Serum lipase levels pre and post Lundh meal: evaluation of exocrine pancreatic status in cystic fibrosis

被引:6
作者
Augarten, A [1 ]
Katznelson, D
Dubenbaum, L
Doolman, R
Sela, BA
Lusky, A
Szeinberg, A
Kerem, BS
Paret, G
Gazit, E
Sack, J
Yahav, Y
机构
[1] Chaim Sheba Med Ctr, Cyst Fibrosis Ctr, IL-52621 Tel Hashomer, Israel
[2] Chaim Sheba Med Ctr, Chem Pathol Inst, IL-52621 Tel Hashomer, Israel
[3] Chaim Sheba Med Ctr, Dept Epidemiol, IL-52621 Tel Hashomer, Israel
[4] Hebrew Univ Jerusalem, Dept Genet, IL-91904 Jerusalem, Israel
关键词
cystic fibrosis; exocrine pancreas; lipase; Lundh meal;
D O I
10.1007/s005990050049
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Determination of pancreatic function is essential in cystic fibrosis. The most-reliable method is by measuring pancreatic enzymes in the duodenum following intravenous or oral stimulation. However, this is invasive, time consuming, and expensive. Indirect tests are non-invasive but lack accuracy. This study examines a simple test which combines pancreatic stimulation by Lundh meal and sequential serum lipase measurements. The test was performed on three groups: group A, 36 cystic fibrosis patients carrying two mutations associated with severe disease and pancreatic insufficiency (Delta F508, W1282X, G542X, N1303K, S549R); group B, 8 compound heterozygote cystic fibrosis patients carrying one mutation causing mild disease with pancreatic sufficiency (3849 + 10 kb C --> T); group C, 17 healthy individuals. Basal lipase levels were 2-16.5, 16.4-73, and 8.5-27.8 U/l in groups A, B, and C, respectively, with some overlapping between groups. There were three patterns of lipase activity(1) consistently low levels (group A) suggested a severely affected insufficient pancreas; (2) normal basal levels followed by a linear rise peaking 30 min after the meal (found in 16 of 17 healthy individuals and 3 patients of group B) reflecting an unaffected sufficient pancreas; (3) elevated lipase levels not influenced by the meal (5 patients of group B). This reflects an ongoing destructive process in the pancreas which will eventually result in conversion from pancreatic sufficiency to pancreatic insufficiency. Hence serum lipase activity prior to and 30 min after Lundh meal is a good indicator of pancreatic status allowing categorization of cystic fibrosis patients as pancreatic insufficient, pancreatic sufficient, or pancreatic sufficient with late conversion to insufficiency.
引用
收藏
页码:226 / 229
页数:4
相关论文
共 18 条
[1]   MILD CYSTIC-FIBROSIS AND NORMAL OR BORDERLINE SWEAT TEST IN PATIENTS WITH THE 3849+10 KB C-]T MUTATION [J].
AUGARTEN, A ;
KEREM, BS ;
YAHAV, Y ;
NOIMAN, S ;
RIVLIN, Y ;
TAL, A ;
BLAU, H ;
BENTUR, L ;
SZEINBERG, A ;
KEREM, E ;
GAZIT, E .
LANCET, 1993, 342 (8862) :25-26
[2]   The significance of sweat Cl/Na ratio in patients with borderline sweat test [J].
Augarten, A ;
Hacham, S ;
Kerem, E ;
Kerem, BS ;
Szeinberg, A ;
Laufer, J ;
Doolman, R ;
Altshuler, R ;
Blau, H ;
Bentur, L ;
Gazit, E ;
Katznelson, D ;
Yahav, Y .
PEDIATRIC PULMONOLOGY, 1995, 20 (06) :369-371
[3]   PATHOPHYSIOLOGY OF GASTROINTESTINAL COMPLICATIONS OF CYSTIC-FIBROSIS [J].
BOROWITZ, D .
SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 15 (05) :391-401
[4]  
CLEGHORN G, 1986, PEDIATRICS, V77, P301
[5]   AGE-RELATED ALTERATIONS IN IMMUNOREACTIVE PANCREATIC LIPASE AND CATIONIC TRYPSINOGEN IN YOUNG-CHILDREN WITH CYSTIC-FIBROSIS [J].
CLEGHORN, G ;
BENJAMIN, L ;
COREY, M ;
FORSTNER, G ;
DATI, F ;
DURIE, P .
JOURNAL OF PEDIATRICS, 1985, 107 (03) :377-381
[6]   DECLINE OF EXOCRINE PANCREATIC FUNCTION IN CYSTIC-FIBROSIS PATIENTS WITH PANCREATIC SUFFICIENCY [J].
COUPER, RTL ;
COREY, M ;
MOORE, DJ ;
FISHER, LJ ;
FORSTNER, GG ;
DURIE, PR .
PEDIATRIC RESEARCH, 1992, 32 (02) :179-182
[7]   IMMUNOCYTOCHEMICAL LOCALIZATION OF THE CYSTIC-FIBROSIS GENE-PRODUCT CFTR [J].
CRAWFORD, I ;
MALONEY, PC ;
ZEITLIN, PL ;
GUGGINO, WB ;
HYDE, SC ;
TURLEY, H ;
GATTER, KC ;
HARRIS, A ;
HIGGINS, CF .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (20) :9262-9266
[8]  
FITZSIMMONS SC, 1982, J PEDIATR, V100, P857
[9]  
GASKIN KJ, 1984, GASTROENTEROLOGY, V86, P1
[10]  
HAMOSH A, 1993, NEW ENGL J MED, V329, P1308