Roberto Ronchetti
Sapienza University of Rome
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The Journal of Allergy and Clinical Immunology | 1990
Roberto Ronchetti; Francesco Macrì; Gianni Ciofetta; Luciana Indinnimeo; Renato Cutrera; Enea Bonci; Giuseppina Antognoni; Fernando D. Martinez
We studied the relationship of serum IgE levels and eosinophil counts with passive smoking in 9-year-old, nonselected children from three Italian towns near Rome. Male children of smoking parents had a significantly higher total count and percentage of eosinophils (p = 0.008) and higher IgE levels (p = 0.01) than male children of nonsmoking parents. Prevalence of eosinophilia (defined as greater than or equal to 4% of total white blood cell count) was significantly correlated with the number of cigarettes smoked by parents among boys (p = 0.003) but not among girls (p = 0.20). There was a significant trend (p = 0.008) for prevalence of eosinophilia to increase with increasing levels of serum IgE. For any given level of serum IgE, the frequency of eosinophilia was higher among children of smoking parents than among children of nonsmoking parents. When parental smoking was studied in a multivariable analysis and after controlling for the other variable, it was still significantly associated with eosinophilia in the children of these smoking parents but not with serum IgE levels. We conclude that parental smoking is associated with a significant enhancement of the expression of the most important markers of allergic sensitization in the children of smoking parents. This is particularly evident for boys and may explain, at least in part, the increased frequency of respiratory symptoms in children of smoking parents.
Pediatric Allergy and Immunology | 2001
Mario Barreto; Maria Pia Villa; Susy Martella; Francesco Ronchetti; Maria T. Darder; Carlo Falasca; Jacopo Pagani; Francesca Massa; Roberto Ronchetti
Asthmatic bronchial inflammation is associated with increased nitric oxide concentrations in exhaled air (eNO). Recent data suggest that this effect arises from atopy. Our aim in this study was to find out whether atopy and sensitization to particular allergens influences eNO levels. A total of 213 subjects (41 asthmatics and 172 controls) (96 boys and 117 girls, 7.3–14 years of age) were studied. Parents completed a questionnaire that sought information on their childrens respiratory symptoms and exposure to tobacco smoke. Subjects underwent skin‐prick tests for the following common allergens: Dermatophagoides pteronyssinus (Dpt), cat fur, Aspergillus fumigatus, Alternaria tenuis, mixed grass, mixed tree pollen, Parietaria officinalis, egg, and cows milk. eNO was collected in 1‐l mylar bags (exhaled pressure 10 cmH2O, flow 58 ml/s) and analyzed by using chemiluminescence. Atopic and non‐atopic children without a history of chronic respiratory symptoms had a similar geometric mean eNO (atopics, n = 28, 11.2 p.p.b.; non‐atopics, n = 96, 10.0 p.p.b.; mean ratio 1.1, 95% confidence interval [CI]: 0.7–1.6). Conversely, atopic asthmatic subjects had significantly higher eNO values than non‐atopic asthmatic subjects (atopics, n = 25, 24.8 p.p.b.; non‐atopics, n = 16, 11.4 p.p.b.; mean ratio 2.2, 95% CI: 1.2–3.9, p= 0.000). In children with rhinitis alone (n = 15) and those with lower respiratory symptoms other than asthma (n = 33), eNO increased slightly, but not significantly, with atopy. eNO levels correlated significantly with Dpt wheal size (r = 0.51) as well with the wheal size for cat, mixed grass, and Parietaria officinalis (r = 0.30–0.29), and with the sum of all wheals (r = 0.47) (p= 0.000). Subjects sensitized only for Dpt (but not those subjects sensitized only for grass pollen or other allergens) showed significantly higher eNO levels than non‐atopic subjects (16.4 p.p.b. vs. 10.2 p.p.b., mean ratio 1.6, 95% CI: 1.1–2.3, p= 0.002). In asthmatic subjects, Dpt sensitization markedly increased eNO levels (Dpt‐sensitized subjects: 28.0 p.p.b.; Dpt‐unsensitized subjects: 12.2 p.p.b.; mean ratio 2.3, 95% CI: 1.5–3.5, p= 0.000). Non‐asthmatic Dpt‐sensitized subjects also had significantly higher eNO values than non‐asthmatic, non‐Dpt‐sensitized subjects (14.2 p.p.b. vs. 10.1 p.p.b.; mean ratio 1.4, 95% CI: 1.1–1.9, p= 0.008). No difference was found between eNO levels in asthmatic subjects and control subjects exposed or unexposed to tobacco smoke. In conclusion, eNO concentrations are high in atopic asthmatic children and particularly high in atopic asthmatics who are sensitized to house‐dust mite allergen.
Pediatric Pulmonology | 1997
Maria Pia Villa; Andrea Dotta; Domenico Castello; Silvana Piro; Jacopo Pagani; Sabrina Palamides; Roberto Ronchetti
A 4‐month‐old baby girl, after a period of apparent good health, began to have aphonia, dyspnea, difficulties with swallowing, cyanosis, apnea, and hypopnea during sleep that resulted in admission to an intensive care unit for intubation and mechanical ventilation. At the age of 9 months she was admitted to our hospital with a possible diagnosis of central hypoventilation syndrome. A polysomnographic study showed apnea and hypopnea (apnea + hypopnea index = 47.1), hypercapnia (mean end‐tidal P co 2 89 ± 15.0 mmHg), and arterial desaturation (mean Sa o 2 91 ± 1.7%; lowest Sa o 2 < 50%; 68% of total sleep time at Sa o 2 below 93%); the study also showed an absent ventilatory response to CO2, absent cardiac responses to apnea during sleep, and right ventricular hypertrophy.
Acta Paediatrica | 2006
Janna G. Koppe; Alena Bartonova; Gabriele Bolte; Marie Louise Bistrup; Chris Busby; Maureen Butter; P. Dorfman; Aleksandra Fucic; David Gee; Peter Van Den Hazel; Vyvyan Howard; Martina Kohlhuber; Marike Leijs; Christofer Lundqvist; Hanns Moshammer; Rima Naginiene; Polyxeni Nicolopoulou-Stamati; Roberto Ronchetti; Georges Salines; Greet Schoeters; Gavin W. ten Tusscher; Max K. Wallis; Moniek Zuurbier
Introduction: All children are exposed to multiple physical, chemical and biological challanges that can result in adverse health effects before and after birth. In this context, the danger of multiple exposures cannot be assessed from a single‐chemical approach as used in classical toxicology. Aim: To open up a ‘negotiation space’ for the problem of multiple exposure to environmental stressors, defined as any physical, chemical or biological entity that can induce an adverse response. In this context, two further questions obtain: to what extent can synergistic risks be assessed, and how far could potential adverse effects be prevented by enhanced regulation?Methods: A discussion of two general approaches is taken: 1 ) the investigation of mixtures such as smoking or air pollution without specifying the individual agents, and 2 ) the investigation of individual substances with a focus on possible interactions in the context of dose to receptor. Results: Although mixtures of compounds can have effects, it may not be possible to ascribe causation to a single compound. Furthermore, cumulative low‐dose insult can, in some circumstances, be more toxic than a single high‐dose exposure, e.g. endocrine disruptive effects of a combination of PCBs and dioxins which disrupt the thyroid hormone status; this tends to contradict elements of classical toxicology,. These cumulative insults may further combine with heavy metals and can disrupt the heme synthesis. It is possible that groups of pollutants could be used to test their cumulative capacity to multiple stress‐susceptible receptor targets as is done in smoking and air pollution. This methodology could be used for further groups of potential pollutants, for example those associated with cleaning products, or cosmetics. Testing individual substances with a focus on interactions means that not only chemicals but also concurrent diseases should be taken into account. We suggest that the enhanced regulation of potential multiple stressors falls into two discrete categories. The first comprises a more precautionary approach (as demonstrated by the banning of chemicals such as some brominated flame retardants in Europe). The second comprises a more ‘permissive’ liberal approach involving the initial study of an individual compound, and subsequent interrogation of that compound in combination with another (as demonstrated by lowering the carcinogenicity of aflatoxin by vaccination against hepatitis B).
Pediatric Allergy and Immunology | 2005
Mario Barreto; Maria Pia Villa; Fabiana Monti; Zuzana Bohmerova; Susy Martella; Marilisa Montesano; Maria T. Darder; Roberto Ronchetti
Although atopy and blood eosinophilia both influence exhaled nitric oxide (eNO) measurements, no study has quantified their single or combined effect. We assessed the combined effect of atopy and blood eosinophilia on eNO in unselected schoolchildren. In 356 schoolchildren (boys/girls: 168/188) aged 9.0–11.5 yr, we determined eNO, total serum IgE, blood eosinophil counts and did skin prick tests (SPT) and spirometry. Parents completed a questionnaire on their childrens current or past respiratory symptoms. Atopy was defined by a SPT > 3 mm and eosinophilia by a blood cell count above the 80th percentile (>310 cells/ml). eNO levels were about twofold higher in atopic–eosinophilic subjects than in atopic subjects with low blood eosinophils [24.3 p.p.b. (parts per billion) vs. 14.1 p.p.b.] and than non‐atopic subjects with high or low blood eosinophils (24.3 p.p.b. vs. 12.2 p.p.b. and 10.9 p.p.b.) (p < 0.001 for both comparisons). The additive effect of atopy and high eosinophil count on eNO levels remained unchanged when subjects were analyzed separately by sex or by a positive history of wheeze (n = 60), respiratory symptoms other than wheeze (n = 107) or without respiratory symptoms (n = 189). The frequency of sensitization to Dermatophagoides (Dpt or Dpf) was similar in atopic children with and without eosinophilia (66.2% and 67.4%, respectively); eosinophilia significantly increased eNO levels in Dp‐sensitized children as well in children sensitized to other allergens. In a multiple linear regression analysis, eNO levels were mainly explained by the sum of positive SPT wheals and a high blood eosinophil count (t = 4.8 and 4.3, p = 0.000), but also by the presence of respiratory symptoms (especially wheeze) and male sex (t = 2.6 and 2.0, p = 0.009 and 0.045, respectively). Measuring eNO could be a simple, non‐invasive method for identifying subjects at risk of asthma in unselected school populations.
Diabetologia | 2000
Maria Pia Villa; G. Multari; Marilisa Montesano; Jacopo Pagani; M. Cervoni; Fabio Midulla; E. Cerone; Roberto Ronchetti
Aims/hypothesis. Patients with diabetes mellitus commonly have cardiovascular autonomic dysfunction and an abnormal ventilatory pattern during sleep. Few data are available on these changes in childhood diabetes. We investigated whether young diabetic children with or without diabetic neuropathy have ventilatory dysfunction during sleep and if so, whether these autonomic changes are related to the duration of diabetes and glycaemic control.¶Methods. We studied 25 children with insulin-dependent diabetes mellitus (19 boys, mean age 7.72 ± 1.99 years). All patients were insulin-dependent at diagnosis; blood samples for HbA1 c assay were collected on the morning before testing and at 3-month intervals during the preceding year. Patients and control subjects (20 age-matched healthy children, 15 boys) underwent overnight polysomnography.¶Results. More diabetic patients than control subjects had sleep apnoeas (p = 0.006); apnoeas in patients also lasted longer (p = 0.07). Patients with poorly controlled diabetes had more apnoeas than patients with well–controlled diabetes and than healthy control subjects (p < 0.0001). Respiratory events during sleep correlated significantly with glycaemic control (r = 0.360; p = 0.09) and with the duration of diabetes (r = 0.430; p = 0.04).¶Conclusion/interpretation. We conclude that respiratory control is compromised very early in children with diabetes. These anomalies are closely related to the duration of diabetes and to glycaemic control. In young children with diabetes, screening of ventilatory control using recording techniques that are simpler than polysomnography could provide an early indication that an adverse cardiopulmonary reaction has begun. [Diabetologia (2000) 43: 696–702]
European Respiratory Journal | 1998
Fabio Midulla; Pm Strappini; V Ascoli; Maria Pia Villa; L Indinnimeo; Carlo Falasca; Susy Martella; Roberto Ronchetti
In an asymptomatic 4 yr old child with radiographic evidence of parenchymal lung disease, bronchoalveolar lavage (BAL) yielded the diagnosis of chronic lipid pneumonia caused by chronic aspiration of mineral oil given as a laxative. BAL analysis showed a marked reduction in the total number of alveolar macrophages; almost 70% of these cells contained intracytoplasmic lipid vacuoles. It also disclosed lymphocytic (cytotoxic/suppressor) alveolitis. A high percentage of lymphocytes expressed antigen markers of activation (human leucocyte antigen (HLA)-DR), CD54 and CD25). BAL analysis 18 months after mineral oil intake revealed that lymphocytes bearing antigen markers of activation had markedly decreased whereas alveolar macrophages (normal and lipid-laden) had increased. A subsequent whole lung BAL was considered unnecessarily invasive in this otherwise healthy child.
Journal of Medical Microbiology | 1998
Carlo Contini; Maria Pia Villa; Roberto Romani; Rocco Merolla; S. Delia; Roberto Ronchetti
A nested polymerase chain reaction (PCR) assay was investigated for detection of Pneumocystis carinii in 96 respiratory tract specimens from 82 children, of whom 28 were immunocompetent but with chronic lung disorders (CLD), eight had AIDS and P. carinii pneumonia (PCP), 16 had AIDS but no respiratory symptoms, and 30 were healthy immunocompetent children. Gomori methenamine silver stain (GMS) and indirect immunofluorescence assay (IFA) were performed in parallel. Of 36 specimens from children with CLD, 12 were P. carinii PCR-positive compared to 10 positive by GMS-IFA. Of eight specimens from children with AIDS and PCP, seven were P. carinii-positive by PCR and six by GMS-IFA, and of 22 specimens from HIV-positive children without respiratory symptoms, two were positive by PCR and none by GMS-IFA. P. carinii DNA was also detected by PCR in blood samples from four children with P. carinii-positive nasopharyngeal aspirates. Specimens from healthy children were negative for P. carinii by both PCR and GMS-IFA. Of the seven children with CLD, who were P. carinii-positive, two had clinical and microbiological improvement with co-trimoxazole treatment, two improved initially but relapsed, and one had P. carinii cysts persistently in follow-up specimens despite co-trimoxazole treatment. These results suggest an association between P. carinii and exacerbations of CLD in childhood, in the absence of HIV infection or other immunodeficiency syndromes.
Acta Paediatrica | 2006
Peter Van Den Hazel; Moniek Zuurbier; Wolfgang Babisch; Alena Bartonova; Marie Louise Bistrup; Gabriele Bolte; Chris Busby; Maureen Butter; Sandra Ceccatelli; Aleksandra Fucic; Wojtec Hanke; Carolina Johansson; Martina Kohlhuber; Marike Leijs; Christofer Lundqvist; Hanns Moshammer; Rima Naginiene; Aw Preece; Roberto Ronchetti; Georges Salines; Margaret Saunders; Greet Schoeters; Nikolaos I. Stilianakis; Gavin W. ten Tusscher; Janna G. Koppe
Background: Facts and hypotheses on the relationship between some childrens diseases or disorders and external stressors during the developmental stage of a child, both prenatally and postnatally are described in literature. In this paper the following changes in patterns and causes of the main childhood illnesses are summarized and recommendations for actions are made.
Acta Paediatrica | 2007
Roberto Ronchetti; Peter Van Den Hazel; Greet Schoeters; Wojtek Hanke; Zusana Rennezova; Mario Barreto; Maria Pia Villa
Numerous studies indicate that low‐level lead poisoning causes mild mental retardation and low IQ scores in children. The general mean lead intake in the adult European population corresponds to a reassuring 14% (0.5–56%) of the tolerable daily intake: at this low level of exposure only few children (less than 10%) have blood lead levels (PbB) higher than 10μg/dl, previously considered the PbB of concern. In more recent years data now suggest that even when ‘the lifetime average blood lead concentration’ is below 10μg/dl an inverse association exists with intelligence quotient (IQ) scores. Two‐thirds (45–75%) of lead in blood, however, comes from long‐term tissue stores and this is especially true for newborn infants and pregnant women. Several data suggest that for lead the main toxic event is prenatal exposure: therefore we should focus our attention on maternal lead stores and whenever possible avoid their mobilization during pregnancy. In this regard we should design appropriate studies to confirm whether dietary supplementations can reduce bone resorption and lead mobilization during pregnancy. The hypothesis that the amount of maternal bone lead stores is the relevant parameter for predicting the level of neurotoxicity of this metal gives some optimism for the future: if we study children whose mothers never underwent high environmental pollution (born after the withdrawal of lead from gasoline) and hence have relatively low bone lead stores we could find that, at the population level, lead has little influence on children IQ scores