Pervasive developmental disorders are a group of neurodevelopmental disorders characterized by impairments in communication, reciprocal social interaction and restricted repetitive behaviors or interests. The term autism spectrum disorders (ASD) has been used to describe their variable presentation. Although the cause of these disorders is not yet known, studies strongly suggest a genetic basis with a complex mode of inheritance. More research is needed to explore environmental factors that could be contributing to the cause of these disorders. The occurrence of ASD has been increasing worldwide, with the most recent prevalence studies indicating that they are present in 6 per 1000 children. The objectives of this article are to provide physicians with relevant information needed to identify and refer children presenting with symptoms suggestive of ASDs to specialized centers early, and to make them feel comfortable in dealing with public concerns regarding controversial issues about the etiology and management of these disorders.

As the rate of autism spectrum disorders rises, parents are searching for answers. In this article, a small study that fueled the belief in an association between autism and vaccines is reviewed, and the scientific evidence regarding the relationship between autism and vaccines is explored.

We compiled data included in the Primal Health Research Database (www.primalhealthresearch.com) to test the hypothesis that when two pathological conditions or personality traits share the same critical period for gene-environment interaction, we should expect further similarities, particularly from clinical and pathophysiological perspectives. The keywords 'autism' and 'anorexia nervosa'(but not bulimia nervosa) lead to studies suggesting that for both conditions the perinatal period is critical. We take this example to look at other possible links between these pathological entities. From a clinical perspective, several teams have independently emphasized the importance of autistic traits in anorexia nervosa. Deficits in the processing of oxytocin have been demonstrated in both cases. Autistic groups have significantly lower blood oxytocin levels than normal groups, and oxytocin levels increase with age in the normal group only. In autistic groups there is a high ratio of intermediates of oxytocin synthesis (OX-T) to the nonapeptide oxytocin (OT). On the other hand, it has been reported that the level of oxytocin in the cerebrospinal fluid of anorexic women is significantly lower than the level of oxytocin in bulimic and control subjects. Scanning data reveal similar asymmetric functions with left hemisphere preponderance in autistic spectrum disorders and anorexia. A comparative study of the mirror neurons systems is another promising avenue for research. Such an accumulation of similarities from a great diversity of perspectives suggests that anorexia nervosa might be considered a female variant of the autistic spectrum. A plausible interpretation is that prenatal exposure to male hormones might protect against the expression of this disease: girls who have a twin brother are at low risk for anorexia nervosa, compared with girls who have a twin sister, and with controls; furthermore genetic linkage analyses do not detect change on the X chromosome. From an overview of the database, the perinatal period appears to be critical for all disorders related to the capacity to love (including love of oneself), to the potential for aggression (including self-destructive behaviours), or to sociability. Is the perinatal period critical for the organisation of the oxytocin system? This is an important question at a time when we learn that the widely used synthetic oxytocin can probably diffuse across the placenta. On the other hand, where the genesis of metabolic types is concerned, it is prenatal life that appears to be critical.

PURPOSE OF REVIEW: Autism is a biologically based disorder of brain development. Genetic factors - mutations, deletions, and copy number variants - are clearly implicated in causation of autism. However, they account for only a small fraction of cases, and do not easily explain key clinical and epidemiological features. This suggests that early environmental exposures also contribute. This review explores this hypothesis. RECENT FINDINGS: Indirect evidence for an environmental contribution to autism comes from studies demonstrating the sensitivity of the developing brain to external exposures such as lead, ethyl alcohol and methyl mercury. But the most powerful proof-of-concept evidence derives from studies specifically linking autism to exposures in early pregnancy - thalidomide, misoprostol, and valproic acid; maternal rubella infection; and the organophosphate insecticide, chlorpyrifos. There is no credible evidence that vaccines cause autism. SUMMARY: Expanded research is needed into environmental causation of autism. Children today are surrounded by thousands of synthetic chemicals. Two hundred of them are neurotoxic in adult humans, and 1000 more in laboratory models. Yet fewer than 20% of high-volume chemicals have been tested for neurodevelopmental toxicity. I propose a targeted discovery strategy focused on suspect chemicals, which combines expanded toxicological screening, neurobiological research and prospective epidemiological studies.

Schultz et al (2008) raised the question whether regression into autism is triggered, not by the measles-mumps-rubella (MMR) vaccine, but by acetaminophen (Tylenol) given for its fever and pain. Considerable evidence supports this contention, most notably the exponential rise in the incidence of autism since 1980, when acetaminophen began to replace aspirin for infants and young children. The impetus for this shift - a Centers for Disease Control and Prevention warning that aspirin was associated with Reye's syndrome - has since been compellingly debunked. If aspirin is not to be feared as a cause of Reyes syndrome, and acetaminophen is to be feared as a cause of autism, can the autism epidemic be reversed by replacing acetaminophen with aspirin or other remedies?

INTRODUCTION: Measles virus causes an estimated 30 million infections and 770,000 deaths a year worldwide, with increased risks of neurological, respiratory, and bleeding complications in survivors. Mumps can cause neurological problems and hearing loss, orchitis with infertility, and pancreatitis. Rubella infection is usually mild, but can lead to fetal death or severe congenital abnormalities if contracted in early pregnancy. The incidence of all three infections has decreased significantly in countries with routine vaccination programmes targeted at these diseases, but decreased vaccination rates are associated with increased risks of infection. METHODS AND OUTCOMES: We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of measles, mumps, and rubella vaccination? We searched: Medline, Embase, The Cochrane Library and other important databases up to July 2006 (Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA). RESULTS: We found 94 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions. CONCLUSIONS: In this systematic review we present information relating to the effectiveness and safety of the following interventions: MMR vaccine, monovalent measles vaccine, monovalent mumps vaccine, and monovalent rubella vaccine.

Revisions to the Centers for Disease Control and Prevention's pediatric immunization guidelines have generated a renewed focus on controversies associated with the nation's childhood vaccination program. Among these issues are adherence with and access to required vaccinations, concerns about individuals' rights in relation to government-mandated vaccinations, ongoing worry about adverse effects associated with immunizations, and questions about how best to protect immunocompromised and ill children. This article addresses these questions and presents strategies that can be used by clinicians to improve adherence with vaccination guidelines.

Although child vaccination rates remain high, some parental concern persists that vaccines might cause autism. Three specific hypotheses have been proposed:(1) the combination measles-mumps-rubella vaccine causes autism by damaging the intestinal lining, which allows the entrance of encephalopathic proteins;(2) thimerosal, an ethylmercury-containing preservative in some vaccines, is toxic to the central nervous system; and (3) the simultaneous administration of multiple vaccines overwhelms or weakens the immune system. We will discuss the genesis of each of these theories and review the relevant epidemiological evidence.

The renin–angiotensin system (RAS) regulates blood pressure mainly via the actions of angiotensin (Ang)II, generated via angiotensin converting enzyme (ACE). The ACE homologue ACE2 metabolises AngII to Ang1-7, decreasing AngII and increasing Ang1-7, which counteracts AngII activity via the Mas receptor. However, ACE2 also converts AngI to Ang1-9, a poorly characterised peptide which can be further converted to Ang1-7 via ACE. Ang1-9 stimulates bradykinin release in endothelium and has antihypertrophic actions in the heart, attributed to its being a competitive inhibitor of ACE, leading to decreased AngII, rather than increased Ang1-7. To date no direct receptor-mediated effects of Ang1-9 have been described. To further understand the role of Ang1-9 in RAS function we assessed its action in cardiomyocyte hypertrophy in rat neonatal H9c2 and primary adult rabbit left ventricular cardiomyocytes, compared to Ang1-7. Cardiomyocyte hypertrophy was stimulated with AngII or vasopressin, significantly increasing cell size by approximately 1.2-fold (P < 0.05) as well as stimulating expression of the hypertrophy gene markers atrial natriuretic peptide, brain natriuretic peptide, β-myosin heavy chain and myosin light chain (2- to 5-fold, P < 0.05). Both Ang1-9 and Ang1-7 were able to block hypertrophy induced by either agonist (control, 186.4 μm; AngII, 232.8 μm; AngII+Ang1-7, 198.3 μm; AngII+Ang1-9, 195.9 μm; P < 0.05). The effects of Ang1-9 were not inhibited by captopril, supporting previous evidence that Ang1-9 acts independently of Ang1-7. Next, we investigated receptor signalling via angiotensin type 1 and type 2 receptors (AT1R, AT2R) and Mas. The AT1R antagonist losartan blocked AngII-induced, but not vasopressin-induced, hypertrophy. Losartan did not block the antihypertrophic effects of Ang1-9, or Ang1-7 on vasopressin-stimulated cardiomyocytes. The Mas antagonist A779 efficiently blocked the antihypertrophic effects of Ang1-7, without affecting Ang1-9. Furthermore, Ang1-7 activity was also inhibited in the presence of the bradykinin type 2 receptor antagonist HOE140, without affecting Ang1-9. Moreover, we observed that the AT2R antagonist PD123,319 abolished the antihypertrophic effects of Ang1-9, without affecting Ang1-7, suggesting Ang1-9 signals via the AT2R. Radioligand binding assays demonstrated that Ang1-9 was able to bind the AT2R (pKi = 6.28 ± 0.1). In summary, we ascribe a direct biological role for Ang1-9 acting via the AT2R. This has implications for RAS function and identifying new therapeutic targets in cardiovascular disease.

We present an empirical scaling law that models the increased energy required for launching a soliton into an optical system with sections of both normal and anomalous dispersion fiber. It is shown that the inclusion of periodic attenuation and amplification can be handled as separate problems, provided that the interval between optical amplifiers is substantially different from the period of the dispersion map. These concepts are illustrated by reference to an example system comprising dispersion-shifted fiber combined with anomalous standard fiber.

We analytically and numerically analyze the occurrence of modulational instability in fibers with periodic changes in the group-velocity dispersion. For small variations, a set of resonances occurs in the gain spectrum. However, large dispersion variations eliminate these resonances and restrict the bandwidth of the fundamental gain spectrum. This research has been motivated by the adoption of dispersion management techniques in long-haul optical communications.

We investigate the stability of dark solitons with respect to periodic amplification by studying sideband generation. It is shown that these sidebands grow exponentially as a result of a four-wave mixing process with the cw background. We derive expressions for the positions of the sidebands and present numerical simulations that are in excellent agreement with the theoretical description. A comparison is made with bright solitons, showing that dark soliton propagation is less perturbed only over very short amplifier chains. We also relate our results to laser cavities and discuss the prospects for dark soliton lasers.

We study analytically and numerically the interaction of adjacent solitons under the influence of a phase modulator. Above a critical value, a bifurcation takes place and the interaction-free lengths are considerably increased.

We identified double and triple antibiotic combinations effective against biofilm-grown Burkholderia cepacia and Pseudomonas aeruginosa sampled from cystic fibrosis (CF) patients undergoing acute pulmonary exacerbations. Sputum bacteria from 110 CF patients were grown as biofilms. Combination antibiotic susceptibility testing was used to test 94 double and triple antibiotic combinations. Biofilm-grown bacterial isolates were less susceptible to antibiotic combinations compared to the same bacterial isolates grown planktonically (P < 0.001). Fifty-nine percent of biofilm-grown B. cepacia isolates and 29% of P. aeruginosa isolates were resistant to all double antibiotic combinations tested. Triple antibiotic combinations were more effective than double antibiotic combinations against biofilms (P < 0.0001). For P. aeruginosa biofilms, the addition of azithromycin or rifampin to otherwise effective antibiotic combinations was frequently associated with antagonism. Bacterial biofilms of CF organisms are highly resistant to antibiotics. This study identified potentially effective antibiotic combinations to guide the empirical treatment of CF pulmonary exacerbations.

Background and purpose:The epithelial sodium channel (ENaC) is a key regulator of airway mucosal hydration and mucus clearance. Negative regulation of airway ENaC function is predicted to be of clinical benefit in the cystic fibrosis lung. The aim of this study was to develop a small animal model to enable the direct assessment of airway ENaC function in vivo.Experimental approach:Tracheal potential difference (TPD) was utilized as a measure of airway epithelial ion transport in the guinea-pig. ENaC activity in the trachea was established with a dose-response assessment to a panel of well-characterized direct and indirect pharmacological modulators of ENaC function, delivered by intra-tracheal (i.t.) instillation.Key results:The TPD in anaesthetized guinea-pigs was attenuated by the direct ENaC blockers: amiloride, benzamil and CF552 with ED(50) values of 16, 14 and 0.2 mug kg(-1)(i.t.), respectively. 5-(N-Ethyl-N-isopropyl) amiloride, a structurally related compound but devoid of activity on ENaC, was without effect on the TPD. Intra-tracheal dosing of the Kunitz-type serine protease inhibitors aprotinin and placental bikunin, which have previously been demonstrated to inhibit proteolytic activation of ENaC, likewise potently attenuated TPD in guinea-pigs, whereas alpha(1)-antitrypsin and soya bean trypsin inhibitor were without effect.Conclusions and implications:The pharmacological sensitivity of the TPD to amiloride analogues and also to serine protease inhibitors are both consistent with that of ENaC activity in the guinea-pig trachea. The guinea-pig TPD therefore represents a suitable in vivo model of human airway epithelial ion transport.British Journal of Pharmacology advance online publication, 22 September 2008; doi:10.1038/bjp.2008.363.

Residual frequency shifts that are due to two-soliton collisions in stepwise exponentially dispersion-tapered fiber are calculated. Two-step dispersion profiles to minimize the frequency shifts and associated timing jitter are specifically identified. These profiles will improve the performance of wavelength-division-multiplexed soliton systems and permit operation with longer amplifier spans over an increased bandwidth.

BACKGROUND:: Extramural vascular invasion (EMVI) is a poor prognostic feature in colorectal cancer. The accuracy of magnetic resonance imaging (MRI) in detecting EMVI and predicting relapse-free survival (RFS) was compared retrospectively with the histological reference standard. METHODS:: Preoperative magnetic resonance images from patients diagnosed with rectal and sigmoid cancer were reviewed and an MRI-EMVI score (range 0 to 4) was assigned. Comparison was made with histology and clinical outcome. RESULTS:: Some 142 patients with a median follow-up of 3.3 (range 0.9-5.7) years were reviewed. Histological EMVI was reported in a quarter of patients. The sensitivity and specificity of MRI detection of EMVI in 94 patients undergoing primary surgery were 62 and 88 per cent respectively. On univariable analysis, RFS at 3 years was 35 per cent for patients with an MRI-EMVI score of 3-4, compared with 74 per cent for those with a score of 0-2 (P < 0.001), similar to values in patients with positive and negative histological EMVI status respectively (34 versus 73.7 per cent; P < 0.001). CONCLUSION:: High MRI-EMVI scores may help in predicting disease relapse. Copyright (c) 2007 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.

BACKGROUND Vaccines are valuable, cost-effective tools for preventing disease and improving community health. Despite the importance and ubiquity of vaccinations, childhood immunization coverage rates vary widely by geography, race, and ethnicity. These differences have been documented for nearly two decades, but their sources are poorly understood. Between 2005 and 2008, immunization staff of the National Association of County & City Health Officials (NACCHO) visited 17 local health department (LHD) immunization programs in 10 states to assess their immunization service delivery (ISD) practices and their impact on community childhood immunization coverage rates. PURPOSE To qualitatively characterize LHD immunization programs and specific organizational factors underlying ISD performance challenges and successes related to community childhood immunization coverage rates. METHODS Case studies were conducted in a convenience sample of 17 geographically and demographically diverse LHDs, predicated on each LHD's childhood immunization coverage rates per data from the National Immunization Survey and/or Kindergarten Retrospective Survey. NACCHO staff selected LHDs with high (> or = 80% up to date [UTD]), moderate (> or = 75% UTD but < 80% UTD), and low (< 75% UTD) coverage rates. All immunization staff members interviewed (n = 112) were included in focus group interviews at each LHD per a standard semi-structured interview script developed by NACCHO staff. Supporting documents from each LHD immunization program were also collected for inclusion in the analysis. Content and thematic analyses of interview transcripts and supporting documents were conducted. RESULTS Two thematic dimensions and six key factors emerged from the data. The dimensions of the themes were success and challenge elements. The organizational factors that were associated with success and/or challenges with regard to improving childhood immunization coverage rates included 1) leadership: organizational leadership and management related to aligning ISD with other child-focused services within the LHD; 2) resources: organizational efforts focused on aligning federal and state ISD financing with local ISD needs; 3) politics: political advocacy and partnering with local community stakeholders, including local political entities and boards of health to better organize ISD; 4) community engagement/coalitions and partnerships: partnerships, coalitions, and community engagement to support local immunization-related decision-making and prioritization; 5) credibility: agency credibility and its ability to influence community attitudes and perspectives on the health department's value in terms of child health; and 6) cultural competency of LHD staff: LHD staff members' perceptions and understandings of its community's cultural, economic, and demographic attributes shaped their responses to and understandings of the community and how they interacted with it in terms of service delivery. DISCUSSION Public health researchers are in a nascent stage of understanding how health department organizational factors may contribute to specific community health outcomes, such as childhood immunization coverage rates. An implicit challenge to LHD immunization programs is to implement strategies that lead to equitable and high vaccination coverage among children, despite shrinking resources and community demographic differences. Community-specific attributes (e.g., poverty, lack of health insurance, or geographic isolation) affect childhood immunization coverage rates, but internal LHD aspects such as leadership and organizational culture also likely have a significant impact.

BACKGROUND The incidence and prevalence of autism have dramatically increased over the last 20 years. Decomposition of autism incidence rates into age, period and cohort effects disentangle underlying domains of causal factors linked to time trends. We estimate an age-period-cohort effect model for autism diagnostic incidence overall and by level of functioning. METHODS Data are drawn from sequential cohorts of all 6 501 262 individuals born in California from 1992 to 2003. Autism diagnoses from 1994 to 2005 were ascertained from the California Department of Development Services Client Development and Evaluation Report. RESULTS Compared with those born in 1992, each successively younger cohort has significantly higher odds of an autism diagnosis than the previous cohort, controlling for age and period effects. For example, individuals born in 2003 have 16.6 times the odds of an autism diagnosis compared with those born in 1992 [95% confidence interval (CI) 7.8-35.3]. The cohort effect observed in these data is stronger for high than for low-functioning children with an autism diagnosis. Discussion Autism incidence in California exhibits a robust and linear positive cohort effect that is stronger among high-functioning children with an autism diagnosis. This finding indicates that the primary drivers of the increases in autism diagnoses must be factors that:(i) have increased linearly year-to-year;(ii) aggregate in birth cohorts; and (iii) are stronger among children with higher levels of functioning.

This article presents a population-based study of early childhood injury mortality following a nonfatal allegation of maltreatment. Findings are based on a unique data set constructed by establishing child-level linkages between vital birth records, administrative child protective services records, and vital death records. These linked data reflect over 4.3 million children born in California between 1999 and 2006 and provide a longitudinal record of maltreatment allegations and death. Of interest was whether children reported for nonfatal maltreatment subsequently faced a heightened risk of unintentional and intentional injury mortality during the first 5 years of life. Findings indicate that after adjusting for risk factors at birth, children with a prior allegation of maltreatment died from intentional injuries at a rate that was 5.9 times greater than unreported children (95% CI [4.39, 7.81]) and died from unintentional injuries at twice the rate of unreported children (95% CI [1.71, 2.36]). A prior allegation to CPS proved to be the strongest independent risk factor for injury mortality before the age of five.

BACKGROUND Studies of season of birth or season of conception can provide clues about etiology. We investigated whether certain months or seasons of conception are associated with increased risk of autism spectrum disorders, for which etiology is particularly obscure. METHODS The study population comprises 6,604,975 children born from 1990 to 2002 in California. Autism cases (n = 19,238) were identified from 1990 through 2008 in databases of the California Department of Developmental Services, which coordinates services for people with developmental disorders. The outcome in this analysis was autism diagnosed before the child's sixth birth date. The main independent variables were month of conception and season of conception (winter, spring, summer, and fall). Multivariate logistic regression models were used to estimate odds ratios (ORs) with their 95% confidence intervals (CIs) for autism by month of conception. RESULTS Children conceived in December (OR = 1.09 [95% CI = 1.02-1.17]), January (1.08 [1.00-1.17]), February (1.12 [1.04-1.20]), or March (1.16 [1.08-1.24]) had higher risk of developing autism compared with those conceived in July. Conception in the winter season (December, January, and February) was associated with a 6%(OR = 1.06, 95% CI = 1.02-1.10) increased risk compared with summer. CONCLUSIONS Higher risks for autism among those conceived in winter months suggest the presence of environmental causes of autism that vary by season.

BACKGROUND Menarche is an important indicator for assessing the developmental status of pubertal girls. Despite its importance, there is no nationwide information on menarcheal age in Turkey. AIM This paper is the first attempt to examine age at menarche for Turkey as a whole. The aim is to present the secular trend of menarcheal age and variations across different socio-demographic groups. METHODS Data were employed from the Turkey Demographic and Health Survey, 2008. Mean menarcheal ages were estimated for birth cohorts and socio-demographic sub-groups. The pace of decline in menarcheal age has been estimated using multiple linear regression analysis, controlling for year of birth and other variables. RESULTS Mean age at menarche was estimated as 13.30 (95% CI = 13.26-13.35). It was estimated as 13.17 years (95% CI 12.95-13.38) for the youngest birth cohort (1989-1993), as opposed to 13.44 (95% CI 13.37-13.52) years for the cohort born in 1959-1968. CONCLUSION Regression analysis indicated a decrease of 1.44 months per decade, providing evidence of a secular trend in menarcheal age in Turkey. Further results suggested childhood place of residence, education, welfare status and number of siblings to be significantly associated with menarcheal age.

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Abstract Weinbruch, Stephan, and Karl-Christian Nordby. Fatal accidents among elite mountaineers: a historical perspective from the European Alps. High Alt. Med. Biol. 11:147-151, 2010.- The lifetime risk of a fatal mountain accident among elite European alpine mountaineers and its time trends are determined by studying a fixed cohort of 390 elite mountaineers listed in the Encyclopaedia of the Alps (Hiebler, 1977). At publication of the encyclopaedia, 158 individuals were still living and were followed up until the end of 2008. The crude lifetime risk of a fatal accident for elite mountaineers is 0.203 [95% confidence interval (CI), 0.165 to 0.246). The difference in mortality between male (0.207; 95% CI: 0.168 to 0.251) and female mountaineers (0.118; 95% CI: 0.033 to 0.343) is not statistically significant. No fatal accidents occurred among elite mountaineers born before 1820. For the birth cohort from 1820 to 1949, the lifetime risk of a fatal accident (male mountaineers only) increased with time from 0.069 (95% CI, 0.019 to 0.220) to 0.375 (95% CI, 0.212 to 0.573). For all time strata, the highest risk of a fatal mountain accident was observed at an age of 30 to 39 yr. The high mortality among elite mountaineers clearly demonstrates that the limits of human performance are reached by these activities. The high risks should be communicated and should motivate risk-reduction efforts for this highly exposed subgroup of mountaineers.

BACKGROUND:: The present study describes the rate and trends of childhood hospitalizations with Kawasaki syndrome (KS) in the United States. METHODS:: Retrospective analysis of hospitalizations with KS among children <18 years of age in the United States using the Kids' Inpatient Database (1997, 2000, 2003, and 2006) and the Nationwide Inpatient Sample (1998-2007). RESULTS:: The KS-associated hospitalization rate for children <5 years of age was 20.8 (95% CI: 18.5-23.1) per 100,000 children in 2006. Annual rates remained constant during the study period, except for a peak in 2005. In 2006, 76.8%(SE = 0.9%) of an estimated 5523 (SE = 289) KS-associated hospitalizations among children <18 years of age were <5 years of age. The mean age for all children at hospitalization was 1.6 years (SE <0.1); 25.7 months (SE = 0.3) for children <5 years of age, and 24.8 months (SE = 0.4) and 27.1 months (SE = 0.5) for boys and girls, respectively. The rate for boys was higher than that for girls (24.2 [95% CI: 21.3-27.1] and 16.8 [95% CI: 14.7-18.9], respectively). The rate for Asian/Pacific Islander children (30.3 [95% CI: 20.2-40.4]) was the highest among the racial groups. CONCLUSIONS:: The national KS-associated annual hospitalization rate for children <5 years of age from 1997 to 2007 was relatively stable and was similar to previously published rates, except for an increase in 2005. Most hospitalizations were in children <3 years of age with few hospitalizations during the first 2 months of age. Children of Asian/Pacific Islander descent had the highest hospitalization rate.

We investigated if shifts in the coding of qualifying conditions in the California Department of Developmental Services (DDS) have contributed to the increase in California children with autism observed in recent years. Qualifying condition codes for mental retardation (MR) and autism in DDS electronic files were compared to hard-copy records for samples of children born 1987, 1990, 1994, and 1997. Contrary to expectations, we did not find evidence of a coding shift from "MR only" to "both MR and autism" or an increase in the proportion of children with coded autism who lacked supportive diagnostic documentation in records (possible "misclassifications"). These results indicate that changes in DDS coding practices are unlikely to explain the increase in DDS clients with autism.

Aim To estimate the prevalence of major birth defects among children with autism, the prevalence of autism in children with birth defects, and the risk for autism associated with having birth defects. Method Retrospective cohort including all children born in Atlanta, GA, USA, 1986 to 1993, who survived to age 3 years and were identified through Georgia vital records. Children with autism and other developmental disabilities residing in Atlanta at ages 3 to 10 years in 1996 were identified through the Metropolitan Atlanta Developmental Disabilities Surveillance Program. Children with major birth defects through age 6 years were identified by the Metropolitan Atlanta Congenital Defects Program. Results Birth defects were found among 6% of children with autism (total n=617; 488 males, 129 females) and was associated with a near twofold increased risk for autism overall. However, the risk magnitude and statistical significance varied by type of birth defect. With any type of birth defect, the risk for autism accompanied by intellectual disability or other developmental disabilities was typically higher than the risk for autism alone. A 6:1 to 8:1 male bias was observed among children with autism and a birth defect. Interpretation Investigation of the association between autism and birth defects is warranted, especially for the role of birth defects in autism among sex-specific or autism subgroups.