俞建輝



[摘要] 目的 探討調理脾胃針法對糖尿病胃輕癱(DGP)患者腦腸肽的調節作用及療效。 方法 選擇72例DGP患者隨機分為聯合組和對照組。兩組患者均予控制飲食、適量運動和控制血糖等基礎治療。兩組患者均予莫沙比利片5 mg/次,3次/d,口服;聯合組患者配合調理脾胃針法針刺治療,兩組均連用8周。比較兩組患者治療前與治療8周后血清VIP和NO指標的變化情況,并進行臨床療效評估。結果 治療8周后,兩組患者血清VIP和NO指標與治療前比較明顯下降(P<0.05或P<0.01),且聯合組治療后VIP和NO指標明顯低于對照組(P<0.05);同時聯合組和對照組治療的總有效率分別為94.44%和77.78%,聯合組明顯高于對照組(χ2=4.18,P<0.05)。 結論 調理脾胃針法聯合西藥莫沙比利治療DGP療效確切,作用機制可能與其能降低血清VIP和NO指標水平、糾正腦腸肽分泌紊亂、促進胃腸動力密切相關。
[關鍵詞] 糖尿病胃輕癱;調理脾胃針法;血管活性腸肽;一氧化氮
[中圖分類號] R246.1 [文獻標識碼] B [文章編號] 1673-9701(2017)06-0123-03
[Abstract] Objective To investigate the regulation and curative effect of regulating spleen-stomach needling on brain-gut peptide in patients with diabetic gastroparesis(DGP). Methods 72 patients with DGP were randomly divided into combination group and control group. Both groups were given basic treatment including controlling diet, moderate exercise and controlling blood glucose.Two groups of patients were treated with moxabiride tablets 5 mg each time, 3 times/d, oral, and the combined group was also given treatment of regulating spleen-stomach needling. The treatment in the two groups both lasted for 8 weeks. The serum VIP and NO indexes were compared between the two groups before and after 8 weeks of treatment, and the clinical curative effect was evaluated. Results After 8 weeks of treatment, the levels of serum VIP and NO in the two groups significantly decreased compared with those before treatment(P<0.05 or P<0.01), and the VIP and NO indexes were significantly lower in the combined group than those in the control group(P<0.05). The total effective rates were 94.44% and 77.78% in the combined group and the control group, respectively, and the total effective rate in combined group was significantly higher than that in the control group(χ2=4.18, P<0.05). Conclusion Regulating spleen-stomach needling method combined with western medicine moxapril in the treatment of DGP is effective, and the mechanism may be closely related to its ability to reduce serum VIP and NO levels, correct brain-gut peptide secretion disorders, and promote gastrointestinal motility.
[Key words] Diabetic gastroparesis; Regulating spleen-stomach needling method; Vasoactive intestinal peptide; Nitric oxide
糖尿病胃輕癱(DGP)是糖尿病較常見的并發癥之一,主要表現為嘔吐、反復呃逆、食后飽脹等胃排空延緩下降相關癥狀,其病情易反復發作,治療處理頗困難[1]。近年來研究已發現血管活性腸肽(VIP)和一氧化氮(NO)等腦腸肽的分泌紊亂參與其整個發病過程,在DGP發病機制中有極其重要的地位[2,3]。近年來我院采用調理脾胃針法治療DGP,療效滿意,進一步研究發現其對血清VIP和NO等腦腸肽具有明顯的調節作用,現報道如下。
1 資料與方法
1.1 臨床資料
選取2014年1月~2016年5月我院針推康復科就診的72例DGP患者。納入標準:(1)以《2型糖尿病防治指南(2007版)》中的診斷為準[4],且病程時間>3年;(2)具有典型癥狀,鋇餐透視示吞鋇超過6 h仍有鋇條在胃內殘留。排除標準:(1)伴糖尿病的急性并發癥,如酮癥酸中毒、低血糖休克和高滲昏迷等;(2)原有肝膽消化道器質性疾病或手術史。按照隨機數字表將患者分為聯合組和對照組。兩組性別、年齡、病程及空腹血糖等比較差異無統計學意義(P>0.05)。見表1。本方案經醫院倫理委員會批準,納入前均簽署知情同意書。
1.2 治療方法
兩組患者予控制飲食、適量運動和控制血糖等基礎治療。兩組患者均予莫沙比利片(江西豪森藥業股份有限公司,規格:5 mg×24片,批號131005)5 mg/次,3次/d,口服;聯合組配合調理脾胃針法針刺治療,取穴:地機、曲池、陰陵泉、三陰交、合谷、豐隆、太沖、足三里、血海、中脘。采用0.30 mm×50 mm和0.30 mm×60 mm針灸針。取仰臥位,穴位常規消毒,針刺深度以得氣為度,得氣后行補瀉手法,其中太沖、合谷、曲池、豐隆采用瀉法;三陰交、陰陵泉、足三里采用補法;中脘、血海、地機采用平補平瀉法;2次/d,每次留針30 min,連用5 d,休息2 d。兩組患者均連用8周。比較兩組患者治療前與治療8周后血清VIP和NO指標的變化情況,并進行臨床療效評估。
1.3 觀察指標
1.3.1血清VIP和NO指標測定 采集晨起空腹患者的靜脈血3 mL,常規低溫2500 r/min,離心10 min分離血清,將分離出上層血清提取,保存于-70℃冰箱。分別采用酶聯免疫吸附實驗(ELISA)法與放射免疫法測定血清VIP和NO指標。
1.3.2 療效評價標準[4] 顯效:癥狀較前明顯好轉,鋇餐透視示胃蠕動基本恢復正常;有效:癥狀較前有所好轉,鋇餐透視示胃蠕動較前加快;無效:癥狀較前無好轉,鋇餐透視示胃蠕動無好轉或加重。除無效均為總有效。
1.4 統計學處理
應用SPSS18.0統計學軟件,計量資料與計數資料分別以均數±標準差(x±s)和率[n(%)]表示,采用t與χ2檢驗,檢驗水準α=0.05。P<0.05為差異有統計學意義。
2 結果
2.1 兩組患者血清VIP和NO指標水平比較
兩組患者治療前血清VIP和NO指標水平比較差異無統計學意義(P>0.05)。治療8周后,兩組患者VIP和NO指標與治療前比較明顯下降(t=3.27、2.89、2.19、2.31,P<0.05或P<0.01),且聯合組治療后VIP和NO指標明顯低于對照組(t=2.29、2.21,P<0.05)。見表2。
2.2 兩組療效比較
治療8周后,聯合組和對照組治療總有效率分別為94.44%和77.78%,聯合組明顯高于對照組(χ2=4.18,P<0.05)。見表3。
3討論
DGP是一種糖尿病并發癥,主要是由于胃排空顯著減慢,胃內液體和固體食物潴留而出現的一系列臨床證候群,其發病率約1.5%~7.5%之間,臨床癥狀以胃運動障礙及胃排空延遲為主。DGP的發病機制十分復雜,至今國內外尚未完全研究明確,隨著對DGP發病機制的深入研究,已發現高血糖毒性、間質細胞數量或功能紊亂、幽門螺桿菌感染、腦腸肽分泌異常、氧化應激、血管內皮功能紊亂、鈉尿肽系統功能異常、神經與微血管病變等因素參與DGP發病過程[5-8],其中VIP和NO等腦腸肽分泌異常在DGP的發病中發揮的作用逐漸引起臨床重視。VIP和NO均為胃腸道分泌的一種抑制性腦腸肽,可抑制胃腸道平滑肌運動,減慢胃腸蠕動和抑制胃排空作用,抑制胃腸動力,抑制腸管對水電解質的轉運,對胃腸運動起負性調節作用[9-16]。因此,抑制VIP和NO的分泌、促進消化道運動有利于DGP的治療[17,18]。
中醫認為DGP屬“消渴兼痞滿”范疇,其病機大多為消渴日久致脾失健運,內生痰濁,痰郁日久,瘀阻脈絡引起,治療應調理脾胃、降逆止嘔和運化有常為主[19,20]。曲池與合谷和胃降逆,調理胃腸;中脘可健脾胃、助運化;足三里,補之能健脾胃,升陽舉陷,瀉之能引胃氣下行,助水谷之運化;陰陵泉健脾升陽,化濕滯;三陰交健脾益氣,調補肝腎,與足三里、中脘相伍,振奮中焦,使清升濁降,與陰陵泉相配,健脾利濕,開通水道;太沖平肝而調肝;豐隆和胃祛濕,潤腸道;血海能引血理血,祛瘀通脈;地機善于活血化瘀。諸穴合用有調理脾胃、使升降有序、健運有常、氣血得化之功效,切合DGP的病理與病機。本研究顯示治療8周后,聯合組血清VIP和NO指標下降程度大于對照組,且總有效率高于對照組,提示調理脾胃針法聯合西藥莫沙比利治療DGP療效確切,其作用機制與其降低血清VIP和NO指標水平、促進胃腸動力密切相關。我們推測認為調理脾胃針法聯合西藥莫沙比利治療DGP可能通過糾正腦腸肽分泌異常、減少VIP和NO等抑制性腦腸肽的分泌,降低血清VIP和NO指標水平,從而促進胃腸蠕動和胃排空,改善胃腸動力,使得脾胃逐漸如常,升降有序,健運有常,切合DGP的病理與病機達到治療目的。但本研究的病例數相對較少,研究時間相對較短,可能結果存在一定的偏差,必要時增加病例數及延長研究時間深入研究探討。
綜上,調理脾胃針法聯合西藥莫沙比利治療DGP療效確切,作用機制可能與其能降低血清VIP和NO指標水平、糾正腦腸肽分泌紊亂、促進胃腸動力密切相關。
[參考文獻]
[1] Nicolas Intagliata BA,Kenneth L,Koch.Gastroparesis in type-diabetes mellitus:Prevalence,etiology,diagnosis,and treatment[J].Current Gastroenterology Reports,2007, 9(4):270-279.
[2] Anitha M,Gondha C,Sutliff R,et al.GDNF rescues hyperglycemia-in-duced diabetic enteric neuropathy through activation of the PI3K/Akt pathway[J]. J Clin Invest,2006, 116(2):344-356.
[3] 吳波,韓萍,周卓.糖尿病胃腸病變與腦腸肽的相關性[J].廣東醫學,2004,25(11):1297-1290.
[4] 中華醫學會糖尿病學分會.中國2型糖尿病防治指南(2007年版)[J].中華醫學雜志,2008, 88(18):1227-1245.
[5] Larson JM,Tavakkoli A,Drane WE,et al.Advantages of azithromycin over erythromycin in improving the gastric emptying half-time in adult patients with gastroparesis[J].Journal of Neurogastroent Erology and Motility,2010,16(4):407-413.
[6] Borg J,Melander O,Johansson L,et al.Gastroparesis is associated with oxytocin deficiency, oesophageal dysmotility with hyper CCKemia,and autonomic neuropathy with hypergas trinemia[J]. BMC Gastroenterol,2009,9(2):17-19.
[7] James AN,Ryan JP,Crowell MD,et al.Regional gastric contractility alterations in a diabetic gastroparesis mouse model-eftects of cholinergic and serotoninergic stimulation[J].AmJ Physiol Gastrointest Liver Physiol,2004,287(3):612-619.
[8] Woerle HJ,Albrecht M,Linke R,et al.Impaired hyperglycemia-induced delay in gastric emptying in patients with type 1 diabetes deficient for iset amyloid polypeptide[J].Diabetes Care,2008,31(2):2325-2331.
[9] He CL,Soffer EE,Ferris CD,et al.Loss of interstitial cells of cajal and inhibitory innervation in insulin-dependent diabetes[J].Gastroenterology,2001,121(2):427-434.
[10] 赫廣玉,劉玉佳,謝曉娜.糖尿病自主神經病變胃輕癱發病機制及診治研究進展[J].中國老年學雜志,2013, 33(6):2987-2990.
[11] 林琳,計敏,趙志泉,等.四種胃腸激素在糖尿病胃動力障礙中的作用[J].現代消化及介入診療,2003,8(2):74-77.
[12] 劉曉娜,吳興全,王富春.胃腸激素與糖尿病胃輕癱發病機制的關系研究進展[J].長春中醫藥大學學報,2016,31(1):209-212.
[13] Sanger GJ,Westaway SM,Barnes AA,et al.GSK962040:A small molecule,selective motilin receptor agonist,effective as a stimulant of human and rabbit gastrointestinal motility[J].Neurogastroenterol Motil,2009,21(6):657-664.
[14] Joseph IM,Kirschner D.A model for the study of helicobater pylori interaction with human gastric acid secretion[J].J Theor Biol,2004,228(1):55-80.
[15] Brzozowski T,Konturek PC,Mierzwa M,et al.Effect of probiotics and triple eradication therapy on the cyclooxygenase(COX)-2 expression,apoptosis,and functional gastric mucosal impairment in Helicobacter pylori-infected Mongolian gerbils[J].Helicobacter,2006,11(2):10-20.
[16] Czaja M,Szarszewski A,Kamińska B,et al.Serum gastrin concentration and changes in G and D cell densities in gastric antrum in children with chronic gastritis[J]. Int J Clin Practm, 2008,62(5):1044-1049.
[17] Wiedemann T,Loell E,Mueller S,et al.Helicobacter pylori cag-Pathogenicity island-dependent early immunological response triggers later precancerous gastric changes in Mongolian gerbils[J]. PLoS One,2009,4(1):e4754.
[18] 于豐彥,周福生,牛麗華,等.糖尿病胃輕癱中醫證候的胃動力相關研究[J].國際醫藥衛生導報,2009,15(4):81-83.
[19] 尚瑩瑩,黃天生,肖定洪.糖尿病胃輕癱中醫理論及臨床研究進展[J].中醫研究,2013,26(1):75-77.
[20] 張萍,劉占芬,王春梅,等.調理脾胃針法治療糖尿病胃輕癱療效觀察[J].中國針灸,2007,27(4):258-260.
(收稿日期:2016-12-27)