中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2009年
6期
584-586
,共3页
杜焕青%刘聪慧%郑艳%侯灵彤
杜煥青%劉聰慧%鄭豔%侯靈彤
두환청%류총혜%정염%후령동
多囊卵巢综合征%C-反应蛋白%胰岛素抵抗%2型糖尿病%白细胞介素-18
多囊卵巢綜閤徵%C-反應蛋白%胰島素牴抗%2型糖尿病%白細胞介素-18
다낭란소종합정%C-반응단백%이도소저항%2형당뇨병%백세포개소-18
Polyeystic ovary syndrome%C-reactive protein%Insulin resistance%Type 2 diabetes%In-terleukin-18
目的 探讨多囊卵巢综合征(PCOS)患者血清CRP及IL-18水平与胰岛素抵抗(IR)的关系.方法 对36例PCOS患者(研究组)及20例正常对照者(对照组)进行血清CRP、IL-18及性激素检测,同时进行葡萄糖耐量试验(OGTT)及胰岛素(INS)释放试验.计算体重指数(BMI)、空腹血糖胰岛素比率(FGIR)、糖负荷120 min血糖胰岛素比率(G120/I120)及稳态模型的胰岛素抵抗指数(HOMA-IR).结果 ①研究组血清睾酮(T)水平及促黄体生成素/促卵泡生成素(LH/FSH)比值均明显高于对照组[分别为(2.77±1.30)nmol/L比(1.21±0.67)nmol/L,2.31±0.87比0.58±0.32,P均<0.05)],研究组logCRP及IL-18均明显高于对照组[分别为0.16±0.20比-0.47±0.38,(0.21±0.08)μg/L比(0.15±0.06)μg/L,P均<0.05];②研究组BMI、空腹INS(I0)均明显高于对照组[30.83±6.65)kg/m2比(22.23±2.68)kg/m2,(35.76±24.11)mU/L比(11.90±5.32)mU/L,P均<0.05],OGTT后60、120 min血糖及INS均明显高于对照组[G60(9.77±2.75)mmol/L比(7.84±2.02)mmol/L,G120(7.97±2.07)mmol/L比(6.24±1.80)mmol/L,I60(228.38±60.16)mU/L比(132.46±60.15)mU/L,I120(172.94±48.39)mU/L比(90.63±39.79)mU/L,P均<0.05];研究组HOMA-IR明显高于对照组(9.59±4.72比3.06±0.82,P<0.05),而FGIR明显低于对照组(0.11±0.04比0.23±0.02,P<0.05);③Pearson相关分析显示,losCRP与BMI、HO-MA-IR呈正相关(r分别为0.5、0.37,P均<0.05),IL-18与BMI、HOMA-IR呈正相关(r分别为0.58、0.61,P均<0.05);排除BMI影响后的偏相关分析显示,logCRP与HOMA-IR仍呈正相关(r=0.46,P<0.05),与FGIR及G120/I120呈负相关(r分别为-0.54、-0.48,P均<0.05).方法 PCOS患者均合并IR,其血清CRP及IL-18水平均明显升高;并且ClIP及IL-18水平与IR程度呈正相关,提示慢性炎症可能参与PCOS的发病,与HOMA-IR有关.
目的 探討多囊卵巢綜閤徵(PCOS)患者血清CRP及IL-18水平與胰島素牴抗(IR)的關繫.方法 對36例PCOS患者(研究組)及20例正常對照者(對照組)進行血清CRP、IL-18及性激素檢測,同時進行葡萄糖耐量試驗(OGTT)及胰島素(INS)釋放試驗.計算體重指數(BMI)、空腹血糖胰島素比率(FGIR)、糖負荷120 min血糖胰島素比率(G120/I120)及穩態模型的胰島素牴抗指數(HOMA-IR).結果 ①研究組血清睪酮(T)水平及促黃體生成素/促卵泡生成素(LH/FSH)比值均明顯高于對照組[分彆為(2.77±1.30)nmol/L比(1.21±0.67)nmol/L,2.31±0.87比0.58±0.32,P均<0.05)],研究組logCRP及IL-18均明顯高于對照組[分彆為0.16±0.20比-0.47±0.38,(0.21±0.08)μg/L比(0.15±0.06)μg/L,P均<0.05];②研究組BMI、空腹INS(I0)均明顯高于對照組[30.83±6.65)kg/m2比(22.23±2.68)kg/m2,(35.76±24.11)mU/L比(11.90±5.32)mU/L,P均<0.05],OGTT後60、120 min血糖及INS均明顯高于對照組[G60(9.77±2.75)mmol/L比(7.84±2.02)mmol/L,G120(7.97±2.07)mmol/L比(6.24±1.80)mmol/L,I60(228.38±60.16)mU/L比(132.46±60.15)mU/L,I120(172.94±48.39)mU/L比(90.63±39.79)mU/L,P均<0.05];研究組HOMA-IR明顯高于對照組(9.59±4.72比3.06±0.82,P<0.05),而FGIR明顯低于對照組(0.11±0.04比0.23±0.02,P<0.05);③Pearson相關分析顯示,losCRP與BMI、HO-MA-IR呈正相關(r分彆為0.5、0.37,P均<0.05),IL-18與BMI、HOMA-IR呈正相關(r分彆為0.58、0.61,P均<0.05);排除BMI影響後的偏相關分析顯示,logCRP與HOMA-IR仍呈正相關(r=0.46,P<0.05),與FGIR及G120/I120呈負相關(r分彆為-0.54、-0.48,P均<0.05).方法 PCOS患者均閤併IR,其血清CRP及IL-18水平均明顯升高;併且ClIP及IL-18水平與IR程度呈正相關,提示慢性炎癥可能參與PCOS的髮病,與HOMA-IR有關.
목적 탐토다낭란소종합정(PCOS)환자혈청CRP급IL-18수평여이도소저항(IR)적관계.방법 대36례PCOS환자(연구조)급20례정상대조자(대조조)진행혈청CRP、IL-18급성격소검측,동시진행포도당내량시험(OGTT)급이도소(INS)석방시험.계산체중지수(BMI)、공복혈당이도소비솔(FGIR)、당부하120 min혈당이도소비솔(G120/I120)급은태모형적이도소저항지수(HOMA-IR).결과 ①연구조혈청고동(T)수평급촉황체생성소/촉란포생성소(LH/FSH)비치균명현고우대조조[분별위(2.77±1.30)nmol/L비(1.21±0.67)nmol/L,2.31±0.87비0.58±0.32,P균<0.05)],연구조logCRP급IL-18균명현고우대조조[분별위0.16±0.20비-0.47±0.38,(0.21±0.08)μg/L비(0.15±0.06)μg/L,P균<0.05];②연구조BMI、공복INS(I0)균명현고우대조조[30.83±6.65)kg/m2비(22.23±2.68)kg/m2,(35.76±24.11)mU/L비(11.90±5.32)mU/L,P균<0.05],OGTT후60、120 min혈당급INS균명현고우대조조[G60(9.77±2.75)mmol/L비(7.84±2.02)mmol/L,G120(7.97±2.07)mmol/L비(6.24±1.80)mmol/L,I60(228.38±60.16)mU/L비(132.46±60.15)mU/L,I120(172.94±48.39)mU/L비(90.63±39.79)mU/L,P균<0.05];연구조HOMA-IR명현고우대조조(9.59±4.72비3.06±0.82,P<0.05),이FGIR명현저우대조조(0.11±0.04비0.23±0.02,P<0.05);③Pearson상관분석현시,losCRP여BMI、HO-MA-IR정정상관(r분별위0.5、0.37,P균<0.05),IL-18여BMI、HOMA-IR정정상관(r분별위0.58、0.61,P균<0.05);배제BMI영향후적편상관분석현시,logCRP여HOMA-IR잉정정상관(r=0.46,P<0.05),여FGIR급G120/I120정부상관(r분별위-0.54、-0.48,P균<0.05).방법 PCOS환자균합병IR,기혈청CRP급IL-18수평균명현승고;병차ClIP급IL-18수평여IR정도정정상관,제시만성염증가능삼여PCOS적발병,여HOMA-IR유관.
Objective To investigate the relationship of sermn C-reactive protein(CRP), IL-18 and insu-lin resistance(IR) in women with polycystic ovary syndrome (PCOS). Methods 36 women with PCOS (study group) and 20 healthy women (control group) were recruited. Serum C RP, IL-18 and sex hormone concentration were tested. Oral glucose tolerance tests (OGTT) and insulin release tests (IR) were conducted in all cases. Body mass index (BMI), fasting glucose to insulin ratio(FGIR), 2-hour glucose to insulin ratio(G120/I120) and homeo-markedly higher T level, LH/FSH ratio , logCRP and IL-18 than control group[(2.77±1.30) nmol/L vs (1.21±0.67) nmol/L, (2.31±0.87) vs (0.58±0.32), (0.16±0.20) vs (-0.47±0.38), (0.21±0.08) μg/L vs vs (22.23±2.68 ) kg/m2, P<0.05] and fasting insulin (I0) concentration [(35.76±24.11) mU/L vs (11.90± 5.32) mU/L, P<0.05)], higher serum glucose (G60=(9.77±2.75) mmol/L vs (7.84±2.02) mmol/L, G120= (7.97+2.07 ) mmol/L vs (6.24±1.80) mmol/L, P<0.05), insulin (I60= (228.38±60.16) mU/L vs (132.46±60.15) mU/L,I120= (172.94±48.39) mU/L vs (90.63±39.79) mU/L,P<0.05 for each) after OGTT and IRT than control group. HOMA-IR increased and FGIR decreased more significantly in study group than controls group (HOMA-IR=(9.59±4.72)vs (3.06±0.82), FGIR=(0.11±0.04) vs (0.23±0.02), HOMA-IR (r=0.5 and 0.37,P<0.05), IL-18 was positively correlatrd with BMI and HOMA-IR (r=0.58 and 0.61, P<0.05). Partial correlation showed that logCRP was positively correlated with HOMA-IR (r=0.46, P< 0.05), but negatively correlated with FGIR and G120/I120(r=-0.54 and -0.48,P<0.05 for all) in test group. Conclusion IR exists in women with PCOS, and their increased serum CRP and IL-18 level shows positive correla-tion with IR,demonstrating that chronic inflammation may participate in the pathogenesis of PCOS, and may have correlation with insulin resistance.
