eLetters published in the past 30 days:

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11 eLetters published for 9 different topic sources.

Articles			eLetters
	ARTICLES: Does Measuring the Changes in TcB Value Offer Better Prediction of Hyperbilirubinemia in Healthy Neonates? Dalal et al. (1 November 2009) [Abstract] [Full text] [PDF]		Prediction of Neonatal Hyperbilirubinemia Michael Kaplan, et al.   (23 November 2009) Read every eLetter to this article
	ARTICLES: Prevalence of Parent-Reported Diagnosis of Autism Spectrum Disorder Among Children in the US, 2007 Kogan et al. (1 November 2009) [Abstract] [Full text] [PDF]		Aluminium and Autism - finally in the same issue of Pediatrics Paul N Thomas   (17 November 2009) Read every eLetter to this article
	COMMENTARIES: When Should Children Be Tested for Genetic Diseases? Trott and Matalon (1 October 2009) [Full text] [PDF]		Should children be tested to detemine carrier status? Jane Karwoski   (7 November 2009) Read every eLetter to this article
	ARTICLES: Pediatric Adverse Drug Events in the Outpatient Setting: An 11-Year National Analysis Bourgeois et al. (1 October 2009) [Abstract] [Full text] [PDF]		Adverse drug reactions to antibiotic use in young children Shih-Wen Huang, et al.   (2 November 2009) Read every eLetter to this article
	COMMENTARIES: Bilirubin Screening for Normal Newborns: A Critique of the Hour-Specific Bilirubin Nomogram Fay et al. (1 October 2009) [Full text] [PDF]		Evidence and Use of Hour-specific Bilirubin Nomogram Vinod K. Bhutani, et al.   (17 November 2009) Losing the forest for the trees Arthur A Strauss   (28 October 2009) Read every eLetter to this article
	ARTICLES: Association of Family History of Autoimmune Diseases and Autism Spectrum Disorders Atladóttir et al. (1 August 2009) [Abstract] [Full text] [PDF]		Autism, Associated Disorders, and Omega 3 Fatty Acids Scott S. Field   (4 November 2009) Read every eLetter to this article
	ARTICLES: Epidemiology of Sexually Transmitted Infections in Suspected Child Victims of Sexual Assault Girardet et al. (1 July 2009) [Abstract] [Full text] [PDF]		Impact of Pubertal Status on Acquistion of STIs Jan E. Paradise, M.D.   (28 October 2009) Read every eLetter to this article
	FROM THE AMERICAN ACADEMY OF PEDIATRICS: Abusive Head Trauma in Infants and Children Christian et al. (1 May 2009) [Abstract] [Full text] [PDF]		Making a Diagnosis of Abusive Head Trauma Cindy W Christian, et al.   (3 November 2009) Avoiding Mistakes F. Edward Yazbak, et al.   (28 October 2009) Read every eLetter to this article
	STATE-OF-THE-ART REVIEW ARTICLE: Pediatric Cardiopulmonary Resuscitation: Advances in Science, Techniques, and Outcomes Topjian et al. (1 November 2008) [Abstract] [Full text] [PDF]		Avoid hypovolaemia for successful CPR David JR Hutchon   (8 November 2009) Read every eLetter to this article

ARTICLES: Does Measuring the Changes in TcB Value Offer Better Prediction of Hyperbilirubinemia in Healthy Neonates? Dalal et al. (1 November 2009) [Abstract] [Full text] [PDF] Does Measuring the Changes in TcB Value Offer Better Prediction of Hyperbilirubinemia... Prediction of Neonatal Hyperbilirubinemia 23 November 2009 Michael Kaplan, Neonatologist Shaare Zedek Medical Center, and Faculty of Medicine of the Hebrew University, Jerusalem, Israel., Cathy Hammerman Send letter to journal: Re: Prediction of Neonatal Hyperbilirubinemia kaplan{at}cc.huji.ac.il Michael Kaplan, et al. To the Editor, We read the paper by Dalal et al (1) on the prediction of neonatal hyperbilirubinemia by predischarge transcutaneous bilirubinometry (TcB) with great interest. The authors concluded that single predischarge TcB measurements were as predictive of hyperbilirubinemia as were TcB dynamics between 2 assessments. Unfortunately, we perceive some deficiencies in design and methodology which may render the authors' conclusions less decisive than they claim. While the predictive factors included objective transcutaneous bilirubin readings, the outcome of the study, i.e. the presence or absence of hyperbilirubinemia post-discharge, was performed subjectively by visual assessment. This is regretful, as the TcB technique was clearly available at the time of the study. Visual assessment of jaundice may be misleading (2), especially in pigmented infants. As a result, some hyperbilirubinemic neonates may have been missed at the time of the return visit. Secondly, we disagree with the authors' concept of using the 2004 phototherapy guidelines of the American Academy of Pediatrics as their definition of hyperbilirubinemia (3). We wish to point out that the graphs included in these guidelines were not devised to define hyperbilirubinemia. However, having adopted the guidelines to categorize which infants became hyperbilirubinemic, these guidelines should have been fully implemented. For each hour of life, there is a choice of 3 levels of serum bilirubin at which phototherapy could be started. This choice depends on gestational age and the presence or absence of risk factors. Phototherapy was indeed started at lower levels of serum bilirubin in direct Coombs' positive ABO incompatible newborns. However, although glucose-6-phosphate dehydrogenase deficiency was screened for in the hyperbilirubinemic neonates, the presence of G-6-PD deficiency was not used to apply phototherapy more rigorously. As a result, some infants who should have been regarded as hyperbilirubinemic, according to the study definition, may not have been included in this category. As the frequency of G-6-PD deficiency in India has recently been estimated at 8-13%, this condition may have contributed significantly to the incidence of hyperbilirubinemia in the study population (4). We are given no information regarding the babies in the study who did have risk factors and in whom a lower threshold of serum bilirubin was applied. Furthermore, additional risk factors, including asphyxia, significant lethargy, temperature instability, sepsis, acidosis or hypoalbuminemia, which the AAP includes among its indications for earlier commencement of phototherapy, are not related to. Thus, the definition of hyperbilirubinemia used in this study may be less useful than a standard serum bilirubin reading greater than the 95th percentile on the hour-of- life-specific bilirubin nomogram. In our opinion, therefore, further study of predischarge TcB dynamics will be necessary before the relative contributions of single or multiple TcB readings to the prediction of subsequent hyperbilirubinemia can be fully determined. Michael Kaplan, MB ChB, Cathy Hammerman, MD, Department of Neonatology, Shaare Zedek Medical Center, Faculty of Medicine of the Hebrew University, Jerusalem, Israel. References 1. Dalal SS, Mishra S, Agarwal R, Deorari AK, Paul V. Does measuring the changes in TcB value offer better prediction of hyperbilirubinemia in healthy neonates? Pediatrics 2009;124:e851-e857. 2. Keren R, Tremont K, Luan X, Cnaan A. Visual assessment of jaundice in term and late preterm infants. Arch Dis Child Fetal Neonatal Ed. 2009;94:F317-322. 3. Subcommittee on Hyperbilirubinemia, American Academy of Pediatrics. Clinical Practice Guideline: Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics 2004;114:297-316. 4. Nkhoma ET, Poole C, Vannappagari V, Hall SA, Beutler E. The global prevalence of glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis. Blood Cells Mol Dis 2009;42:267-278. Conflict of Interest: None declared

ARTICLES: Prevalence of Parent-Reported Diagnosis of Autism Spectrum Disorder Among Children in the US, 2007 Kogan et al. (1 November 2009) [Abstract] [Full text] [PDF] Prevalence of Parent-Reported Diagnosis of Autism Spectrum Disorder Among Children... Aluminium and Autism - finally in the same issue of Pediatrics 17 November 2009 Paul N Thomas, Pediatrician Integrative Pediatrics Send letter to journal: Re: Aluminium and Autism - finally in the same issue of Pediatrics Paulthomasmd{at}aol.com Paul N Thomas Autism was 1 - 2 per 10,000 in the early 1980's when I trained. We have seen the prevalence rise to 1:650 then 1:150 and now 1:91. When we got the mercury out of the vaccines in 2001 there was no change and in fact rates have continued to rise. Alas we moved the Hep B vaccine around that time from teens to newborns. Many Vaccines have a lot of aluminium (eg 330 micrograms in most DTaP's, 250 micrograms in the Hep B and Hep A etc.). The November issue has the article on Aluminium in preterm infants and later bone health. In this article there is mention of the FDA recommended limit of aluminium exposure to <5 micrograms/Kg per day. Clearly our Hep B vaccines in newborns exceed this exposure ten-fold or more. Is it not time we re-consider the routine Hep B vaccine to infants whose mothers are hep B - negative and or/immune and have no risk factors? Most babies in my practice are not sexually active or using IV drugs. The precuationary principle should be sufficient to prevent us from routinely injecting the known neurotoxin aluminium into every baby in this country. Conflict of Interest: None declared

COMMENTARIES: When Should Children Be Tested for Genetic Diseases? Trott and Matalon (1 October 2009) [Full text] [PDF] When Should Children Be Tested for Genetic Diseases? Should children be tested to detemine carrier status? 7 November 2009 Jane Karwoski, Adjunct Professor Department of Psychology, University of Nevada, Las Vegas Send letter to journal: Re: Should children be tested to detemine carrier status? Jane.Karwoski{at}unlv.edu Jane Karwoski Tarini et al (1) and Trott and Matalon (2) have suggested that childhood testing for adult-onset hereditary disease be reconsidered. Genetic testing of minors for another reason, to determine carrier status, also deserves reappraisal. Similar to testing for adult-onset disorders, it has been generally discouraged by professional organizations, although viewpoints have differed regarding the ethics involved and the psychosocial effect such testing might have on children (3-8). Now that genetic testing can be obtained privately through self-referral, physicians are no longer gatekeepers to this service. By arranging for testing, however, pediatricians can retain their counseling role and exercise a positive influence on the use and interpretation of test results. Parental requests for carrier determination may arise out of a desire "to help their children adjust to the knowledge of their carrier status" (9, p. 209). But parent and child could differ radically in the meaning and implications the same information has for them and, consequently, in their notion of how best to adjust. Parents might interpret an offspring's risk as much higher than would the child because of a particular cognitive error known as the availability heuristic (10). This shortcut method of reasoning makes unlikely events that have actually happened, and are therefore more available to consciousness, seem more likely. Those who have personally experienced a rare event are prone to see the future probability of the event as substantially higher than a purely objective estimate would indicate. Thus, if making this error, parents who have experienced the birth of an affected child will perceive the likelihood of a grandchild being affected as unacceptably high, irrespective of any computed risk factor. They may wish to protect their daughters at all costs from the ordeal they themselves are experiencing, exerting undue pressure upon the child's reproductive hopes, dreams, or plans. The trauma associated with their own childbearing experience can even cause them to view parenting, in general, as too risky to "take the chance" of bearing children. This can be the case whether carrier testing returns a positive result or is unable to return a confident negative result. One or both parents might, for instance, exert pressure toward a life without children, or without biological children, which could lead to foreclosure of child-bearing possibilities for their offspring. Such an influence would place constraints on a child's current self-concept, later decision making, and freedom in selection of a marital partner (11). It is therefore crucial that the physician help all family members examine the meaning and implications various test results could have. Accordingly, testing in and of itself, is neither good nor bad. Rather, it is the meaning of the test and test results within each particular family context that determines how genetic testing might affect minor children (12). The importance of carrier determination lies not in mere information, but in the way that information "maintains or alters how the individual views himself [or herself] both as an integral person and as a social creature" (13, p. 167). Teaching responsible reproductive behavior is a laudable parental goal. But, when parents invest possible carrier status with great salience, negative implications, and fear, they may come to feel that the end (avoiding the disorder in the next generation) justifies the means (depriving adolescents and young adults of control over their own future reproductive decision making). While rooted in loving concern for the lives of their children and potential grandchildren, an overly zealous effort to curtail the risk as they perceive it may move parents to act in a counterproductive manner. When asked to facilitate carrier determination testing for a child, the discerning physician will obtain a baseline knowledge of the attitudes of each parent and the minor involved. One useful question might be, "If the test indicates that your child does carry disorder X, how would that affect your feelings about her bearing children?" Parents who have themselves experienced chance turning against them through the birth of an affected child, may indicate a desire that their daughter would avoid childbearing. If so, they could be led to consider the fact that difficult decisions must be self-motivated if they are not to cause potentially harmful distress. Research in educational psychology has demonstrated that autonomous control is a significant characteristic of motivated decisions. Control promotes interest, confidence, and self-worth (14, pp. 222-227). Preempting the personal choice of future adults is a route fraught with hazards. At one extreme, youths might react with complete denial of any desire for children of their own. At the opposite extreme, they may rebelliously disregard any and all risks associated with sexual activity. Physicians are uniquely situated to mitigate pressure on children by helping parents find a way to facilitate a child's adjustment and yet avoid usurping control over reproductive decisions that, in the future, will rightfully belong to their child. References 1. Tarini BA, Singer D, Clark SJ, Davis MM. Parents' interest in predictive genetic testing for their children when a disease has no effective treatment. Pediatrics. 2009;124(3). Available at: www.pediatrics.org/cgi/content/full/124/3/e432 2. Trott AA, Matalon R. When should children be tested for genetic diseases? Pediatrics. 2009;124(4). Available at: www.pediatrics.org/cgi/content/full/124/4/e807 3. American Society of Human Genetics, Board of Directors; American College of Medical Genetics, Board of Directors. Points to consider: ethical, legal, and psychosocial implications of genetic testing in children and adolescents. Am J Hum Genet. 1995;57(5):1233–1241 4. Borry P, Goffin T, Nys H, Dierickx K. Attitudes regarding carrier testing in incompetent children: a survey of European clinical geneticists. Eur J Hum Genet. 2007;15(12):1211–1217 5. Clarke A. The genetic testing of children: report of a working party of the Clinical Genetics Society (UK). J Med Genet. 1994;31(10):785–797 6. Wehbe RM, Spiridigliozzi GA, Heise EM, Dawson DV, McConkie-Rosell A. When to tell and test for genetic carrier status: Perspectives of adolescents and young adults from fragile X families. Am J Hum Genet A. 2009;149A(6):1190–1199. 7. Ross LF, Moon MR. Ethical issues in genetic testing of children. Arch Pediatr Adolesc Med. 2000;154(9):873-879 8. Wertz DC, Fanos JH, Reilly PR. Genetic testing for children and adolescents: who decides? JAMA. 1994;272(11):875-881 9. McConkie-Rosell A, Spiridigliozzi GA, Rounds K, Dawson DV, Sullivan JA, Burgess D, Lachiewicz AM. Parental attitudes regarding carrier testing in children at risk for fragile X syndrome. Am J Med Genet A. 1999;82(3):206–211. 10. Tversky A, Kahneman D. Availability: a heuristic for judging frequency and probability. Cogn Psychol. 1973;5(2):207–232 11. Kay E, Kingston H. Feelings associated with being a carrier and characteristics of reproductive decision making in women known to be carriers of X-linked conditions. J Health Psychol. 2002;7(2):169–181 12. McConkie-Rosell A, Spiridigliozzi GA. "Family matters": a conceptual framework for genetic testing in children. J Genet Couns. 2004:13(1): 9–29 13. Sorenson JR. Some social and psychologic issues in genetic screening. In: Bergsma D, ed. Ethical, Social and Legal Dimensions of Screening for Human Genetic Diseases. New York, NY: Stratton; 1974:165-184 14. Paris SG, Turner JC. Situated motivation. In: Pintrich PR, Brown DR, Weinstein CE, eds. Student Motivation, Cognition, and Learning: Essays in Honor of Wilbert J. McKeachie. Hillsdale, NJ: Lawrence Erlbaum; 1994:213-237 Conflict of Interest: None declared

ARTICLES: Pediatric Adverse Drug Events in the Outpatient Setting: An 11-Year National Analysis Bourgeois et al. (1 October 2009) [Abstract] [Full text] [PDF] Pediatric Adverse Drug Events in the Outpatient Setting: An 11-Year National Analysis Adverse drug reactions to antibiotic use in young children 2 November 2009 Shih-Wen Huang, M.D. University of Florida, Department of Pediatrics, N/A Send letter to journal: Re: Adverse drug reactions to antibiotic use in young children huangsw{at}peds.ufl.edu Shih-Wen Huang, et al. Letter to the Editor: We read with interest the article entitled “Pediatric Adverse Drug Events in the Outpatient Setting: An 11-Year National Analysis” by Bourgeois et al. (Pediatrics. 2009;124:e744–e750).1 The authors reported a spectacular number of clinical and emergency room visits related to adverse drug events (ADEs) in children. They stated in their discussion (and showed in Figure 1) that children 0 to 4 years old made up the majority of ADE patients, with 13.2 visits per 1000 persons. Of these, 56% presented with dermatologic symptoms, suggesting that a large number of the reactions were allergic in nature. Figure 1 in the paper showed that antimicrobial agents were most often responsible for the ADEs, and, although the authors did not state it implicitly, they seemed to strongly imply that ADEs in that age group, as evidenced by reports of skin rash, were largely due to sensitivity to antimicrobials. They concluded that age -specific approaches for monitoring and preventing ADEs may be most effective. While we agree with their conclusion, we disagree that ADEs in children between 0 and 4 years of age are largely the result of sensitivity to antibiotics. The results of our earlier study of skin rashes related to antibiotic use in young children2 do not support this contention. In that study, we reported on 86 consecutive children presenting at our allergy clinic over a period of 5 years,2 80% of whom were under the age of 3. All of the patients had taken antibiotics in the form of a liquid suspension; the majority had taken either penicillin or cephalosporin. The onset of skin rash normally occurred within 3 to 5 days after ingesting the suspension. Twenty percent of the patients had never taken antibiotics in the past, but, interestingly, 33% of them had a history of reactions to the dyes contained in drugs or drinks. In our study, the results of both skin test and RAST were negative for drugs. The patients were then given an oral challenge of a dye-free antibiotic suspension or the original suspension of antibiotics after they recovered from infections, and none showed a reaction. We therefore concluded that the cause of the skin rash was not sensitivity to antimicrobials in the original antibiotic suspensions. Furthermore, the skin rashes of the patients upon presentation at our clinic were mostly bright erythema; a few had urticaria. We also observed that the majority of our children did not look ill in spite of the presence of extensive skin rashes.2 These clinical features are in sharp contrast to those typically seen with drug allergies, in which intolerable pruritus, irritability, and loss of quality of life (e.g., poor sleep or poor appetite) are the norms. In considering other diagnoses, we initially speculated that the drug -related rashes were related to viral exanthem; however, we found that not all of the patients had viral illness. We then suspected that perhaps excipients such as dyes, flavorings, or preservatives in the suspension were the cause; however, patients later tolerated the dyes contained in the original drugs. We then wondered whether the skin reactions could have been due to a transient biochemical changes. Studies by Buhl et al.3 and Andre et al.4 had proposed this new hypothesis in trying to explain reports of rashes found in many HIV patients given sulfa drugs for the prevention or treatment of Pneumocystitis carinii. While they were unable to confirm that the rashes were due to sensitivity to the drugs, the authors also measured the blood level of glutathione (GSH), and found that patients with skin rashes had a significantly lower level of GSH. GSH is known to be a powerful antioxidant that serves as a scavenger of toxic, reactive metabolites created by drugs or excipients such as dyes, but its levels can fluctuate during periods of stress such as during an infection. The authors concluded that the rashes seen after sulfa drug use were likely due to a transient state GSH deficiency. In our study, 17 of 28 (61%) patients had GSH levels below two standard deviations of the mean of the value for normal adults at the peak of infection. Since they later were able to tolerate dyes or food colorings after they fully recovered from infection, we believe that similar transient GSH deficiencies might have occurred in the children who developed rashes during treatment with antimicrobial suspensions. It would be interesting to know if the cases presented by Bourgeois et al. had similar levels of GSH, especially those in the same age group. We agree that all patients who present with skin rashes related to drugs require a careful workup that includes oral challenge. If the reactions are found to be the result of sensitivity to excipients such as dyes, then a dye-free, compounded form of the drug should be substituted instead of abandoning the useful antimicrobials altogether. These efforts will not only result in better patient care, but will also help to reduce medical costs significantly. References 1. Bourgeois FT, Mandl KD, Valim C et al. Pediatric drug events in the outpatient setting: An 11-year national analysis. Pediatrics 2009;124:e744–e750. 2. Huang SW, Borum PR. Study of skin rashes after antibiotic use in young children. Clin Pediatr. 1998;37:601–608. 3. Buhl R, Jaffe HA, Holroyd KJ, et al. Systemic glutathione deficiency in symptom- free HIV-seropositive individuals. Lancet. 1991;ii:431–433. 4. Andre JAM, Ven VD, Kooperman PP, et al. Adverse reactions to cotrimoxazole in HIV Infections. Lancet. 1991;ii:431–433. Conflict of Interest: None declared

COMMENTARIES: Bilirubin Screening for Normal Newborns: A Critique of the Hour-Specific Bilirubin Nomogram Fay et al. (1 October 2009) [Full text] [PDF] Bilirubin Screening for Normal Newborns: A Critique of the Hour-Specific Bilirubin... Evidence and Use of Hour-specific Bilirubin Nomogram 17 November 2009 Vinod K. Bhutani, Professor of Pediatrics Stanford University School of Medicine, Lois Johnson, Children's Hospital of Philadelphia Send letter to journal: Re: Evidence and Use of Hour-specific Bilirubin Nomogram bhutani{at}stanford.edu Vinod K. Bhutani, et al. The breakthrough and innovative contribution of predictive value of routine predischarge total serum bilirubin (TSB) measured at time of the universal metabolic screen is its use as an hour-specific (instead of day-specific) risk designation for developing post-discharge clinically significant hyperbilirubinemia (specifically: TSB levels ± 95th percentile for age in hours) during the first postnatal week rather than by dependence on visual assessment of jaundice [1]. Such levels of hyperbilirubinemia have been deemed significant and are generally considered to require close supervision, possible further evaluation, and sometimes intervention if brain damage is to be prevented without resort to exchange transfusion. Careful reading of this manuscript emphasizes that the risk designation does not predict kernicterus or the decision to use phototherapy. The designated risk zones guide post-discharge follow-up. In an attempt to anticipate risk of an errant experience for a newborn who unexpectedly develops significant hyperbilirubinemia, newborns who crosses percentile tracks required a closer supervision. As provided in legend of Table 3, the nomogram can be used at geographic sites with different prior probabilities of significant hyperbilirubinemia to calculate site-specific risk assessment. In independent studies, Stevenson et al have reported on the reliable performance of the nomogram in a large-scale multinational study [2]; Keren et al have addressed and argued against evidence of spectrum or verification biases in a re-analysis of the cohort from the population reported to construct the nomogram [3, 4]. Recently, Keren et al supported the predictive accuracy of alternative risk-assessment strategies used to screen for the risk of significant neonatal hyperbilirubinemia using transcutaneous measurements on the TSB nomogram [5]. The difficulties encountered by practitioners with “false negatives” in the low-risk zone (not designated as a “no-risk” zone) relate to the limitations of TcB measurements to substitute for TSB [6] and possibly due to tissue bilirubin dynamics; inappropriate use of bovine albumin serum during TSB assay [7] and its continued usage outside the US; poor calibrated performance of certain devices [8]. Thankfully, the College of American Pathologists has been diligent in ensuring a better inter- laboratory performance of TSB assay [9, 10]. Clearly, the answer is not to have sub-cohorts of predictive nomograms based on diet, race, gender, ethnicity, overt or covert hemolysis, altitude, geographical distance from the equator, season, assay or institution. Based on lessons learned and reported in our study and those to yet come, a better universal predictive bilirubin nomogram based on accurate TSB/TcB measurements would be welcome. References: 1. Bhutani VK, Johnson L, Sivieri EM. Predictive ability of a predischarge hour-specific serum bilirubin for subsequent significant hyperbilirubinemia in healthy term and near-term newborns Pediatrics. 1999;103:6-14. 2. Stevenson DK, Fanaroff AA, Maisels MJ, et al. Prediction of hyperbilirubinemia in near-term and term infants. Pediatrics. 2001; 108:31– 39 3. Keren R, Bhutani VK, Luan X, Nihtianova S, Cnaan A, Schwartz SJ. Identifying newborns at risk of significant hyperbilirubinemia. Arch Dis Child 90:415-21, 2005. 4. Keren R and Bhutani VK, Predischarge Risk Assessment for Severe Neonatal Hyperbilirubinemia. NeoReviews. 2007; 8(2): e68 5. Keren R, Luan X, Friedman S, Saddlemire S, Cnaan A, Bhutani VK. A comparison of alternative risk-assessment strategies for predicting significant neonatal hyperbilirubinemia in term and near-term infants. Pediatrics. 2008;121(1):e170-9. 6. Maisels MJ, Bhutani VK, Bogen D, Newman TB, Stark AR, Watchko JF. Hyperbilirubinemia in the newborn infant > or =35 weeks' gestation: an update with clarifications. Pediatrics. 2009;124(4):1193-8. 7. Lo SF, Doumas BT, Ashwood ER; College of American Pathologists. Bilirubin proficiency testing using specimens containing unconjugated bilirubin and human serum: results of a College of American Pathologists study. Arch Pathol Lab Med. 2004;128(11):1219-23 8. Lo SF, Jendrzejczak B, Doumas BT. Total or neonatal bilirubin assays in the Vitros 5,1 FS: hemoglobin interference, hemolysis, icterus index. Clin Chem. 2007;53(4):799-800 9. Lo SF, Jendrzejczak B, Doumas BT; College of American Pathologists. Laboratory performance in neonatal bilirubin testing using commutable specimens: a progress report on a College of American Pathologists study. Arch Pathol Lab Med. 2008;132(11):1781-5. 10. Lo SF, Kytzia HJ, Schumann G, Swartzentruber M, Vader HL, Weber F, Doumas BT. Interlaboratory comparison of the Doumas bilirubin reference method. Clin Biochem. 2009;42(12):1328-30. Conflict of Interest: None declared Bilirubin Screening for Normal Newborns: A Critique of the Hour-Specific Bilirubin... Losing the forest for the trees 28 October 2009 Arthur A Strauss, Neonatologist Miller Children's Hospital, Long Beach CA Send letter to journal: Re: Losing the forest for the trees astrauss{at}memorialcare.org Arthur A Strauss Dr. Newman's angst about the state of bilirubin screening and the goal of preventing both acute and chronic bilirubin encephalopathy is understandable. Pediatricians and the AAP have missed the boat for decades as a recent review of the same subject suggested (1). TSB or TcB are lousy surrogates for kernicterus risk as Dr. Bhutani aptly documented in the review and elsewhere. All the articles and commentaries in the Journal (October 2009) are discussing the relative cost-effectiveness of using a screening program that is using the wrong screening tool; the debate therefore centers around the cost of case - finding - is it $5M vs $10M or $100M for kernicterus case prevented? It's no wonder that the US Preventive Services Task Force cannot find evidence to support the 2004 AAP Guidelines. In the meantime, the poor pediatrician is left to the mercy of the expert witness and attorney who can use this unworthy lab test to their advantage, while we subject more and more babies to unnecessary treatment (albeit relatively benign phototherapy). 1) Wennberg, et al; Pediatrics; 117 : 474-85, February 2006 Conflict of Interest: None declared

ARTICLES: Association of Family History of Autoimmune Diseases and Autism Spectrum Disorders Atladóttir et al. (1 August 2009) [Abstract] [Full text] [PDF] Association of Family History of Autoimmune Diseases and Autism Spectrum Disorders Autism, Associated Disorders, and Omega 3 Fatty Acids 4 November 2009 Scott S. Field, pediatrician Field Pediatrics, P.C. Send letter to journal: Re: Autism, Associated Disorders, and Omega 3 Fatty Acids scottfieldmd{at}gmail.com Scott S. Field Dear Editor: Recent articles in this journal [1-3] shed more light on associations and potential etiologies of autism. Maternal (but not paternal) depression and other psychiatric disorders [1], celiac disease and rheumatoid arthritis [2] were all associated with increased rates of autism. Omega 3 fatty acids (n-3 FAs) have been useful in treating mental and autoimmune problems [4-7]. Deficiencies of n-3 FAs causing those conditions in mothers might also explain their children developing autism. Celiac disease is linked genetically to type 1 diabetes (T1D) [8] and causes malabsorption. Malabsorption of n-3 FAs might explain the significant occurrence of autism in children born to mothers with celiac disease [2]. Maternal and paternal family histories of schizophrenia [1] and T1D [2] increased children’s risk for autism. Increased intake of n-3 FAs has been beneficial in preventing T1D [9] and treating schizophrenia [4]. Perhaps the genes involved in those two disorders involve n-3 FA metabolism or expression. There is a strong association between childhood-onset-schizophrenia and autism [10]. The only gastrointestinal problems Ibrahim, et. al. [3] found in association with autism were constipation and picky diets. They attributed the dietary habits to the autism without considering that the autism might be caused by the dietary habits. The authors did recognize that “Autistic behaviors are coincidentally [maybe not] first recognized by many parents at the same time that infants are weaned from breast milk and formulas...” A recent study [11] found that children with autism compared to controls had much lower levels of mercury in their blood, explained by the fact that they ate less fish. Fish is the best source of neuro-beneficial n-3 FAs. There is some evidence that n-3 FA supplementation may be beneficial in treating autism [12,13]. More importantly, n-3 FAs are essential nutrients instrumental in normal brain development and should be at least considered for their potential to prevent autism [14,15]. References: 1. Daniels, JL, Forssen, U, Hultman, CM, et. al. Parental psychiatric disorders associated with autism spectrum disorders in the offspring. Pediatrics. 2008;121(5):e1357-e1362 (doi:10.1542/peds.2007-2296) 2. Atladottir, HO, Pedersen, MG, Thorsen, P, et. al. Association of family history of autoimmune diseases and autism spectrum disorders. Pediatrics. 2009;124(2):687-694 3. Ibrahim, SH, Voigt, RG, Katusic, SK, et. al. Incidence of gastointestinal symptoms in children with autism: A population-based study. Pediatrics. 2009;124(2):680-686 4. Arvindakshan, M, Ghate, M, Ranjekar, PK, et. al. Supplementation with a combination of omega-3 fatty acids and antioxidants (vitamins E and C) improves the outcome of schizophrenia. Schizophr Res. 2003;62(3):195-204 5. Su, KP, Huang, SY, Chiu, CC, et. al. Omega-3 fatty acids in major depressive disorder. A preliminary double-blind, placebo-controlled trial. Eur Neuropsychopharmacol. 2003;13(4):267-271 6. Simopoulos, AP. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002;21(6):495-505 7. Berbert, AA, Kondo, CR, Almendra, CL, et. al. Supplementation of fish oil and olive oil in patients with rheumatoid arthritis. Nutrition. 2005;21(2):131-136 8. Smyth, DJ, Plagnol, V, Walker, NM, et. al. Shared and distinct genetic variants in type 1 diabetes and celiac disease. N Engl J Med. 2008;359(26):2767-2777 9. Stene, LC, and Joner, G. Use of cod liver oil during the first year of life is associated with lower risk of childhood-onset type 1 diabetes: a large, population-based, case-control study. Am J Clin Nutr. 2003;79(5):1128-1134 10. Rapoport, J, Chavez, A, Greenstein, D, et. al. Autism spectrum disorders and childhood-onset schizophrenia: clinical and biological contributions to a relation revisited. J Am Acad Child Adolesc Psychiatry. 2009;48(1):10-18 11. Hertz-Picciotto, I, Green, PG, Delwiche, L, et. al. Blood mercury concentrations in CHARGE study children with and without autism. Environ Health Perspect (Oct 19, 2009) http://dx.doi.org/10.1289/ehp.0900736 (accessed October 23, 2009) 12. Amminger, GP, Berger, GE, SchAofer, MR, et. al. Omega-3 fatty acids supplementation in children with autism: a double-blind randomized, placebo-controlled pilot study. Biol Psychiatry. 2007;61(4):551-553 13. Meiri, G, Bichovsky, Y, and Belmaker, RH. Omega 3 fatty acid treatment in autism. J Child Adolesc Psychopharmacol. 2009;19(4):449-451 14. Saugstad, LF. Infantile autism: a chronic psychosis since infancy due to synaptic pruning of the supplementary motor area. Nutr Health. 2008;19(4):307-317 15. Clark-Taylor, T, and Clark-Taylor, BE. Is autism a disorder of fatty acid metabolism? Possible dysfunction of mitochondrial beta-oxidation by long chain acyl-CoA dehydrogenasae. Med Hypotheses. 2004;62(6):970-975 Conflict of Interest: None declared

ARTICLES: Epidemiology of Sexually Transmitted Infections in Suspected Child Victims of Sexual Assault Girardet et al. (1 July 2009) [Abstract] [Full text] [PDF] Epidemiology of Sexually Transmitted Infections in Suspected Child Victims of Sexual... Impact of Pubertal Status on Acquistion of STIs 28 October 2009 Jan E. Paradise, M.D., Department of Pediatrics Signature Medical Group, Brockton, MA Send letter to journal: Re: Impact of Pubertal Status on Acquistion of STIs jeparadise{at}hotmail.com Jan E. Paradise, M.D. To the editor: In their impressive, multicenter study, Dr. Girardet and colleagues highlight their observation that "...10 girls with normal examinations also received a diagnosis of an STI, 1 of whom tested positive for gonorrhea...A positive test for gonorrhea in a child with normal examination findings was unanticipated.." Although this report provides data concerning the age distribution of the children who were tested for sexually transmitted infections, it does not provide data concerning their pubertal status. Approximately one- third of the children were 11 to 13 years old. Presumably, that group included a number of post-pubertal girls and boys. It seems likely that some girls were post-menarchal. In girls, lower genital tract infections with gonorrhea and chlamydia are vaginal in location before puberty but localize to the cervix after puberty.(ref 1) Regarding infection caused by Trichomonas, clinical experience and some research reports suggest that, in the absence of estrogenized vaginal mucosa, girls do not acquire vaginitis even if they are exposed to the organism. To allow fuller interpretation of this excellent study and to maximize its contribution to clinical decision-making, the incidence of STIs in the study subjects should be analyzed according to their pubertal status. In particular, this analysis is needed for gonococcal, chlamydial, and trichomonal infections in girls, since the manifestations of these infections are clearly influenced by girls' pubertal status. 1. Gutman L, "Gonococcal diseases in infants and children." In Holmes KK, et al, eds. Sexually Transmitted Diseases, 3rd Edition. NY: McGraw-Hill, 1999, p. 1149. Conflict of Interest: None declared

FROM THE AMERICAN ACADEMY OF PEDIATRICS: Abusive Head Trauma in Infants and Children Christian et al. (1 May 2009) [Abstract] [Full text] [PDF] Abusive Head Trauma in Infants and Children Making a Diagnosis of Abusive Head Trauma 3 November 2009 Cindy W Christian, Pediatrician The Children's Hospital of Philadelphia, The University of Pennsylvania School of Medicine, Robert Block, MD Send letter to journal: Re: Making a Diagnosis of Abusive Head Trauma christian{at}email.chop.edu Cindy W Christian, et al. We thank Drs. Yazbak and Innis for their attention to the AAP policy statement "Abusive Head Trauma in Infants and Children". They correctly emphasize the primary points from the statement: a careful medical history and appropriate examinations, including laboratory and radiologic studies, will inform the final diagnosis chosen from a carefully considered differential. While the statement was not intended to review the differential diagnosis of abusive head trauma, the authors of the statement and members of the Committee on Child Abuse and Neglect are aware of both uncommon diseases that may present with symptoms similar to those of abusive head trauma, and theoretical diseases that are purported to mimic abuse despite the lack of sound science to support that contention. We must recognize that abusive head trauma often goes undiagnosed by unsuspecting physicians, putting infants and children at continued risk and further harm. Ascribing traumatic injuries to unproven hypotheses of causation can do the same. Conflict of Interest: None declared Abusive Head Trauma in Infants and Children Avoiding Mistakes 28 October 2009 F. Edward Yazbak, Peditatrician TL Autism Research, Co-author Michael D Innis, Hematologist Send letter to journal: Re: Avoiding Mistakes tlautstudy{at}aol.com F. Edward Yazbak, et al. In “Abusive Head Trauma in Infants and Children”1 Christian, Block and the Committee on Child Abuse and Neglect recommended that the “Shaken Baby Syndrome”2 be renamed “Abusive Head Trauma”. The authors were careful to stress that pediatricians had “a responsibility to consider alternative hypotheses when presented with a patient with findings suggestive of AHT”, that such a diagnosis is only made “after consideration of all the clinical data” and that “restraint is required until the medical evaluation has been completed” It is imperative to heed this advice as all the signs and symptoms attributed to Shaken Baby Syndrome/Abusive Head Trauma can in fact result from other causes that include a deficiency in various nutrients such as Vitamins C and K.3,4,5 Having reviewed many cases where innocent parents were suspected of child abuse and emotionally and financially ruined, we agree with the authors that as long as the infant is safe in the hospital, a rush to judgment is not justified. We believe that in addition to a very careful physical examination, a “meticulous medical history taking” must include a comprehensive review of the pregnancy, delivery and the infant’s past history including the listing of recent vaccinations. In addition, we do have concerns about diagnostic mishaps continuing to occur if screening is only “performed when indicated”. It is therefore wiser to consider the following laboratory investigations as “routine” and to perform them as early as possible in such cases: • CBC to exclude a blood dyscrasia • PTT, aPTT, PIVKA-II test and Undercarboxylated Osteocalcin to exclude Vitamin K Deficiency, a recognized cause of hemorrhage, bruising and bone lesions5,6 • Fibrin, fibrin degradation products and Factor XIII for further evidence of a coagulopathy • Serum ascorbate & blood histamine for evidence of Vitamin C Deficiency3,4 • Urinary organic acid and serum carnitine as a screen for a metabolic disorder. By doing so, everyone can be protected and terrible mistakes, at the worst possible times, can be prevented. References 1.Christian CW, Block R; Committee on Child Abuse and Neglect; American Academy of Pediatrics. Abusive Head Trauma in Infants and Children Pediatrics. 2009 May;123(5):1409-11. 2. Ludwig S, Warman M. Shaken baby syndrome: a review of 20 cases. Ann Emerg Med. 1984;13(2):104–107 3. Clemetson CAB Was it “shaken baby” or a varient of Barlow’s disease? J Am Phys Surg 2004:9:78-80 4. Clemetson CA Elevated blood histamine caused by vaccinations and Vitamin C deficiency may mimic the shaken baby syndrome. Med Hypotheses. 2004;62(4):533-6 5. Innis MD. Vitamin K Deficiency Disease. Jour Orthomol Med.2008:23; 15-20 6. Rutty GN, Smith M, Malia RG. Late Form Hemorrhagic Disease of the Newborn. A Fatal Case Report with Illustrations of Investigations Which May Assist Avoiding the Mistaken Diagnosis of Child Abuse. Am J Forensic Med Path 1999;20(1):48-51 Conflict of Interest: None declared

STATE-OF-THE-ART REVIEW ARTICLE: Pediatric Cardiopulmonary Resuscitation: Advances in Science, Techniques, and Outcomes Topjian et al. (1 November 2008) [Abstract] [Full text] [PDF] Pediatric Cardiopulmonary Resuscitation: Advances in Science, Techniques, and Outcomes Avoid hypovolaemia for successful CPR 8 November 2009 David JR Hutchon, Consultant Obstetrician Memorial Hospital, Darlington, UK Send letter to journal: Re: Avoid hypovolaemia for successful CPR djrhutchon{at}hotmail.co.uk David JR Hutchon Sir, In 1958 Professor G S Dawes of Oxford wrote at the end of one of his numerous reports of animal investigations “It was concluded that the maintenance of the circulation is of primary importance in anoxia.” Even then there was evidence to support more emphasis of circulation and less on oxygenation. Dawes had previously described the recovery of a neonate after 40 minutes of complete anoxia. It is well recognised that the young brain can withstand hypoxia a lot better than the mature brain however even in the neonate 40 minutes of compete hypoxia has never been associated a normal outcome. These lambs were subjected to 40 minutes of complete anoxia by occlusion of the umbilical cord, which was then released allowing the placental circulation to recover. The lambs were never at risk of hypovlaemia as the compartment volumes and pulmonary circulation were unchanged from the fetal state. It was from these results that he was able to conclude that circulation was of primary importance. Contrast this with the normal management of human birth, especially when asphyxia or hypoxia of the neonate is anticipated. The circulation may already be compromised by hypoxia. Hypoxia is commonly due to cord compression. This prevents the oxygenated blood returning from the placenta and results in congestion in the placenta and hypovolaemia in the fetus. Once the baby is born the compression will be released and the appropriate blood volume return to the neonate. Unfortunately this return of blood from the placenta is usually prevented by the rapid application of the cord clamp to enable the baby to be handed over to the pediatrician for cardio-pulmonary resuscitation. Ventilation of the lungs, the fall in pulmonary vascular resistance, and the filling of the pulmonary vascular tree simply aggravates the hypovolaemia. No amount of adjustment of the ratio of heart compression to ventilation can improve the cardiac output and cerebral circulation. By the time hypovolaemia is recognised and corrected permanent damage from a failure of circulation may have already occurred. “Untying” the umbilical cord at birth may help to maintain the circulation of primary importance. If cardiac compression is necessary, the technique will not be compromised by hypovolaemia. Reference Dawes GS, Mott JC, Shelley HJ. The importance of cardiac glycogen for the maintenance of life in foetal lambs and new-born animals during anoxia. J Physiol (1959) 146,516-538 Conflict of Interest: None declared