Publications by authors named "Anna Hogendorf"

20 Publications

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Clinical heterogeneity among pediatric patients with autoimmune type 1 diabetes stratified by immunoglobulin deficiency.

Pediatr Diabetes 2021 Apr 10. Epub 2021 Apr 10.

Department of Pediatrics, Oncology, and Hematology, Medical University of Łódź, Łódź, Poland.

Background: Type 1 diabetes (T1D) may coexist with primary immunodeficiencies, indicating a shared genetic background.

Objective: To evaluate the prevalence and clinical characteristics of immunoglobulin deficiency (IgD) among children with T1D.

Methods: Serum samples and medical history questionnaires were obtained during routine visits from T1D patients aged 4-18 years. IgG, IgA, IgM, and IgE were measured by nephelometry and enzyme-linked immunosorbent assay (ELISA). IgG and IgM deficiency (IgGD, IgMD) were defined as IgG/IgM >2 standard deviations (SD) below age-adjusted mean. IgE deficiency was defined as IgE <2 kIU/L. IgA deficiency (IgAD) was defined as IgA >2 SD below age-adjusted mean irrespective of other immunoglobulin classes (absolute if <0.07 g/L, partial otherwise) and as selective IgAD when IgA >2 SD below age-adjusted mean with normal IgG and IgM (absolute if <0.07 g/L, partial otherwise).

Results: Among 395 patients (53.4% boys) with the median age of 11.2 (8.4-13.7) and diabetes duration 3.6 (1.1-6.0) years, 90 (22.8%) were found to have hypogammaglobulinemia. The IgGD and IgAD were the most common each in 40/395 (10.1%). Complex IgD was found in seven patients. Increased odds of infection-related hospitalization (compared to children without any IgD) was related to having any kind of IgD and IgAD; OR (95%CI) = 2.1 (1.2-3.7) and 3.7 (1.8-7.5), respectively. Furthermore, IgAD was associated with having a first-degree relative with T1D OR (95%CI) = 3.3 (1.4-7.6) and suffering from non-autoimmune comorbidities 3.3 (1.4-7.6), especially neurological disorders 3.5 (1.2-10.5).

Conclusions: IgDs frequently coexist with T1D and may be associated with several autoimmune and nonimmune related disorders suggesting their common genetic background.
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http://dx.doi.org/10.1111/pedi.13208DOI Listing
April 2021

Broad phenotypic spectrum of germ line 7p12.1 microdeletions encompassing the IKZF1 gene includes predisposition to acute lymphoblastic leukemia.

Genes Chromosomes Cancer 2021 Feb 18;60(2):79-87. Epub 2020 Nov 18.

Department of Pediatrics, Oncology and Hematology, Medical University of Lodz, Lodz, Poland.

Microdeletions of 7p12.1 encompassing the IKZF1 gene locus are rare, with few cases reported. The common phenotype includes intellectual disability, overgrowth, and facial dysmorphism accompanied, albeit rarely, by congenital anomalies. Haploinsufficiency of IKZF1 predisposes individuals to childhood acute lymphoblastic leukemia (ALL). In this study, we comprehensively analyzed the frequency of 7p12.1 deletions among 4581 Polish individuals who underwent chromosomal microarray testing for unexplained developmental delay, intellectual disability, and/or congenital anomalies. Two unrelated individuals (0.04%) with a de novo interstitial 7p12.1 microdeletion encompassing IKZF1 were identified. One developed ALL. Analysis of the incidence and the phenotype of constitutional 7p12.1 microdeletion, which based on the previously annotated patients data in public databases and literature reports, revealed 21 cases including five patients diagnosed with ALL.
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http://dx.doi.org/10.1002/gcc.22914DOI Listing
February 2021

HLA-A gene variation modulates residual function of the pancreatic β-cells in children with type 1 diabetes.

Pediatr Endocrinol Diabetes Metab 2020 ;26(2):73-78

Department of Pediatrics, Oncology and Hematology, Medical University of Lodz, Poland.

Aim Of The Study: The study aimed to analyze an association between the HLA-A gene variation and a risk of type 1 diabetes development and to evaluate the association of HLA class I and class II alleles with β-cell destruction.

Material And Methods: A group of 108 children with type 1 diabetes were genotyped in HLA-A, -DRB1, and -DQB1 genes using hybridization with oligonu-cleotides probes. Plasma C-peptide concentration was assessed by radioimmunoassay method.

Results: No differences in allele HLA-A distribution between type 1 diabetes patients and healthy individuals were found. Among "low C-peptide"(< 0.28 pmol/ml) individuals, the frequency of HLA-A*02 allele was 41.3%, whereas only one HLA-A*26 allele was detected in this group (0.7%). Conversely, among "high C-peptide"( 0.28 pmol/ml) probands the prevalence of A*02 allele was 19.7% (Pc = 0.008, OR = 1.4, 95% CI: 1.2-1.7) and A*26 10.5 % (Pc < 0.007, OR = 0.15, 95% CI: 0.02-0.9). Genotype analysis showed that A*02/*02 and A*02/X children were more likely to have "low" C-peptide at the onset compared to those with non-A*02/non-A*02 genotype (p = 0.008, OR = 1.6, 95% CI: 1.3-2.0 and p = 0.015, OR = 1.4, 95% CI: 1.1-1.9, respectively). A02 phenotype individuals had lower median C-peptide (0.17 pmol/ml) than non-A02 patients (0.26 pmol/ml, p = 0.008). Median C-peptide was higher in the A26-positive group comparing to A26-negative (0.40 and 0.20, respectively, p = 0.04). No association between HLA class II and C-peptide levels was observed.

Conclusions: HLA-A alleles are not associated with disease development nevertheless strongly influence a residual pancreatic β-cell function. The results suggest a different role of HLA class I and class II in type 1 diabetes pathogenesis.
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http://dx.doi.org/10.5114/pedm.2020.95617DOI Listing
May 2021

A cross-sectional study of patients referred for HNF1B-MODY genetic testing due to cystic kidneys and diabetes.

Pediatr Diabetes 2020 05 29;21(3):422-430. Epub 2020 Jan 29.

Department of Biostatistics and Translational Medicine, Medical University of Lodz, Lodz, Poland.

Background/objectives: Patients referred for HNF1B testing present very heterogeneous phenotypes. Despite suggestive characteristics, many do not harbor mutations in HNF1B. Our objective was to evaluate the clinical characteristics of probands referred for HNF1B genetic testing through a nationwide monogenic diabetes screening program.

Methods: Probands tested for HNF1B mutations in the 2005-2018 period (N = 50) were identified in the Polish Monogenic Diabetes Registry, which prospectively recruits primarily pediatric patients and their families on a nationwide scale. Variants that had been reported pathogenic were reassessed using criteria of the American College of Medical Genetics and Genomics (ACMG). A structured medical interview was performed with all available individuals, their parents, and/or their physicians. For each patient, HNF1B score was calculated based on available clinical information.

Results: The study group numbered 36 unrelated probands (28% lost to follow-up): 14 with pathogenic or likely-pathogenic variants in HNF1B, one with a variant of uncertain significance, and 21 negative for HNF1B mutations. Presence of cystic kidneys (OR = 9.17, 95% CI:1.87-44.92), pancreatic abnormalities (OR = 15, 95% CI:1.55-145.23), elevated liver enzymes (OR = 15, 95% CI:1.55-145.23) best discriminated HNF1B-positive cases from the negative ones. Presence of impaired glucose tolerance coupled with kidney disease in the proband and one parent was also highly predictive for HNF1B mutations (OR = 11.11, 95% CI:1.13-109.36). HNF1B-score with recommended cutoff distinguished patients with and without HNF1B findings with 100% sensitivity and 47.6% specificity. Addition of four clinical variables to select patients based on HNF1B score improved specificity to 71.4% (95% CI:47.8%-88.7%) while retaining 100% sensitivity.

Conclusions: Detailed medical interview may enable more accurate patient selection for targeted genetic testing.
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http://dx.doi.org/10.1111/pedi.12959DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217165PMC
May 2020

Serum Level of Soluble CD226 Receptor in Healthy Individuals is Highly Variable and Associated with Age.

Iran J Immunol 2019 Mar;16(1):92-95

Department of Pediatrics, Diabetology, Endocrinology and Nephrology, Medical University of Lodz, Poland.

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http://dx.doi.org/10.22034/IJI.2019.39410DOI Listing
March 2019

Achieving target levels for vascular risk parameters in Polish school-age children with type 1 diabetes - a single center study.

J Pediatr Endocrinol Metab 2018 Oct;31(10):1073-1079

Department of Pediatrics, Oncology, Hematology and Diabetology, Medical University of Lodz, Lodz, Poland.

Background Therapeutic goals have been established to decrease the risk of long-term complications of type 1 diabetes (T1DM). The effects of these guidelines should be constantly evaluated. Hence, the present study examines the frequency at which children with T1DM treated by one of the Polish reference centers complied with the therapeutic targets issued in 2014 by the International Society for Pediatric and Adolescent Diabetes (ISPAD) and by the Diabetes Poland (PTD). Methods A retrospective analysis (years 2011-2014) was performed in patients with T1DM aged 6.5-18 years, with diabetes duration >12 months and no change of insulin regimen within 6 months. Collected data included insulin therapy regimen, weight, height, blood pressure, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG) and glycated hemoglobin (HbA1c) level from the last hospitalization. Results The records of 447 patients (260 boys, 299 treated with insulin pump) were analyzed. All ISPAD goals were achieved by 123 (27.5%) patients, but only 43 (9.6%) met all PTD targets. Optimal HbA1c was achieved by 224 (50.1%) according to ISPAD criteria (HbA1c<7.5%) and by 87 (19.6%) patients according to PTD (HbA1c≤6.5%). Obesity was diagnosed in 11.6% of the patients; 19.7% of the patients were overweight. In logistic regression, patient age was the only independent predictor of failing to achieve complete T1DM control (p=0.001, OR=1.12 [1.05-1.23]) and optimal HbA1c (p=0.01, OR=1.1 [1.0-1.2]) according to ISPAD guidelines. Moreover, girls had a greater risk of failing body mass index (BMI) targets (PTD: p=0.002, OR=2.16; ISPAD: p=0.0001, OR=3.37) and LDL-C targets (p=0.005, OR=1.8) than boys. Conclusions Overall, control of vascular risk factors in Polish children with T1DM is unsatisfactory. While too few children are achieving the HbA1c target set by PTD, it is possible that such strict national target helps half of the Polish school-age patients achieve ISPAD-issued aim which is more liberal. High prevalence of overweight among children with T1DM warrants initiatives focused not only on glycemic control but also on motivation of patients to lead a healthy lifestyle.
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http://dx.doi.org/10.1515/jpem-2018-0098DOI Listing
October 2018

Coexisting psoriasis affects the clinical course of type 1 diabetes in children.

Pediatr Endocrinol Diabetes Metab 2017 ;23(3):139-145

Department of Biostatistics and Translational Medicine, Medical University of Lodz, Department of Paediatrics, Oncology, Haematology and Diabetology, Medical University of Lodz.

Introduction: Literature reports link psoriasis with insulin resistance characteristic for type 2 diabetes. However, this condition may also affect the clinical course of type 1 diabetes (T1D).

Aim: To investigate whether children with type 1 diabetes mellitus (T1D) and psoriasis have a different course of diabetes.

Methods: We evaluated patients diagnosed with T1D in the years 2002-2011 for the presence of psoriasis and matched them 1:10 with T1D-only patients by sex and duration of diabetes using propensity score. We collected T1D-onset parameters and metabolic control surrogates from six months after T1D diagnosis.

Results: We identified 14 patients with psoriasis and matched 140 controls, of whom 129 (68 boys) were eligible for the analysis. At onset T1D+psoriasis patients showed higher concentration of C-peptide than controls (median: 0.38ng/ml vs 0.15ng/ml, p=0.02). Six months later, they had non-significantly lower HbA1c (6.0 vs 6.6%, p=0.11), TC (143mg/dl vs 159mg/dl, p=0.14) HDL (54.5mg/dl vs 59mg/dl, p=0.11).

Conclusions: Patients with T1D and psoriasis present higher endogenous insulin secretion at T1D onset and a tendency for better glycemic control during the first 6 months.
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http://dx.doi.org/10.18544/PEDM-23.03.0085DOI Listing
July 2018

Alcohol and cigarette use among adolescents with type 1 diabetes.

Eur J Pediatr 2017 Jun 5;176(6):713-722. Epub 2017 Apr 5.

Department of Pediatrics, Oncology, Hematology and Diabetology, Medical University of Lodz, ul. Sporna 36/50, 91-738, Lodz, Poland.

In this study, we compare the prevalence of alcohol and cigarette use among Polish adolescents with type 1 diabetes mellitus (T1DM) (n = 209), aged 15-18 years, with that of a large cohort of their healthy peers, using standardized questionnaire used in the European School Survey Project on Alcohol and Drugs (ESPAD). The lifetime, previous year, and past 30-day prevalence of alcohol consumption was high among adolescents with T1DM but lower than in the controls (82.8 vs 92.0%, 71.7 vs 85.6%, and 47.5 vs 69.7%, respectively, p < 10). The lifetime and 30-day prevalence of cigarette use was also lower among patients than the controls (54.6 vs 65.5%, p = 0.001 and 27.3 vs 35.9%, p = 0.012, respectively). Patients who admitted smoking exhibited worse metabolic control than non-smokers (p < 0.0001) and had a higher chance of developing diabetic ketoacidosis. The incidence of severe hypoglycemia was higher among those who reported getting drunk in the previous 30 days (p = 0.04) and lifetime smoking (p = 0.01).

Conclusions: Although alcohol and cigarette consumption is lower than in controls, it is common among teenagers with type 1 diabetes, effecting metabolic control and causing the risk of acute diabetes complications. Better prevention strategies should be implemented in this group of patients in their early teen years. What is Known: • Substance use remains a significant cause of morbidity and mortality among teenagers with type 1 diabetes. • Current medical literature contains inconsistent data on the prevalence of alcohol and cigarette use among adolescents with type 1 diabetes, mostly due to methodological problems with conducting such surveys. What is New: • Methodological approach: we used a validated questionnaire from the European School Survey Project on Alcohol and Other Drugs (ESPAD) and compared the results to a large national control group of 12,114 healthy students who took part in ESPAD in 2011.
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http://dx.doi.org/10.1007/s00431-017-2895-yDOI Listing
June 2017

Breaking the Taboo: Illicit Drug Use among Adolescents with Type 1 Diabetes Mellitus.

J Diabetes Res 2016 29;2016:4153278. Epub 2015 Dec 29.

Department of Pediatrics, Oncology, Hematology and Diabetology, Medical University of Lodz, 91-738 Lodz, Poland.

Background: The aim of the study was to explore the prevalence of illicit drug use in a group of Polish adolescents with type 1 diabetes (DM1) in comparison with a national cohort of their healthy peers.

Methods: Two hundred and nine adolescents with DM1, aged 15-18 years, were studied in 2013 with an anonymous questionnaire prepared for the European School Survey Project on Alcohol and Other Drugs (ESPAD). The control group was a representative sample of 12114 students at the same age who took part in ESPAD in 2011. Metabolic control was regarded as good if self-reported HbA1c was <8% or poor if HbA1c was ≥8%.

Results: Lifetime prevalence of illicit drug use was lower among adolescents with DM1 than in the control group [58 (28%) versus 5524 (46%), p = 10(-5)]. Cannabis preparations were the most frequently used substances [38 (18.3%) versus 3976 (33.1%), p = 10(-5)], followed by tranquilizers, sedatives, and amphetamine. Lifetime and last 12-month use of cannabis were associated with poorer glycemic control (HbA1c ≥ 8%), p < 0.01 and 0.02, respectively.

Conclusions: Adolescents with DM1 report using illicit drugs to a lesser extent than their healthy peers. The use of cannabis is associated with a poorer metabolic control in teens with DM1.
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http://dx.doi.org/10.1155/2016/4153278DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4709623PMC
December 2016

Alkaptonuria in a boy with type 1 diabetes mellitus, vitiligo, autoimmune thyroiditis and immunoglobulin A deficiency - a case report.

Pediatr Endocrinol Diabetes Metab 2016 ;22(2):71-75

Department of Pediatrics, Oncology, Hematology and Diabetology, Medical University of Lodz, Lodz.

We present a 15-year-old Caucasian boy with an exceptional coincidence of a rare monogenic metabolic disease - alkaptonuria (AKU) and a cluster of autoimmune disorders: type 1 diabetes (T1DM), autoimmune thyroiditis (AIT), vitiligo, insulin infusion induced lipoatrophy and immunoglobulin A deficiency (IgAD) Alkaptonuria and type 1 diabetes in a child, especially in such an interesting coincidence with other autoimmune conditions, has not been reported so far. Our investigation, including comprehensive genetic evaluation using next generation sequencing technology, shows that alkaptonuria and T1DM were independently inherited. We also show that alkaptonuria in its pre-ochronotic phase seems to have no effect on the course of diabetes.
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http://dx.doi.org/10.18544/PEDM-22.02.0054DOI Listing
November 2017

Atypical phenotypic features among carriers of a novel Q248X nonsense mutation in the HNF1B gene.

Endokrynol Pol 2015 ;66(1):15-21

Department of Paediatrics, Oncology, Haematology and Diabetology, Medical University of Lodz, Poland.

Introduction: Hepatocyte transforming factor 1B-maturity onset diabetes mellitus of the young (HNF1B-MODY) is an autosomal dominant type of monogenic diabetes caused by a mutation in the gene encoding hepatocyte nuclear factor 1beta (HNF-1beta). The aim of this study was to determine if a HNF1B gene mutation was responsible for a dominantly inherited form of diabetes mellitus among the members of a three-generation Polish family.

Material And Methods: The index subject was a 13-year-old boy with metabolic syndrome, spina bifida occulta, posterior urethral valves, congenital ureteropelvic junction obstruction, and a family history of diabetes of autosomal dominant trait of inheritance. We performed clinical and laboratory examinations of his family and sequenced the HNF1B gene.

Results: A novel Q248X mutation (nucleotide C to T transition at position 742 of the exon 3 of HNF1B gene, resulting in stop codon formation) was identified. Phenotypes of family members sharing this mutation are highly variable, and include previously known abnormalities of the urinary system and pancreas, diabetes mellitus of variable onset and severity, hyperinsulinaemia, insulin resistance, metabolic syndrome, elevated aminotransferases, hyperbilirubinemia, hyperamylasemia, short stature and cataracts. To the best of our knowledge, spina bifida occulta, pectus carinatum, and splenomegaly have not been previously reported.

Conclusions: Our results broaden the spectrum of HNF1B gene mutations and HNF1B-MODY-related phenotypes.
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http://dx.doi.org/10.5603/EP.2015.0004DOI Listing
January 2017

Chromosome 18q deletion syndrome with autoimmune diabetes mellitus: putative genomic loci for autoimmunity and immunodeficiency.

Pediatr Diabetes 2016 Mar 18;17(2):153-9. Epub 2014 Nov 18.

Department of Pediatrics, Oncology, Hematology and Diabetology, Medical University of Lodz, Lodz, Poland.

A girl with 18q deletion syndrome was diagnosed with autoimmune diabetes mellitus and Hashimoto's thyroiditis at the age of 3 yr. In addition, the girl suffered from recurrent infections due to immunoglobulin A and IgG4 deficiency. She was also found to have CD3+CD4+FoxP3+, CD3+CD4+FoxP3+CD25+, and CD3+CD4+CD25+CD127 regulatory T cells deficiency. The exceptional coincidence of the two autoimmune disorders occurring at an early age, and associated with immune deficiency, implies that genes located on deleted 19.4 Mbp region at 18q21.32-q23 (chr18:58,660,699-78,012,870) might play a role in the pathogenesis of autoimmunity leading to β cell destruction and diabetes.
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http://dx.doi.org/10.1111/pedi.12235DOI Listing
March 2016

Factor XIII deficiency in Henoch-Schönlein purpura - report on two cases and literature review.

Dev Period Med 2014 Jul-Sep;18(3):318-22

Department of Pediatrics, Oncology, Hematology and Diabetology, Medical university of Lodz, 36/50 Sporna St. 91-738 Lodz, Poland, phone +48 505-979-152, +48 42 617-77-50, fax: +48 42 617 77 98, e-mail:

Factor XIII (FXIII) deficiency is a rare, inherited or acquired coagulation disorder that potentially precipitates fatal haemorrhage. We report two consecutive pediatric patients with Henoch-Schönlein purpura (HSP) and symptomatic decrease in FXIII. The possible FXIII deficiency should be kept in mind by every doctor taking care of patients with HSP, in spite of normal value of routine coagulation tests.
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October 2014

Is there any association between secretory IgA and lactoferrin concentration in mature human milk and food allergy in breastfed children.

Med Wieku Rozwoj 2013 Jan-Mar;17(1):47-52

Department of Pediatrics, Hematology and Diabetology Medical University of Lodz, Łódź, Poland.

Background: Breastfeeding is recommended as a protective method against the development of allergy. However, some studies have reported an increased risk of allergies development in breastfed infants of atopic mothers, which implies that atopic mothers may have an altered composition of breast milk.

Aim: The aim of the study was to determine the concentration of secretory immunoglobulin A (S-IgA) and lactoferrin in human mature milk and to evaluate the association between the levels of these proteins in breast milk with food allergy in children, depending on the allergy status of the breastfeeding mother.

Material And Methods: Medical data was collected from birth to 24 months of age from 84 mother-child pairs participating in an EU-funded project "EuroPrevall - The prevalence, cost and basis of food allergy across Europe". The diagnosis of food allergy in children was based on the positive result of a double-blind placebo-controlled food challenge (DBPCFC). S-IgA and lactoferrin levels were measured in the whey of mature breast milk with commercial enzyme-linked immunosorbent assay (ELISA) kits. Statistical analysis (the U Mann-Whitney and Kruskal-Wallis tests as well as the Spearman's rank correlation coefficient) was performed using STATISTICA 8.0 PL (Statsoft, Tulsa, USA).

Results: Ten out of eighty four participating children had positive skin prick tests (SPT) and/or sIgE to food antigens and in 7 (8.4%) DBPCFC confirmed food allergy. the median concentration of S-IgA was 476,83 μg/ml (range 6.51-1359.61 μg/ml). the median concentration of Lf was 15.68 μg/ml (range 11.68-36.43 μg/ml). The concentrations of S-IgA and Lf showed a moderate, negative, correlation R=-0.28; p=0.05.

Conclusions: Mature breast milk of mothers of children with food allergy and of healthy children showed similar concentrations of both proteins. The level of S-IgA in the mature milk of mothers with atopic allergy was significantly lower, compared to non-atopic mothers. More studies are needed to reveal the mystery of the lack of protective effect of breastfeeding on allergy development in children.
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August 2013

[Can the concentration of immunomodulating factors in mature breastmilk be associated with food allergy in breastfed children?].

Med Wieku Rozwoj 2012 Apr-Jun;16(2):104-8

Klinika Pediatrii, Onkologii, Hematologii i Diabetologii Uniwersytetu Medycznego w Łodzi, ul. Sporna 36/50, Łódź, Poland.

Objectives: The aim of the study was to determine the concentration of such immunomodulating factors as transforming growth factor beta1 (TGF-β1), interleukin 10 (IL-10), tumor necrosis factor alpha (TNF-α) in mature human milk and to relate the levels of the above mentioned cytokines in mature breast milk to the occurence of food allergy in children during the first 24 months of life.

Materials And Methods: Data on breastfeeding, symptoms of food allergy in children and breast milk samples were collected prospectively from birth to 24 months of age from 84 mothers participating in the Polish birth cohort of "EuroPrevall" study, in the years 2005-2007. Cytokine levels were measured in the whey with commercial enzyme-linked immunosorbent assays (ELISA) kits.

Results: Ten out of the eighty four (11.9%) participating children had positive SPT and/or sIgE to food antigens. In 7 out of 84 (8.4%) children DBPCFC confirmed the diagnosis of food allergy. The median concentration of TGF-β1 was 21.94 pg/ml (range 10.47-83.19), TNF-α 1.46 pg/ml (range 0.35-16.50), IL- 101.83 pg/ml (range 0.58-31.04). There was a positive correlation between the concentration of IL-10 and TGF-β1. The level of TNF-α correlated positively with the duration of lactation (p=0.04). There was no significant difference between the concentration of IL-10, TGF-β1, TNF-α, in the mature breast milk of mothers of children with symptoms of allergy and positive SPT and/or sIgE, mothers of children with positive DBPCFC and in the milk of mothers of control children.

Conclusions: There was no significant difference between the concentration of IL-10, TGF-β1, TNF-α, in the mature breast milk of mothers of children with food allergy and in the breast milk of mothers of control children.
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April 2013

Breastfeeding in primary prevention of atopic diseases - is it really protective?

Authors:
Anna Hogendorf

Med Wieku Rozwoj 2011 Oct-Dec;15(4):487-92

Klinika Pediatrii, Onkologii, Hematologii i Diabetologii, Uniwersytet Medyczny w Łodzi, ul. Sporna 36/50, Łódź.

The role of human milk in the development of allergic sensitization remains controversial, especially in view of the difficulty to perform randomized clinical trials as well as methodological differences in the existing data. The incapability of human milk to prevent from allergic phenotype may be ascribed to genetic predisposition, environmental factors and also to differences in the immune contents of human milk, resulting in a lack of oral tolerance development. This article presents controversial results of recently published studies and current recommendations regarding the role of breastfeeding in allergy prevention.
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May 2012

Unequal contribution of familial factors to autoimmunity and clinical course of childhood diabetes.

Pediatr Endocrinol Diabetes Metab 2012 ;18(4):130-6

Department of Paediatrics, Medical University of Lodz, Poland.

Introduction: collection of family history of diabetes mellitus (DM) is commonly performed when this illness is diagnosed in children. However the significance of gleaned information may differ depending on the affected family members.

Aim Of The Study: this study was performed in order to describe detailed familial history of DM in patients and to evaluate the impact of it on the natural course of childhood DM.

Material And Methods: After exclusion of patients with confirmed monogenic basis of the disease or type 2 diabetes, the study group numbered 989 diabetic children. The data on detailed family history of DM among the first- and second- degree relatives, age at the onset of DM, recent percentage of glycated hemoglobin (HbA1c), presence of diabetes-related antibodies and the highest observed fasting c-peptide level were collected.

Results: Having siblings with DM was linked to early onset of diabetes in the study group (mean difference -2.83 95% confidence interval [cI] -4.24 to -1.42). Dominant mode of inheritance, particularly from the maternal side was significantly associated with diabetes onset at an older age. Children of diabetic mothers developed diabetes at a mean age of 10.83 in comparison to those without family history of DM - 8.75 years (p=0.0228). However, children whose mothers had any type of DM, had a significantly higher level of glycated hemoglobin than the others (8.34 vs 7.56%, p=0.0315). Additionally, a rising number of units of the family tree affected by any type of diabetes was associated with later onset of diabetes in children (p for trend = 0.0452).

Conclusion: Familial factors influence the natural course of childhood diabetes, but their contribution is not equal, showing more pronounced effects of maternal factors.
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November 2013

Non-coding glucometers among pediatric patients with diabetes: looking for the target population and an accuracy evaluation of no-coding personal glucometer.

Pediatr Endocrinol Diabetes Metab 2011 ;17(2):57-63

Department of Pediatrics, Oncology, Hematology, and Diabetology Medical University of Lodz, Poland.

Introduction: Self-monitoring of blood glucose (SMBG) is one of the cornerstones of diabetes management.

Aim Of The Study: To evaluate the potential for miscoding of a personal glucometer, to define a target population among pediatric patients with diabetes for a non-coding glucometer and the accuracy of the Contour TS non-coding system.

Material And Methods: Potential for miscoding during self-monitoring of blood glucose was evaluated by means of an anonymous questionnaire, with worst and best case scenarios evaluated depending on the responses pattern. Testing of the Contour TS system was performed according to guidelines set by the national committee for clinical laboratory standards.

Results: Estimated frequency of individuals prone to non-coding ranged from 68.21% (95% 60.70- 75.72%) to 7.95% (95%CI 3.86-12.31%) for the worse and best case scenarios respectively. Factors associated with increased likelihood of non-coding were: a smaller number of tests per day, a greater number of individuals involved in testing and self-testing by the patient with diabetes. The Contour TS device showed intra- and inter-assay accuracy -95%, linear association with laboratory measurements (R2=0.99, p <0.0001) and consistent, but small bias of -1.12% (95% Confidence Interval -3.27 to 1.02%). Clarke error grid analysis showed 4% of values within the benign error zone (B) with the other measurements yielding an acceptably accurate result (zone A).

Conclusions: The Contour TS system showed sufficient accuracy to be safely used in monitoring of pediatric diabetic patients. Patients from families with a high throughput of test-strips or multiple individuals involved in SMBG using the same meter are candidates for clinical use of such devices due to an increased risk of calibration errors.
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October 2011

[Optimization of monogenic diabetes screening programme--initial report on recruitment efficacy of the TEAM project].

Pediatr Endocrinol Diabetes Metab 2010 ;16(2):73-6

Klinika Pediatrii, Onkologii, Hematologii i Diabetologii Uniwersytetu Medycznego w Łodzi.

Introduction: Due to the lack of precise diagnostic criteria, current search strategy for monogenic diabetes is predominantly based on atypical clinical course of diabetes and intuition of the attending physician. Yet another issue is the common view that monogenic diabetes is rare. It discourages from performing deepened diagnostics and makes it difficult to gain experience necessary to select appropriate patients for genetic examination.

Aim Of The Study: Estimating the true incidence of patients with a high probability of monogenic background of the disease and compare their search strategies based on clinical practice or structured databases.

Material And Methods: The authors compared the current strategy of selecting candidates for screening with a directed search strategy based on immunologic (lack of islet autoantibodies), functional (presence or complete lack of c-peptide at onset and follow-up) and familial (dominant pattern of inheritance) criteria. The number of patients selected for the screening was chosen as efficacy measure selected among 1281 diabetic patients diagnosed and treated between 1983-2009.

Results: Screening based on clinical assessment yielded 37 patients (2.9%) chosen for genetic screening. Criteria used by the physicians were based on up-to-date guidelines and unusual clinical course. Active search of the database according to predefined criteria resulted in selecting: 121 patients (9.4%) with likely monogenic background of diabetes (71 - lack of autoantibodies, 8 - normal C-peptide, 6 - lack of both c-peptide and autoantibodies, 36 - diabetes in at least one parent). The difference in screening efficacy was statistically significant (p <0.0001).

Conclusions: Periodic reevaluation of patients' data allows a significant increase in the number of candidates subjected to genetic screening and potentially achieving beneficial therapeutic effects by means of pharmacogenetics.
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October 2010