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1.
J Allergy Clin Immunol Pract ; 7(6): 1970-1985.e4, 2019 Jul - Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30877075

RESUMO

BACKGROUND: Although autoimmunity and hyperinflammation secondary to recombination activating gene (RAG) deficiency have been associated with delayed diagnosis and even death, our current understanding is limited primarily to small case series. OBJECTIVE: Understand the frequency, severity, and treatment responsiveness of autoimmunity and hyperinflammation in RAG deficiency. METHODS: In reviewing the literature and our own database, we identified 85 patients with RAG deficiency, reported between 2001 and 2016, and compiled the largest case series to date of 63 patients with prominent autoimmune and/or hyperinflammatory pathology. RESULTS: Diagnosis of RAG deficiency was delayed a median of 5 years from the first clinical signs of immune dysregulation. Most patients (55.6%) presented with more than 1 autoimmune or hyperinflammatory complication, with the most common etiologies being cytopenias (84.1%), granulomas (23.8%), and inflammatory skin disorders (19.0%). Infections, including live viral vaccinations, closely preceded the onset of autoimmunity in 28.6% of cases. Autoimmune cytopenias had early onset (median, 1.9, 2.1, and 2.6 years for autoimmune hemolytic anemia, immune thrombocytopenia, and autoimmune neutropenia, respectively) and were refractory to intravenous immunoglobulin, steroids, and rituximab in most cases (64.7%, 73.7%, and 71.4% for autoimmune hemolytic anemia, immune thrombocytopenia, and autoimmune neutropenia, respectively). Evans syndrome specifically was associated with lack of response to first-line therapy. Treatment-refractory autoimmunity/hyperinflammation prompted hematopoietic stem cell transplantation in 20 patients. CONCLUSIONS: Autoimmunity/hyperinflammation can be a presenting sign of RAG deficiency and should prompt further evaluation. Multilineage cytopenias are often refractory to immunosuppressive treatment and may require hematopoietic cell transplantation for definitive management.

2.
Am J Hum Genet ; 104(3): 422-438, 2019 Mar 07.
Artigo em Inglês | MEDLINE | ID: mdl-30773277

RESUMO

SPONASTRIME dysplasia is an autosomal-recessive spondyloepimetaphyseal dysplasia characterized by spine (spondylar) abnormalities, midface hypoplasia with a depressed nasal bridge, metaphyseal striations, and disproportionate short stature. Scoliosis, coxa vara, childhood cataracts, short dental roots, and hypogammaglobulinemia have also been reported in this disorder. Although an autosomal-recessive inheritance pattern has been hypothesized, pathogenic variants in a specific gene have not been discovered in individuals with SPONASTRIME dysplasia. Here, we identified bi-allelic variants in TONSL, which encodes the Tonsoku-like DNA repair protein, in nine subjects (from eight families) with SPONASTRIME dysplasia, and four subjects (from three families) with short stature of varied severity and spondylometaphyseal dysplasia with or without immunologic and hematologic abnormalities, but no definitive metaphyseal striations at diagnosis. The finding of early embryonic lethality in a Tonsl-/- murine model and the discovery of reduced length, spinal abnormalities, reduced numbers of neutrophils, and early lethality in a tonsl-/- zebrafish model both support the hypomorphic nature of the identified TONSL variants. Moreover, functional studies revealed increased amounts of spontaneous replication fork stalling and chromosomal aberrations, as well as fewer camptothecin (CPT)-induced RAD51 foci in subject-derived cell lines. Importantly, these cellular defects were rescued upon re-expression of wild-type (WT) TONSL; this rescue is consistent with the hypothesis that hypomorphic TONSL variants are pathogenic. Overall, our studies in humans, mice, zebrafish, and subject-derived cell lines confirm that pathogenic variants in TONSL impair DNA replication and homologous recombination-dependent repair processes, and they lead to a spectrum of skeletal dysplasia phenotypes with numerous extra-skeletal manifestations.

3.
Pediatr Blood Cancer ; 66(4): e27602, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30609294

RESUMO

Allogeneic hematopoietic stem cell transplantation is curative for primary immunodeficiencies. Bone marrow from an unaffected human leukocyte antigen (HLA)-identical sibling donor is the ideal graft source. For minor donors, meaningful consent or assent may not be feasible, and permission from parents or legal guardians is considered acceptable. Adverse events, albeit extremely small, can be associated with bone marrow harvest in pediatric donors. Donor safety concerns potentially increase with multiple bone marrow harvests. Very little is known about multiple bone marrow harvests from pediatric donors. We describe the ethical considerations and clinical decision-making in an unusual clinical situation where three patients with the same primary immunodeficiency were HLA identical to one another and their younger sibling, who underwent bone marrow harvests three times between 1.3 and 4 years of age, resulting in successful transplantation for all three patients. We hope that this experience will provide guidance to providers and families in a similar situation.

4.
Tunis Med ; 96(10-11): 672-677, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30746660

RESUMO

INTRODUCTION: Primary Immunodeficiency (PIDs) is a set of 330 rare hereditary diseases that increase susceptibility to infections, allergies, autoimmunity, and neoplasia. North American registries give higher prevalence than Maghreb ones, whereas consanguinity is high. The purpose of this study is to compare prevalence and coverage rate of Maghreb PID registries with estimates based on USA. METHODS: We searched the prevalence of PIDs in the Maghreb registers. Next, we estimated the expected values based on recent publications. Finally, we calculated the coverage rate of the Maghreb registries compared to the new estimates and we evaluated the impact of consanguinity. RESULTS: The total number is N1 = 2456 patients. The current Maghreb PID Prevalence is 2.56 / 100,000 inhabitants (population of 94,804,694 Million in 2017). Tunisia leads with a prevalence of 8.70 followed by Morocco 2.09, Libya 1.65 and Algeria 1.46/100.000 habitants. We did not find values for Mauritania. If we extrapolate the prevalence of the USA to the Maghreb population, the number of patients in the Maghreb would be N2 = 27,588 and the coverage rate (N1 / N2) would be 8.90%. This low coverage rate is however better than the World average (1.21%), that of Latin America 1.19% and Africa 0.36%. The Maghreb prevalence is close to that of the Arab world 2.04 / 100,000 (population of 391,449,544 in 2017). Using the incidence found in the USA, the number of patients would be 9765 new patients per year in the Maghreb and 40,319 in Arab countries. CONCLUSION: PID Maghreb patients number is very low compared to global estimates, whereas consanguinity is very high. Special attention should be given to PIDs by governments and research teams in this region.


Assuntos
Síndromes de Imunodeficiência/epidemiologia , África/epidemiologia , África do Norte/epidemiologia , Argélia/epidemiologia , Ásia/epidemiologia , Consanguinidade , Europa (Continente)/epidemiologia , Humanos , Síndromes de Imunodeficiência/genética , Incidência , Oriente Médio/epidemiologia , Marrocos/epidemiologia , Prevalência , Sistema de Registros/estatística & dados numéricos , Estatística como Assunto/normas , Tunísia/epidemiologia , Estados Unidos/epidemiologia
5.
Adv Med Educ Pract ; 7: 597-602, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27799840

RESUMO

BACKGROUND: Food allergy is an increasing public health burden, and is considered among the most common chronic noncommunicable diseases in children. Proper diagnosis and management of food allergy by a health care provider is crucial in keeping affected children safe while simultaneously averting unnecessary avoidance. OBJECTIVE: The rationale of the study was to estimate the knowledge of pediatric residents and academic general pediatric fellows with regard to food allergies in children. METHODS: A cross-sectional and prospective study was carried out at Hamad Medical Corporation, the only tertiary care, academic and teaching hospital in the State of Qatar. The study took place between January 1, 2015 and September 30, 2015. RESULTS: Out of the 68 questionnaires distributed, 68 (100%) were returned by the end of the study. Among the participants, 15 (22%) were in post-graduate year-1 (PGY-1), 16 (23.5%) in PGY-2, 17 (25%) in PGY-3, 12 (16%) in PGY-4, and 8 (12%) were academic general pediatric fellows. Our trainees answered 60.14% of knowledge based questions correctly. In the section of treatment and management of food allergy in childhood, 23 (34%) of respondents' main concern when taking care of a patient with food allergies was making sure the patient is not exposed to food allergen, while 22 (33%) reported no concerns. In the section of treatment and management of food allergy in childhood, 22 (33%) of participants reported no concerns in taking care of a child with food allergy, while 23 (34%) of respondents' main concern was making sure the patient is not exposed to food allergen. In the teaching and training section, 56% of participants stated that they have not received formal education on how to recognize and treat food allergies, while 59% claimed not being trained on how to administer injectable epinephrine. Furthermore, approximately 60% of all participants expressed the need of additional information about recognizing and treating food allergies and recommended certification and regulation of food allergy training for all residents. CONCLUSION: There is an appreciable lack of knowledge in identifying food allergy and managing anaphylaxis reaction in children, among pediatric residents. Robust efforts should be implemented by attending immunologists to improve the lack of knowledge and improve the trainee's confidence when facing such cases.

7.
Blood ; 128(17): 2135-2143, 2016 10 27.
Artigo em Inglês | MEDLINE | ID: mdl-27557945

RESUMO

Cell motility, division, and structural integrity depend on dynamic remodeling of the cellular cytoskeleton, which is regulated in part by actin polymerization and depolymerization. In 3 families, we identified 4 children with recurrent infections and varying clinical manifestations including mild neutropenia, impaired wound healing, severe stomatitis with oral stenosis, and death. All patients studied had similar distinctive neutrophil herniation of the nuclear lobes and agranular regions within the cytosol. Chemotaxis and chemokinesis were markedly impaired, but staphylococcal killing was normal, and neutrophil oxidative burst was increased both basally and on stimulation. Neutrophil spreading on glass and cell polarization were also impaired. Neutrophil F-actin was elevated fourfold, suggesting an abnormality in F-actin regulation. Two-dimensional differential in-gel electrophoresis identified abnormal actin-interacting protein 1 (Aip1), encoded by WDR1, in patient samples. Biallelic mutations in WDR1 affecting distinct antiparallel ß-strands of Aip1 were identified in all patients. It has been previously reported that Aip1 regulates cofilin-mediated actin depolymerization, which is required for normal neutrophil function. Heterozygous mutations in clinically normal relatives confirmed that WDR1 deficiency is autosomal recessive. Allogeneic stem cell transplantation corrected the immunologic defect in 1 patient. Mutations in WDR1 affect neutrophil morphology, motility, and function, causing a novel primary immunodeficiency.


Assuntos
Citoesqueleto de Actina/patologia , Síndromes de Imunodeficiência/patologia , Transtornos Leucocíticos/genética , Proteínas dos Microfilamentos/genética , Neutrófilos/patologia , Criança , Eletroforese em Gel Bidimensional , Feminino , Predisposição Genética para Doença , Humanos , Immunoblotting , Síndromes de Imunodeficiência/imunologia , Transtornos Leucocíticos/imunologia , Transtornos Leucocíticos/patologia , Masculino , Espectrometria de Massas , Proteínas dos Microfilamentos/deficiência , Proteínas dos Microfilamentos/imunologia , Microscopia Confocal , Mutação , Neutrófilos/imunologia , Linhagem
8.
Blood ; 128(1): 45-54, 2016 07 07.
Artigo em Inglês | MEDLINE | ID: mdl-27129325

RESUMO

Adenosine deaminase (ADA) deficiency is a rare, autosomal-recessive systemic metabolic disease characterized by severe combined immunodeficiency (SCID). The treatment of choice for ADA-deficient SCID (ADA-SCID) is hematopoietic stem cell transplant from an HLA-matched sibling donor, although <25% of patients have such a donor available. Enzyme replacement therapy (ERT) partially and temporarily relieves immunodeficiency. We investigated the medium-term outcome of gene therapy (GT) in 18 patients with ADA-SCID for whom an HLA-identical family donor was not available; most were not responding well to ERT. Patients were treated with an autologous CD34(+)-enriched cell fraction that contained CD34(+) cells transduced with a retroviral vector encoding the human ADA complementary DNA sequence (GSK2696273) as part of single-arm, open-label studies or compassionate use programs. Overall survival was 100% over 2.3 to 13.4 years (median, 6.9 years). Gene-modified cells were stably present in multiple lineages throughout follow up. GT resulted in a sustained reduction in the severe infection rate from 1.17 events per person-year to 0.17 events per person-year (n = 17, patient 1 data not available). Immune reconstitution was demonstrated by normalization of T-cell subsets (CD3(+), CD4(+), and CD8(+)), evidence of thymopoiesis, and sustained T-cell proliferative capacity. B-cell function was evidenced by immunoglobulin production, decreased intravenous immunoglobulin use, and antibody response after vaccination. All 18 patients reported infections as adverse events; infections of respiratory and gastrointestinal tracts were reported most frequently. No events indicative of leukemic transformation were reported. Trial details were registered at www.clinicaltrials.gov as #NCT00598481.


Assuntos
Adenosina Desaminase/deficiência , Agamaglobulinemia/terapia , Terapia Genética , Recuperação de Função Fisiológica , Retroviridae , Imunodeficiência Combinada Severa/terapia , Adenosina Desaminase/genética , Adenosina Desaminase/imunologia , Agamaglobulinemia/genética , Agamaglobulinemia/imunologia , Agamaglobulinemia/mortalidade , Linfócitos B/imunologia , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD8-Positivos/imunologia , Criança , Pré-Escolar , Intervalo Livre de Doença , Feminino , Humanos , Lactente , Masculino , Imunodeficiência Combinada Severa/genética , Imunodeficiência Combinada Severa/imunologia , Imunodeficiência Combinada Severa/mortalidade , Taxa de Sobrevida
9.
Sci Immunol ; 1(6)2016 12 16.
Artigo em Inglês | MEDLINE | ID: mdl-28783691

RESUMO

Recombination-activating genes 1 and 2 (RAG1 and RAG2) play a critical role in T and B cell development by initiating the recombination process that controls the expression of T cell receptor (TCR) and immunoglobulin genes. Mutations in the RAG1 and RAG2 genes in humans cause a broad spectrum of phenotypes, including severe combined immunodeficiency (SCID) with lack of T and B cells, Omenn syndrome, leaky SCID, and combined immunodeficiency with granulomas or autoimmunity (CID-G/AI). Using next-generation sequencing, we analyzed the TCR and B cell receptor (BCR) repertoire in 12 patients with RAG mutations presenting with Omenn syndrome (n = 5), leaky SCID (n = 3), or CID-G/AI (n = 4). Restriction of repertoire diversity skewed usage of variable (V), diversity (D), and joining (J) segment genes, and abnormalities of CDR3 length distribution were progressively more prominent in patients with a more severe phenotype. Skewed usage of V, D, and J segment genes was present also within unique sequences, indicating a primary restriction of repertoire. Patients with Omenn syndrome had a high proportion of class-switched immunoglobulin heavy chain transcripts and increased somatic hypermutation rate, suggesting in vivo activation of these B cells. These data provide a framework to better understand the phenotypic heterogeneity of RAG deficiency.

10.
J Clin Invest ; 125(11): 4135-48, 2015 Nov 02.
Artigo em Inglês | MEDLINE | ID: mdl-26457731

RESUMO

Patients with mutations of the recombination-activating genes (RAG) present with diverse clinical phenotypes, including severe combined immune deficiency (SCID), autoimmunity, and inflammation. However, the incidence and extent of immune dysregulation in RAG-dependent immunodeficiency have not been studied in detail. Here, we have demonstrated that patients with hypomorphic RAG mutations, especially those with delayed-onset combined immune deficiency and granulomatous/autoimmune manifestations (CID-G/AI), produce a broad spectrum of autoantibodies. Neutralizing anti-IFN-α or anti-IFN-ω antibodies were present at detectable levels in patients with CID-G/AI who had a history of severe viral infections. As this autoantibody profile is not observed in a wide range of other primary immunodeficiencies, we hypothesized that recurrent or chronic viral infections may precipitate or aggravate immune dysregulation in RAG-deficient hosts. We repeatedly challenged Rag1S723C/S723C mice, which serve as a model of leaky SCID, with agonists of the virus-recognizing receptors TLR3/MDA5, TLR7/-8, and TLR9 and found that this treatment elicits autoantibody production. Altogether, our data demonstrate that immune dysregulation is an integral aspect of RAG-associated immunodeficiency and indicate that environmental triggers may modulate the phenotypic expression of autoimmune manifestations.


Assuntos
Autoanticorpos/imunologia , Autoantígenos/imunologia , Doenças Autoimunes/imunologia , Citocinas/imunologia , Proteínas de Ligação a DNA/deficiência , Doença Granulomatosa Crônica/imunologia , Proteínas de Homeodomínio/imunologia , Proteínas Nucleares/deficiência , Imunodeficiência Combinada Severa/imunologia , Adolescente , Adulto , Animais , Anticorpos Neutralizantes/sangue , Anticorpos Neutralizantes/imunologia , Especificidade de Anticorpos , Autoanticorpos/sangue , Doenças Autoimunes/genética , Criança , Pré-Escolar , RNA Helicases DEAD-box/imunologia , Proteínas de Ligação a DNA/genética , Modelos Animais de Doenças , Feminino , Doença Granulomatosa Crônica/genética , Doença Granulomatosa Crônica/terapia , Proteínas de Homeodomínio/genética , Humanos , Lactente , Helicase IFIH1 Induzida por Interferon , Masculino , Camundongos , Camundongos Endogâmicos , Proteínas Nucleares/genética , Imunodeficiência Combinada Severa/genética , Imunodeficiência Combinada Severa/terapia , Receptores Toll-Like/agonistas , Receptores Toll-Like/imunologia , Viroses/imunologia , Adulto Jovem
12.
Case Rep Pediatr ; 2014: 516256, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25161792

RESUMO

Eliciting proper family medical history is critical in decreasing morbidity and mortality in patients with primary immunodeficiency disorders (PIDs). Communities with a common practice of consanguinity have a high rate of PIDs. We are presenting 2 cases where digging deeply into the family medical history resulted in the diagnosis of Omenn syndrome, a possibly fatal entity if not managed in a reasonable period.

13.
Blood ; 124(13): 2046-50, 2014 Sep 25.
Artigo em Inglês | MEDLINE | ID: mdl-25139357

RESUMO

Identification of the molecular etiologies of primary immunodeficiencies has led to important insights into the development and function of the immune system. We report here the cause of combined immunodeficiency in 4 patients from 2 different consanguineous Qatari families with similar clinical and immunologic phenotypes. The patients presented at an early age with fungal, viral, and bacterial infections and hypogammaglobulinemia. Although their B- and T-cell numbers were normal, they had low regulatory T-cell and NK-cell numbers. Moreover, patients' T cells were mostly CD45RA(+)-naive cells and were defective in activation after T-cell receptor stimulation. All patients contained the same homozygous nonsense mutation in IKBKB (R286X), revealed by whole-exome sequencing with undetectable IKKß and severely decreased NEMO proteins. Mutant IKKß(R286X) was unable to complex with IKKα/NEMO. Immortalized patient B cells displayed impaired IκBα phosphorylation and NFκB nuclear translocation. These data indicate that mutated IKBKB is the likely cause of immunodeficiency in these 4 patients.


Assuntos
Códon sem Sentido , Quinase I-kappa B/genética , Imunodeficiência Combinada Severa/genética , Imunodeficiência Combinada Severa/imunologia , Família , Feminino , Homozigoto , Humanos , Lactente , Masculino , Imunodeficiência Combinada Severa/diagnóstico , Imunodeficiência Combinada Severa/terapia , Resultado do Tratamento
14.
Pediatrics ; 126(2): e465-9, 2010 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-20603253

RESUMO

Physicians caring for infants in the first months of life need to know the normal ranges for absolute lymphocyte counts (ALCs) during that age. Any ALC <2500/microL is potentially pathogenic in early infancy and should be evaluated. We report the case of a 4-month-old white girl with a 2-month history of an oral ulcer, intermittent fever, recurrent otitis, decreased appetite, weight loss, and a new respiratory illness with hypoxemia. She had been in an in-home day care since birth. The patient's primary care physician had seen her frequently and obtained blood counts, but her persistent lymphopenia had not been appreciated. The infant was ultimately diagnosed with T(-)B(-)NK(+) (lacking both B and T lymphocytes and having primarily natural killer [NK] cells), recombinase-activating gene 2 (RAG2)-deficient severe combined immunodeficiency (SCID). However, because she had already developed 2 difficult-to-treat viral infections (parainfluenza 3 and adenovirus), she did not survive long enough to receive a bone marrow transplant. Newborn screening would not only have made the diagnosis at birth but would have led to measures to protect her from becoming infected before she could receive a transplant. Newborn screening would also reveal the true incidence of SCID and define the range of conditions characterized by severely impaired T-cell development. Until screening for SCID and other T-cell defects becomes available for all neonates (either by quantifying T-cell receptor excision circles in Guthrie spots or using other tests that quantify T cells), all pediatricians should know the normal range for ALCs according to age. Recognition of the characteristic lymphopenia of SCID can facilitate early diagnosis.


Assuntos
Triagem Neonatal , Imunodeficiência Combinada Severa/diagnóstico , Linfócitos B/fisiologia , Proteínas de Ligação a DNA/genética , Feminino , Humanos , Lactente , Recém-Nascido , Células Matadoras Naturais/fisiologia , Contagem de Linfócitos , Proteínas Nucleares/genética , Imunodeficiência Combinada Severa/genética , Imunodeficiência Combinada Severa/fisiopatologia , Linfócitos T/fisiologia
15.
Pediatr Hematol Oncol ; 26(8): 566-72, 2009 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-19954366

RESUMO

We report 3 children who developed persistent antibody depletion and abnormal response to bacteriophage after rituximab treatment for autoimmune cytopenias. Whether these patients have developed immunodeficiency secondary to an underlying disease process, to rituximab, or both, is not understood. Rituximab is an efficacious drug for a number of pediatric conditions. However, some patients who receive the drug have prolonged suppression or absence of B-cell function. Families should be counseled of this possibility prior to therapy. Patients should have baseline measurement of quantitative immunoglobulins and specific antibody levels and should be monitored for long term changes in immune function after rituximab.


Assuntos
Anticorpos Monoclonais/efeitos adversos , Síndromes de Imunodeficiência/induzido quimicamente , Pancitopenia/tratamento farmacológico , Anticorpos/sangue , Anticorpos/efeitos dos fármacos , Anticorpos Monoclonais Murinos , Doenças Autoimunes/complicações , Doenças Autoimunes/tratamento farmacológico , Bacteriófagos/imunologia , Criança , Feminino , Humanos , Imunossupressão , Lactente , Masculino , Pancitopenia/complicações , Pancitopenia/imunologia , Rituximab
16.
Ann Allergy Asthma Immunol ; 100(4): 377-83, 2008 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-18450125

RESUMO

BACKGROUND: The Centers for Disease Control and Prevention (CDC), the American Academy of Family Practice, and the American Academy of Pediatrics published guidelines for judicious antibiotic use: antibiotics are injudicious for the treatment of short-term purulent rhinorrhea, otitis media with effusion, and acute wheezy bronchitis. OBJECTIVE: To determine how academic, pediatric, and adult clinical allergists differed in use of antibiotics for upper respiratory tract infections (URIs). METHODS: Surveys were sent to 424 allergists in private clinical practice and 156 allergists in academic settings. Three clinical pediatric vignettes were described. Questions about possible antibiotic use followed. Vignettes were as follows: simple URI in a toddler, the same child with short-duration green rhinorrhea, and the same child with otitis media with effusion. RESULTS: Of 580 mailed surveys, 358 were returned, for an overall response rate of 61.7%. Thirty-nine of these surveys did not meet inclusion criteria, reducing the response rate to 55.0%. Of these, 47.0% (n=150) were familiar with the guidelines: 85.3% answered that they usually adhered to them in practice. The academic allergist respondents demonstrated the best adherence to the guidelines for the 3 vignettes, followed closely by the clinical pediatric allergist respondents. For the population surveyed, adult clinical allergists were more likely than the other 2 groups to prescribe antibiotics for a simple URI (P < .001) and for a URI with short-duration green rhinorrhea (P = .004). CONCLUSIONS: Academic allergists adhered to the CDC guidelines more closely than did adult allergists. Pediatric allergists in clinical practice were in agreement with the academic allergists. Despite self-reported knowledge of the CDC guidelines, many adult allergists in clinical practice did not adhere to them in their answers to the questions after several vignettes.


Assuntos
Antibacterianos/uso terapêutico , Fidelidade a Diretrizes , Padrões de Prática Médica , Infecções Respiratórias/tratamento farmacológico , Alergia e Imunologia/normas , Centers for Disease Control and Prevention (U.S.) , Feminino , Humanos , Masculino , Médicos , Guias de Prática Clínica como Assunto , Estados Unidos
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