is an expert in gastroesophageal reflux disease and aerodigestive disorders. Yvan Vandenplas MD, PhD: YV is an expert in gastroesophageal reflux disease. Maartje Singendonk MD: MS is an expert in esophageal physiology. Michael Cabana MD: MC is a pediatrician with expertise in consensus guideline Carlo Di Lorenzo MD: CD is an expert in pediatric motility disorders and gastroesophageal reflux disease Frederic Gottrand MD: FG is an expert in esophagitis and gastroesophageal reflux disease Sandeep Gupta MD: SG is an expert in esophageal diseases. Miranda Langendam PhD: ML is aguideline methodologist Annamaria Staiano MD: AS is an expert in pediatric motility disorders and gastroesophageal reflux disease. Nikhil Thapar MD: NT is an expert in pediatric motility disorders. Neelesh Tipnis MD: NT is an expert in pediatric motility disorders. Merit Tabbers MD, PhD: MT is an expert in gastroesophageal reflux disease.
Gastroesophageal reflux (GER), defined as passage of gastric contents into the esophagus, and GER disease (GERD), defined as symptoms or complications of GER, are common pediatric problems encountered by both primary and specialty medical providers. Clinical manifestations of GERD in children include vomiting, poor weight gain, dysphagia, abdominal or substernal pain, esophagitis and respiratory disorders. The GER Guideline Committee of the North American Society for Pediatric Gastroenterology and Nutrition has formulated a clinical practice guideline for the management of pediatric GER. The GER Guideline Committee, consisting of a primary care pediatrician, two clinical epidemiologists (who also practice primary care pediatrics) and five pediatric gastroenterologists, based its recommendations on an integration of a comprehensive and systematic review of the medical literature combined with expert opinion. Consensus was achieved through Nominal Group Technique, a structured quantitative method. The Committee examined the value of diagnostic tests and treatment modalities commonly used for the management of GERD, and how those interventions can be applied to clinical situations in the infant and older child. The guideline provides recommendations for management by the primary care provider, including evaluation, initial treatment, follow-up management and indications for consultation by a specialist. The guideline also provides recommendations for management by the pediatric gastroenterologist. This document represents the official recommendations of the North American Society for Pediatric Gastroenterology and Nutrition on the evaluation and treatment of gastroesophageal reflux in infants and children. The American Academy of Pediatrics has also endorsed these recommendations. The recommendations are summarized in a synopsis within the article. This review and recommendations are a general guideline and are not intended as a substitute for clinical judgment or as a protocol for the management of all patients with this problem.
This clinical practice guideline for the diagnosis and treatment of acute hematogenous osteomyelitis (AHO) in children was developed by a multidisciplinary panel representing Pediatric Infectious Diseases Society (PIDS) and the Infectious Diseases Society of America (IDSA). This guideline is intended for use by healthcare professionals who care for children with AHO, including specialists in pediatric infectious diseases, orthopedics, emergency care physicians, hospitalists, and any clinicians and healthcare providers caring for these patients. The panel’s recommendations for the diagnosis and treatment of AHO are based upon evidence derived from topic-specific systematic literature reviews. Summarized below are the recommendations for the diagnosis and treatment of AHO in children. The panel followed a systematic process used in the development of other IDSA and PIDS clinical practice guidelines, which included a standardized methodology for rating the certainty of the evidence and strength of recommendation using the GRADE (Grading of Recommendations Assessment, Development and Evaluation) approach. A detailed description of background, methods, evidence summary and rationale that support each recommendation, and knowledge gaps can be found online in the full text.
ABSTRACT. Fatal lead encephalopathy has disappeared and blood lead concentrations have decreased in US children, but approximately 25% still live in housing with deteriorated lead-based paint and are at risk of lead exposure with resulting cognitive impairment and other sequelae. Evidence continues to accrue that commonly encountered blood lead concentrations, even those less than 10 g/dL, may impair cognition, and there is no threshold yet identified for this effect. Most US children are at sufficient risk that they should have their blood lead concentration measured at least once. There is now evidence-based guidance available for managing children with increased lead exposure. Housing stabilization and repair can interrupt exposure in most cases. The focus in childhood lead-poisoning policy, however, should shift from case identification and management to primary prevention, with a goal of safe housing for all children.
An immunohistochemical analysis of skin biopsies was performed in 18 patients with cutaneous lupus erythematosus (LE), using the alkaline phosphatase and monoclonal anti-alkaline phosphatase method (APAAP). The study group was subdivided on the basis of clinical criteria into 10 patients with chronic discoid LE (CDLE) and eight patients with subacute cutaneous LE (SCLE). Using a panel of monoclonal antibodies the following results were obtained: (i) ICAM-1 was expressed on epidermal keratinocytes, dermal inflammatory cells, and endothelial cells in most biopsies, whereas LFA-1 was confined to the dermis. Attachments between keratinocytes or endothelial cells and activated T lymphocytes via ICAM-1/LFA-1 may be a possible mechanism of target/effector recognition in cutaneous LE. (ii) HLA-DR was expressed on epidermal keratinocytes and cells of the dermal infiltrate, but not on endothelial cells. HLA-DR+ cells probably function as antigen-presenting cells, leading to major histocompatibility complex-restricted cellular cytotoxicity in cutaneous LE. (iii) Interleukin 2 receptor expression on dermal inflammatory cells was weak, indicating non-specific activation of T lymphocytes. (iv) The dermal inflammatory cells were T lymphocytes, mainly of the helper/inducer subtype. B lymphocytes were rarely found in the dermis. In general, no significant immunohistochemical differences were found between CDLE and SCLE, suggesting that these variants represent clinical subtypes rather than different pathogenetic entities.
Molds are multicellular fungi that are ubiquitous in outdoor and indoor environments. For humans, they are both beneficial (for the production of antimicrobial agents, chemotherapeutic agents, and vitamins) and detrimental. Exposure to mold can occur through inhalation, ingestion, and touching moldy surfaces. Adverse health effects may occur through allergic, infectious, irritant, or toxic processes. The cause-and-effect relationship between mold exposure and allergic and infectious illnesses is well known. Exposures to toxins via the gastrointestinal tract also are well described. However, the cause-and-effect relationship between inhalational exposure to mold toxins and other untoward health effects (eg, acute idiopathic pulmonary hemorrhage in infants and other illnesses and health complaints) is controversial and requires additional investigation. In this report we examine evidence of fungal-related illnesses and the unique aspects of mold exposure to children. Mold-remediation procedures are also discussed.
BACKGROUND
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