Defective thymopoiesis and poor peripheral homeostatic replenishment of T-helper cells cause T-cell lymphopenia in cirrhosis.

BACKGROUND & AIMS: Depletion of circulating CD4(+) T-helper (Th) lymphocytes, especially naive Th cells, is common in cirrhosis. Little is known about the pathogenetic mechanisms involved in Th-cell depletion in cirrhosis. We investigated the mechanisms involved in circulating Th-cell lymphopenia in cirrhosis. METHODS: Circulating naive and memory Th cells were analyzed by flow cytometry in 60 patients with cirrhosis and 40 sex- and age-matched healthy controls. Thymopoiesis, apoptosis, cell activation, and proliferation were assessed through CD31, annexin-V, HLA-DR and Ki-67 expression, respectively. Lipopolysaccharide (LPS)-binding protein (LBP) and spleen size were measured as indicators of bacterial translocation and splenic pooling, respectively. RESULTS: Compared to controls, patients showed reduced numbers of Th cells involving a greater depletion of the naive than memory Th-cell compartment (2.7- vs. 1.5-fold, respectively). Recent thymic emigrants were diminished (p < 0.01), and each patient had a lower number of CD31(+) naive Th cells than the matched-control. Spontaneous and induced apoptosis (Annexin-V(+)) of Th cells was increased in patients. Activated (HLA-DR(+)) and proliferating (Ki-67(+)) memory Th cells were increased in patients (p < 0.01), and they directly correlated with plasma LBP (p < 0.05) and negatively with naive Th cells (p < 0.01), respectively. Naive Th cells were inversely correlated (p < 0.01) with their frequencies of apoptosis and of activated memory Th cells, LBP, and spleen size. On multivariate analysis, defective thymic generation of naive Th cells, increased memory Th-cell activation, and splenomegaly were independently associated with Th-cell depletion. CONCLUSIONS: Th-cell immunodeficiency in cirrhosis is explained by a universal defect in thymopoiesis exacerbated by splenic pooling and activation-driven cell-death induced by bacterial translocation.

The association between serum IGF-1 and neonatal growth and disease in a NICU / 소아과

PURPOSE: The objective of this study was to establish the serum IGF-1 level in newborn infants, and investigate its association with growth and diseases. METHODS: In a retrospective study, serum IGF-1 levels were measured for newborn infants admitted to NICU at Kyungpook University Hospital from March 2007 to July 2007. Birth data, disease history, and hospital course were obtained from medical records. RESULTS: Of 52 blood samples obtained at birth, serum IGF-l levels in 30 preterm infants (31.6+/-27.3 ng/mL) were lower than in 22 full-term infants (53.4+/-40.0 ng/mL; P<0.05). In sick full-term infants, serum IGF-1 levels (46.0+/-40.2 ng/mL) were lower than in healthy full-term infants (64.1+/-39.5 ng/mL; P<0.05). In preterm infants, there were no differences in IGF-1 levels between healthy (33.2+/-23.3 ng/mL) and sick infants (30.6+/-30.4 ng/mL); however, IGF-1 levels in both sick and healthy preterm infants were lower than in healthy full-term infants. Among infants admitted after 8 days of life, serum IGF-1 levels were higher in infants who gained weight (70.8+/-36.2 ng/mL) than in infants who lost weight (13.3+/-19.9 ng/mL; P<0.01); however IGF-1 levels showed no difference between gender or method of delivery. CONCLUSION: The study showed lower IGF-l levels in preterm infants than in full-term infants. Additionally, the IGF-l level in infants with weight loss was lower than in infants with weight gain. These results indicate that serum IGF-1 is associated with gestational age and postnatal growth.