Immunoglobulin isotypes in childhood asthma

Immunoglobulin isotypes (IgG, IgA, IgM, IgD, IgE) in serum were investigated in 64 Libyan children with mild to moderately severe asthma (age: 1–12 years; sex: 39 males, 25 females) (Group A) and in 57 healthy Libyan children (age: 1–12 years; sex; 30 males, 27 females (Group B). The patients were classified according to age into three groups (A1: 1–3 years; A2: >3–5 years; A3: >5–12 years); according to disease activity into two groups (AA: active disease; NA: inactive disease); and according to age plus disease activity into six groups (AA1, NA1; AA2, NA2; AA3, NA3). The healthy children were also divided according to age into three groups (B1: 1–3 years; B2: >3–5 years; B3: >5–12 years). IgG, IgA, IgM and IgD were measured by radial immunodiffusion method and IgE was estimated by enzyme immunoassay technique utilizing immunokits from bioMerieux France. Serum levels of IgG, IgD and IgE were elevated significantly in patients compared to controls (A vs B: p<0.05) while IgA and IgM levels were normal (p>0.05). IgG and IgD levels were raised in A3 (p<0.05), while IgD levels were raised in both A2 and A3 (p<0.05) and IgE was elevated in all age groups (p<0.05). However, IgG was elevated significantly in AA only, while IgD and IgE levels were high in both AA and NA (p<0.05) and IgE was even considerably higher in AA compared to NA (p<0.02). Further elevated levels were observed for IgG in AA3 only (p<0.05), for IgD in NA2 (p<0.01), AA3 (p<0.01) and NA3 (p<0.05) and IgE was much higher in patients with active disease than with inactive disease in all age groups (p<0.05). The fact that asthmatic attack in majority of our patients can be explained as mediated through IgE and the possibilities that IgG and IgD may play roles as aetiopathogenetic or protective regulatory factors in childhood asthma are discussed.     

高免疫球蛋白D伴周期性发热综合征1例病例报告

目的 提高对高IgD伴周期性发热综合征（HIDS）的认识。 方法 回顾性总结1例儿童HIDS病例的临床特征、实验室检查、血清IgD、MVK酶和MVK基因检测结果。 结果 6岁7个月男孩,2岁起病,呈周期性发作性发热,每2~4周发热1次,每次持续3~7 d。发热时伴腹痛,腹泻,关节疼痛,肝脾肿大。发热时未用抗生素经退热对症治疗,体温可恢复正常。发热时WBC、N和CRP升高,热退后可降至正常。免疫接种后有发热和感染史。经全面检查排除感染性、风湿性及血液肿瘤相关疾病。MVK基因分析发现外显子11,c.1129G>A,p.V377I,为杂合型错义突变,外显子9,c.790_791insC,p.Leu264fsX12,为杂合型插入突变(首次报道的新突变)。患儿血清IgD（1 084 μg·mL-1）显著高于正常参照值（<100 μg·mL-1）。MVK酶(23 ng·mL-1）低于正常参照值（50～300ng·mL-1）。本文病例临床特征典型,HIDS诊断明确。 结论 婴儿期起病的周期性发作性发热,需警惕HIDS可能,免疫接种后发热是重要的诊断线索,检测血清IgD和MVK酶水平是重要诊断依据,MVK基因突变可明确诊断。     

Hyperimmunoglobulinemia D and periodic fever syndrome (HIDS) in a child with normal serum IgD,but increased serum IgA concentration

This report describes a boy with hyperimmunoglobulinemia D and periodic fever syndrome (HIDS). The serum IgD level was normal, but the serum IgA concentration was markedly elevated. In addition, he had a history of orchitis on two occasions, a previously unreported manifestation of HIDS. This report expands the clinical and laboratory features associated with HIDS and serves to emphasize that a normal serum IgD level does not exclude the diagnosis of HIDS.     

Tendonitis in variant hyperimmunoglobulinaemia D and periodic fever syndrome—a rare disease with a new symptom

Hyperimmunoglobulinaemia D syndrome (HIDS) is defined as recurrent fever, generalised lymphadenitis, abdominal pain, arthritis and raised polyclonal serum IgD >100 IU/ml. The cause is a mutation in the mevalonate kinase gene. Other periodic fever syndromes are known. We report a new patient and describe orbital tendonitis as a hitherto unreported symptom Conclusion: Without any underlying cause, the tendonitis must be seen as new symptom of variant hyperimmunoglobulinaemia D syndrome. We speculate that the inflammation of the Tenon spatium is similar to the process of inflammation of the connective tissue in the joint in hyperimmunoglobulinaemia D syndrome where deposits of C3 and IgM are present. Variant hyperimmunoglobulinaemia D syndrome can be present in one family.     

Pseudo-periodic disease with hyperimmunoglobulinemia D: a never-ending story with probable prenatal onset]

Diagnosis of inflammatory non-infectious diseases with a neonatal onset is often retrospective. It may lead to aggressive and iatrogenic procedures. PATIENT: A 6-year-old boy was suffering, since birth, from recurrent febrile attacks including rashes, gastrointestinal manifestations and inflammatory joint involvement. This syndrome, partially improved with steroids, could have been of antenatal onset. Since the age of 4 years, the patient is considered as having hyper-IgD syndrome (HIDS). DISCUSSION: HIDS must be distinguished from familial Mediterranean fever. Patients suffer from recurrent fever concomitant to inflammatory joint involvement, abdominal distress, skin lesions, swollen lymph nodes and hepatosplenomegaly (especially seen in children). All patients have high serum IgD (> 100 UI/mL) and IgA levels. Nevertheless, a high IgD level is not specific. Our case could also be part of the CINCA (chronic, infantile, neurological, cutaneous and articular) syndrome, which includes similar early manifestations associated with a constant neurological and frequent ophthalmological involvement and epiphyseal changes; to date, these last three manifestations are not present in our patient. CONCLUSION: HIDS and CINCA syndrome are not known to be modified by any effective therapeutic agent. When presenting at birth, these inflammatory diseases must be considered as entities with a rarely described potential severity.     

Latent coeliac disease in a child with epilepsy, cerebral calcifications, drug-induced systemic lupus erythematosus and intestinal folic acid malabsorption associated with impairment of folic acid transport across the blood-brain barrier

A 15-year-old boy with epilepsy and cerebral calcifications, treated with valproic acid, ethyl phenylbarbiturate and ethosuximide, was referred for drug induced systemic lupus erythematosus. Anti-gliadin (AGA) and anti-endomysium (EMA) antibody tests were both positive (EMA titre 1:50). Endoscopic duodenal biopsy showed intense chronic inflammation without villous atrophy or crypt hyperplasia. The child was discharged with a gluten-containing diet. The follow-up showed an increase in EMA titre (1:200) and the persistence of AGA. After 15 months, a second endoscopic intestinal biopsy showed flat mucosa and villous atrophy. Three serum folic acid determinations showed 1.8, 2.4, 2.0 ng/ml (reference range 2.5–16.9 ng/ml) prior to the two intestinal biopsies, but returned to normal levels (11.8 ng/ml) after a gluten-free diet and oral supplementation together. Two years later, the frequency of epileptic seizures was unchanged despite ongoing anti-epileptic treatment and a gluten-free diet. As cerebral calcification and epilepsy are reminiscent of the findings in congenital folate malabsorption, oral loading tests with 5 mg folic acid were carried out and showed impaired intestinal absorption and a defect in the transport across the blood-brain barrier. Low CSF folate levels (13.9 and 12.6 ng/ml, reference range 15–40 ng/ml) and an alteration in the CSF/serum folate ratio (1.43 and 1.16, normal ratio 3:1) were also found as well as increased levels of cystathionine both in CSF (40 μmol/l, reference range 18–28 μmol/l) and in serum (32 μmol/l, reference value <0.10 μmol/l). Conclusion Impairment of intestinal folic acid absorption with a defect in folic acid transport across the blood-brain barrier has been demonstrated in a case of epilepsy and cerebral calcifications associated with coeliac disease. Received: 12 November 1998 / Accepted: 29 February 2000     

A family with a novel TSH receptor activating germline mutation (p.Ala485Val)

Autosomal dominant nonautoimmune hyperthyroidism (ADNAH) is caused by gain of function mutations in the TSH receptor (TSHr) gene and characterized by toxic thyroid hyperplasia with a variable age of onset in the absence of thyroid antibodies and clinical symptoms of autoimmune thyroid disease in at least two generations. We report here a Turkish family with a novel TSHr gene mutation with distinct features all consistent with ADNAH. Thyroid function tests of the proband were as follows: free T3: 13.1 pg/ml (N: 1.8–4.6); free T4: 5.1 ng/dl (N: 0.9–1.7); TSH: 0.01 μIU/ml (N: 0.2–4.2); and TSH receptor antibody: 2 IU/ml (N: 0–10). A heterozygous missense mutation in exon 10 of the TSHr gene (c.1454C>T) resulting in the substitution of valine for alanine at codon 485 (p.Ala485Val) was found in the father and his son and daughter. This mutation had arisen de novo in the father. Functional studies of the novel TSHr germline mutation demonstrated a higher constitutive activation of adenyl cyclase than wild type without any effect on phospholipase C activity. In conclusion, our data indicate that gain of function germline mutations in the TSHr gene should be investigated in families with members suffering from thyrotoxicosis and progressive growth of goiter, but without clinical and biochemical evidence of autoimmune thyroid disease. In addition, patients harboring the same mutation of the TSHr gene may show wide phenotypic variability with respect to the age at onset, and severity of hyperthyroidism and thyroid growth.     

Validation of cardiac output measurement by ultrasound dilution technique with pulmonary artery thermodilution in a pediatric animal model

Novel COstatus system (Transonic Systems, Inc., NY), based on ultrasound dilution (UD), works off in situ arterial and central venous catheters in pediatric patients to measure cardiac output (CO). The purpose of the present study was to validate CO measurement by UD (COUD) with pulmonary artery (PA) thermodilution (COTD) in a prospective animal study. Ten anesthetized pigs (16–45 kg) were instrumented with pediatric PA, central venous, and peripheral artery catheters. For COUD measurements, normothermic saline (0.5–1.0 ml/kg body weight, up to a maximum of 30 ml) was injected into the venous limb of an arteriovenous loop that was connected between in situ catheters. For COTD measurements, 5–10 ml cold saline was injected into the PA catheter. Sixty-four averaged sets were obtained for comparison. COTD mean was 2.98 ± 1.21 l/min (range 1.33–6.29), and COUD mean was 2.68 ± 1.16 l/min (range 1.33–5.85). This study yielded a correlation r = 0.96, COUD = 0.91*(COTD) − 0.04 l/min; bias was 0.3 l/min with limits of agreement as −0.39 to 0.99 l/min; and the percentage error was 23.73% between the methods. CO measurements by UD agreed well with thermodilution measurements in the pediatric swine model.     

A further case of renal tubular dysgenesis surviving the neonatal period

Renal tubular dysgenesis is a critical disorder characterized by the Potter phenotype and severe hypotension in the early neonatal period. We herein report a 3-year-old female with renal tubular dysgenesis. Endocrinological studies showed a high plasma renin activity (over 49.2 ng/ml/h; normal range 2.0–15.2), high active renin concentration (1,823.5 pg/ml; normal range 2.4–21.9), and low angiotensin-converting enzyme (ACE) concentration (1.7 U/l; normal range 8.3–21.4). Taken together, these findings suggested an abnormality of the ACE gene, ACE. Direct sequencing analysis revealed two novel deletions in the coding region of ACE. We conclude that hormonal analysis of the renin-angiotensin system can aid in identifying the responsible genes and help with efficient gene analysis and pathophysiological considerations.     

Bedside detection of low systemic flow in the very low birth weight infant on day 1 of life

We aimed to assess the relationship between the clinical and biochemical parameters of perfusion and superior vena cava (SVC) flow in a prospective observational cohort study of very low birth weight (VLBW) infants. Newborns with congenital heart disease were excluded. Echocardiographic evaluation of SVC flow was performed in the first 24 h of life. Capillary refill time (forehead, sternum and toe), mean blood pressure, urine output and serum lactate concentration were also measured simultaneously. Thirty-eight VLBW infants were examined. Eight patients (21%) had SVC flow less than 40 ml/kg/min. There was a poor correlation between the capillary refill time (in all sites), mean blood pressure, urine output and SVC flow. The correlation coefficient for the serum lactate concentration was r = −0.28, p = 0.15. The median serum lactate concentration was 3.5 (range 2.8–8.5) vs. 2.7 (range 1.2–6.9) mmol/l (p = 0.01) in low flow versus normal flow states. A serum lactate concentration of >2.8 was 100% sensitive and 60% specific for detecting a low flow state. Combining a capillary refill time of >4 s with a serum lactate concentration of >4 mmol/l had a specificity of 97% for detecting a low SVC flow state. Serum lactate concentrations are higher in low SVC flow states. A capillary refill time of >4 s combined with serum lactate concentrations >4 mmol/l increased the specificity and positive and negative predictive values of detecting a low SVC flow state.     

A novel mutation and unusual clinical features in a patient with immune dysregulation,polyendocrinopathy, enteropathy,X-linked (IPEX) syndrome

We report a patient with immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome with a novel splicing mutation of the FOXP3 gene. The patient is a boy, born at 39 + 2 weeks gestation with a birth weight of 3,280 g. The family history was unremarkable. He was well until 11 months of age, when he was diagnosed with type 1 diabetes mellitus. The level of urine C-peptide was 0.58 μg/day (normal range, 44–116 μg/day). Glutamic acid decarboxylase autoantibody was not detected, but a high level of anti-insulin antibody (50 IU/mL; normal range, <5 IU/mL) was noted. This patient presented with unusual clinical features, including pure red cell aplasia, membranous glomerulopathy, and posterior reversible encephalopathy syndrome after a vaccination against influenza A H1N1 virus. The diagnosis of IPEX was made when the patient was 11 years old, which is quite late compared with typical cases. Conclusion: Although IPEX syndrome is usually a disease of infancy, it should not be ruled out solely on the basis of age. IPEX presentation is so variable that it should be suspected in a male child with one or more autoimmune disorders and severe infections.     

Diphtheria, tetanus and pertussis antibodies in 10-year-old children before and after a booster dose of three toxoids: implications for the timing of a booster dose

In an open study, 502 10-year-old children, who had received primary vaccination against diphtheria and tetanus in infancy and had varying histories of pertussis disease and vaccination, were vaccinated with diphtheria-tetanus vaccine (DT) alone or with the addition of 20 µg or 40 g of pertussis toxoid. Diphtheria toxin neutralising antibodies, pertussis toxin IgG and tetanus toxoid IgG antibodies were measured before and 1 month after the booster. All toxoids were highly immunogenic. In pertussis toxoid recipients, median levels of pertussis toxin IgG increased to 16.5 U/ml (DTaP20) and to 36 U/ml (DTaP40) in children with non-detectable (<1 U/ml) antibodies before vaccination and to >400 U/ml in children (both DTaP20 and DTaP40) with detectable antibodies before vaccination. A total of 60 children (12%) with non-detectable (<0.01 IU/ml) diphtheria antibodies and 36 children (7%) with non-detectable (<0.01 IU/ml) tetanus antibodies before the booster had lower median antibody concentrations post-vaccination than children with detectable antibodies before the booster (diphtheria: 5.12 vs. 20.48 IU/ml; tetanus: 4.0 vs. 10.0 IU/ml). There were no differences in diphtheria and tetanus antibodies after vaccination between children who did and did not receive pertussis toxoid. Conclusion:10-year-old children with non-detectable diphtheria and tetanus antibodies before the booster had lower post-vaccination antibodies than those with detectable antibodies before the booster indicating a poor immunological memory. Addition of pertussis toxoid to diphtheria-tetanus vaccine did not affect the antibody responses to diphtheria and tetanus toxoids when the three toxoids were combined as a booster. Even though immunity to diphtheria and tetanus was only estimated by surrogate markers (serum antitoxin antibodies) the results indicate that a lower age for the booster dose of diphtheria-tetanus vaccine or diphtheria-tetanus acellular pertussis vaccine should be considered.     

The relationship between procollagen-III-peptide and the severity of esophageal varices in children with biliary atresia after Kasai operation

Biliary atresia (BA) is a common cause of infantile cholestasis. Disease progression leads to intra hepaticfibrosis, and thus to the development of PH and EV. Our objective has been to study the relationship between procollagen-III-peptide (PIIIP) and the severity of EV in children with BA after Kasai operation. Children below 15 years of age (n=29) with BA after a Kasai operation were evaluated for EV by endoscopy. Healthy (n=26) children of the same age and sex distribution who participated in the hepatitis B vaccination program served as the controls. Serum PIIIP was determined by radioimmunoassay. The BA patients were classified on the basis of severity of EV (Paquet's classification) into three groups: group 1 (n=15) had grade 0, group 2 (n=8) grade 1–2, and group 3 (n=6) grade 3–4 EV. In group 3, serum PIIIP (2.9 ± 1.3 IU/ml) was significantly higher than in group 2 (1.5 ± 0.4 IU/ml) (P < 0.05). Serum PIIIP levels were increased in group 2 compared with group 1 (1.2 ± 0.4 IU/ml) and in group 1 compared with the control group (1.2 ± 0.2 IU/ml), but this difference was not significant. PIIIP levels increased with severity of the EV in the BA patients. Hence, high PIIIP levels may serve as a non invastive indicator of EV developing in postoperative BA patients. Accepted: 8 January 2001     

Eisenmangelan?mie als Leitsymptom einer glutensensitiven Enteropathie bei einem 16-j?hrigen M?dchen

Wir berichten über ein 16-j?hriges M?dchen, bei dem im Rahmen einer Blutbilduntersuchung wegen einmalig aufgetretener Gelenkbeschwerden erstmalig eine ausgepr?gte Eisenmangelan?mie aufgefallen war (H?moglobinkonzentration 6,2 g/dl, mittleres korpuskul?res Volumen (MCV) 66,4 fl, Serumeisenkonzentration 19 μg/l). Familien- und Eigenanamnese waren unauff?llig. Nachdem es unter oraler Eisensubstitution zu keinem ad?quaten H?moglobinanstieg kam, wurden zum Ausschluss okkulter Blutungen – ausgel?st durch intermittierend aktive Blutungsquellen – sowie zum Ausschluss einer Malabsorption eine Koloskopie und eine ?sophago-Gastro-Duodenoskopie durchgeführt. Die histologische Untersuchung des Duodenalbiopsates zeigte eine hochgradige Zottenatrophie mit Kryptenhyperplasie und intraepithelialer Lymphozytose. Die Gliadin-Antik?rper (IgG 375 U/ml, IgA 647 U/ml), Transglutaminase-Antik?rper (743 U/ml) und Antik?rper gegen Retikulin (1:5120) waren deutlich erh?ht. Unter einer glutenfreien Di?t und Fortführung der Eisensubstitution kam es zu einem deutlichen Anstieg der H?moglobinkonzentration auf 10,9 g/dl innerhalb von 8 Wochen.     

Plasma levels of interleukin-6 and interleukin-10 in preterm neonates evaluated for sepsis

In a prospective study, plasma interleukin-6 (IL-6) and interleukin-10 (IL-10) levels were measured by enzyme-linked immunosorbent assay in 45 premature neonates (25–34 weeks gestational age) with signs and symptoms of suspected sepsis at 0, 12 and 24 h; C-reactive protein (CRP) was measured at 0–24 h after enrolment. Six subjects were excluded due to insufficient blood sampling. The remaining 39 neonates were assigned to one of three groups: 25 newborns with sepsis (blood culture positive), seven with pneumonia (positive results on broncho-alveolar lavage fluid culture and characteristic chest radiography) and seven with necrotising enterocolitis (NEC) (characteristic intestinal and radiological signs according to the criteria of Bell et al.). A group of 20 healthy preterm neonates represented control subjects. On admission, higher levels of IL-6, IL-10 and CRP were observed in neonates with sepsis: IL-6 (median 1500 pg/ml, range 487–10000 pg/ml), IL-10 (median 113 pg/ml, range 70–196 pg/ml), CRP (median 22 mg/l, range 4–80 mg/l); pneumonia: IL-6 (median 1500 pg/ml, range 747–8000 pg/ml, IL-10 (median 84 pg/ml, range 76–92 pg/ml), CRP (median 10 mg/l, range 8–33 mg/l) and NEC: IL-6 (median 6650 pg/ml, range 1595–7950 pg/ml), IL-10 (median 80 pg/ml, range 61–147 pg/ml), CRP (median 3 mg/l, range 2.8–8 mg/l) as compared to controls (IL-6 median 208 pg/ml, range 198–349 pg/ml; IL-10 median 36 pg/ml, range 19–50 pg/ml; CRP median <2 mg/l) (P < 0.05). In neonates with sepsis, IL-6 levels were significantly correlated with IL-10 levels (r=0.65; P=0.04) at the time of the second sample. The highest IL-6 levels were observed at onset, while IL-10 was predominant 12 h later. On admission, IL-10 and CRP levels were significantly higher in non-survivors (IL-10 median 507 pg/ml, range 422–753 pg/ml; CRP median 123 mg/l, range 20–219 mg/l) than in survivors (IL-10 median 76 pg/ml, range 61–143 pg/ml; CRP median 8 mg/l range 3–46 mg/l), while IL-10 levels were significantly higher (P < 0.05) also 12 h after admission (non-survivors: IL-10 median 600 pg/ml, range 538–800 pg/ml; survivors: IL-10 median 74 pg/ml, range 53–161 pg/ml). IL-6 and IL-10 levels were significantly correlated with CRP levels on admission (r=0.45; P=0.05). Conclusion Preterm neonates with sepsis, pneumonia or necrotising enterocolitis showed increased interleukin-6, interleukin-10 and C-reactive protein levels. High interleukin-10 concentration was associated with mortality and could be an early indicator of prognosis. Received: 21 November 2000 / Accepted: 23 January 2001     

Serum osteocalcin has limited usefulness as a diagnostic marker for rickets

Serum alkaline phosphatase (AP), the bone fraction of which is secreted by osteoblasts, is elevated in rickets. Both normal and elevated levels of serum osteocalcin (OC), a bone-specific marker secreted by osteoblasts, have been reported in rickets. Expression of the OC gene is enhanced by 1,25-dihydroxyvitamin D (1,25(OH)₂D) in experimental models. This study assessed serum OC levels in 14 controls and 41 patients with active rickets divided into a phosphopenic (n=20) and a calciopenic (n=21) group. Phosphopenic subjects were older (9.5 versus 5.7 years, P=0.03) with higher median serum calcium level (2.35 versus 2.16 mmol/l, P=0.0002) and serum 25-hydroxyvitamin D level (15.4 versus 10.4 ng/l, P=0.003); and lower serum phosphate (0.80 versus 1.51 mmol/l, P=0.0001), serum 1,25(OH)₂D (43.0 versus 95.6 pg/ml, P=0.0001) and intact serum parathyroid hormone level (45.0 versus 141.5 ng/l, P=0.01) than calciopenic subjects. There were no differences in median serum AP (774 versus 1430 IU/l, P=0.17) and OC (14.5 versus 13.4 ng/ml, P=0.6) between the two groups. The mean OC value for the 41 rickets subjects was 15.1 ± 6.2 ng/ml and 17.4 ± 7.8 ng/ml for the 14 control subjects. In the face of markedly elevated serum AP levels in the rickets subjects, all of the serum OC values in the study fell within two standard deviations of the mean for normals. There was no association between serum OC and 1,25-(OH)₂D in either the phosphopenic or the calciopenic group. Conclusion These results show that serum osteocalcin levels are not elevated in all forms of active rickets and that, unlike serum alkaline phosphatase, serum osteocalcin cannot be used in the diagnosis of rickets. Received: 24 September 1999 / Accepted: 23 March 2000     

Usefulness of serum levels of phenobarbitone in control of epilepsy

Phenobarbitone on account of economy and safety still ranks as the foremost drug in the management of epilepsy in India. Fortyfive children with epileptic seizures receiving phenobarbitone as the sole drug were studied. Effective serum levels lie between 15–40 μgg/ml. Side effects appeared over levels of 40 μg/ml. Numerous seizure before instituting treatment, focal type of seizures, presence of mental retardation are factors which signal poorer chances of control. No relationship could be established between nutritional status and serum levels.     

Effect of low and moderate doses of recombinant human erythropoietin on the haematological response in premature infants on a high protein and iron intake

There is no consensus regarding protein intake and the doses of recombinant human erythropoietin (r-HuEpo) and iron in the treatment of anaemia of prematurity (AOP). This open, randomized study has compared the effectiveness of 50 IU r-HuEpo/kg with that of 100 IU/kg, both given subcutaneously thrice weekly. In addition, two different protein supplements have been compared; lyophilized human milk protein and a commercial cow’s milk product. Total protein intake was 3 g/kg per day. Daily iron dose was 18–36 mg. “Healthy” preterm infants (n = 32, birth weight: 800–1400 g, gestational age ≤ 31 weeks) were studied from age 3 to 8 weeks. The two protein regimens yielded no differences in body growth, reticulocyte count or Hb concentration. In both r-HuEpo dose groups increased number of reticulocytes followed start of treatment; higher levels were, however, found in the group receiving 100 IU/kg. Mean Hb concentration plateaued at 12 g/dl for infants receiving 100 IU/kg, at 11 g/dl in the 50 IU/kg group. Even though serum levels of ferritin and transferrin saturation indicated no iron deficiency, soluble transferrin receptor increased in both groups, more rapidly and to higher levels in the 100 IU/kg group. In addition, the number of infants having more than 8% hypochromic red cells increased in both groups. Conclusions Commercial cow’s milk protein added to human milk was as good as human milk protein supplementation in supporting growth and erythropoiesis. Fifty IU/kg r-HuEpo thrice weekly during AOP stimulated erythropoiesis significantly, but less so than 100 IU/kg. Even when using high oral doses of iron to preterms receiving r-HuEpo, our data suggested a certain degree of iron deficient erythropoiesis. Received: 20 January 1996 / Accepted: 2 February 1996     

Serum concentration of granulocyte colony stimulating factor in term and preterm infants

We measured serum granulocyte colony stimulating factor (GCSF) concentration and absolute neutrophil count in four groups of infants: (1) 15 healthy term newborn infants; (2) 21 healthy preterm newborn infants, with mean (SD) birth weight 1583 (533) g, and gestational age 32.0 (3.8) weeks; (3) 5 infected newborn infants; (4) 22 6-month-old control infants. Median (range) serum GCSF concentration was 132.2 (41.5–176.0) pg/ml in term infants, 51.5 (1.8–175.7) pg/ml in preterm infants and 138.9 (54.1–449.8) pg/ml in 6-month-old control infants, with a significant reduction in preterm infants, as compared to term and control infants. GCSF levels were significantly higher in the infected infants, as compared to healthy neonates. Conclusion A significant positive relationship was found in term and preterm infants between serum GCSF concentration and gestational age or birth weight. No relationship was found between serum GCSF concen tration and neutrophil count. The low GCSF baseline levels may contribute to the increased incidence and severity of infection in preterm infants. Received: 17 May 1996 and in revised form: 20 July 1996 / Accepted: 29 July 1996