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Irina Pateva

Other affiliations: Boston Children's Hospital
Bio: Irina Pateva is an academic researcher from Case Western Reserve University. The author has contributed to research in topics: Medicine & Intensive care medicine. The author has an hindex of 4, co-authored 6 publications receiving 39 citations. Previous affiliations of Irina Pateva include Boston Children's Hospital.

Papers
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Journal ArticleDOI
01 Jan 2017-Medicine
TL;DR: The case of a patient who was diagnosed with hepatoblastoma at an atypical age of presentation for this type of malignancy, who later had disease recurrence and after undergoing treatment with different modalities, ultimately died of his disease.

18 citations

Journal ArticleDOI
01 Jan 2015
TL;DR: In this article, the authors compared the relationship between maternal and infants' body iron in smokers and non-smokers in a large matched-pair cohort and found that women who smoked had lower sTfR, higher ferritin and higher body iron compared to nonsmoking women.
Abstract: Background Maternal smoking has been known to have a negative impact on the well being of the developing fetus. Prenatal smoking has been associated with premature births, low birth weight and with certain birth defects. Small research studies have also found a negative correlation between maternal smoking and neonatal body iron. Objectives To study and compare the relationship between maternal and infants' body iron in smokers and non-smokers in a large matched-pair cohort. Methods This was a prospective cohort study involving 144 mothers - 72 smokers and 72 non-smokers and their respective infants. Samples were obtained from maternal and infants' cord blood at delivery for Serum transferrin receptor (sTfR) and ferritin levels. Serum TfR and ferritin were measured by RAMCO ELISA and RIA assays. Total Body Iron (TBI) was calculated using the sTfR/ferritin ratio in a previously described formula by Cook et al. Results Women who smoked had lower sTfR, higher ferritin and higher body iron compared to nonsmoking women. In contrast to their respective mothers, we found a small, but statistically significant negative correlation between smoking and infants' total body iron. The number of packs per day smoked was also negatively correlated with infants' ferritin and total body iron. Lower birth weight was noted in babies of smokers compared to nonsmokers (mean /- SD =3270 +/-475 vs. 3393 g +/- 475 g, p=0.03). Conclusion Women who smoked during pregnancy had higher iron stores but their newborn infants had lower iron stores than those of non-smoking mothers. The more packs per day (PPD) and more days smoked during pregnancy led to lower total body iron of the babies. There may be a negative dose-dependent response between fetal smoke exposure and infant iron stores.

17 citations

Journal ArticleDOI
15 Nov 2013-Blood
TL;DR: Mothers who smoked during pregnancy had higher iron stores but their newborn infants had lower iron stores than those of non-smoking mothers, and there may be a negative dose-dependent response between fetal smoke exposure and infant iron stores.

8 citations

Journal ArticleDOI
TL;DR: A brief review of all the pediatric cases and clinical studies of post‐HSCT HLH along with a critical evaluation of its various diagnostic criteria suggests a need for formulating disease‐specific diagnostic criteria for post-HS CT HLH.
Abstract: HLH occurring after HSCT is a relatively rare disease. Many conditions may mimic or trigger HLH in post-HSCT period (eg, cytokine release syndrome, engraftment syndrome, graft rejection/failure, acute graft-vs-host disease, infections systemic inflammatory response syndrome/sepsis, and thrombotic microangiopathy). Moreover, this period is usually marked by febrile illness, cytopenia, and a "cytokine storm" leading to elevation of inflammatory biomarkers like ferritin and sCD25. These parameters overlap with the diagnostic criteria for HLH. Such confounding factors make the management of post-HSCT HLH quite challenging. We illustrate this critical issue with case report of a patient who was diagnosed with HLH after allogeneic HSCT for tAML. He received MP and CsA for HLH but VP-16 was not administered due to fear of severe myelosuppression. Fortunately, he responded well to treatment and remains in remission to date. We recommend caution while using HLH-94/HLH-2004 guidelines for the diagnosis and management of post-HSCT HLH. In this article, we pinpoint these issues with a brief review of all the pediatric cases and clinical studies of post-HSCT HLH along with a critical evaluation of its various diagnostic criteria. Finally, based on the limitations of current diagnostic criteria, we suggest a need for formulating disease-specific diagnostic criteria for post-HSCT HLH.

6 citations

Journal ArticleDOI
TL;DR: Key information about diagnosis of lymphedema, associated conditions and syndromes, and current treatment modalities is reviewed.
Abstract: Lymphedema in children is rare; however, it is usually a progressive and chronic condition. Accurate diagnosis of lymphedema in the pediatric population often takes several months and sometimes is delayed for years. Lymphedema can be isolated or associated with genetic syndromes, thus it is very important to identify the correct diagnosis, to select carefully which patients to refer for genetic testing, and to initiate appropriate treatment in a timely fashion. In this article, we review key information about diagnosis of lymphedema, associated conditions and syndromes, and current treatment modalities.

4 citations


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Journal ArticleDOI
TL;DR: It is proposed that clinical trials are warranted to clarify the impact of dietary or pharmacological iron reduction on the development of metabolic disorders.
Abstract: Dietary advice is the cornerstone in first-line treatment of metabolic diseases. Nutritional interventions directed at these clinical conditions mainly aim to (a) improve insulin resistance by reducing energy-dense macronutrient intake to obtain weight loss and (b) reduce fluctuations in insulin secretion through avoidance of rapidly absorbable carbohydrates. However, even in the majority of motivated patients selected for clinical trials, massive efforts using this approach have failed to achieve lasting efficacy. Less attention has been given to the role of micronutrients in metabolic diseases. Here, we review the evidence that highlights (a) the importance of iron in pancreatic beta-cell function and dysfunction in diabetes and (b) the integrative pathophysiological effects of tissue iron levels in the interactions among the beta cell, gut microbiome, hypothalamus, innate and adaptive immune systems, and insulin-sensitive tissues. We propose that clinical trials are warranted to clarify the impact of dietary or pharmacological iron reduction on the development of metabolic disorders.

77 citations

Journal ArticleDOI
TL;DR: The treatment of HB started from one and the same therapy for all patients and aimed at increased treatment individualization, but the future seems to lie in biology-driven patient-tailored therapies.
Abstract: Introduction : Hepatoblastoma (HB) is the most common primary malignant liver neoplasm in children. Its increasing survival rate is related to the progress in modern imaging, surgical techniques, and new chemotherapy regimens. Clinical approach : One of the past achievements was the development of the pretreatment extension of disease (PRETEXT) system. Gradually, the HB therapeutic approach has become more individualized with better stratification of patients. Controversies : These include the need for preoperative chemotherapy and its optimal duration; intensity of preoperative chemotherapy required for locally advanced cases (PRETEXT 4); optimal surgical treatment for locally advanced tumors: aggressive hepatic resections versus liver transplantation; the role of postoperative chemotherapy in the post-transplant setting; the timing and role of metastasectomy in patients with disseminated disease who undergo partial liver resection; and the prognostic significance of several HB pathology variants. Hepatoblastoma biology : Beta-catenin mutations and the beta-catenin/Wnt pathway play an important role in HB development. There have been at least two molecular signatures in HB published. Unluckily, all of these findings are based on relatively small clinical series and require confirmation. Conclusion : The treatment of HB started from one and the same therapy for all patients and aimed at increased treatment individualization, but the future seems to lie in biology-driven patient-tailored therapies.

45 citations

Journal ArticleDOI
TL;DR: PAE altered fetal iron distribution independent of maternal iron status in rats, and the elevated iron content of fetal liver suggests that PAE may have limited iron availability for fetal erythropoiesis and brain development.
Abstract: Background Prenatal alcohol exposure (PAE) causes neurodevelopmental disabilities, and gestational iron deficiency (ID) selectively worsens learning and neuroanatomical and growth impairments in PAE. It is unknown why ID worsens outcomes in alcohol-exposed offspring. Objective We hypothesized that PAE alters maternal-fetal iron distribution or its regulation. Methods Nulliparous, 10-wk-old, Long-Evans rats were mated and then fed iron-sufficient (100 mg Fe/kg) or iron-deficient (≤4 mg Fe/kg) diets. On gestational days 13.5-19.5, dams received either 5.0 g ethanol/kg body weight (PAE) or isocaloric maltodextrin by oral gavage. On gestational day 20.5, maternal and fetal clinical blood counts, tissue mineral and iron transport protein concentrations, and hepatic hepcidin mRNA expression were determined. Results In fetal brain and liver (P 300% (P Conclusions PAE altered fetal iron distribution independent of maternal iron status in rats. The elevated iron content of fetal liver suggests that PAE may have limited iron availability for fetal erythropoiesis and brain development. Altered fetal iron distribution may partly explain why maternal ID substantially worsens growth and behavioral outcomes in PAE.

35 citations

Journal ArticleDOI
TL;DR: Clinical applications of iron homeostasis and the effects of cigarette smoke are detailed in this article, particularly in relation to lung conditions that favour the upper lobes, such as emphysema and lung cancer.
Abstract: Respiratory disease accounts for a large proportion of emergency admissions to hospital and diseaseassociated mortality. Genetic association studies demonstrate a link between iron metabolism and pulmonary disease phenotypes. IREB2 is a gene that produces iron regulatory protein 2 (IRP2), which has a key role in iron homeostasis. This review addresses pathways involved in iron metabolism, particularly focusing on the role of IREB2. In addition to this, environmental factors also influence phenotypic variation in respiratory disease, for example inhaled iron from cigarette smoke is deposited in the lung and causes tissue damage by altering iron homeostasis. The effects of cigarette smoke are detailed in this article, particularly in relation to lung conditions that favour the upper lobes, such as emphysema and lung cancer. Clinical applications of iron homeostasis are also discussed in this review, especially looking at the pathophysiology of chronic obstructive pulmonary disease, lung cancer, pulmonary infections and acute respiratory distress syndrome. Promising new treatments involving iron are also covered.

26 citations