新生儿HIE血清IL-6、IL-8与TNF-α动态变化及临床意义探讨

为探讨新生儿缺氧缺血性脑病 (HIE)外周血IL -6、IL -8与TNF -α变化的临床意义 ,采用放射免疫法 ,对生后 1天 ( 2 4小时内 )、3天及 7天检测了 40例HIE患儿及 40例正常新生儿外因血IL 6、IL 8与TNF α水平。结果显示 ,与正常新生儿比较 ,HIE患儿生后 1天血清IL -6水平分别为 ( 5 2 6± 2 4 5 )对 ( 80 2± 2 9 4)ng L(P <0 0 1) ,IL -8分别为 ( 0 47± 0 13)对 ( 0 6 8± 0 16 ) μg L(P <0 0 1) ,TNF -α分别为( 1 18± 0 31)对 ( 0 91± 0 30 ) μg L(P <0 0 1) ,而且病情越重改变越明显 ;至生后 1周IL -6、TNF -α恢复至正常 ,与对照组水平相比P >0 0 5 ,而IL -8则仍显著低于正常新生儿 (P <0 0 1)。因此 ,认为围产期窒息与HIE患儿外周血IL -6与IL -8水平减低 ,TNF -α水平升高 ;它们可能参与了新生儿缺氧缺血性脑损伤的某些发病过程。     

缺铁性贫血患儿T辅助细胞的免疫与调控

为研究缺铁性贫血患儿T辅助细胞 (TH)的细胞调控及免疫功能。对 2 0 0 2年 1月至 2 0 0 2年 1 2月住院患儿进行TH 细胞检测 ,同时设正常健康儿童 2 8人为对照组。对两组儿童应用ELISA法检测白细胞介素 2 (IL 2 )及γ干扰素 (INF γ)水平 ,用单细胞内染色法检测TH1、TH2 百分率。结果 :缺铁贫血患儿IL 2 ( 1 6 55± 2 87ug L)水平明显降低 ,与对照组IL 2 ( 2 4 73± 4 37ug L)比较差异有显著意义 (t =8 6 2 ,P <0 0 1 ) ;INF γ( 4 75 6± 2 7 1pg mL)水平也明显降低 ,与对照组IFNγ( 6 54 0 7± 1 4 6 4pg mL)比较 ,差异有极其显著性意义 (t =7 4 2 ,P <0 0 1 ) ;缺铁性贫血患儿TH1百分率( 1 2 2 4± 2 51 % )亦明显低于对照组TH1百分率 ( 1 6 6 7± 2 73% ) ,经t检验差异亦有极显著意义 (t=6 89,P <0 0 1 ) ;缺铁性贫血患儿TH2 百分率明显升高 (t=5 37,P <0 0 5)。结果表明 :缺铁贫血患儿机体TH1细胞数量及功能低下 ,TH1 TH2 值下降 ,TH1、TH2 极化异常 ,导致细胞毒性T细胞 (CTL)介导的细胞免疫功能受到抑制     

新生儿缺氧缺血性脑病血清IL-8水平变化研究

目的　白细胞介素 8(IL 8)为缺血 /再灌注时炎症细胞的释放产物 ,并可引起细胞损伤。该研究旨在探讨IL 8是否参与新生儿缺氧缺血性脑病 (HIE)脑缺血 /再灌注损伤。方法　采用双抗体夹心ELISA法检测5 0例HIE患儿 (HIE组 ,其中轻度HIE 1 8例 ,中度HIE 1 7例 ,重度HIE 1 5例 ;合并感染者 2 9例 ,未合并感染者 2 1例 )、30例正常新生儿 (正常对照组 )及 2 0例患感染性疾病无HIE患儿 (感染组 )血清IL 8水平 ,HIE患儿经治疗后复查血清IL 8。结果　HIE组血清IL 8水平高于对照组 (2 1 .5 2± 9.5 9pg/mlvs 1 4 .4 3± 4 .84 pg/ml) ,差异有显著性 (P <0 .0 1 ) ;重度HIE患儿血清IL 8水平高于轻度HIE组 (2 6 .0 7± 1 3.83pg/mlvs 1 7.5 6± 6 .5 2pg/ml) ,差异有显著性 (P <0 .0 5 ) ,与中度HIE组比较 (2 1 .71± 5 .6 5 pg/ml) ,差异无统计学意义 (P >0 .0 5 ) ;HIE患儿治疗后IL 8水平较治疗前下降 (1 4 .5 3± 4 .87pg/mlvs 2 2 .6 0± 7.0 6 pg/ml) ,差异有显著性 (P <0 .0 1 ) ;有感染合并症HIE患儿血清IL 8水平高于无感染合并症患儿及感染组患儿依次为 2 3.79± 1 1 .0 4pg/ml,1 8.38± 6 .0 7pg/ml,1 8.2 2± 8.0 1 pg/ml,差异有显著性 (P <0 .0 5 )。结论　新生儿HIE时血清IL 8升高 ,病情越重升高越显著     

急性中枢神经系统感染患儿脑脊液中IL-6和TNF水平的测定及临床意义

目的　探讨急性中枢神经系统感染患儿脑脊液 (CSF)中白细胞介素 - 6 (IL - 6 )和肿瘤坏死因子(TNF)水平的变化及临床意义。方法　采用ELISA法对 5 0例初诊为中枢神经系统感染患儿 ,其中化脓性脑膜炎(PM ) 1 8例 ,病毒性脑膜脑炎 (VE) 32例 ,进行了CSF中IL - 6和TNF水平测定 ,并与 1 2例对照组测定值进行比较。结果　PM组患儿CSF中IL - 6和TNF水平 (分别为 746± 499pg/ml和 5 6 5± 371 pg/ml)明显高于VE组 (分别为 1 6 5± 1 76 pg/ml和 75± 73pg/ml)和对照组 (分别 1 0± 1 7pg/ml和 2 1± 2 6pg/ml) (均 P <0 .0 0 1 ) ,VE组CSF中IL - 6和TNF水平亦明显高于对照组 (分别P <0 .0 1和P <0 .0 5 )。患儿CSF中IL - 6和TNF水平与脑脊液白细胞计数之间相关性分析 ,未见显著性意义。结论　IL - 6和TNF参与了急性中枢神经系统感染的病理生理过程 ,CSF中IL - 6和TNF的测定可能对化脓性脑膜炎和病毒性脑膜脑炎的鉴别具有一定的意义。     

IL-13、SccAg与毛细支气管炎关系的研究

目的　探讨白细胞介素 13(IL 13)、鳞状细胞癌抗原 (SccAg)及免疫球蛋白E(IgE)与毛细支气管炎 (简称毛支 )发病机制的关系。方法　用ELISA法检测 36例毛支患儿、2 6例哮喘患儿、4 0例肺炎患儿及 33例正常儿童血清IL 13、SccAg及IgE水平 ,并对结果进行统计学处理。 结果　 (1)毛支患儿发作期血清IL 13(10 4 91± 18 0 5 )ng/L及SccAg(2 4 9± 0 38)ng/ml水平显著高于缓解期(85 15± 17 98)ng/L ,(2 30± 0 34)ng/ml及正常对照组 (77 2 7± 18 16 )ng/L ,(2 2 9± 0 34)ng/ml(P<0 0 5 ) ,而缓解期与正常对照组间无显著性差异 (P >0 0 5 )。 (2 )毛支发作期患儿血清IgE水平(370 91± 6 9 2 6 )kU/L显著高于缓解期 (189 4 6± 70 36 )kU/L(P <0 0 5 ) ,两组均显著高于正常对照组 (15 1 6 6± 70 17)kU/L(P <0 0 5 )。 (3)毛支发作期患儿血清IL 13、SccAg及IgE水平显著低于哮喘发作期 (14 7 0 0± 2 3 78)ng/L ,(3 0 1± 0 37)ng/ml,(6 5 9 5 2± 70 5 1)kU/L(P <0 0 0 1)。 (4 )毛支患儿发作期血清IL 13、SccAg及IgE水平显著高于肺炎组 (80 74± 18 0 8)ng/L ,(2 31± 0 35 )ng/ml,(15 2 87± 6 6 91)kU/L(P <0 0 5 )。 (5 )毛支患儿发作期血清IL 13水平与SccAg、IgE及SccAg与IgE水     

新生儿感染性黄疸血浆组织因子和组织因子途径抑制物含量的变化

目的　探讨新生儿感染性黄疸患儿血浆组织因子 (TF)和组织因子途径抑制物 (TFPI)含量的变化及其意义。方法　运用酶联免疫吸附法 (ELISA)测定 8例非感染性高胆红素血症新生儿 (对照组 )及 2 1例感染性黄疸新生儿 (感染组 )血浆TF和TFPI水平。结果　感染组的血浆TFPI含量和TF含量显著高于对照组 [TFPI( 2 1 0± 4 3 )、( 16 2± 1 9) μg/L ,P <0 0 1;TF ( 177± 79)、( 5 1± 2 4)ng/L ,P <0 0 1];TFPI/TF比值显著低于对照组 ( 13 7± 61、3 19± 67,P <0 0 1)。根据患儿血清胆红素 (SB)浓度 ,将 2 1例感染性黄疸新生儿分为胆红素重度增高感染组 (SB≥ 2 0 5 2 μmol/L ,n =10 )和胆红素轻度增高感染组 (SB <2 0 5 2 μmol/L ,n =11) ,两组间TFPI水平差异无显著性 (P >0 0 5 )。胆红素重度增高感染组TF水平高于胆红素轻度增高感染组 [( 2 16± 79)、( 141± 63 )ng/L ,P <0 0 1],而TFPI/TF低于胆红素轻度增高感染组 ( 10 0± 3 0、171± 74,P <0 0 1)。结论　感染可引起新生儿体内抗凝与促凝作用的平衡失调。黄疸可提高血浆TF水平 ,加重感染新生儿体内抗凝与促凝作用的失衡     

中性粒细胞粘附分子CD11b表达对新生儿败血症早期诊断价值的研究

目的　观察新生儿败血症中性粒细胞粘附分子CD11b表达的规律 ,并评价其在新生儿败血症早期诊断中的价值。方法　将 5 1例临床疑似败血症的新生儿根据其临床表现及WBC、PLT、血浆CRP和未成熟中性粒细胞数与中性粒细胞总数比值 (I/T)四项指标 ,分为败血症和可疑败血症两组。采用全血流式细胞术检测患儿和 15例正常对照组新生儿中性粒细胞CD11b的平均荧光强度 (MFI)。结果　败血症组 2 3例 ,可疑败血症组 2 8例。两组中性粒细胞CD11b分别为 (32 0± 189)、(4 5 6± 2 13)MFI,均显著低于正常对照组的 (10 90± 338)MFI(t分别为 - 9 0 1、- 7 5 6 ,P均 <0 0 0 1) ,败血症组又低于可疑败血症组 ,差异有显著性 (t=- 2 39,P <0 0 5 )。高CRP组患儿CD11b为 (2 11± 16 4 )MFI,低于低CRP组的 (5 0 5± 2 6 5 )MFI,差异有显著性 (t=2 6 4 ,P <0 0 5 )。中性粒细胞CD11b≤ 6 0 0MFI对疑似败血症新生儿诊断的敏感性、特异性、阳性和阴性预测值分别为 86 3%、10 0 %、10 0 %、6 8 2 % ,CD11b检测阳性率为 86 3% ,高于血培养的阳性率 (17 6 % ) ,差异有显著性 (χ2 m=31 2 ,P <0 0 5 )。结论　新生儿败血症中性粒细胞粘附分子CD11b表达下调 ,其下调与感染严重程度有一定关系。中性粒细胞CD11b的动态检测对早期     

肺炎患儿血清β_2-微球蛋白及白细胞介素-2水平变化

目的　探讨小儿肺炎时免疫功能的变化。方法　采用放射免疫分析法测定 12 8例肺炎患儿血清β2 微球蛋白 (β2 MG)及白细胞介素 2 (IL 2 )水平 ,并与 38例健康儿童相比较。结果　轻、重型肺炎血 β2 MG水平分别为 (3.0 8± 0 .72 )mg/L ,(3.5 6± 0 .5 3)mg/L ,明显高于对照组 (1.83± 0 .5 7)mg/L ,P <0 .0 1;IL 2水平分别为 (2 .13± 0 .84)ng/L ,(1.95± 0 .79)ng/L较对照组 (5 .31± 1.2 4)ng/L显著降低 ,P <0 .0 1。结论　肺炎患儿细胞免疫功能较健康儿童低下。     

新生儿HIE脐血IL-6、IL-8与TNF-α变化及临床意义探讨

为探讨新生儿缺氧缺血性脑病 ( HIE)脐血 IL - 6、IL - 8与 TNF-α的变化及临床意义 ,应用放射免疫法检测了 4 0例 HIE患儿 IL- 6、IL- 8与 TNF- α水平 ,并与 4 0例正常新生儿比较。结果显示与正常新生儿比较 ,HIE患儿与正常对照儿相比脐血IL - 6水平分别为 ( 61.0 4± 2 3 .0 6)对 ( 91.83± 3 7.5 4 ) ng/L ( P<0 .0 1) ,IL - 8分别为( 0 .3 4± 0 .0 9)对 ( 0 .2 6± 0 .0 7) μg/L( P<0 .0 1) ,TNF- α分别为 ( 1.0 3± 0 .3 0 )对 ( 0 .83± 0 .3 1) μg/L( P<0 .0 1) ;而且病情越重改变越明显。因此 ,我们认为 ,围产期窒息与HIE患儿脐血 IL - 6水平减低、IL - 8与 TNF-α水平升高有关 ;它们可能参与了新生儿缺氧缺血性脑损伤的某些发病过程     

新生儿HIE、感染性疾病及早产儿IL-2、IL-6检测

目的　 探讨新生儿缺氧缺血性脑病 (HIE)、感染性疾病及早产儿血清白细胞介素 2 (IL 2 )、白细胞介素 6(IL 6)检测值的变化及临床意义 ,间接了解新生儿部分特异性及非特异性免疫功能。 方法 　选择 3 3 1例住院新生儿 ,分为HIE组、感染组、早产儿组 ,与 3 0例健康新生儿对照 ,采用酶联免疫吸附法 (ELISA)检测血清IL 2、IL 6的水平 ,进行对比分析。 结果 　①患病新生儿IL 2明显低于正常新生儿 ,P <0 0 1,有高度显著性差异 ,其中早产儿组最低仅为 1 3 5pg/ml;②感染组IL 6增高最为明显 ,与健康对照组相比 ,P <0 0 1,有高度显著性差异 ,其中 2 5例败血症患儿的IL 6均 >5 0pg/ml。 结论 　①新生儿感染性疾病、HIE及早产儿的免疫方面受到不同程度的损伤 ,介导特异性免疫的IL 2检测值低于健康新生儿 ;②本文首次报道早产儿IL 2检测值 ;③感染组介导天然免疫的IL 6高于健康新生儿 ,认为可作为早期诊断新生儿败血症的指标。     

Allergic factors associated with the development of asthma and the influence of cetirizine in a double-blind, randomised, placebo-controlled trial: First results of ETA®

There is a common progression known as the allergic march from atopic dermatitis to allergic asthma. Cetirizine has several antiallergic properties that suggest a potential effect on the development of airway inflammation and asthma in infants with atopic dermatitis. Methods. Over a two year period, 817 infants aged one to two years who suffered from atopic dermatitis and with a history of atopic disease in a parent or sibling were included in the ETAC^® (Early Treatment of the Atopic Child) trial, a multi-country, double-blind, randomised, placebo-controlled trial. The infants were treated for 18 months with either cetirizine (0.25mg/ kg b.i.d.) or placebo. The number of infants who developed asthma was compared between the two groups. Clinical and biological assessments including analysis of total and specific IgE antibodies were performed. Results. In the placebo group, the relative risk (RR) for developing asthma was elevated in patients with a raised level of total IgE (≥ 30 kU/I) or specific IgE (≥ 0.35 kUA/I) for grass pollen, house dust mite or cat dander (RR between 1.4 and 1.7). Compared to placebo, cetirizine significantly reduced the incidence of asthma for patients sensitised to grass pollen (RR = 0.5) or to house dust mite (RR = 0.6). However, in the population that included all infants with normal and elevated total or specific IgE (intention-to-treat - ITT), there was no difference between the numbers of infants developing asthma while receiving cetirizine or placebo. The adverse events profile was similar in the two treatment groups. Discussion. Raised total IgE level and raised specific IgE levels to grass pollen, house dust mite or cat dander were predictive of subsequent asthma. Cetirizine halved the number of patients developing asthma in the subgroups sensitised to grass pollen or house dust mite (i.e. 20% of the study population). In view of the proven safety of the drug, we propose this treatment as a primary pharmacological intervention strategy to prevent the development of asthma in specifically sensitised infants with atopic dermatitis.     

Bibliometric data: a disaster for many non-American biomedical journals

Bibliometric data published by the Institute of Scientific Information in Philadelphia (ISI), and which was previously discussed in Acta Paediatrica , has increasingly been used despite all the relevant and severe criticism that has been raised against this method of evaluating individual research results and grading scientific journals. It is obvious that the present trend regarding the use of bibliometric data as a basis for priorities and funding of research and for the promotion of individual scientists favours American-oriented research projects at the expense of those that are based on concepts of predominantly European relevance.

Conclusion: For the future of non-American research, it is important that no single super-power, i.e. the USA, should dominate scientific priorities. The condition for efficient European competition is that European Centres with high levels of competence for creative research and training of scientists from all over the world are established. In addition, it is important that the results of European research are published in prestigious European journals, as was the situation before World War II.     

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孤独症谱系障碍(autistic-spectrum disorders,ASDs)近年来患病率逐年攀升至1%左右,其症状往往伴随终生,成为严重威胁儿童健康和发展的神经发育性疾患;注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是儿童期最常见的精神障碍,国内报道患病率为4.13%～5.83%,其症状可延续至青少年期,甚至到成年期[1]。这两类精神障碍在成年期的临床表现、共患病、治疗策略和预后与儿童期有哪些不同呢?本文通过回顾相     

Infiltrations of Epstein-Barr virus-carrying cells in granular lymphocyte-proliferative disorders corresponding to chronic active Epstein-Barr virus infection

A 21-year-old man with granular lymphocyte-proliferative disorders (GLPD) associated with chronic active Epstein-Barr virus (EBV) infection is described. Chromosomal analyses revealed several clonal abnormalities and two of them were mainly repetitious. High copy numbers of monoclonal EBV genome were also detected in the proliferative large granular lymphocytes (LGLs), indicating the monoclonal expansion of EBV-infected LGLs. The patient had an indolent course for several years, and there was no evidence of infiltrations of his bone marrow until the end stage. At autopsy, microscopic studies revealed marked infiltrations of LGL in the liver and spleen, and the infiltrating cells were NK-cell immunophenotype. The infiltrated LGLs showed latency I.     

LUTEINIZING HORMONE RECEPTOR MUTATIONS IN DISORDERS OF SEXUAL DEVELOPMENT AND CANCER

Human male sexual development is regulated by chorionic gonadotropin (CG) and luteinizing hormone (LH). Aberrant sexual development caused by both activating and inactivating mutations of the human luteinizing hormone receptor (LHR) have been described. All known activating mutations of the LHR are missense mutations caused by single base substitution. The most common activating mutation is the replacement of Asp-578 by Gly due to the substitution of A by G at nucleotide position 1733. All activating mutations are present in exon 11 which encodes the transmembrane domain of the receptor. Constitutive activity of the LHR causes LH releasing hormone-independent precocious puberty in boys and the autosomal dominant disorder familial male-limited precocious puberty (FMPP). Both germline and somatic activating mutations of the LHR have been found in patients with testicular tumors. Activating mutations have no effect on females. The molecular genetics of the inactivating mutations of the LHR are more variable and include single base substitution, partial gene deletion, and insertion. These mutations are not localized and are present in both the extracellular and transmembrane domain of the receptor. Inactivation of the LHR gives rise to the autosomal recessive disorder Leydig cell hypoplasia (LCH) and male hypogonadism or male pseudohermaphroditism. Severity of the clinical phenotype in LCH patients correlates with the amount of residual activity of the mutated receptor. Females are less affected by inactivating mutation of the LHR. Symptoms caused by homozygous inactivating mutation of the LHR include polycystic ovaries and primary amenorrhea.     

EXCITING NEW TREATMENT APPROACHES FOR PATHYPHYSIOLOGIC MECHANISMS OF SICKLE CELL DISEASE

During the past several decades, our understanding of the complex pathophysiology of vasoocclusion associated with sickle cell disease has improved greatly. Interaction of genes, hemoglobin molecules, red cell membrane and metabolic changes, cell-cell interactions and cell-plasma interactions, red cell adhesion to vascular endothelium, activation of coagulation, and vascular reactivity play a role in vaso occlusion. Penicillin prophylaxis of pneumococcal infections and appropriate use of blood transfusions and other supportive measures improved survival of sickle cell patients. Hydroxyurea made a major impact on sickle cell therapy when it was shown to decrease acute painful episodes, acute chest syndrome, and the need for blood transfusion in adults. Significant experience in the use of hydroxyurea has been accumulated in older children. The benefits and risks of hydroxyurea for younger children and long-term risks in all patients will be evaluated in future investigations. Other promising therapies include butyrate compounds, clotrimazole, magnesium supplementation, poloxamer 188, antiadhesion agents, anticoagulant approaches, and nitric oxide. Hemopoietic transplantation remains the only curative therapy. However, several transgenic mouse models are available for studies of gene therapy or other treatment approaches on biochemical, cellular, and pathologic effects of mutant genes.     

Personality profiles and heart rate variability (vagal tone) in children with recurrent abdominal pain

The aim of the study was to explore psychological factors and autonomic activity in children with recurrent abdominal pain and to compare them with those in a control group of healthy children. The Personality Inventory for Children was used for assessment of developmental, emotional and psychosocial factors in 25 children with recurrent abdominal pain (age, 7-15 y). Parasympathetic and sympathetic functions in these children and in 23 healthy control subjects (age, 7-13 y) were also investigated, non-invasively using a computerized polygraph. Vagal tone (parasympathetic function) was indexed by calculation of respiratory sinus arrhythmia in beats/min. Skin conductance (sympathetic function) was recorded by the constant current method. On the Personality Inventory for Children, 16 patients had high scores on somatic concern. Several patients had scores in the clinical range for depression, withdrawal and anxiety, but the mean scores for these personality profile scales were well within the normal range of healthy children. Interestingly, there was a spike on the L (Lie)-scale for most of the patients and 15 patients had scores above or close to the clinical cut-off value. As compared with the scores in healthy children, vagal tone and sympathetic tone were normal. Conclusion: Many children with recurrent abdominal pain have scores in the clinical range for depression, withdrawal, anxiety and L-scale indicating coping problems, denial and a trend towards somatic concern that may contribute to the evolution of abdominal pain. Autonomic nerve activity was not disturbed in these children.     

alpha -SMOOTH MUSCLE ACTIN DISTRIBUTION IN THE PULMONARY VASCULATURE COMPARING HYPOPLASTIC AND NORMAL FETAL LUNGS

We investigated the intra-acinar pulmonary vascular muscularization in the developing human fetal lung between the 17th and 24th gestational weeks, that is, during the canalicular phase of lung development. Fifteen hypoplastic and 25 normal developed lungs were included in this study using monoclonal alpha -smooth muscle (sm) actin antibodies for smooth muscle detection. Computer-aided image analysis was performed for morphometrical measurements and statistical evaluation. Alphasm-actin-immunoreactive intra-acinar vessels down to a luminal diameter of less than 10 mu m were detected in hypoplastic as well as in normally developed lungs. Crucial differences presented as follows: significantly higher density of intra-acinar vessels, especially due to alpha -sm-actin-negative vessels less than 30 mu m in luminal diameter, in the control group; significantly higher alpha -sm-actin immunoreactivity per section unit as well as per vessel in the hypoplastic lung group. As suggested by others, alpha-sm-actin-positive cells of the intra-acinar vessel wall in the developing human lung were demonstrated to be smooth muscle cells, their immediate precursors, and pericytes. We conclude that the increased alpha -sm-actin immunoreactivity represents muscularization of the vessel wall in functional terms and may be regarded as one structural cause among others for the establishment of persistent fetal circulation in hypoplastic lungs.     

Understanding infant formula

The World Health organisation recommends breast feeding infants for the first six months of life. When this breast feeding does not occur either through parental choice or medical need, infant formulas will be required. There is a bewildering array of formulas on the UK market for many different requirements. When faced with an unsettled infant many parents (and healthcare professionals) will experiment with the infant formula available and then attend the paediatric clinic looking for help and advice. It is therefore essential that paediatricians understand what milks are available and what the key differences between different products are. This review attempts to provide a simple guide through many of the formulations currently available in the UK; and offers advice for the dietary management of the child with extra calorie requirements, infants with cow's milk protein allergy, gastro oesophageal reflux disease, apparent unresolved hunger and infantile colic. Whatever the underlying condition, there is likely to be an infant formula that is suitable in this generation of ever expanding formulations.