200(8):2905-2914.
[31] Wang Y,de Vallière C,Imenez Silva PH,et al. The proton-activated receptor GPR4 modulates intestinal inflammation [J]. J Crohns Colitis,2018,12(3):355-368.
[32] Wang Z,Vaughan TY,Zhu W,et al. Gab2 and Gab3 redundantly suppress colitis by modulating macrophage and CD8+ T-cell activation [J]. Front Immunol,2019, 10:486.
[33] Paiatto LN,Silva FGD,Yamada ?魣T,et al. Adoptive transfer of dendritic cells expressing CD11c reduces the immunological response associated with experimental colitis in BALB/c mice [J]. PLoS One,2018,13(5):e0196994.
[34] Singh V,Yeoh BS,Nilsen-Hamilton M,et al. Data on IL-10R neutralization-induced chronic colitis in Lipocalin 2 deficient mice on BALB/c background [J]. Data Brief,2017,11:588-592.
[35] Xiang J,Zhang Y,Bao D,et al. c-Abl regulates gastrointestinal muscularis propria homeostasis via ERKs [J]. Sci Rep,2017,7(1):3563.
[36] Percy DH,Barthold SW. Pathology of laboratory rodents and rabbits [M]. Ames(IA):Blackwell Publishing,2007.
[37] Ward JM,Anver MR,Haines DC,et al. Inflammatory large bowel disease in immunodeficient mice naturally infected with Helicobacter hepaticus [J]. Lab Anim Sci,1996,46(1):15-20. |
|
|
|