IGF binding proteins in growth-retarded children with chronic renal failure

Changes in the normal hormonal regulation of linear growth which lead to growth failure in children with chronic renal failure (CRF) are not well understood. Previous studies indicate that serum levels of growth hormone and IGF-I and II are normal or elevated in this population; and that serum levels of poorly defined inhibitors of IGF action are increased. Using a recently developed RIA for the 25-kD IGF-binding protein (IGF-BP25), we report significant elevations of this protein in children with CRF when compared to age- and sex-matched controls. IGF-BP25 levels correlate positively with IGF-binding activity in both populations, indicating that the RIA reflects levels of bioactive protein. Although the variation of serum IGF-BP25 with chronologic age and IGF levels are preserved in CRF, the quantitative interrelationships are disrupted. Levels of the 53-kD IGF-binding protein, an IGF-binding protein derived from the high mol wt IGF complex, were also found to be elevated in the CRF population and, unlike in the control population, did not vary with age or IGF levels. IGF-BP25 has been shown to inhibit IGF mitogenic action in vitro. Our finding of elevated levels of IGF-BP25 in children with CRF suggests that this protein may play a role in the growth retardation of pediatric chronic renal failure. The significance of the elevated IGF-BP53 levels in CRF remains uncertain.     

Early developmental changes in IGF-I, IGF-II, IGF binding protein-1, and IGF binding protein-3 concentration in the cerebrospinal fluid of children

IGF-I and IGF-II are ubiquitously expressed growth factors that have profound effects on the growth and differentiation of many cell types and tissues, including cells of the CNS. In biologic fluids, most IGFs are bound to one of six IGF binding proteins (IGFBPs 1-6). Increasing evidence strongly supports a role for IGF-I in CNS development, as it promotes neuronal proliferation and survival. However, little is known about IGF-I and its homolog IGF-II and their carrier proteins, IGFBPs, during the neonatal period in which brain size increases dramatically, myelination takes place, and neurons show limited capacity to proliferate. Herein, we have determined the concentrations of IGF-I, IGF-II, IGFBP-1, and IGFBP-3 in cerebral spinal fluid (CSF) samples that were collected from children who were 1 wk to 18 y of age. The concentrations of IGF-I, IGFBP-1, and IGFBP-3 in CSF from children <6 mo of age were significantly higher than in older children, whereas IGF-II was higher in the older group. This is in contrast to what is observed in the peripheral circulation, where IGF-I and IGFBP-3 are low at birth and rise rapidly during the first year, reaching peak levels during puberty. Higher concentrations of IGF-I, IGFBP-1, and IGFBP-3 in the CSF of very young children suggest that these proteins might participate in the active processes of myelination and synapse formation in the developing nervous system. We propose that IGF-I and certain IGFBPs are likely necessary for normal CNS development during critical stages of neonatal brain growth and development.     

Serum levels of insulin-like growth factor (IGF)-I, free IGF-I, IGF binding protein (IGFBP)-1, IGFBP-3 and insulin in obese children.

In simple obesity, spontaneous and stimulated growth hormone (GH) secretions are diminished. However, this diminished GH secretion does not result in decreased somatic growth in obese children. Although the increased insulin level, low insulin-like growth factor binding protein (IGFBP)-1 and the resulting increase of bioavailability of insulin-like growth factor I (IGF-I) have been suggested as being involved, the exact mechanism has not yet been established. We investigated serum IGF-I, free IGF-I, IGFBP-1, IGFBP-3 and insulin levels in 36 obese and 39 non-obese healthy children. Insulin and IGFBP-3 were significantly higher in the obese group than in the control group (p < 0.05, p = 0.001, respectively). IGF-I, free IGF-I, free IGF-I/IGF-I and IGFBP-1 levels in the obese children were not significantly different from those in the control group. A positive correlation was found between body mass index (BMI) and IGF-I in the obese children (r = 0.30, p = 0.05). IGFBP-3 levels correlated positively with IGF-I (r = 0.44, p < 0.005), and free IGF-I levels (r = 0.37, p = 0.05) in the obese children. A negative correlation was found between IGFBP-1 and insulin levels (r = -0.30, p = 0.05) in the obese children. We concluded that normal growth in obese children might be maintained through normal IGF-I and increased IGFBP-3 levels, which are stimulated by increased insulin levels or nutritional factors or by increased responsiveness to GH.     

Short stature with normal growth hormone and elevated IGF-I

We report on a Japanese girl with short stature, malar hypoplasia, up-slanting palpebral fissures, blue sclerae and thin, stiff and slightly brownish hair. Short stature started in utero and her psychomotor development was normal. Menarche appeared at 13 years 8 months. Height at 14 years 5 months was 132 cm (–4.6 SD). Her growth hormone (GH) sleep pattern and responses to insulin,l-dopa, arginine, propranolol-glucagon and growth hormone-releasing hormone were normal. Plasma insulin-like growth factor I (IGF-I) was high (2170–4860 units/l) and increased from 4860 to 7080 units/l 20 h after biosynthetic GH injection. Gel infiltration patterns of the free and protein-bound IGF-I in plasma from the patient were not different from the controls; IGF-I fraction of the high and low molecular weight binding protein and the non-protein bound fraction were 75.5%, 15.8% and 8.7%, respectively. IGF-I from the patient showed normal bioactivities when determined by [³⁵S]sulphate and [³H]thymidine uptake into cultured rat chondrocytes, and by [³H]thymidine and [³H]-aminoisobutyric acid uptake into the patient's skin fibroblasts. IGF-I binding to cultured skin fibroblasts from the patient was comparable to that of controls. These results suggest that tissue specific defects of IGF-I receptors may be the cause of increased IGF-I levels in the patient.     

Insulin-like growth factors I and II and their binding proteins in human milk: effect of heat treatment on IGF and IGF binding protein stability.

Insulin-like growth factors (IGF-I and -II) are peptide growth factors that contribute to the growth-promoting properties of human milk. IGFs in extra cellular fluids are associated with high-affinity binding proteins (IGFBPs). In this study, IGF-I and -II, and IGFBPs in human milk were characterized, and the stability of the IGFs and IGFBPs to heat treatment was investigated. IGF-I and -II were quantified by radioimmunoassays of acid-chromatographed samples, and IGFBPs were characterized using Western ligand blotting. The concentration (mean +/- SD) of IGF-I in human milk was 1.5 +/- 0.5 micrograms/L, compared to 2.7 +/- 0.7 micrograms/L for IGF-II. Heat treatment did not significantly affect either IGF-I or -II content. Human milk contains a single, nonglycosylated, IGFBP, with an apparent Mr of 31 k, which was immunoprecititable by an antibody to IGFBP-2. Stability of the IGFBP to heat treatment was assessed and was not significantly affected by heat treatment. Therefore, both IGF-I and -II, and the IGFBP in human milk appear to be stable under heat treatment conditions routinely used for processing banked human milk.     

短期吸入小剂量糖皮质激素对哮喘患儿骨转换指标影响的研究

目的研究短期吸入小剂量糖皮质激素对哮喘儿童骨转换指标的影响。方法对８例无激素治疗史哮喘儿童持续吸入二丙酸倍氯米松（ＢＤＰ）２００～３００μｇ／ｄ,疗程１～２个月。疗程开始与结束时分别检测血清钙、磷、碱性磷酸酶、骨钙素及尿羟脯氨酸／肌酐比值。结果吸入ＢＤＰ１～２个月后患儿血清骨钙素水平下降了２０５６％,Ｐ＜００５,而血钙、磷、碱性磷酸酶水平和尿羟脯氨酸／肌酐比值无明显改变。结论短期内吸入ＢＤＰ２００～３００μｇ／ｄ有可能发生骨生成抑制。有必要对血清骨钙素水平进行长期动态观察     

Leptin, insulin-like growth factor (IGF)-I and IGF binding protein-3 levels in children with constitutional delay of growth

This study was planned in order to investigate the role of insulin-like growth factor-I (IGF-I), IGF binding protein-3 (IGFBP-3) and leptin, the product of the ob gene synthesized by fat tissue cells, in constitutional delay of growth and puberty (CDGP) which is the most frequent cause of short stature in children. This study was conducted on 80 children with CDGP aged 6-15 years, and 60 healthy children served as controls. Serum IGF-I, IGFBP-3, insulin and plasma leptin levels were measured by immunoradiometric assay. Mean IGF-I and leptin levels were significantly lower in the CDGP group compared with the controls, but the mean IGFBP-3 level was not different in the two groups. Mean leptin levels were 3.72 +/- 2.29 in CDGP and 4.68 +/- 3.08 in the control group (p <0.05). There was a statistically significant relationship between leptin levels and height, weight, and body mass index. Leptin levels were also correlated with chronological age, bone age and height age. When evaluated according to pubertal status, a significant difference was found in IGF-I, leptin and IGFBP-3 levels between prepubertal and pubertal groups. Leptin levels were significantly different in the prepubertal CDGP group compared with controls but in the pubertal CDGP group only IGF-I levels were significantly different from controls. As the weight of children with CDGP was lower than in the control group, it is postulated that the reason for short stature and pubertal delay may be this decrease in weight which is also the cause of low levels of leptin and IGF-I.     

Ghrelin, leptin and IGF-I levels in breast-fed and formula-fed infants in the first years of life

AIM: To establish ghrelin, leptin and IGF-I serum levels in breastfed (BF) and formula-fed (FF) infants during the first period of life. METHODS: A cross-sectional study was conducted on fasting blood venous samples obtained from exclusively BF (n=106) and FF (n=100) infants to measure total ghrelin (RIA test), leptin (RIA test) and IGF-I (chemiluminescence). Anthropometrical measurements of weight, length and cranial circumference were performed. RESULTS: During the first 4 mo of life, FF infants compared to BF ones showed higher ghrelin levels (2654.86 vs 2132.96 pg/ml; p<0.032), higher IGF-I levels (3.73 vs 3.15 ng/ml; p=0.00) and lower leptin levels (0.68 vs 1.16 ng/ml; p<0.04). Leptin values were higher in females than in males (0.80 vs 0.47 ng/ml; p<0.03), while no gender-related difference was found for ghrelin and IGF-I. No differences were found in anthropometrical measurements comparing the two groups of infants. A multiple regression analysis showed an inverse correlation between ghrelin and leptin values (p<0.04) and between IGF-I and leptin levels (p=0.00). CONCLUSION: Our finding suggests that breastfeeding influences hormones such as ghrelin, leptin and IGF-I in infancy, mainly during the first 4 mo of life. Further evidence is needed to confirm and clarify the role of a protective link from mother to infants as seen in our observations.     

Feto-maternal interaction of IGF-I and its binding proteins in fetal growth.

Elevated levels of maternal IGF-I and IGF-binding proteins IGFBP-1 are regulated by placental hormones rather than pituitary control during pregnancy. Maternal IGF-I promotes fetal growth by stimulating nutrient transfer to fetus through placenta and IGFBP-1 suppresses fetal growth by inhibiting IGF-I binding to receptors in placenta. Since IGF-I and IGFBP-1 are produced in placenta and decidua, respectively, fetal growth is regulated by these substances in the locally formed paracrine system.     

IGF-I, IGF-II, IGF binding protein 1, and C-peptide in second trimester amniotic fluid are dependent on gestational age but do not predict weight at birth.

Previous data suggested that small for gestational age newborns have increased levels of IGF binding protein 1 (IGFBPI) in amniotic fluid (AF) at 15-16 wk of pregnancy. In this study, we developed an RIA for IGFBP1 and measured IGFBP1 concentrations in 209 AF samples with normal fetal karyotype between 14 and 20 wk; we measured IGF-I, IGF-II, and C-peptide in the same samples. Concentrations of these growth-modulating factors were all positively correlated with gestational age at sampling (p < 0.0001). After correcting for gestational age, AF IGFBP1 remained strongly correlated with IGF-I and IGF-II (both p < 0.0001); their concentrations were many times higher in AF than in cord serum during the third trimester. None of the growth-modulating factors in AF correlated with birth weight, after correction for gestational age; birth weight percentile distribution was comparable in two groups of newborns who had AF values of IGF-I, IGF-II, IGFBP1, or C-peptide that were either less than or equal to the 50th percentile or more than the 50th percentile at sampling. However, placenta weight and the placenta weight to birth weight percentage were negatively correlated with AF IGF-I, IGF-II, and IGFBP1; placenta weight to birth weight percentage was lower in pregnancies with IGFBP1 values more than the 50th percentile compared with those less than or equal to the 50th percentile at sampling. In conclusion, AF concentrations of IGFBP 1 increase gradually between 14 and 20 wk gestational age and correlate with IGF-I and IGF-II levels; high IGFBP1 levels do not predict small for gestational age newborns, but are associated with lower placenta weight.     

Changes in bone markers in children with asthma during inhaled budesonide and nedocromil treatments

We evaluated serum and urinary markers of bone turnover in 14 children with asthma during inhaled budesonide and nedocromil treatments. Both the markers of formation (serum carboxy- and aminoterminal propeptides of type I procollagen and serum osteocalcin) and the markers of degradation (serum carboxy-terminal telopeptide of type I collagen and urinary pyridinium cross-links) decreased (p < 0.05) during budesonide treatment for 6 months. During inhaled nedocromil treatment (for the following 6 months), the markers returned to the normal levels. These transient decreases in the markers of both formation and degradation of bone suggest that inhaled budesonide may slightly decrease the bone turnover rate. However, normal “coupling” between formation and degradation seemed to operate, e.g. a change in one resulted in a corresponding change in the other, so that net bone loss did not necessarily occur.     

Basal and stimulated levels of growth hormone, insulin-like growth factor-I (IGF-I), IGF-I binding and IGF-binding proteins in beta-thalassemia major

A significant percentage of children with beta-thalassemia major shows retardation in longitudinal growth as they progress towards puberty due to skeletal dysplasia, endocrine gland hypofunction or trace element deficiencies. The aim of this study was to evaluate GH/IGF-I secretion and action in prepubertal patients with beta-thalas-semia major. Eight prepubertal patients with short stature (group A) and seven prepubertal patients with normal stature (group B) were studied. Basal and stimulated (after administration of the hexapeptide Hexarelin) GH levels were measured with IRMA (Nichols); IGF-I and IGFBP-3 levels were measured with RIA (Nichols). IGF-I binding proteins (IGFBPs) were analyzed qualitatively with Western ligand blot. IGF-I binding to B-lymphocytes of the patients was also measured with competitive binding studies using human recombinant IGF-I and 125I-IGF-I (Amersham). Basal GH levels did not differ statistically between the groups. Peak GH levels after Hexarelin stimulation test were higher in group A (A: 27.9 +/- 15.6 ng/ml vs B: 9.1 +/- 4.7 ng/ml) (Wilcoxon test, p < 0.05). IGF-I levels in the two groups were low-normal and comparable (A: 168.0 +/- 81.6 ng/ml vs B: 126.6 +/- 25.5 ng/ml). IGFBP-3 levels were low in both groups (A: 1.21 +/- 0.27 microg/ml vs B: 1.08 +/- 0.20 microg/ml). Western ligand blot did not reveal any discernible difference in IGFBPs. However, IGF-I binding on B-lymphocytes was at least 20% lower in group A compared to group B (t-test, p < 0.01). IGF-I binding inversely correlated with peak GH levels (r = -0.54, p < 0.05). Patients in group A were older and chronological age correlated with IGF-I levels (r = 0.53, p < 0.05) whereas it inversely correlated with IGF-I binding (r = -0.63, p < 0.05). Moreover, patients in group A had higher ferritin levels. No correlation was found between ferritin levels, desferrioxamine dose/compliance or liver enzyme levels and the parameters of the GH axis studied. However, desferrioxamine dose x years correlated with IGFBP-3 (r = 0.56, p < 0.05) and correlated inversely with IGF-I binding (r = -0.74, p < 0.01). In conclusion, we have shown adequate GH secretion, higher secretive capacity after the administration of Hexarelin and lower IGF-I binding in prepubertal beta-thalassemic patients with short stature. Whatever the cause, reduced IGF-I action has to be considered when treating beta-thalassemic patients with short stature.     

Indications, limitations and pitfalls in the determination of human growth hormone, IGF-I and their binding proteins

Deviations from normal growth are a major part of Pediatric Endocrinology. The principal post-natal growth promoting hormones are pituitary growth hormone (GH) and insulin-like growth factor-I (IGF-I). The GH-IGF-I axis has many links and portals, the secrets of which have been disclosed in recent years by scientific advances (genetic and biochemical technologies). In this article, we describe the players in the GH axis, the auxological indications for performing GH evaluation tests, enumerate the most frequently used tests and discuss the laboratory tests which help to define the pathological entities along the GH axis. Emphasis is put on the limitations of methods used, lack of standards, norms and the possible errors in diagnosis and treatment indications that may evolve. As both hGH and IGF-I immunoassay measurements represent cornerstones in the diagnosis and monitoring of the different etiological entities presenting with short stature, clinicians must have an insight into the variability and limitations of these analytical techniques. Interpretation of biochemical results without proper reference data and without knowledge of the assay-inherent characteristics inevitably leads to misdiagnosis, unnecessary further testing and treatment and imposes a burden on the child, family and the health care system.     

单纯性肥胖症儿童血清内脂素、促酰化蛋白水平测定及其临床意义

目的 探讨血清内脂素(visfatin)和促酰化蛋白(ASP)与单纯性肥胖症儿童发病的关系及其对肥胖症防治的意义.方法 研究对象共86例,男57例,女29例;年龄7～15岁.其中单纯性肥胖儿童40例;超重儿童22例;健康对照儿童24例.采用酶联免疫吸附法检测各组儿童血清visfatin、ASP水平.结果 1.肥胖组血清visfatin与健康对照组和超重组相比,分别增加了49.80％(P＜0.05)、35.88％ (P ＜0.05).肥胖组血清ASP与健康对照组和超重组相比,分别增加了7.34％ (P ＜0.01)和5.57％(P＜0.05).超重组和健康对照组血清visfatin及ASP比较差异均无统计学意义.2.肥胖组体质量指数(BMI)、总胆固醇、三酰甘油、低密度脂蛋白、空腹血糖、空腹胰岛素、胰岛素抵抗指数均高于健康对照组,差异均有统计学意义(P均＜0.05);肥胖组高密度脂蛋白和胰岛素敏感指数明显低于健康对照组,差异均有统计学意义(P均＜0.05);肥胖组BMI、空腹胰岛素、胰岛素抵抗指数均高于超重组,差异均有统计学意义(P均＜0.01).3.相关性分析:血清visfatin与BMI、三酰甘油均呈正相关(r =0.218,P＜0.05;r =0.500,P＜0.01).血清ASP与BMI、总胆固醇和三酰甘油均呈正相关(r=0.268,P＜0.05;r =0.250,P＜0.05;r =0.427,P＜0.01).结论 Visfatin和ASP与肥胖关系密切,均参与肥胖儿童体内脂质代谢紊乱的发生.检测血清visfatin和ASP水平将有助于判断儿童肥胖症的发展趋势,有助于评价肥胖儿童未来发生糖尿病、心血管疾病的危险程度.     

癫痫发作后患儿血清和脑脊液中神经元特异性烯醇化酶S-100β蛋白髓鞘碱性蛋白的变化

目的　探讨癫痫发作是否引起脑损伤 ,生化标志物能否作为癫痫发作后脑细胞损伤早期诊断的指标。方法　应用电化学发光法和酶联免疫反应法测定癫痫发作后 2 4h内患儿血清和脑脊液 (CSF)中神经元特异性烯醇化酶 (NSE)、S 10 0 β蛋白 (S 10 0 β)、髓鞘碱性蛋白 (MBP)水平的含量。 结果　癫痫非反复发作组血清和CSF中NSE、S 10 0 β含量明显高于对照组 ,差异有非常显著性 (均 P <0 .0 1) ;癫痫反复发作组血清和CSF中NSE、S 10 0 β含量又明显高于非反复发作组 ,差异有显著性 (均 P <0 .0 5 ) ;持续状态组血清和CSF中NSE、S 10 0 β含量亦显著高于非反复发作组 ,差异有非常显著性 (均P <0 .0 1) ;但癫痫反复发作组与持续状态组比较 ,血清和CSF中NSE、S 10 0 β含量差异均无显著性意义 (均 P >0 .0 5 )。各组血清和CSF中MBP含量与对照组相比差异无显著性(均P >0 .0 5 )。结论　癫痫发作后 2 4h内血清和CSF中NSE和S 10 0 β已明显升高 ,两者均能作为癫痫发作后脑细胞损伤的早期指标 ;MBP不能作为癫痫发作后脑细胞损伤的早期诊断指标。     

肺炎支原体肺炎患儿支气管肺泡灌洗液和血清中肺表面活性蛋白的变化及意义

目的：研究肺表面活性蛋白在小儿肺炎支原体肺炎（MPP）血清和支气管肺泡灌洗液（BALF）中的变化及意义。方法：根据肺CT结果将47例MPP患儿分为两组：单侧病变组（n=32）和双侧病变组（n=15）。采用ELISA法检测两组患儿BALF和血清中肺表面活性蛋白A、B、C、D（SP-A、B、C、D）的含量。血清与BALF中SP-A、B、C、D含量的相关性采用Spearman秩相关分析。结果：两组患儿中,主病变侧或病变侧BALF中 SP-A、B、C、D含量显著高于次病变侧或健侧BALF和血清中SP-A、B、C、D含量（P＜0.01）。单侧病变组患儿血清中SP-A、B、C含量显著低于健侧BALF中含量（P＜0.01 或0.05）,而血清中SP-D含量与健侧BALF中SP-D含量差异无统计学意义（P＞0.05）。双侧病变组患儿血清中SP-A、B、C、D含量与次病变侧BALF中SP-A、B、C、D含量相比,差异无统计学意义（P＞0.05）。Spearman秩相关分析显示,双侧病变组患儿中血清SP-D含量与主病变侧BALF中SP-D含量呈密切正相关（P＜0.01）。结论：血清中SP-D可作为反映小儿社区获得性肺炎肺组织感染损伤严重程度的生化指标。     

Clinical utility of insulin-like growth factor-I (IGF-I) and IGF binding protein-3 measurements in paediatric practice

Measurements of serum insulin-like growth factor-I (IGF-I) and its major binding protein, IGFBP-3, are utilised in the routine clinical management of short children. In this review, the value of such measurements in the diagnosis of primary and secondary IGF-I deficiency is presented. The achievement of optimal growth while maintaining IGF-I within the normal range is the goal of GH treatment schedules used in a range of growth disorders, and thus data on IGF-I monitoring during initiation and maintenance phases of GH treatment are discussed. Comment is also made on the relationship between levels of IGF-I and IGFBP-3 in the population with regard to risks for cancer and cardiovascular disease.IGF-I and IGFBP-3 are important parameters to measure as one part of the process of managing short children. It is proposed that improving the clinical value of IGF measurement may involve measurement of specific prohormones and E-peptides, to get closer to the pool of GH dependent IGF-I.     

慢性心力衰竭患儿心型脂肪酸结合蛋白的变化及临床意义

目的：通过前瞻性观察慢性心力衰竭（CHF）患儿血浆心型脂肪酸结合蛋白（h-FABP）的水平变化及其与心功能的关系,探讨其在CHF中的临床价值。方法：36例CHF患儿（CHF组）纳入研究,其中心内膜弹力纤维增生症16例（EFE组）,扩张型心肌病20例（DCM组）。选择同期30例健康儿童作为对照组。血浆h-FABP浓度测定采用酶联免疫吸附法（ELISA）,并以心脏超声心动图测量心脏指数、左室短轴缩短率及左室射血分数。结果：CHF患儿血浆h-FABP浓度明显高于对照组（21.7±4.3 ng/mL vs 6.2±1.7 ng/mL, P＜0.01）,且心力衰竭程度越重,h-FABP浓度升高越明显（P＜0.01）。EFE、DCM两组h FABP水平均高于对照组（P＜0.01）。CHF患儿h-FABP水平与左室射血分数、心脏指数及左室短轴缩短率均呈明显负相关（分别r=-0.65、-0.64、-0.71,均P＜0.01）。结论：CHF患儿的血浆h-FABP浓度明显升高,血浆h FABP浓度与心力衰竭的严重程度相关。血浆h-FABP浓度可作为评估心力衰竭及其严重程度的一个指标。     

阻塞性睡眠呼吸暂停低通气综合征患儿C-反应蛋白变化及意义

目的探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患儿血浆C-反应蛋白(CRP)的变化。方法检测40例OSAHS患儿及27例健康对照儿童的血浆CRP与血生化指标,完成多导睡眠监测(PSG)。结果中重度OSAHS组的血浆CRP较对照组和轻度OSAHS组明显增高,并且CRP与呼吸暂停低通气指数(AHI)呈正相关(r=0.824,P<0.01),与最低指脉氧饱和度(SaO2)呈负相关(r=-0.802,P<0.01)。CRP值升高的患儿中,出现白天嗜睡和(或)学习障碍者占82.3%,而CRP正常的儿童,有此症状者仅占46.0%。结论中重度OSAHS患儿CRP增高,并且与AHI和SaO2相关联。CRP增高在白天嗜睡和(或)学习障碍的儿童表现更为明显。