The prevalence and etiology of anemia among HIV-infected children in India

In this report, the prevalence and multifactorial etiology of anemia among Indian human immunodeficiency virus (HIV)-infected children are described. HIV-infected children aged 2–12 years were prospectively enrolled in 2007–2008. Measured parameters included serum ferritin, vitamin B₁₂, red-cell folate, soluble transferrin receptor, and C-reactive protein. Children received antiretroviral therapy (ART), iron and, folate supplements as per standard of care. Among 80 enrolled HIV-infected children (mean age 6.8 years), the prevalence of anemia was 52.5%. Etiology of anemia was found to be iron deficiency alone in 38.1%, anemia of inflammation alone in 38.1%, combined iron deficiency and anemia of inflammation alone in 7.1%, vitamin B₁₂ deficiency in 7.1%, and others in 9.5%. Median iron intake was 5.7 mg/day (recommended dietary allowance 18–26 mg/day). Compared to nonanemic children, anemic children were more likely to be underweight (weight Z-score −2.5 vs. -1.9), stunted (height Z-score −2.6 vs. -1.9), with lower CD4 counts (18% vs. 24%, p < 0.01), and higher log viral load (11.1 vs. 7.1, p < 0.01). Hemoglobin (Hb) improved significantly among those who started ART (baseline Hb 11.6 g/dl, 6-month Hb 12.2 g/dl, p = 0.03). Children taking ART combined with iron supplements experienced a larger increase in Hb compared to those receiving neither ART nor iron supplements (mean Hb change 1.5 g/dl, p < 0.01). Conclusion Anemia, particularly iron deficiency anemia and anemia of inflammation, is highly prevalent among children with HIV infection. Micronutrient supplements combined with ART improved anemia in HIV-infected children.     

Estimated intake levels of methylmercury in children, childbearing age and pregnant women in a Mediterranean region, Murcia, Spain

Methylmercury (MeHg) is a bioaccumulable toxin in the trophic chain and a powerful neurotoxin during fetal and child development. Consumption of contaminated fish and shellfish is a principal environmental source of MeHg exposure. This study was designed to assess the Hg and estimated MeHg intake in vulnerable groups of the Murcia region, a Mediterranean part of Spain, compared with international regulations. A validated food frequency questionnaire was used to assess seafood consumptions in 320 children younger than 10 years, 301 women of childbearing age, and 537 pregnant women. Hg concentrations were measured in the most consumed fish products by cold vapor generation–atomic fluorescence spectrometry. The weekly intake of MeHg (μg/kg bw/week) was 2.60 (95% CI = 2.10–3.10) in children 1–5 years, 2.65 (95% CI = 2.26–3.03) in children 6–10 years, 0.98 (95% CI = 0.89–1.07) in women of childbearing age, and 0.88 (95% CI = 0.81–0.95) in pregnant women. The main exposure to MeHg, especially in young children, is related to intake of bluefin tuna and swordfish. Fifty-four percent of children aged 1–10 years, 10% of pregnant women, and 15% of women of childbearing age exceed the Joint Expert Committee on Food Additives provisional tolerable weekly intake of MeHg. In the Murcia region, where fish is a central component of the diet, the focus should be on educating vulnerable populations to reorient fish consumption in order to lower the amount of Hg incorporated with the diet as well as to reduce Hg emissions into the environment.     

Measurement of reticulocyte hemoglobin content to diagnose iron deficiency in Saudi children

Iron deficiency and iron deficiency anemia are common conditions in children, especially in developing countries. It is often difficult for the pediatrician to know which indices should be used in the diagnosis of these conditions in children. Reticulocyte hemoglobin (Hb) content (CHr) has been shown to be an accurate indicator of anemia, however whether its use suits the situation in developing countries or not is unclear. The aim of this study was to evaluate the value and effectiveness of using CHr as a method to diagnose iron deficiency and iron deficiency anemia in Saudi children. The samples for the study were collected from 305 children suspected to have anemia. Complete blood count, transferrin saturation (Tfsat), ferritin, circulating transferrin receptor (TfR) and CHr were measured. Three groups were defined, iron deficiency (Tfsat <20%, Hb >11 g/dL; n=120), iron deficiency anemia (Tfsat <20%, Hb <11 g/dL; (n=73) and controls (Tfsat >20%; n=112). The anemic group had significantly lower macrocytic anemia (MCV), mean corpuscular hemoglobin (MCH) and CHr. All of the variables in the anemia group were significantly lower than those of the control group except for the ferritin level. Compared to the control group, the iron deficiency group also showed significantly lower values except for transferrin receptor and the ferritin levels. CHr levels of <26 pg correlated well with anemic states. CHr together with a complete blood count may provide an alternative to the traditional hematologic or biochemical panel for the diagnosis of iron deficiency and iron deficiency anemia in young children and is cost-effective in developing countries. A CHr cut-off level of 26 pg is considered to be a reasonable indicator of anemic states.     

Microcytic anemia in children: parallel screening for iron deficiency and thalassemia provides a useful opportunity for thalassemia prevention in low- and middle-income countries

Abstract

Microcytic anemia in children is commonly attributed to iron deficiency without attempting to find the cause. Inadequate investigations to exclude hemoglobinopathies lead to missed opportunities for identification of thalassemia carriers. Here we aim to describe the relative contribution of iron deficiency and thalassemia to microcytic anemia in children. This hospital-based prospective study was conducted at the Colombo North Teaching Hospital, Ragama, Sri Lanka. All newly diagnosed patients with microcytic anemia were recruited and data were collected using an interviewer-administered questionnaire. Full blood count, blood film, serum ferritin, c-reactive protein, quantification of hemoglobin sub-types and α-globin genotype were performed using 4?ml of venous blood. A total of 104 children (Male- 60.5%) were recruited. Iron deficiency was the cause for anemia in 49% whilst 16% and 10% had α- and β-thalassemia trait respectively. Seven (6.7%) children had co-existing iron deficiency and thalassemia trait while two coinherited α- and β-thalassemia trait. Children with β-thalassemia trait had significantly higher red cell count and lower mean corpuscular volume compared to children with iron deficiency. However, none of the red cell parameters were significantly different between children with α-thalassemia trait and iron deficiency. Iron deficiency contributes only to half of children with microcytic anemia; one-fourth had thalassemia trait. Co-existence of iron deficiency and thalassemia trait or co-inheritance of α- and β-thalassemia trait were found in 9%. Parallel investigation of children with microcytic anemia to diagnose iron deficiency and thalassemia provides an opportunity to identify thalassemia carriers which is beneficial for thalassemia prevention.     

The prevalence of anemia in adolescents: a study from Turkey

A cross-sectional method was used to study a group of 400 high school students in Kocaeli, Turkey, aged 14 to 16 years, identified among 17,812 high school students. Students from 10 high schools were selected using a random sampling method. Whole blood counts were performed as a screening test for anemia. Serum ferritin levels and, when necessary, hemoglobin electrophoresis were determined for anemic students. Iron medication was prescribed for iron deficiency and genetic counseling was given to adolescents with thalassemia trait. Out of 338 participating students (mean age, 14.72+/-0.71 y), anemia (hemoglobin <12 g/dL for girls and <13 g/dL for boys) was detected in 17/174 girls (9.7%) and 6/164 boys (3.6%). Iron deficiency anemia was detected in 20/23 (86.9%) of anemic children [15/17 (88.2%) girls and 4/6 (66.6%) boys]. Of 23 students with anemia 2 had beta-thalassemia trait and 2 had both iron deficiency, and beta-thalassemia trait. Etiology of anemia could not be defined in 1 student. The prevalence of adolescent anemia in Kocaeli is almost equal to that in developed countries.     

Factors associated with syndemic anemia and stunting among children in Myanmar: A cross-sectional study from a positive deviance approach

BackgroundAnemia and stunting in children are detrimental to the prospects of a normal, healthy upbringing. Having similar risk factors and serious consequences, the syndemic aspect of these two ailments is mostly underrated, and positive deviant (PD) factors that ensure non-anemic status in stunted children have not been studied to date.MethodsThis study aimed to identify PD factors that have potential to prevent syndemic anemia among stunted children aged 6–59 months in Myanmar. This was a cross-sectional secondary analysis of the Myanmar Demographic and Health Survey (DHS) data conducted in 2016, applying the PD concept, where children who were stunted without anemia were considered as PDs.ResultsAmong 1248 stunted children, those who had the syndemic condition were compared with their PD peers in terms of maternal characteristics as well as socioeconomic and health-related factors. Multivariable logistic regression analyses were used to identify the determinants of syndemic state. The results showed that three out of every five stunted children were anemic. The syndemic risk was decreased among children of maternal age groups 20–34 years and 35–44 years: [aOR] = 0.19, 95% CI = 0.05–0.69; p = 0.012, and aOR = 0.19, 95% CI = 0.05–0.75; p = 0.018, respectively. Moderately stunted children (aOR = 0.53, 95% CI = 0.34–0.81; p = 0.004) and children who were not currently breastfed (aOR = 1.56, 95% CI = 1.01–2.41; p = 0.044) were less likely to develop the syndemic condition.ConclusionMaternal age, stunting severity, breastfeeding duration, and maternal anemic status are strong predictors in determining hemoglobin concentrations among stunted children. This study suggests that nutritional interventions targeting PD factors could represent syndemic action in improving child health.     

High birth prevalence of sickle cell disease in Northwestern Tanzania

1 Background

Worldwide, hemoglobinopathies affect millions of children. Identification of hemoglobin disorders in most sub‐Saharan African countries is delayed until clinical signs of the disease are present. Limited studies have been conducted to understand their prevalence and clinical presentation among newborns in resource‐limited settings.

2 Methodology

This was a prospective cohort study. Newborns (aged 0–7 days) at two hospitals in Northwestern Tanzania were enrolled and followed prospectively for 6 months. Clinical and laboratory information were collected at baseline. Participants were screened for hemoglobinopathies using high‐performance liquid chromatography. Clinical and laboratory follow‐up was performed at 3 and 6 months for those with hemoglobinopathies as well as a comparison group of participants without hemoglobinopathies.

3 Results

A total of 919 newborns were enrolled. Among these, 1.4% (13/919) had sickle cell anemia or Hb S/β⁰‐thalassemia (Hb FS), and 19.7% (181/919) had sickle cell trait or Hb S/β⁺ thalassemia (Hb FAS). Furthermore, 0.2% (two of 919) had β⁺‐thalassemia. Red cell indices compared between Hb FS, Hb FAS, and Hb FA were similar at baseline, but hemoglobin was lower and red cell distribution width was higher in children with Hb FS at 3‐ and 6‐month follow‐up. Febrile episodes were more common for children with Hb FS at 3‐ and 6‐month follow‐up.

4 Conclusion

The prevalence of sickle cell disease among neonates born in Northwestern Tanzania is one of the highest in the world. Newborn screening is needed early in life to identify neonates with hemoglobinopathies so that clinical management may commence and morbidity and mortality related to hemoglobinopathies be reduced.     

A community study of clinical traits and risk factors for human metapneumovirus and respiratory syncytial virus infection during the first year of life

Human metapneumovirus (hMPV) and respiratory syncytial virus (RSV) are important respiratory pathogens with similar symptomatology. The aim of this prospective birth cohort study was to identify risk factors for an hMPV or RSV infection during the first year of life in unselected healthy children. We followed 217 children from birth to 1 year of age. Nasal swabs and symptom diaries were collected monthly. Anti-hMPV and anti-RSV IgG antibodies by age 1 year were detected by ELISA, and nasal swabs were analysed for hMPV and RSV by RT-PCR. Logistic regression was used for risk factor analysis. Anti-hMPV IgG was found in 38 children (17.5%), and anti-RSV IgG in 172 children (79%). Risk factors for being anti-hMPV IgG-positive were: (1) being born in the spring (OR = 2.36; 95% CI:1.06–5.27), and (2) having older siblings (OR = 3.82; 95% CI:1.75–8.34). Risk factors for being anti-RSV IgG-positive were: (1) gestational age <38 weeks (OR = 3.39; 95% CI:1.42–8.05), (2) increasing paternal age (OR = 1.85 per 5 yrs; 95% CI:1.28–2.68), and (3) wall-to-wall carpeting (OR = 3.15; 95% CI:1.29–7.68). Being born in the spring was associated with decreased odds of being anti-RSV IgG-positive (OR = 0.27, 95% CI:0.09–0.85). Risk factors for RSV hospitalisation (n = 11) were: (1) older siblings (OR = 4.49; 95% CI: 1.08–18.73) and (2) smoking in the household (OR = 5.06; 95% CI: 1.36–18.76). Exclusive breastfeeding for the first 14 days of life protected against hospitalisation (OR = 0.21; 95% CI:0.06–0.79). In conclusion, this study identifies risk factors for mild and asymptomatic hMPV infections in infancy.     

Iron deficiency in proteinuric children with nephrotic syndrome: A cross-sectional pilot study

Massive proteinuria in nephrotic syndrome causes depletion of various proteins. Iron deficiency can occur due to urinary loss of iron, transferrin, and soluble transferrin receptors. We conducted this cross-sectional study of 52 children with proteinuric nephrotic syndrome, aged 1–12 years (mean 7.1 ± 2.7 years). Hemoglobin (Hb), RBC indices (MCV, MCH, MCHC), percentage of hypochromic RBCs (Hypo-He), reticulocyte hemoglobin content (Ret-He), and serum ferritin were examined. Seven (13%) patients had iron deficiency anemia and another 10 (19%) exhibited iron deficiency. A higher proportion of children with steroid-resistant disease had anemia than did steroid-sensitive children (P = 0.076). Thus, children with nephrotic syndrome may have iron deficiency (32.7%), which needs to be screened.     

Leukocyte DNA damage in children with iron deficiency anemia: effect of iron supplementation

Iron deficiency is frequently associated with anemia. Iron is a transition-metal ion, and it can induce free radical formation, which leads to formation of various lesions in DNA, proteins, and lipids. The aim of this study was to investigate baseline oxidative DNA damage and to clarify the role of the administration of a therapeutic dose of iron on DNA oxidation in children with iron deficiency anemia (IDA). Twenty-seven children with IDA and 20 healthy children were enrolled in the study. Leukocyte DNA damage (strand breaks and Fpg-sensitive sites) was assessed using comet assay before and after 12 weeks of daily iron administration. Before the iron administration, the frequency of DNA strand breaks in the children with IDA was found to be lower than those in the control group (P < 0.05), but there was not a significant difference for frequency of Fpg-sensitive sites. After 12 weeks of iron administration, the frequency of both DNA strand breaks and Fpg-sensitive sites were found to be increased (P < 0.01). No significant association was determined between DNA damage parameters and hemoglobin, hematocrit, serum iron, total iron binding capacity, and ferritin. In conclusion, basal level of DNA strand breaks is at a low level in children with IDA. After iron administration, DNA strand breaks and Fpg-sensitive sites, which represent oxidatively damaged DNA, increased. However, this increase was unrelated to serum level of iron and ferritin.     

Lipoprotein lipase gene polymorphisms and risks of childhood obesity in Chinese preschool children

Childhood obesity is increasingly prevalent in the community and is related to many adult diseases. Lipoprotein lipase (LPL) plays a central role in dyslipidemia, and polymorphisms of the LPL gene may result in the disturbance in the lipid’s metabolism. The aim of this study is to test the hypothesis that genetic variants of LPL and serum lipid levels are associated with the risk of childhood obesity. We genotyped +495T > G and PvuII T > C in an LPL gene and measured the serum lipid levels in a case–control study of 124 obese children and 346 frequency-matched normal controls in preschool Chinese children. The variant genotypes of LPL +495GG and PvuII CC were associated with a significantly increased risk of childhood obesity [adjusted odds ratio (OR) = 2.39, 95% CI = 1.09–5.23 for +495 GG; adjusted OR = 2.00, 95% CI = 1.04–3.83 for PvuII CC], compared with their wild-type genotypes, respectively. In addition, compared with the lower serum level cut off by the control median, the higher level of serum triglyceride (TG) (>0.59 mmol/L) was associated with a 1.32-fold increased risk of childhood obesity, and the higher level of high density lipoprotein cholesterol (HDLC) (>1.14 mmol/L) was associated with a 36% decrease in risk of childhood obesity. Furthermore, the median levels of TG were higher in obese children carrying LPL +495TT/TG and PvuII TT/CT genotypes than those in controls, the HDLC levels were lower in obese children carrying LPL +495TG and PvuII CT/CC genotypes than those in controls. In conclusion, the LPL gene +495T > G and PvuII T > C polymorphisms may modulate the magnitude of dyslipidemia in Chinese early-onset obesity.     

Characteristics of pediatric patients with enterovirus meningitis and no cerebral fluid pleocytosis

Human non-polio enterovirus (EV) is the most important cause of aseptic meningitis in children. Only a few studies report the lack of cerobrospinal fluid (CSF) pleocytosis in children with confirmed EV meningitis; however, the characteristics of these children have not been well defined. This paper describes the clinical and laboratory features of EV meningitis in children with no CSF pleocytosis. Clinical, laboratory, and virological data of Dutch patients <16 years diagnosed with EV meningitis, between 2003 and 2008, were analyzed retrospectively. Data of children with and without CSF pleocytosis were compared. A total of 149 children were infected with EV. Patients presented mainly with fever (n = 113), malaise (n = 43), abdominal pain (n = 47), and irritability (n = 61). Of the 60 patients with EV meningitis, 23 had no pleocytosis. Those who lacked CSF pleocytosis were younger [odds ratio (OR) 1.00; 95% confidence interval (CI) 1.000–1.002; p = 0.001], had experienced drowsiness more (OR 9.60; 95% CI 2.24–41.15; p = 0.002), had lower white blood cell counts (OR 0.73; 95% CI 0.61–0.89; p = 0.001), and had higher C-reactive protein (OR 1.13; 95% CI 1.03–1.23; p = 0.006) than those with pleocytosis. Conclusion. These findings show that EV meningitis occurs in the absence of CSF pleocytosis, particularly in young infants, meaning that EV meningitis in this age group cannot be solely excluded by the absence of CSF pleocytosis. They also confirm the importance of genome detection in the diagnosis of EV meningitis in young infants.     

Programmed death-1 (PD-1) gene polymorphisms lodged in the genetic predispositions of Kawasaki Disease

The purpose of this study is to investigate the association of programmed death-1 gene (PD-1) polymorphisms with genetic predispositions to Kawasaki disease (KD). A total of 73 patients with KD and 100 healthy controls were enrolled from 2007 to 2008. Two single nucleotide polymorphisms of the PD-1 gene, rs41386349 and rs2227981, were analyzed. Higher T allele frequency of rs41386349 was found in the patient group than the control group (p = 0.007, odds ratio (OR) = 1.9, 95% CI = 1.2–2.9). PD-1 rs2227981 polymorphism was not significant in patients with KD comparing with the control group (p = 0.4, OR = 1.2 (0.8–1.9)). Furthermore, no difference of PD-1 polymorphisms between patients with coronary artery dilatation (CAD) and those without CAD was found. Our data support the possibility that PD-1 gene polymorphism may be related with the genetic susceptibility of KD in Korean population.     

Risk factors for severe RSV-induced lower respiratory tract infection over four consecutive epidemics

Variability in severity among different respiratory syncytial virus (RSV) seasons may influence hospital admission rates for RSV-induced lower respiratory tract infection (LRTI) in young children. The aim of the present study was to identify through logistic regression analysis, risk factors associated with higher likelihood to acquire RSV-induced LRTI, in children with symptoms severe enough to lead to hospital admission. Over four consecutive RSV seasons (2000–2004), records from children <4 years of age admitted for RSV-induced LRTI (“cases”) were compared with those from children with LRTI not due to RSV and not requiring hospitalization (“controls”). 145 “case-patients” and 295 “control-patients” were evaluated. Independent from the severity of the four epidemic seasons, seven predictors for hospitalization for RSV infection were found in the bivariate analysis: number of children in the family, chronological age at the onset of RSV season, birth weight and gestational age, birth order, daycare attendance, previous RSV infections. In the logistic regression analysis, only three predictors were detected: chronological age at the beginning of RSV season [aOR = 8.46; 95% CI:3.09–23.18]; birth weight category [aOR = 7.70; 95% CI:1.29–45.91]; birth order (aOR = 1.92; 95% CI:1.21–3.06). Conclusions: Independent from the RSV seasonality, specific host/environmental factors can be used to identify children at greatest risk for hospitalization for RSV infection.     

Antibody persistence for 3?years following two doses of tetravalent measles–mumps–rubella–varicella vaccine in healthy children

Two doses of a varicella-containing vaccine in healthy children <12 years are suggested to induce better protection than a single dose. Persistence of immunity against measles, mumps, rubella, and varicella as well as varicella breakthrough cases were assessed 3 years after two-dose measles, mumps, rubella, and varicella (MMRV) vaccination or concomitant MMR (Priorix™) and varicella (Varilrix™) vaccination. Four hundred ninety-four healthy children, 12–18 months old at the time of the first dose, received either two doses of MMRV vaccine (GlaxoSmithKline Biologicals) 42–56 days apart (MMRV, N = 371) or one dose of MMR and varicella vaccines administered simultaneously at separate sites, followed by another MMR vaccination 42–56 days later (MMR + V, N = 123). Three hundred-four subjects participated in 3-year follow-up for persistence of immunity and occurrence of breakthrough varicella (MMRV, N = 225; MMR + V, N = 79). Antibodies were measured by ELISA (measles, mumps, rubella) and immunofluorescence (varicella). Contacts with individuals with varicella or zoster and cases of breakthrough varicella disease were recorded. Three years post-vaccination seropositivity rates in subjects seronegative before vaccination were: MMRV-measles, 98.5% (geometric mean titer [GMT] = 3,599.6); mumps, 97.4% (GMT = 1,754.5); rubella, 100% (GMT = 51.9); varicella, 99.4% (GMT = 225.5); MMR + V-measles, 97.0% (GMT = 1,818.8); mumps, 93.8% (GMT = 1,454.6); rubella, 100% (GMT = 53.8); and varicella, 96.8% (GMT = 105.8). Of the subjects, 15–20% reported contact with individuals with varicella/zoster each year. After 3 years, the cumulative varicella breakthrough disease rate was 0.7% (two cases) in the MMRV group and 5.4% (five cases) in the MMR + V group. Conclusion: Immunogenicity of the combined MMRV vaccine was sustained 3 years post-vaccination. (208136/041/NCT00406211).     

Attention-deficit hyperactivity disorder in children chronically exposed to high level of vehicular pollution

The purpose of this study is to explore whether sustained exposure to vehicular air pollution affects the behavior and activities of children. The prevalence of attention-deficit hyperactivity disorder (ADHD) was assessed in two childhood populations. In a cross-sectional study 969 school-going children (9–17 years) and 850 age- and sex-matched children from rural areas were assessed, following the criteria of Diagnostic and Statistical Manual of conduct disorders (DSM-IV) of American Pediatric Association. Data of ambient particulate matter with a diameter of less than 10 μm (PM₁₀) were obtained from Central Pollution Control Board and aerosol monitor. ADHD was found in 11.0% of urban children in contrast to 2.7% of the control group (p < 0.001). Major risk factors were male gender, lower socioeconomic status, 12–14 year age group, and PM₁₀ level in breathing air. ADHD was more prevalent among boys both in urban and rural areas. It was prevalent among 18.0% of the boys enrolled in Delhi against 4.0% of the girls, giving a male/female ratio of 4.5:1. Inattentive type of ADHD was predominant followed by hyperactive–impulsive type and combined type of ADHD. Controlling potential confounder, ambient PM₁₀ level was positively correlated with ADHD (OR = 2.07; 95% CI, 1.08–3.99). Conclusion: The results of this study point to a possible association between air pollution and behavioral problems in children. Though gender, socioeconomic status, and age play a very important factor in ADHD prevalence, the association is highest and strongest between particulate pollution and prevalence of ADHD.     

Clinical presentation of celiac disease and the diagnostic accuracy of serologic markers in children

There has been growing recognition of a changing clinical presentation of celiac disease (CD), with the manifestation of milder symptoms. Serologic testing is widely used to screen patients with suspected CD and populations at risk. The aim of this retrospective analysis was to evaluate the clinical presentation of CD in childhood, assess the diagnostic value of serologic tests, and investigate the impact of IgA deficiency on diagnostic accuracy. We evaluated 206 consecutive children with suspected CD on the basis of clinical symptoms and positive serology results. Ninety-four (46%) had biopsy-proven CD. The median age at diagnosis of CD was 6.8 years; 15% of the children were <2 years of age. There was a higher incidence of CD in girls (p = 0.003). Iron deficiency and intestinal complaints were more frequent in children with CD than those without CD (61% vs. 33%, p = 0.0001 and 71% vs. 55%, p = 0.02, respectively), while failure to thrive was less common (35% vs. 53%, p = 0.02). The sensitivity of IgA tissue transglutaminase (IgA-tTG) was 0.98 when including all children and 1.00 after excluding children with selective IgA deficiency. The specificity of IgA-tTG was 0.73 using the recommended cut-off value of 20 IU, and this improved to 0.94 when using a higher cut-off value of 100 IU. All children with CD and relative IgA deficiency (IgA levels that are measurable but below the age reference [n = 8]) had elevated IgA-tTG. In conclusion, CD is frequently diagnosed in school-age children with relatively mild symptoms. The absence of intestinal symptoms does not preclude the diagnosis of CD; many children with CD do not report intestinal symptoms. While the sensitivity of IgA-tTG is excellent, its specificity is insufficient for the diagnostic confirmation of a disease requiring life-long dietary restrictions. Children with negative IgA-tTG and decreased but measurable IgA values are unlikely to have CD.     

Total serum bilirubin levels during the first 2 days of life and subsequent neonatal morbidity in very low birth weight infants: a retrospective review

To determine the relationship between total serum bilirubin (TSB) during the first 2 days of life and subsequent neonatal morbidity in very low birth weight (VLBW, less than 1500 g) infants. We performed a prospective study of 582 VLBW infants born between July 1, 2005 and December 31, 2009. TSB was measured in umbilical cord blood (UCB), at 24 and 48 h after birth. Demographic and clinical characteristics of infants in hospital were recorded. The interaction between TSB variables during the first 48 h of life and subsequent neonatal morbidity were assessed in logistic regression analyses adjusted for multiple risk factors. It was found that TSB in UCB was in a negative correlation with occurrence of respiratory distress syndrome (RDS) [OR 0.626, 95% confidence interval (95% CI): 0.446–0.879, p = 0.007], and there was also a negative correlation between TSB in UCB and occurrence of intraventricular hemorrhage (IVH) [OR 0.695, 95% CI 0.826–0.981, p = 0.020]. However, TSB in UCB positively correlated with hyperbilirubinemia [OR 2.471, 95% CI 1.326–3.551, p = 0.012], and TSB at 24 h after birth was also in a positive correlation with early onset sepsis (EOS) [OR 1.299, 95% CI 1.067–1.582, p = 0.011]. VLBW infants with low TSB levels in UCB were more likely to develop RDS and IVH, and those with low TSB levels in UCB were less likely to develop hyperbilirubinemia. Infants with high TSB levels at 24 h after birth were more likely to develop EOS. The protective effect of raised TSB in UCB with respect to RDS and IVH warrants further investigation.     

Cardiovascular response in Anemia

Objective: To study the functional consequences of nutritional anemia by evaluating the exercise performance in these children.Methods: The study was conducted on 30 each of anemic and normal children of both sexes aged between 7 and 14 years. Relevant history was taken, and detailed examination was done. These children were classified according to severity of anemia based on hemoglobin estimation as mild (10–11.9 g/dl), moderate (7–9.9 g/dl) and normal (>12g/dl). Children with severe anemia (Hb <7g/dl), heart disease, non-nutritional anemia, acute febrile or respiratory illness were excluded. The subjects were tested on Mortara X Scribe colour stress treadmill using the modified Bruce protocol. Continuous computerised electrocardiographic analysis was done. The parameters studied included heart rate, systolic blood pressure, double product (DP = HRxSBP), ECG changes, metabolic equivalents (METS) and exercise duration. The end point of the test was a HR of 170/min (non-fatigue group) or inability to perform further (fatigue group). Statistical analysis was done by appropriate tests.Results: Fifteen children each with mild and moderate anemia and 30 age-matched controls were enrolled in the study. There was no significant difference in the resting HR, exercise duration or DP between the cases and controls. Thirty-one children reached the target HR (non-fatigue group). The end-point HR was significantly lesser among the anemic children in the fatigue group (P 0.04). The percent gain of SBP, at peak exercise (P 0.0007) and recovery SBP as percent of resting SBP (p 0.006) were significantly more in the anemic children, more so in the mildly anemic ones. Lesser METS was achieved by anemics as compared to controls (P 0.04). ECG changes occurred significantly more often in anemic children, 53.8% of those with changes being moderately anemic, the main abnormality being ST depression. None developed arrhythmia during exercise testing.Conclusion: The cardiovascular response to physical exercise is compromised in children with nutritional anemia and hence these children may never attain their full potential in various school activities. Prevention of anemia should be a priority in school going children