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1.
Eur Thyroid J ; 11(5)2022 Oct 01.
Article in English | MEDLINE | ID: mdl-35900797

ABSTRACT

Introduction: Infants of mothers with autoimmune hypothyroidism (AH) are at risk of developing late-onset hypothyroidism, often escaping at newborn screening. This condition might be caused both by the action of maternal antibodies and/or by maternal treatment. Objectives: The aim of this study is to evaluate the prevalence of AH in the mothers of children born in Veneto region, Italy, and to define what is the most appropriate management for these newborns. Methods: Newborns of six different hospitals with a mother suffering from AH and with negative neonatal screening for congenital hypothyroidism (CH) were included in the study. Between 15 and 20 days of life, we collected a serum sample for the evaluation of thyroid function (thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3)) and anti-thyroid antibodies. On the same occasion, a capillary blood sampling was performed for a second screening test. Results: Maternal AH has a prevalence of 3.5%. A total of 291 newborns were enrolled from November 2019 to May 2021. Whereas the 11.4% of infants had a slight elevated serum TSH (>6 mU/L) and required a follow-up, only 2 children presented an elevated TSH level at the second screening test. One of these, with the gland in situ, showed persistently elevated serum TSH levels and required treatment with levothyroxine. Conclusions: Maternal AH rarely caused neonatal thyroid dysfunction. We suggest to reassess newborns from mothers with AH 15 days after birth by means of a second neonatal screening test. This procedure avoids false negatives due to maternal thyroid status, is less invasive and cheaper than the serum TSH evaluation, and prevents a long follow-up.

2.
Int J Pediatr Obes ; 6 Suppl 1: 42-5, 2011 Sep.
Article in English | MEDLINE | ID: mdl-21905815

ABSTRACT

INTRODUCTION: In humans, using adipose tissue to store fat represents the most effective means to 'store' energy. On the whole and over an extended period of time, intake of energy has exceeded energy expenditure and where previously the excess of energy was regularly turned over through physical activity, this crucial circle has now been broken. In this way obesity ascribed to either 'overeating' or 'under-activity'. Central adiposity poses a major risk for chronic diseases such as hypertension, cardiovascular diseases and diabetes, and possibly mortality. Predictors and potential factors underlying the development of excess adiposity were well studied and established with emphasis on fat mass. OBJECTIVE: When studying the development of body composition, bone mass, fat mass and lean mass should be considered together. The purposes of the present paper are to briefly analyze the methodologies used to estimate the lean mass (LM), understanding the interrelationship between fat mass (FM) and LM and underline the importance of LM during growth. RESULTS: As muscle and adipose tissue are closely linked anatomically, biologically and pathologically, the interrelationship between these two tissues is of great importance in understanding the pathogenesis and development of diseases related to obesity and physical activity/inactivity. LM estimation, and LM programming could show several implications for the early origin of obesity. CONCLUSION: Measurements of lean mass may improve the capacity to tailor nutrition, treatment and management to metabolic criteria. This approach could offer a unique opportunity of putting lean mass in the first line keeping in mind that this metabolic active tissue need to be preserved when obesity prevention and treatment are considered.


Subject(s)
Adiposity/physiology , Body Composition/physiology , Child Development/physiology , Energy Metabolism/physiology , Obesity/metabolism , Adipose Tissue/growth & development , Adipose Tissue/metabolism , Birth Weight/physiology , Bone and Bones/metabolism , Child , Humans , Infant, Newborn , Motor Activity/physiology , Muscle, Skeletal/growth & development , Muscle, Skeletal/metabolism , Obesity/physiopathology , Obesity/prevention & control
3.
J Matern Fetal Neonatal Med ; 23 Suppl 3: 80-3, 2010 Oct.
Article in English | MEDLINE | ID: mdl-20925457

ABSTRACT

The origins of asthma might be traced back to events occurring during fetal life. Reduced lung development has been shown to be a risk factor both for viral induced wheeze and allergic asthma. The evidence for a causal relationship between exposure to environmental tobacco smoke, chemical domestic products for cleaning, outdoor pollutants, and reduction in lung function is quite strong. Reduced maternal intake of vitamin E, vitamin D, and zinc, or increased use of paracetamol during pregnancy is associated with increased wheezing outcomes in children. The odds ratio for asthma onset is also increased in infants born from mothers with oligohydramnios, chorioamnionitis, hypertension, preeclampsia, diabetes and exposed to stressful events. The risk of developing allergic asthma is increased if the child is exposed in the first months of life to synthetic bedding and is enhanced by allergen exposure and an inadequate barrier function of the skin. In conclusion, several lines of evidence support the concept of fetal programming and very early life events in the development of the different phenotypes of asthma. Since some environmental triggers can be easily avoided and some protective factors can be easily implemented all efforts should be made to prevent intrauterine insults and early sensitization.


Subject(s)
Asthma/etiology , Fetal Diseases , Infant, Newborn, Diseases/etiology , Asthma/congenital , Asthma/diagnosis , Asthma/embryology , Disease Susceptibility , Female , Fetal Diseases/diagnosis , Fetal Diseases/immunology , Humans , Hypersensitivity/congenital , Hypersensitivity/embryology , Hypersensitivity/etiology , Infant, Newborn , Infant, Newborn, Diseases/diagnosis , Infant, Newborn, Diseases/immunology , Lung/embryology , Lung/growth & development , Lung/immunology , Lung/pathology , Pregnancy , Prenatal Exposure Delayed Effects/diagnosis , Prenatal Exposure Delayed Effects/immunology , Prenatal Exposure Delayed Effects/pathology
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