Outcomes of HIV-infected orphaned and non-orphaned children on antiretroviral therapy in western Kenya

OBJECTIVES: Determine outcome differences between orphaned and non-orphaned children receiving antiretroviral therapy (ART). DESIGN: Retrospective review of prospectively recorded electronic data. SETTING: Nine HIV clinics in western Kenya. POPULATION: 279 children on ART enrolled between August 2002 and February 2005. MAIN MEASURES: Orphan status, CD4%, sex- and age-adjusted height (HAZ) and weight (WAZ) z scores, ART adherence, mortality. RESULTS: Median follow-up was 34 months. Cohort included 51% males and 54% orphans. At ART initiation (baseline), 71% of children had CDC clinical stage B or C disease. Median CD4% was 9% and increased dramatically the first 30 weeks of therapy, then leveled off. Parents and guardians reported perfect adherence at every visit for 75% of children. Adherence and orphan status were not significantly associated with CD4% response. Adjusted for baseline age, follow-up was significantly shorter among orphaned children (median 33 vs. 41 weeks, P = 0.096). One-year mortality was 7.1% for orphaned and 6.6% for non-orphaned children (P = 0.836). HAZ and WAZ were significantly below norm in both groups. With ART, HAZ remained stable, while WAZ tended to increase toward the norm, especially among non-orphans. Orphans showed identical weight gains as non-orphans the first 70 weeks after start of ART but experienced reductions afterwards. CONCLUSIONS: Good ART adherence is possible in western rural Kenya. ART for HIV-infected children produced substantial and sustainable CD4% improvement. Orphan status was not associated with worse short-term outcomes but may be a factor for long-term therapy response. ART alone may not be sufficient to reverse significant developmental lags in the HIV-positive pediatric population.     

CTLA4 gene polymorphisms and soluble CTLA4 protein in Behcet's disease

Cytotoxic T lymphocyte antigen 4 (CTLA4; CD152) is a costimulatory molecule expressed on activated T cells that plays a key inhibitory role during T lymphocyte activation. The gene encoding for CTLA4 has been suggested as a candidate for conferring susceptibility to autoinflammatory diseases. We investigated the polymorphisms of the CTLA4 gene [promoter region (−1722 T/C, −1661 A/G and −318 C/T) and exon 1 (+49 G/A)] and the differences of serum soluble sCTLA4 levels in 285 patients with Behcet's disease (BD) and 287 controls. The frequency of the CTLA4 −1661 GG genotype was significantly higher in BD patients than in controls [ P  = 0.019, odds ratio (OR) = 5.2, 95% confidence interval (CI) = 1.13–23.86]. Also, the genotype frequency for CTLA4 −1722 TC was significantly higher ( P  = 0.014, OR = 1.8, 95% CI = 1.13–2.99), while CTLA4 −1722 CC was significantly lower ( P  = 0.018, OR = 0.4, 95% CI = 0.20–0.87) in BD patients with ocular lesions compared with patients without this symptom. Serum sCTLA4 levels in BD patients were significantly lower, especially in BD patients with the CTLA4 +49 G allele, than those in healthy controls ( P  < 0.05). Although our understanding of the role of the CTLA4 gene and its protein product in BD is incomplete, these results suggest that single nucleotide polymorphisms of the promoter and exon regions in the CTLA4 gene are candidates that predispose to BD and that sCTLA4 may be related to the immunological abnormalities and disease expressions associated with BD.     

Serum 25-hydroxyvitamin D and IgE – a significant but nonlinear relationship

Background:  Hormonal vitamin D system affects the determination of T-cell responses. It is unknown if there is an association between vitamin D status and allergic conditions. Our aim was to investigate differences in serum IgE concentrations by vitamin D status [measured by 25(OH)D] and by a genetic variation in a key vitamin D activation enzyme (CYP27B1) previously shown to be associated with type 1 diabetes.
Methods:  9377 participants in the 1958 British birth cohort completed a biomedical assessment at 45 years of age ; 7288 eligible participants had data on 25(OH)D and IgE, with 6429 having further information on CYP27B1 genotype (−1260C>A).
Results:  There was a nonlinear association between 25(OH)D and IgE ( P -value for curvature = 0.0001). Compared with the reference group with the lowest IgE concentrations [25(OH)D 100–125 nmol/l], IgE concentrations were 29% higher (95% CI 9–48%) for participants with the 25(OH)D <25 nmol/l, and 56% higher (95% CI 17–95%) for participants with 25(OH)D >135 nmol/l (adjusted for sex, month, smoking, alcohol consumption, time spent outside, geographical location, social class, PC/TV time, physical activity, body mass index and waist circumference). CYP27B1 genotype was associated with both 25(OH)D (difference for A vs. C allele: 1.88%, 95% CI 0.37–3.4%, P  = 0.01) and IgE concentrations (−6.59%, −11.6% to −1.42%, P  = 0.01).
Conclusions:  These data suggest that there may be a threshold effect with both low and high 25(OH)D levels associated with elevated IgE concentrations. The same CYP27B1 allele that is protective of diabetes was associated with increased IgE concentrations.     

Effect of polymorphism in insulin locus and HLA on type 1 diabetes in four ethnic groups in Israel

This study examined a possible association of the insulin ( INS ) gene with type 1 diabetes (T1D) in patients and controls from four ethnic groups in Israel. We analyzed the distribution of −23 Hph I single nucleotide polymorphism (SNP) T/A alleles that correspond to INS variable number of tandem repeat short class I alleles (26–63 repeats) and class III alleles (141–209 repeats), respectively. The −23 Hph I T/T genotype was found to be positively associated with T1D in three Jewish groups (Yemenites: 93.9% patients vs 68.8% controls, P  = 0.0002; Ashkenazi: 80.6% vs 50.8%, P  < 10⁻⁴; Ethiopians: 75% vs 40.5%, P  = 0.002). The Yemenite healthy controls have the highest frequency of T allele from all Jewish groups studied (83.5% vs 68.8% in Ashkenazi and 64.3% in Ethiopians). The high frequency of a susceptibility allele in the Yemenites is in line with the high incidence of T1D in this population. No association was observed between T1D and the INS gene in Israeli Arabs studied (70.6% vs 66.7%). Variable incidence of T1D among different ethnicities in Israel is largely attributed to heterogeneous genetics. Human leukocyte antigen (HLA) results of our previous studies describing the susceptibility and protective haplotypes were used for combined analysis to determine possible interaction between the HLA and INS loci. Only in the Ashkenazi group such interaction was presented with statistical significance.     

Circulating levels of sTNFR and discrepancy between cytotoxicity and immunoreactivity of TNF-α in patients with visceral leishmaniasis

Objectives To study the influence of soluble tumour necrosis factor (TNF) receptors (sTNFR) on bioactivity and immunoreactivity of TNF-α in patients with visceral leishmaniasis (Kala-azar) and to examine the association between circulating levels of sTNFR type I and type II with clinical manifestations of the disease.
Methods   Ten patients with Kala-azar were enrolled. Plasma samples for TNF-α and sTNFR were obtained on days 0, 7 and 21–28 of antimonial therapy. Bioactivity of TNF-α was measured by cytotoxicity to L-929 cells and immunoreactivity by enzyme-linked immunosorbent assay (ELISA). sTNFR-I and sTNFR-II were measured by ELISA.
Results   Measured by ELISA, TNF-α was detected at baseline in all patients (range from 22.3 to 163 pg/mL) and showed a linear decline over time on therapy ( r  = −0.49, P  = 0.007). In contrast, when measured by cytotoxicity assay, TNF-α was detected in only one patient at baseline (193 pg/mL) and in four patients at the end of therapy (38.7, 95, 133 and 232 pg/mL) and there was no linear association between TNF-α and duration of therapy ( r  = −0.18, P  = 0.45). sTNFR-I and sTNFR-II were detected in all patients before therapy. There was a strong positive correlation between plasma concentrations of sTNFR-I and sTNFR-II ( r  = 0.8, P  = 0.006). Levels of sTNFR-I and sTNFR-II declined exponentially with time on therapy.
Conclusions   We concluded that sTNFR-I and sTNFR-II are related to disease activity in patients with Kala-azar and that these circulating receptors may interfere with the biological activity of TNF-α in patients with Kala-azar.     

Asthma, body mass, gender, and Hispanic national origin among 517 preschool children in New York City

Background:  Striking differences in asthma prevalence have been reported among Hispanic adults and children living in different cities of the USA. Prevalence is highest among those of Puerto Rican and lowest among those of Mexican origin. We hypothesized that body size would mediate this association.
Methods:  Parents of children in New York City Head Start programs completed a questionnaire including demographic factors, health history, a detailed history of respiratory conditions, lifestyle, and home environment. Children's height and weight were measured in home visits. Logistic regression was used to model the association of asthma with body mass index percentile (<85th percentile, gender/age specific vs ≥85th percentile, gender/age specific), national origin, and other factors.
Results:  Of 517 children at mean age of 4.0 ± 0.6 years, 34% met the study criteria for asthma, and 43% were above the 85th percentile. Asthma was strongly associated with non-Mexican national origin, male gender, allergy symptoms, and maternal asthma, and marginally with body size. The odds of asthma among boys of non-Mexican origin was 5.9 times that among boys of Mexican origin [95% confidence interval (CI): 2.9–12.2]; the comparable odds ratio (OR) among girls was 1.8 (95% CI: 0.9–3.6). Body mass was associated with asthma among girls [OR = 2.0 (95% CI: 1.1–3.7)], but not boys [OR = 1.4 (95% CI: 0.8–2.6)].
Conclusions:  The association of asthma with both body mass and national origin was gender-specific among the children in our study. Ours is one of the first studies to report on pediatric asthma in different Hispanic populations in the same city, by gender.     

IL3 variant on chromosomal region 5q31-33 and protection from recurrent malaria attacks

Using segregation analyses, control of malaria parasites has previously been linked to a major gene within the chromosomal region 5q31-33, but also to complex genetic factors in which effects are under substantial age-dependent influence. However, the responsible gene variants have not yet been identified for this chromosomal region. In order to perform association analyses of 5q31-33 locus candidate single nucleotide polymorphisms (SNPs), 1015 children were recruited at the age of 3 months and followed monthly until the age of 2 years in an area holoendemic for Plasmodium falciparum malaria in Ghana. Quantitative (incidence rates of malaria episodes) and qualitative phenotypes (i.e. 'more than one malaria episode' or 'not more than one malaria episode') were used in population- and family-based analyses. The strongest signal was observed for the interleukin 3 gene (IL3) SNP rs40401 (P = 3.4 × 10(-7), P(c)= 1.4 × 10(-4)). The IL3 genotypes rs40401(CT) and rs40401(TT) were found to exert a protective effect of 25% [incidence rate ratio (IRR) 0.75, P = 4.1 × 10(-5)] and 33% (IRR 0.67, P = 3.2 × 10(-8)), respectively, against malaria attacks. The association was confirmed in transmission disequilibrium tests (TDT, qTDT). The results could argue for a role of IL3 in the pathophysiology of falciparum malaria.     

Genetic variation in ORM1-like 3 (ORMDL3) and gasdermin-like (GSDML) and childhood asthma

Background:  A genome-wide association study identified ORM1-like 3 (orosomucoid 1-like 3, ORMDL3 ) as an asthma candidate gene. Single nucleotide polymorphisms (SNPs) in the region including ORMDL3 on chromosome 17q21 were related to childhood asthma risk and ORMDL3 expression levels in Europeans.
Objective:  We examined whether polymorphisms in ORMDL3 and the adjacent gasdermin-like ( GSDML ) gene associated with asthma in the genome-wide association study are related to childhood asthma and atopy in a Mexico City population.
Methods:  We genotyped rs4378650 in ORMDL3 and rs7216389 in GSDML in 615 nuclear families consisting of asthmatic children aged 4–17 years and their parents. Atopy was determined by skin prick tests to 25 aeroallergens.
Results:  Individuals carrying the C allele of rs4378650 or the T allele of rs7216389 had increased risk of asthma [relative risk (RR) = 1.73, 95% confidence interval (CI) 1.19–2.53, P  = 0.003 for one or two copies of rs4378650 C, and RR = 1.64, 95% CI 1.12–2.38, P  = 0.009 for one or two copies of rs7216389 T). Linkage disequilibrium between the two SNPs was high ( r ² = 0.92). Neither of the SNPs was associated with the degree of atopy. A meta-analysis of five published studies on rs7216389 in nine populations gave an odds ratio for asthma of 1.44 (95% CI, 1.35–1.54, P  < 0.00001).
Conclusions:  Our results and the meta-analysis provide evidence to confirm the finding from a recent genome-wide association study that polymorphisms in ORMDL3 and the adjacent GSDML may contribute to childhood asthma.     

Ambient ozone modifies the effect of tumor necrosis factor G-308A on bronchitic symptoms among children with asthma

Background:  Tumor necrosis factor (TNF)-α has a recognized role in respiratory pathophysiology. One genetic variant (G-308A) in the promoter region affecting the expression of this cytokine may contribute to airway inflammatory diseases, but the studies on bronchitic symptoms were still inconclusive. Because ozone produces oxidative stress, increased airway TNF, and inflammation, the associations of the TNF-308 polymorphism with bronchitic symptoms may vary by ambient ozone exposure.
Methods:  We studied associations of TNF-308 genotype with bronchitic symptoms among asthmatic children in Children's Health Study. The association of TNF G-308A polymorphism with bronchitic symptoms was investigated and we also determined whether the associations vary with ambient ozone exposure.
Results:  Asthmatic children with TNF-308 GG genotype had a significantly reduced risk of bronchitic symptoms with low-ozone exposure (adjusted OR: 0.53; 95% CI: 0.31–0.91). The risk was not reduced in children living in high-ozone communities (adjusted OR: 1.42; 95% CI: 0.75–2.70). This difference in genotypic effects between low- and high-ozone environments was statistically significant among asthmatics ( P for interaction = 0.01), but insignificant among nonasthmatic children.
Conclusion:  Our findings suggest a role of gene–environmental interactions on the occurrence of bronchitic symptoms among children with asthma.     

GWAS reveals new recessive loci associated with non-syndromic facial clefting

We have applied a GWAS to 40 consanguineous families segregating cases of non-syndromic cleft lip with or without cleft palate (NS CL/P) (a total of 160 affected and unaffected individuals) in order to trace potential recessive loci that confer susceptibility to this common facial malformation. Pedigree-based association test (PBAT) analyses reported nominal evidence of association and linkage over SNP markers located at 11q25 (rs4937877, P = 2.7 × 10⁻⁶), 19p12 (rs4324267, P = 1.6 × 10⁻⁵), 5q14.1 (rs4588572, P-value = 3.36 × 10⁻⁵), and 15q21.1 (rs4774497, P = 1.08 × 10⁻⁴). Using the Versatile Gene-Based Association Study to complement the PBAT results, we found clusters of markers located at chromosomes 19p12, 11q25, and 8p23.2 overcome the threshold for GWAS significance (P < 1 × 10⁻⁷). From this study, new recessive loci implicated in NS CL/P include: B3GAT1, GLB1L2, ZNF431, ZNF714, and CSMD1, even though the functional association with the genesis of NS CL/P remains to be elucidated. These results emphasize the importance of using homogeneous populations, phenotypes, and family structures for GWAS combined with gene-based association analyses, and should encourage. other researchers to evaluate these genes on independent patient samples affected by NS CL/P.     

Association between the SUMO4 M55V (A163G) polymorphism and susceptibility to type 1 diabetes: A meta-analysis

Objective

The aim of this study was to determine whether the SUMO4 M55V (A163G) polymorphism confers susceptibility to type 1 diabetes (T1D).

Methods

A meta-analysis was conducted on the association between the SUMO4 M55V polymorphism and T1D using; (1) allelic contrast (G vs. A), and the (2) recessive (GG vs. GA+AA), (3) dominant (GG+GA vs. AA), and (4) additive models (GG vs. AA).

Results

Thirteen separate studies were considered in the meta-analysis, which in total included 5915 patients and 6660 controls, and five European and eight Asian sample populations. Europeans had a higher prevalence of the G allele than Asians (50.4% vs. 30.2%). Meta-analysis of the SUMO4 M55V polymorphism showed an association between T1D and the SUMO4 G allele in all study subjects (OR = 1.236, 95% CI = 1.112–1.373, p = 7.9 × 10⁻⁶), and stratification by ethnicity indicated a highly significant association between the SUMO4 G allele and T1D in Asians (OR = 1.303, 95% CI = 1.169–1.452, p = 1.78 × 10⁻⁷) and a marginal association with T1D in Europeans (OR = 1.177, 95% CI = 1.000–1.386, p = 0.050). Furthermore, significant associations were found between the SUMO4 M55V polymorphism and T1D and all study subjects, Europeans, and Asians using the dominant model (OR = 1.239, 95% CI = 1.144–1.342, p = 1.4 × 10⁻⁸; OR = 1.156, 95% CI = 1.051–1.271, p = 0.003; OR = 1.461, 95% CI = 1.262–1.691, p = 3.8 × 10⁻⁸, respectively).

Conclusions

This meta-analysis indicates that the SUMO4 M55V polymorphism confers susceptibility to T1D in Asians and Europeans.     

The efficacy of sublingual immunotherapy for house dust mites respiratory allergy: results of a GA²LEN meta-analysis

Recent meta-analyses documented the efficacy and safety of sublingual immunotherapy (SLIT) in patients with allergic rhinitis (AR) and asthma (AA). Although SLIT appeared globally effective, the sub-analyses for single allergens provided uncertain results. This study is aimed to investigate the efficacy of SLIT with house dust mite (HDM) extracts in AR and AA through an updated reassessment of randomized controlled trials. Electronic databases were searched up to March 31, 2008, for randomized DBPC trials, assessing the efficacy of SLIT in AR and AA due to HDM sensitization. Outcomes were symptom scores and rescue medications use. For AR, eight studies fulfilled the selection criteria. A significant reduction in symptoms of AR (SMD −0.95; CI 95%−1.77 to −0.14 P  = 0.02) was found in 194 patients (adults and children) receiving SLIT compared to 188 receiving placebo. For AA, with nine studies, similar results were found for symptoms (SMD −0.95; CI 95%−1.74 to −0.15 P  = 0.02) in 243 patients (adults and children) receiving SLIT compared to 209 receiving placebo. A reduction in rescue medication use was found for AR (SMD −1.88; CI 95%−3.65 to −0.12 P  = 0.04) in 89 patients, and AA (SMD −1.48; CI 95%−2.70 to −0.26 P  = 0.02) in 202 patients. A relevant inter-study heterogeneity was detected. Promising evidence of efficacy for SLIT, using mite extract in allergic patients suffering from AR and AA, are herein shown. These findings suggest that more data are needed, derived from large-population-based high quality studies, and corroborated by objective outcomes, mainly for AA.     

Investigations into the role of ST2 in acute asthma in children

The ST2 gene is a member of the interleukin-1 receptor family and is located on chromosome 2q12, an area of the genome that has been associated with asthma. The soluble product of the ST2 gene, serum ST2 (sST2), has previously been shown to be elevated in adult asthmatic patients. This study investigated the potential role of ST2 in children with acute asthma. Children aged 2–16 years ( n  = 186) were recruited on presentation with acute asthma in the emergency department. Blood was obtained on presentation and during convalescence. Variables assessed included sST2 levels, a comprehensive assembly of clinical parameters and two polymorphisms in the ST2 gene, −26999G/A, located in the distal promoter region, and ala78glu polymorphism, on exon 3. The A allele of the −26999G/A polymorphism occurred more frequently in asthmatics compared with an unselected control group ( P  = 0.031). Serum ST2 levels were substantially higher during acute asthma compared with levels after the attack: 0.29 ng/ml (95% confidence interval: 0.23–0.36) and 0.14 ng/ml (0.12–0.17), respectively ( P  = 0.001) and were inversely related to eosinophil counts during an acute asthma attack ( P  = 0.002). The −26999AA genotype, as well as the AC haplotype, was associated with asthma severity scores ( P  = 0.05 and 0.02) compared with the −26999GA and GG genotypes. Serum ST2 levels were not associated with any of the studied genotypes or haplotypes. The observed associations of ST2 genotypes and haplotypes with acute asthma and asthma severity scores as well as the phenotypic differences associated with ST2 polymorphisms suggest that ST2 may play a role in the pathophysiology of asthma.     

Associations between TNFSF4 and TRAF1-C5 gene polymorphisms and systemic lupus erythematosus: A meta-analysis

Objective

The aim of this study was to determine whether tumor necrosis factor superfamily 4 (TNFSF4) and TNF receptor-associated factor 1-complement 5 (TRAF1-C5) polymorphisms confer susceptibility to systemic lupus erythematosus (SLE).

Methods

The authors conducted meta-analyses on associations between polymorphisms of the TNFSF4 (rs2205960, rs1234315, rs10489265) and TRAF1-C5 (rs10818488, rs3761847) genes and SLE susceptibility, using fixed and random effects models.

Results

A total of 21 comparative studies were included in this meta-analysis; meta-analysis showed an association between the minor allele of rs2205960 of TNFSF4 and SLE in all study subjects (odds ratio [OR] = 1.356, 95% confidence interval [CI] = 1.275–1.442, p < 1.0 × 10⁻⁹). Meta-analysis revealed an association between the minor alleles of rs1234315 and rs10489265 of TNFSF4 and SLE in Asians (OR = 1.366, 95% CI = 1.295–1.440, p < 1.0 × 10⁻⁹; OR = 1.463, 95% CI = 1.208–1.771, p = 9.7 × 10⁻⁵). The minor allele of rs10818488 of TRAF1-C5 was found to be significantly associated with SLE in Europeans (OR = 1.210, 95% CI = 1.115–1.313, p = 5.0 × 10⁻⁶). The association p-values remained significant after multiple corrections.

Conclusions

This meta-analysis confirms that TNFSF4 polymorphisms are associated with susceptibility to SLE in Asians and Europeans. An association was found between the rs10818488 polymorphism of TRAF1-C5 and susceptibility to SLE in Europeans.     

Urbanization and child growth in Nepal

The growth of children (0–60 months) of rural-to-urban migrant women was studied in a population of carpet-making workers in a peri-urban community of Kathmandu, Nepal. Mean height-for-age (HAZ) and weight-for-age (WAZ) z-scores are compared for two groups of children belonging to recent urban migrant women (resident <5 years) and to long-term migrants (resident ⩾5 years). The process of urbanization and adaptation to the city environment was explored by examining cohort differences in health care utilization, diarrheal morbidity, breastfeeding practices, demographic, and socioeconomic characteristics. On average, both children of recent and long-term migrants have moderate-to-severe linear growth retardation after 12 months of age. There is, however, a statistically significant difference in mean HAZ and WAZ scores between children depending on maternal length of urban residence status; children of long-term migrants have better growth status compared to children of recent migrants. Nevertheless, there are no significant differences between long-term and recent migrant families in terms of socioeconomic characteristics and selected biobehavioral practices which have been associated with modernization and adaptation to an urban environment. It is concluded that the process of adaptation to an urban environment cannot be explained by standard biobehavioral indicators of modernization and requires further consideration. Am. J Hum. Biol. 10:307–315, 1998. © 1998 Wiley-Liss, Inc.     

Gene expression profiles of meningiomas are associated with tumor cytogenetics and patient outcome

Cytogenetic analysis is a powerful tool for predicting recurrence in meningiomas, even among histologically benign/grade I tumors. Despite this, no study has been reported in which the impact of tumor cytogenetics on the gene expression profiles (GEP) has been analyzed in meningiomas. Here, we analyzed the GEP of 47 tumors and correlated them with the most clinical relevant cytogenetic subgroups of meningiomas, as confirmed through the analysis of 172 patients. Additionally three normal meningeal samples were also studied.
Overall, our results show a clear association between the clinically relevant cytogenetic subgroups of meningiomas including diploid tumors (n = 18), isolated −22/22q− (n = 12), del(1p36) alone (n = 4) and complex karyotypes associated with del(1p36) and/or −14q (n = 13) and their GEP. Accordingly, based on the expression of 85 genes (40 of which were coded in the altered chromosomes used for patient stratification) the cytogenetic class of the tumor could be predicted with an error of <1%, a clear association being found between the GEP and patient outcome ( P  = 0.03) but not tumor histopathology.
In summary, we show a clear association between GEP of neoplastic cells and clinically relevant cytogenetic subgroups of meningiomas.     

Preoperative Mannan-Binding Lectin Pathway and Prognosis in Colorectal Cancer

Background:  Deficiency of the mannan-binding lectin (MBL) pathway of innate immunity leads to increased susceptibility to infections. In patients with colorectal cancer, postoperative infection is associated with poor prognosis. The aim of the present study was to evaluate (1) the relation between the MBL pathway and postoperative infectious complications and survival of patients resected for colorectal cancer and (2) the role of MBL as acute phase reactant compared to CRP.
Methods:  Preoperative MBL concentration, MBL/MBL-associated serine protease (MASP) activity and CRP were determined in serum from 611 patients and 150 healthy controls. The patients were observed for 8 years. Postoperative infections, recurrence and survival were recorded.
Results:  The MBL pathway components were increased in the patients ( P  < 0.0001) compared to healthy controls. Low MBL levels were predictive of pneumonia ( P  = 0.01), and pneumonia ( n  = 87) was associated with poor survival ( P  = 0.003, HR = 1.5, 95% CI 1.1–1.9). MBL and MBL/MASP activity could not predict postoperative overall infections. MBL showed no correlation (spearman's ρ = 0.02, 95% CI −0.06–0.10) with CRP.
Conclusions:  Low preoperative MBL levels are predictive of pneumonia, which is associated with poorer survival. MBL concentration and MBL/MASP activity was not predictive of other postoperative infections or long-term prognosis. MBL apparently is not a surrogate measure of CRP.     

Plasma adiponectin level and sleep structures in children with Prader–Willi syndrome

Adiponectin, an adipose tissue-derived hormone, has been negatively related to obstructive sleep apnea syndrome. Besides sleep apnea, children with Prader–Willi syndrome (PWS) may have excessive daytime sleepiness and rapid eye movement (REM) sleep abnormality. The aim of this study is to determine whether changes in sleep structures are related to plasma adiponectin levels in PWS. Correlations between adiponectin level and sleep variables were analyzed in 28 children with PWS and 18 controls. Overnight polysomnography was performed. The fasting plasma adiponectin levels were higher in the children with PWS than in the controls ( P  =   0.0006). In the PWS, Epworth sleepiness scale was significantly higher ( P  =   0.002); sleep latency ( P  =   0.003) and REM latency ( P  =   0.001) were significantly shortened; the apnea–hypopnea index (AHI) was significantly increased ( P  =   0.0001); and the duration of non-rapid eye movement (NREM) sleep stages 3 and 4 was decreased ( P  =   0.005). Multiple regression analysis revealed correlations between the adiponectin level and the total sleep time ( β  = 0.688, P  =   0.009), AHI ( β  = 1.274, P  =   0.010), REM latency ( β  = −0.637, P  =   0.021) and the percentage of NREM sleep ( β  = −7.648, P  =   0.002) in PWS. In children with PWS, higher plasma adiponectin levels were independently associated with several sleep variables, which was not observed in the control group. These results suggest a potential influence of elevated adiponectin level on the sleep structures in PWS.