key: cord-0920351-qja1v2j7 authors: Bermejo, JF; Muñoz‐Fernandez, MA title: Severe Acute Respiratory Syndrome in children: a clue to better understanding the disease and advancing towards solutions date: 2007-01-02 journal: Acta Paediatr DOI: 10.1111/j.1651-2227.2004.tb03034.x sha: 9ae0cda21be9a473c02b977408d52ff1de68d18c doc_id: 920351 cord_uid: qja1v2j7 nan PUFAs intake and human content relationship during the first month of lactation. Clin Nutrition 2001; 20: 393-7 9. Pugo-Gunsam P, Guesnet P, Subratty AH, Rajcoomar Severe Acute Respiratory Syndrome in children: a clue to better understanding the disease and advancing towards solutions Sir, Severe Acute Respiratory Syndrome (SARS) is a disease caused by a new coronavirus that has generated worldwide concern. In the adult population, respiratory distress is the main cause of mortality. In our view, there is an open question: what is the underlying cause of evolution to respiratory distress: a viral direct cytopathic damage, an immune-mediated damage in response to the viral infection or both? Evidence of immune implication in SARS pathogenesis comes from autopsies (1), which show a pronounced increase in macrophages in the alveoli and the interstitium of the lung and haemophagocytosis (thought to be in relation with an incorrect regulation of T lymphocytes and cytokines). Therefore, pro-inflammatory cytokines released by stimulated macrophages in the alveoli could have a prominent role in SARS pathogenesis. Additionally, reports coming from China testing levels of cytokines on serum and blood samples show that most pro-inflammatory cytokines are elevated during the early phase of SARS (2) . Pre-existing comorbidity, particularly diabetes, is related to an increased mortality, but immuno-supressive states such as HIV infection are not. It is supposed that the virus comes from an animal host. On this basis, it does not seem to be hazardous to suppose an incorrect or exacerbated immune response against this non-common virus. At this point, the first reports about SARS in paediatric patients reveal a surprising conclusion: to date, there have been no reported case fatalities in children with this disease, in contrast with the 774 deaths registered in adults. The severity is much milder and the clinical progression much less aggressive in young children, while adolescents (12 y or older) resemble adults in their clinical features. In general, younger children do not require oxygen supplementation or immunosupressors and do not develop radiographic findings consistent with acute respiratory distress syndrome (3) (4) (5) (6) . The benign course of SARS in children presents several implications. (1) It discards an important direct viral cytopathic component for respiratory distress: children would be the most affected patients given the immaturity of their immune system. (2) On the other hand, severity of the disease is worst in patients with an adult immune system. This implies that immune response plays a fundamental role in the evolution to distress. (3) The role that immunomodulators could play in therapy acquires more relevance, such as phosphodiesterase inhibitors (i.e. pentoxifylline), due to their activity-decreasing pro-inflammatory cytokines (7) , or inhaled corticoids, aimed at exerting a local immunomodulation. The misuse of systemic glucocorticoids and antibiotics in SARS has lead to secondary infections, pathological fractures and avascular necrosis. Teophylline and Nedocromil sodium are drugs capable of preventing inflammatory cell recruitment into the airway wall. An early instauration of an immunomodulatory therapy guided for the levels of proinflammatory cytokines could aid in preventing the instauration of respiratory distress. (4) The design of vaccines should avoid those SARS coronavirus antigens that could lead to an immune-mediated inflammatory damage. (5) The animals used to test any vaccine have to be adults. If they are too young, it would be logical to find no adverse effects. (6) Paediatricians should be aware of mild symptomatic children who could transmit the virus to close adult contacts (patients with a more severe course), and confirm any case suspicious of SARS. In conclusion, children present particular features that could aid our understanding of adult SARS. Lung pathology of fatal severe acute respiratory syndrome Dynamic changes in blood cytokine levels as clinical indicators in severe acute respiratory syndrome Severe acute respiratory syndrome in children: experience in a regional hospital in Hong Kong Clinical presentations and outcome of severe acute respiratory syndrome in children Children hospitalized with severe acute respiratory syndrome-related illness in Toronto Severe acute respiratory syndrome (SARS) in a paediatric cluster in Singapore Pentoxifylline and severe acute respiratory syndrome (SARS): a drug to be considered How reliable is clinical assessment in neonatal jaundice?Dear Sir, We have read with great interest the article by Riskin et al. (1) , which appeared in a recent issue of the journal. The authors have investigated the value of eye measurement (so-called "Bili Eye") in predicting the serum total bilirubin levels in 283 healthy term newborns at 63.8 ± 21.6 h of life. They have reported a very significant positive correlation between bilirubin clinical assessments (8.8 ± 2.3 mg/dl) and serum total bilirubin (STB) levels (8.8 ± 2.4 mg/dl), although the 95% CI of the observers' mean estimations is not zero despite such sensitive assessments. We have some comments about the methodology and conclusions of the study.Although it is stated that there were intra-and interobserver variations in estimations of bilirubin, we cannot observe these variations in each physician's assessments. Further, there seem to be no significant differences between inter-observer estimations (rvalues between 0.622 and 0.795). If the primary aim of the study was to bring alternatives to use hourspecific nomograms (2) (3) (4) , then it should be strictly and statistically defined how experienced and how well trained a clinical neonatal practitioner should be, to use or to have a "Bili Eye". And, finally, how could the authors conclude that "using this method STB levels need to be measured only in significantly jaundiced babies" while they did not compare newborns with and without significant hyperbilirubinaemia? However, we wonder, and one might easily conclude that the value of "Bili Eye" remains to be determined in significantly jaundiced newborns (with STB levels of !12-13 mg/ dl), considering the absence of any significant correlation even between zone-to-zone clinical assessment and STB levels of !12 mg/dl (5) . The efficacy of "Bili Eye"