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The prevalence of gastrointestinal abnormalities in individuals with ASDs is incompletely understood.

The reported prevalence of gastrointestinal symptoms in children with ASDs has ranged from 9% to 70% or higher (Table 4 ). 13 , 16 25 Prospective descriptive reports from autism clinics have described significant gastrointestinal symptoms in at least 70% of patients, 22 data that might reflect a referral bias. In contrast, secondary analysis of a UK database indicated that the prevalence of gastrointestinal symptoms was no different in children with ASDs compared with children without ASDs (9%) at the time of their initial ASD diagnosis. 16

View this table:
TABLE 4

Prevalence of Gastrointestinal Symptoms in Individuals With ASDs

Most of these studies had 1 or more methodologic limitations, in particular a lack of appropriate (nonrelated) control groups. Despite the limitations in type and quality of available evidence, the preponderance of data were consistent with the likelihood of a high prevalence of gastrointestinal symptoms and disorders associated with ASDs.

The panel agreed that to unequivocally answer the important question of prevalence of gastrointestinal dysfunction in this population, prospective multicenter studies need to be performed by using validated instruments and outcome measures administered to persons with a diagnosis of ASD established by accepted methods and appropriate control groups. Population-based studies are also needed to avoid referral bias and overestimation of the prevalence of gastrointestinal symptoms in patients with ASDs.

Statement 4

Some health care providers and researchers have proposed that certain gastrointestinal pathologies are specific to individuals with ASDs. An immune or inflammation-mediated mechanism specific to ASDs, possibly vaccine-triggered in the setting of abnormal immune function or increased gut permeability (“leaky gut”), has been hypothesized to underlie the gastrointestinal disorders seen in individuals with ASDs, mainly on the basis of a finding of ileal nodular lymphoid hyperplasia (NLH) and/or chronic colitis seen on colonoscopy.

In 1998, Wakefield et al reported an association between ileocolitis and developmental regression in 12 children and coined the term “autistic enterocolitis.” From the same uncontrolled study they reported NLH of the ileum and colon as an abnormal finding in most children with ASDs. However, similar findings are known to be present in children with typical development, as well as children with food allergies and immunodeficiencies. The significance of these findings, therefore, is unclear. Wakefield et al also proposed a causal relation between measles, mumps, and rubella (MMR) vaccination and autism, a suggestion that was later retracted by many of the original authors.

Other study-design limitations in these reports included flawed control groups, lack of validated and standardized definitions, and speculative interpretation of results. In summary, published reports have not established the presence of a unique gastrointestinal pathophysiology specific to ASDs.

Statement 5

Altered intestinal permeability was reported in 9 of 21 (43%) children with ASDs and 0 of 40 healthy age-matched controls. The authors of the study speculated that the alteration might be the mechanism for increased passage of food-derived peptides through a damaged gut mucosa. Increased permeability (or a “leaky gut”) has been cited as having a key role in various hypotheses regarding the biology of ASDs, including excess opiate activity, diminished peptidase activity, and immune dysfunction. Some investigators have reported decreased serum sulfate levels in children with ASDs and hypothesized a link between such deficits and increased gut permeability.

The available literature has not confirmed the presence of abnormal gastrointestinal permeability in individuals with ASDs, and the presence of increased intestinal permeability has not been correlated with an underlying gastrointestinal disorder or neuropsychiatric manifestations. Studies to date have had methodologic limitations including small subject populations and poor controls; properly powered prospective studies with appropriate controls are needed.

Statement 6

An emerging literature suggests that individuals with ASDs and gastrointestinal symptoms may be at higher risk for problem behaviors than those with ASDs who do not have gastrointestinal symptoms. Problem behaviors are recurrent behaviors that interfere with an individual's functioning; their occurrence often affects family and community members as well. Problem behaviors are the single most important factor in determining quality of life for individuals with ASDs and their caretakers. Vocal and motor behaviors, including problem behaviors such as self-injury and aggression, as well as overall changes in state of being (eg, sleep disturbance or irritability), may be behavioral manifestations of abdominal pain or discomfort in persons with ASDs (Table New Arrival Sale Online Womens Black tie up sequin embellished espadrilles River Island Cheap For Nice Sale Online Shop Cheap Sale Shop Buy Online New BH0C8
).

The evaluation of individuals with ASDs and gastrointestinal symptoms can be complex. Sleep disturbances and the other problem behaviors mentioned above may indicate abdominal discomfort. In turn, abdominal discomfort, as well as other symptoms (constipation, flatulence, bloating, diarrhea, straining), may be manifestations of neurenteric dysregulation or IBS. A diagnosis of exclusion, IBS is difficult to distinguish from other underlying conditions without invasive testing. For the patient who is not losing weight, has no blood in the stool, and has normal findings on a complete blood count and urinalysis, evaluations are recommended in the order described in Table 3 . No evidence-based guidelines are available to guide the evaluation. For this reason, primary care physicians, psychiatrists, psychologists, pediatricians, and gastroenterologists may need to work together to improve the evaluation and treatment of gastrointestinal symptoms in individuals with ASDs.

Statement 7

Clinical practice guidelines for the management of ASDs have not included routine consideration of potential gastrointestinal problems. As previously noted, for individuals with ASDs, symptoms associated with gastrointestinal disorders, especially pain, may function as setting events for problem behaviors. In this context, a setting event is any gastrointestinal symptom that influences how a person will respond to a given environment. For example, the presence of pain (a gastrointestinal setting event) can result in simple daily tasks and routines being perceived by the child as much more aversive than would be the case if the child were healthy and free of pain. As a consequence, these tasks and routines now trigger bouts of severe problem behavior as the child attempts to escape from the now-aversive situation. Once the gastrointestinal condition has been treated successfully, it is likely that pain will diminish, the situation will be perceived as less aversive, and the child will, therefore, no longer be motivated to engage in problem behavior. A review of both gastrointestinal symptoms and behaviors clinically associated with gastrointestinal problems (see Tables 2 and 3 ), along with other potential sources of pain and discomfort (such as ear, dental, urologic, musculoskeletal, and cutaneous problems), should be incorporated into the clinical behavioral assessment.

The presence of gastrointestinal symptoms and/or related behaviors (Table 3 ), regardless of whether they are clearly temporally related to problem behavior, should be considered a strong and urgent indication for medical investigation. Clinical judgment will determine if medical investigation should precede or occur concurrently with behavioral and/or psychopharmacologic intervention; the latter, however, should never substitute for medical investigation. Clearly, reliable biomarkers of gastrointestinal function are needed to identify those individuals who are highly likely to have conditions that may respond to medical or surgical intervention. Until such biomarkers are shown to be helpful, clinicians with expertise in both medical and behavioral interventions should work together on an integrated care plan.

Recognition that abdominal pain and discomfort can function as a setting event has important implications for the treatment of problem behavior. First, time-consuming behavioral treatments that address only psychosocial triggers and consequences for problem behavior may likely be ineffective. Behavioral treatments that promote means of communication in the affected individual may be more effective. For example, it would be extremely useful, from the standpoint of medical diagnosis, to teach a child to identify the location and type of pain that he or she is currently experiencing. Second, the individual can be taught skills for coping with task demands appropriately during moments of pain or discomfort, and psychosocial environments that have become aversive because of gastrointestinal pain can be restructured to attenuate their aversive properties. Third, if the gastrointestinal disorder is recognized and medical treatment is effective, the problem behaviors may diminish. When abdominal pain or discomfort is a setting event, psychotropic medications are likely to be ineffective and may even aggravate the problem if they have adverse gastrointestinal effects.

Statement 8

The clinical presentation of gastrointestinal disorders in individuals with ASDs may differ from that of individuals with typical development. For example, behavioral alterations can complicate the diagnosis of GERD in persons with compromised communication skills. Expert clinicians have observed that aggressive and self-injurious behavior may be the primary clinical manifestations of GERD in individuals with ASDs, but these symptoms are frequently attributed to nonmedical causes. As a result, manifestations may go unrecognized as signs and symptoms of GERD and, importantly, may go untreated. Caregivers should be informed about atypical manifestations of gastrointestinal disorders. Greater awareness of this association by health care providers may result in these conditions being diagnosed and treated in more affected individuals. Additional research is needed to evaluate the usefulness of adding behavior to screening for gastrointestinal problems in persons with ASDs.

Educational programs designed to increase awareness of medical conditions that can go unrecognized because of atypical symptom presentation should be a priority at meetings of professional societies such as the American Academy of Pediatrics, American Academy of Family Physicians, and National Association of Pediatric Nurse Practitioners.

Statement 9

Nutritional deficiencies have been reported in patients with ASDs, which is not surprising because of the narrow food preferences of many affected individuals and/or purported therapeutic diets that might be nutritionally inadequate. In a study of 36 children with ASDs, regardless of unrestricted or restricted diet, essential amino acid deficiencies consistent with poor protein nutrition occurred more frequently than in age- and gender-matched controls. Low dietary intake of calcium and vitamin D and iron deficiency have been implicated in compromised bone development and sleep disturbances, respectively, in children with ASDs receiving an unrestricted or restricted diet. Resources for general nutritional guidance are available that may be helpful for families.

Statement 10

It is recommended that pediatricians routinely monitor anthropometry as part of the evaluation of children with ASDs. Abnormalities in nutritional status (wasting, stunting) or changes in growth rate should alert the clinician to inadequate growth and the possibility of inadequate caloric intake or poor nutritional quality of the diet, malabsorption, or maldigestion. Any child whose growth is of concern should be referred to a nutritionist, preferably one who is familiar with nutritional support for individuals with ASDs.

In addition to nutritional inadequacy, children with ASDs have the potential to be obese. In a retrospective review of charts from 1992 to 2003 in children aged 3 to 18 years with ASDs, the prevalence rates of at risk for overweight (BMI ≥ 85th percentile) and overweight (BMI ≥ 95th percentile) were 35.7% and 19.0%, respectively. These prevalence data are similar to rates in children aged 6 to 19 years in the general population of 31.0% and 16.0% for at risk for overweight and overweight, respectively, in 1999–2002. However, children with ASDs in the 12- to 19-year age range were reported to have 80% and 50% rates of being at risk for overweight and overweight, respectively, compared with 30.9% and 16.1%, respectively, in the general population.

Statement 11

Dietary modifications such as removal of milk for symptoms of lactose intolerance may be approached empirically, as with any other pediatric patient with consistent symptoms. The data on the value of specific diets being effective in the treatment of individuals with ASDs are difficult to assess. Many dietary modifications are believed to have a beneficial outcome, although placebo effects are likely to be high in this setting. The few studies in the literature are difficult to interpret without adequate control groups.

Statement 12

Few studies have examined the effects of a casein-free diet, a gluten-free diet, or combined GFCF diet on the behavior of individuals with ASDs. To our knowledge, only 1 double-blind placebo-controlled study has been published to date.

In this double-blind crossover trial of GFCF or typical diet in 15 children with ASDs, there were no differences in measures of severity of ASD symptoms, communication, social responsiveness, and urinary peptide levels after 12 weeks. Nevertheless, after being informed of the results, 9 parents wanted to continue the diet and reported positive subjective clinical changes while their child was on the GFCF diet. Study limitations included the small sample size and heterogeneity, concerns about compliance and possible dietary infractions by study subjects, and lack of a direct observational outcome measure.

Parents need information to help plan a balanced diet within the restrictions imposed by the chosen diet. Given the real hardships associated with implementation of a strict GFCF diet, additional studies are needed to assess risk factors and possible markers that identify individuals who might benefit from these diets. The panel emphasized that parents and care providers should agree on objective measures, which ideally are to be evaluated by blinded observers, to assess the intervention effect as well as a reasonable time frame before embarking on restrictive or unusual diets. The current literature does not permit a recommendation as to the length of a trial of dietary intervention. In the absence of data, any trial will need to be long enough to ensure that variability in behavior is not responsible for the perceived diet response.

For patients with ASDs, a detailed history should be obtained to identify potential associations between allergen exposure and gastrointestinal and/or behavioral symptoms.

Analysis of the sequences from individual IgM + , Syndecan‐1‐expressing plasmablasts revealed the presence of mutations in the Sμ region, the majority of which were C to T transitions involving the AID hotspot motif WRC ( Table I ; Supplementary Figure S4 ). Importantly, this spectrum of mutations was dependent on AID, as similarly sorted cells from Aicda −/− cells exhibited no such mutations. The background mutations likely reflect Taq polymerase error. A total of 7% of IgM + plasmablasts have AID‐dependent mutations; given that only 21% of IgG1 + cells have AID‐dependent mutations, we estimate the fraction of IgM + cells passing through the CSR/SHM state to be 33% (7% normalized by 21%). This is a lower bound since we expect that sorting for cells that have not switched experimentally selects for a population that expressed AID for a shorter time. These single‐cell data substantiate the kinetic‐control scenario in the sense that a large fraction of IgM + plasma cells (cells that never completed CSR) followed a developmental trajectory through a state of transient AID activity accompanied by a probabilistic opportunity for CSR/SHM prior to terminal differentiation.

View this table:
Table 1. Analysis of AID‐dependent mutations in sorted B cells

To directly test a causal role for Irf4 expression levels in controlling B cell fate, we developed an experimental system that would afford control of Irf4 expression in naive primary B cells. We constructed a tet‐inducible system ( Beard et al , 2006 ) as follows; a cassette containing a tetracycline‐regulatable Irf4 transgene was recombined at a neutral, defined position downstream of the CollagenA1 locus using Flp‐mediated homologous recombination in ES cells ( Supplementary Figure S5 ). These cells were engineered to express the tetracycline‐dependent transactivator (M2rtTA) from the Rosa26 locus. Suitable ES cell clones ( Supplementary Figure S5 ) were used to transmit the tet‐regulatable Irf4 allele through the germline. When crossed to the Irf4 +/− background, both endogenous and transgene expression of Irf4 combine to attain higher than wild‐type expression levels. In contrast, when crossed to the Irf4 −/− background, Irf4 gene expression can be uncoupled from BCR as well as CD40 signaling, and a lower range of expression of IRF‐4 can be induced and maintained because the transgene is the sole source. In this way, the inducible‐ Irf4 allele enables a wide dynamic range of IRF‐4 production.

We first tested the dynamics of alternate cell fate choice as a consequence of inducing IRF‐4 expression in cells containing an endogenous wild‐type Irf4 allele. We purified B cells from the Irf4 ‐inducible mouse (on the Irf4 +/− background) and stimulated them with CD40L and IL‐4 in the presence of varying concentrations of a high‐affinity analog of tetracycline, doxycycline (DOX). Strikingly, increasing Irf4 expression levels induced by DOX resulted in markedly enhanced plasma‐cell generation that occurred at the expense of CSR ( Outlet Sale Online Womens Zeching Rubber Boots Giesswein Shop For Cheap Price Wiki Cheap Price Clearance Cheap Real kJTqDfVR
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). The lower panel shows the amount of IRF‐4 expression achieved by DOX at day 3 of differentiation. We next measured the effects of exogenously controlled Irf4 expression on the dynamics of network components ( Figure 5B and C ). At early time points, Pax5, Bach2 and AID are all induced to comparable levels regardless of DOX concentration, consistent with the kinetic‐control scenario. Downregulation of the CSR factors occurs only as Blimp‐1 levels rise at later time points.

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