1、 s K ? 1 H,bV, =# YO By 8 ,4Ug 82 UhB9FbFPG #O #$ /O s ?,yg iO F,#1O bFPG 8. 2 mmol/ L, B%s ? ? 9 , FFPGaHOM A- ISd9il,g FFPG (r8. 2 mmol/ L,g FFINSvF, Bg 8$ /O s ?,OB% ? YVs O bWeir 10G O% ?MFPG 1“,N O ,N OB% 9Fb O db# O byg iO F,#g 8 O dbb2 h PG 0 Sb L, Uh 0 _ UhMV,5 6bTA U F2 h PGd9il, $I30/$G 30
2、O wL/ (vF, FAs, 5* =MO s 9F, PS,81 Xs,wg 8O s ?sb8 ,Bg 8O F, HiOB%s ?s,yNg 8#*B% ?_# ,i |Mn bV1 g vF8FPGa2 haFINSa2 hO aHOMA- IR HOMA-IAIaHOMA-ISa$I30/ $G30aINSAUC1 ( x ? s)Table 1 Comparison of FPG, 2 h PG, FINS, 2 h INS, HOMA- IR, HOMA- IAI, HOMA- IS, $I30/$G30,INSAUC in Obesity and Control Groups
3、( x?s)FYn FPG( mmol/ L) 2 h PG(mm ol/ L) FINS( mU/ L) 2 h INS( mU/ L) HOMA-IR HOMA-IAI HOMA-IS $I30/ $G30 INSAUCg F62 4. 6? 0. 5 5. 9? 1. 2 14. 0? 8. 8 50. 4? 34. 2 0. 9? 0. 6 - 4. 0? 0. 6 5.4? 0. 6 3. 0? 1. 2 5. 0? 0. 6vF22 4. 4? 0. 8 5. 2? 1. 1 7. 0? 3. 7 15. 2? 14 0. 2? 0. 4 - 3. 0? 0. 4 5.2? 0.
4、9 1. 8? 1. 7 4. 0? 0. 7t/V 2 1. 35 2. 68 6.42 6. 66 7. 49 - 7. 49 1. 90 4. 02 6. 74P 0. 05 0. 05 , i:,.g O F1“ J . 4 2$D, 2006, 11( 1) : 37- 38. 8 +, , 9 ,.g OB% ?O M J .:D, 2006, 33( 3) : 393- 396. 9o, .2 UhOB% ?4 J . “5 = S, 2006, 23( 1) : 38- 40. 10 W eir GC, Bonner- Weir S . Five stages of evolv
5、ing B- cell dysfunc-tion during progression to diabetes J . Diabetes , 2004, 53( suppl 3) :S 16- S 21.(I := , 3, q, V, V 3 =,Z_ ?/Ab先天性肾上腺皮质增生症 5例刘志刚,吴红艳,黄长军(西安交通大学医学院第一附属医院儿科, 西安710061)K1 “ 45? / F 9 3 Ma)# n bZE 95 5? / F 9 3“5 b3 3VC , ( ga a| a* “,Q |sa , ; U17 %?A 64 , OKa )# L iVC; 5 / FCT , (
6、A U / F9vb5 ( 9 , m | M“ 2 bT 3 2 4 M, 9 n 3?S( 性征; 21-羟化酶;肾上腺皮质激素ms | R725. 8 DS M B cI| 1003- 515X( 2006) 20- 1386- 025? / F 9 3( congenital adrenal hyperplasia,CAH) n 8 L.h, / F o 5? J bnCAHsY21- a11B- a3B- %? _ a17A- J 1b “5 ?s() a y(Ka )aVCb7B?s ; a y8 ?h,h f ,OKbCAH8 (n M -42 d 10 b#1386# L8 S
7、 “521 20 2006 M10 J Appl Clin Pediatr, Vol. 21 No. 20, Oct. 20061 8 T; 3VB 8, 33 d 38 T=, 1 M - (v34 b 8 ( Tb二a临床表现 3 o 3VC ,|gvaU 7 g|1 b ( a* “,+Y ga a|, 3 7 dC |sa , b 32 , 1 % ,! 4,! , 1 M =Q3Q,2Q; 1 10 3|Yv,Ca#t2, ?r, 2bpvl# (b三a实验室检查 5 )( 120 127 mmol/ L) 3 ,K( 6. 18 6. 38 mmol/ L) 4 , o( 93.
8、2 mmol/ L)1 ; U 4 ;m_4 , 2 KVC( ToUaQ- TW ) , 2 mvb4 U17 %? ( 6( 59. 4 116. 6 Lmol/ 24 h,13. 9 55. 5Lmol / 24 h) ; 5 U17? (b5 ? s, 3 , 1 , 1 b4 _ ( A 6: x 23. 28 31. 0 IU / L( 112 IU / L) ,8 3 19. 0 21. 45 IU / L( 5 10 IU / L) ,h, M s0 3Z, v CAH C,7 ?h|, / F 5 ? s sE,Q T P/ m 7-ad db KK,8“ 3VC, 3 VJ
9、a |sa a8 9/a a )aKa , # H, Vy 7 ;d 31VCL* , 36C8* +, 4 5 A,|a| 5i - F9v,p, - -, o 3;d?a G , 21- C b 3VC| *Ca* a 3F a -4 -; o VCa?a #b 3 o? 3* 4b二a早期诊断 1 “5VC, 3VC ,|gv, IEB N( M -Vv)PCAH, QC |sa , H VT “5,iM1 L i_ bQC |sa , 3,$5? .N h, “5D =N;a VPh A17-#24 h U17 %? b17 %? 8 =K, CAHA 6bF5 / FCT (A Us
10、, 1NbG “5VCS 8s Y, P mg - VxbEB N TX 3V 8, V (14 20 17- i %zyFM F( HLA)_, V 21- C7T -,38 E17- V 5b三a治疗 h v,# H N 8 3 11b ?* a#* , V 3* ?Z,8 3# 3?b _ V 50 mg/ ( m2#d) 8 25 mg/ ( m2#d) b 10 20 mg/ ( m2#d) , (s3QbC / F # 3 f H _ V 4 Vr100mg/ ( m2#d)bXT+T 3?8 Vr b D C2 4 mg/ ( m2#d) ,s2Qb 0. 250 0. 375
11、mg/ ( m2#d) , 1Q/ db?C _ V 3Y D Cl,# Hi P _V 8K V & 6b V3,i V 3 o“+bL oR6 12|s M“ b* # m KD m HW2 6 7b21- J VBy E 8bF3 T0# 2 M, 3?S -8 AYb ID 1E +, . 21- C16 J .D, 2005, 20( 2) : 76. 2 d , !.5? / F 9 34 J . “5$Y,2005, 20( 8) : 470. 3l , .5? / F 9 3# J. L8 S “5, 2006, 21( 8) : 510- 513. 4B ,= +,b ,.
12、M -5? / F 938?Y J .S L8 S, 2006, 21 ( 4) : 272-273. 5 ,.8 S M .6.: 3,2005: 493- 497. 6 Khadilkar V, Khadilkar A, Maskati G. Impact of availability of oralhydrocortisone on grow th of children w ith CAH J . Indian J Pediatr ,2005, 72( 4) : 301- 303. 7 Joint L, W PES / ESPE CAH Working Group. Consensu
13、s statement on21- hydroxylase deficiency from the Lawson W ilkins Pediatric En-docrine S ociety and the European S ociety for Paediatric Endocrinology J .J Clin Endocr inol Metab, 2002, 87( 9) : 4048- 4053. 8 M erke DP, Bornstein SR. Congenital adrenal hyperplasia J. Lancet,2005, 365( 18) : 2125- 2136.(I :)#1387# L8 S “521 20 2006 M10 J Appl Clin Pediatr, Vol. 21 No. 20, Oct. 2006
