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Robert Booy - One of the best experts on this subject based on the ideXlab platform.
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long term immunological follow up of children with haemophilus influenzae serotype b vaccine failure in the united kingdom
Clinical Infectious Diseases, 2009Co-Authors: Shamez N Ladhani, Paul T Heath, Mary Ramsay, Mary P E Slack, Elizabeth Kibwana, Andrew J Pollard, Robert BooyAbstract:BACKGROUND It is not known how long children with Haemophilus influenzae serotype b (Hib) vaccine failure retain protective Hib antibody concentrations after infection. The objective of this study was to determine Hib antibody concentrations in children several years after infection and to identify risk factors for low antibody concentrations. METHODS The families of children from the United Kingdom who developed invasive Hib disease after prior immunization with Hib conjugate vaccine (i.e., Hib vaccine failure) from October 1992 through December 2005 were asked to complete a questionnaire. A blood sample was also obtained from each child. RESULTS Of 323 families approached, 260 (80.5%) returned a completed questionnaire, and 175 (54.2%) children provided a blood sample. The median age at follow-up was 8.4 years (interquartile range [IQR], 6.2-15.4 years), and the median duration of follow-up was 4.1 years (IQR, 3.5-9.7 years). Twenty-seven children (16.1%) had been born prematurely and/or had an underlying medical condition, and 18 (10.8%) had Immunoglobulin Deficiency. The median Hib antibody concentration was 0.70 microg/mL (IQR, 0.22-5.8 microg/mL). Overall, 95 children (56.9%) had antibody concentrations <1.0 microg/mL, and 27 (16.2%) had antibody concentrations <0.15 microg/mL. All 3 children with Down syndrome and 10 (42%) of 24 children aged <5 years at follow-up had Hib antibody concentrations <0.15 microg/mL. An antibody concentration <0.15 microg/mL was independently associated with underlying conditions, young age at onset of Hib disease, and shorter time from Hib disease to follow-up. CONCLUSIONS More than one-half of the children with Hib vaccine failure had antibody concentrations below those considered to confer long-term protection, which suggests that these children might be at further risk of invasive Hib disease and would benefit from another dose of Hib vaccine.
Mehnaaz S Khuroo - One of the best experts on this subject based on the ideXlab platform.
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diffuse duodenal nodular lymphoid hyperplasia a large cohort of patients etiologically related to helicobacter pylori infection
BMC Gastroenterology, 2011Co-Authors: Naira S Khuroo, Mehnaaz S KhurooAbstract:Nodular lymphoid hyperplasia of gastrointestinal tract is a rare disorder, often associated with immunoDeficiency syndromes. There are no published reports of its association with Helicobacter pylori infection. From March 2005 till February 2010, we prospectively followed all patients with diffuse duodenal nodular lymphoid hyperplasia (DDNLH). Patients underwent esophagogastroduodenoscopy with targeted biopsies, colonoscopy, and small bowel video capsule endoscopy. Duodenal nodular lesions were graded from 0 to 4 based on their size and density. Patients were screened for celiac sprue (IgA endomysial antibody), Immunoglobulin abnormalities (Immunoglobulin levels & serum protein electrophoresis), small intestine bacterial overgrowth (lactulose hydrogen breath test), and Helicobacter pylori infection (rapid urease test, and histological examination of gastric biopsies). Patients infected with Helicobacter pylori received sequential antibiotic therapy and eradication of infection was evaluated by 14C urea breath test. Follow up duodenoscopies with biopsies were performed to ascertain resolution of nodular lesions. Forty patients (Males 23, females 17; mean age ± 1SD 35.6 ± 14.6 years) with DDNLH were studied. Patients presented with epigastric pain, vomiting, and weight loss. Esophagogastroduodenoscopy showed diffuse nodular lesions (size varying from 2 to 5 mm or more) of varying grades (mean score ± 1SD 2.70 ± 0.84) involving postbulbar duodenum. Video capsule endoscopies revealed nodular disease exclusively limited to duodenum. None of the patients had Immunoglobulin Deficiency or small intestine bacterial overgrowth or positive IgA endomysial antibodies. All patients were infected with Helicobacter pylori infection. Sequential antibiotic therapy eradicated Helicobacter pylori infection in 26 patients. Follow up duodenoscopies in these patients showed significant reduction of duodenal nodular lesions score (2.69 ± 0.79 to 1.50 ± 1.10; p < 0.001). Nodular lesions showed complete resolution in 5 patients and significant resolution in remaining 21 patients. Patients with resistant Helicobacter pylori infection showed no significant reduction of nodular lesions score (2.71 ± 0.96 to 2.64 ± 1.15; p = 0.58). Nodules partially regressed in score in 2 patients, showed no interval change in 10 patients and progressed in 2 patients. We report on a large cohort of patients with DDNLH, etiologically related to Helicobacter pylori infection.
Shamez N Ladhani - One of the best experts on this subject based on the ideXlab platform.
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long term immunological follow up of children with haemophilus influenzae serotype b vaccine failure in the united kingdom
Clinical Infectious Diseases, 2009Co-Authors: Shamez N Ladhani, Paul T Heath, Mary Ramsay, Mary P E Slack, Elizabeth Kibwana, Andrew J Pollard, Robert BooyAbstract:BACKGROUND It is not known how long children with Haemophilus influenzae serotype b (Hib) vaccine failure retain protective Hib antibody concentrations after infection. The objective of this study was to determine Hib antibody concentrations in children several years after infection and to identify risk factors for low antibody concentrations. METHODS The families of children from the United Kingdom who developed invasive Hib disease after prior immunization with Hib conjugate vaccine (i.e., Hib vaccine failure) from October 1992 through December 2005 were asked to complete a questionnaire. A blood sample was also obtained from each child. RESULTS Of 323 families approached, 260 (80.5%) returned a completed questionnaire, and 175 (54.2%) children provided a blood sample. The median age at follow-up was 8.4 years (interquartile range [IQR], 6.2-15.4 years), and the median duration of follow-up was 4.1 years (IQR, 3.5-9.7 years). Twenty-seven children (16.1%) had been born prematurely and/or had an underlying medical condition, and 18 (10.8%) had Immunoglobulin Deficiency. The median Hib antibody concentration was 0.70 microg/mL (IQR, 0.22-5.8 microg/mL). Overall, 95 children (56.9%) had antibody concentrations <1.0 microg/mL, and 27 (16.2%) had antibody concentrations <0.15 microg/mL. All 3 children with Down syndrome and 10 (42%) of 24 children aged <5 years at follow-up had Hib antibody concentrations <0.15 microg/mL. An antibody concentration <0.15 microg/mL was independently associated with underlying conditions, young age at onset of Hib disease, and shorter time from Hib disease to follow-up. CONCLUSIONS More than one-half of the children with Hib vaccine failure had antibody concentrations below those considered to confer long-term protection, which suggests that these children might be at further risk of invasive Hib disease and would benefit from another dose of Hib vaccine.
Xia Liu - One of the best experts on this subject based on the ideXlab platform.
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iga and igg hypogammaglobulinemia in waldenstrom s macroglobulinemia
Haematologica, 2010Co-Authors: Zachary R. Hunter, Bryan Ciccarelli, Robert Manning, Christopher J Patterson, C. A. Hanzis, Leukothea Ioakimidis, Megan Lewicki, Hsuiyi Tseng, Ping Gong, Xia LiuAbstract:Background Hypogammaglobulinemia is common in Waldenstrom’s macroglobulinemia. The etiology of this finding remains unclear, but it has been speculated to be based on tumor-induced suppression of the ‘uninvolved’ Immunoglobulin productionDesign and Methods We evaluated the incidence of IgA and IgG hypogammaglobulinemia in 207 untreated patients with Waldenstrom’s macroglobulinemia and investigated the associated clinicopathological findings and impact of therapy. We also sequenced eight genes (AICDA, BTK, CD40, CD154, NEMO, TACI, SH2D1A, UNG) implicated in Immunoglobulin Deficiency in 19 Waldenstrom’s macroglobulinemia patients with IgA and/or IgG hypogammaglobulinemia.Results At baseline 63.3%, 58.0% and 49.3% of the 207 patients had abnormally low serum levels of IgA, IgG, or both. No association between IgA and IgG hypogammaglobulinemia and disease burden, serum IgM levels, β2-microglobulin, International Prognostic Scoring System score, or incidence of recurrent infections was observed, although the presence of adenopathy and/or splenomegaly was associated with a lower incidence of hypogammaglobulinemia. Lower IgA and IgG levels were associated with disease progression in patients managed with a ‘watch and wait’ strategy. IgA and/or IgG levels remained abnormally low despite response to treatment, including complete remissions. A missense mutation in the highly conserved catalytic site of UNG was observed in a patient with hypogammaglobulinemia, warranting further study of this pathway in Waldenstrom’s macroglobulinemia.Conclusions IgA and IgG hypogammaglobulinemia is common in Waldenstrom’s macroglobulinemia and persists despite therapeutic intervention and response. IgA and IgG hypogammaglobulinemia does not predict the risk of recurrent infections in patients with Waldenstrom’s macroglobulinemia, although lower levels of serum IgA and IgG are associated with disease progression in Waldenstrom’s macroglobulinemia patients being managed with a ‘watch and wait’ strategy.
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iga and igg hypogammaglobulinemia does not predict for recurrent infection risk and persists despite therapeutic response in patients with waldentrom s macroglobulinemia
Blood, 2009Co-Authors: Zachary R. Hunter, Bryan Ciccarelli, Robert Manning, Christopher J Patterson, C. A. Hanzis, Megan Lewicki, Hsuiyi Tseng, Ping Gong, Thea Ioakimidis, Xia LiuAbstract:Abstract 1947 Poster Board I-970 Recurrent infections are commonly observed among patients with WM, and may be related to the presence of IgA and IgG hypogammaglobulinemia. The etiology for this finding remains unclear, and has been speculated to be on the basis of tumor-induced suppression. We therefore evaluated the incidence of IgA and IgG hypogammaglobulinemia in 207 untreated WM patients and addressed the associated clinicopathological findings, and impact of therapy. The median age of these patients was 60, median IgM was 2,910, and median bone marrow (BM) infiltration was 40%. Of these patients, 131 (63.3%) and 120 (58.0%) patients demonstrated decreased serum IgA and IgG levels respectively, while 102 (49.3%) of these patients were abnormally low for both. BM infiltration, serum IgM levels, complete blood counts, absolute lymphocyte counts, b2-microglobulin, or the WM International Prognostic Scoring System score had no impact on the odds ratio of having IgA or IgG, or both IgA or IgG hypogammaglobulinemia by logistic regression analysis. The presence of adenopathy and/or splenomegaly was surprisingly associated with a lower incidence of hypogammaglobulinemia (p≤0.03). The presence of IgA, IgG or both IgA and IgG hypogammaglobulinemia did not predict for the occurrence of recurring infections, which were nearly all respiratory in nature and consisted of sinus (n=53; 25.85%), bronchial (n=16; 7.80%), unspecified upper respiratory tract (n=14; 6.83%), and pneumonic (n=7; 3.41%) infections. Lower IgA and IgG levels were however associated with disease progression in watch and wait patients. To understand the impact of WM directed therapeutic intervention on uninvolved Immunoglobulin levels, we analyzed changes in IgA and IgG levels in a cohort of 93 patients who underwent treatment for WM. With a median follow-up of 12 months, no significant recovery in the median IgA and IgG levels was observed with any therapy during the course of follow-up, including in those patients who had follow-up in excess of 1 (n=46), 2 (n=25), and 3 (n=8) or more years post-therapy, and in those achieving a major remission including complete response. Lastly, we sequenced 8 genes (AICDA; BTK; CD40; CD154; NEMO, TACI, SH2D1A, UNG) implicated in Immunoglobulin Deficiency in 19 WM patients with IgA and/or IgG hypogammaglobulinemia. We observed an intronic variation at position c.1056-6T>C in 2 patients, and a hemizygous missense mutation at c.337G>A in another patient for NEMO, as well as a heterozygous missense mutation at c.425A>T in the highly conserved catalytic site of UNG for one patient. The results of these studies demonstrate that IgA and IgG hypogammaglobulinemia is common, and does not predict for recurrent infection risk in WM. Moreover, IgA and IgG hypogammaglobulinemia persists despite therapeutic intervention and response. These studies highlight the importance for further investigations into the IgA and IgG hypogammaglobulinemia of WM, as well as the signaling pathways involved in B-cell differentiation and Immunoglobulin heavy chain class switching in the pathogenesis of WM. Disclosures: No relevant conflicts of interest to declare.
Nancy E Messonnier - One of the best experts on this subject based on the ideXlab platform.
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prevention and control of haemophilus influenzae type b disease recommendations of the advisory committee on immunization practices acip
MMWR. Recommendations and reports : Morbidity and mortality weekly report. Recommendations and reports Centers for Disease Control, 2014Co-Authors: Elizabeth C Briere, Lorry G. Rubin, Amanda C Cohn, Thomas A Clark, Pedro L Moro, Nancy E MessonnierAbstract:This report compiles and summarizes all recommendations from CDC's Advisory Committee on Immunization Practices (ACIP) regarding prevention and control of Haemophilus influenzae type b (Hib) disease in the United States. As a comprehensive summary of previously published recommendations, this report does not contain any new recommendations; it is intended for use by clinicians, public health officials, vaccination providers, and immunization program personnel as a resource. ACIP recommends routine vaccination with a licensed conjugate Hib vaccine for infants aged 2 through 6 months (2 or 3 doses, depending on vaccine product) with a booster dose at age 12 through 15 months. ACIP also recommends vaccination for certain persons at increased risk for Hib disease (i.e., persons who have early component complement deficiencies, Immunoglobulin Deficiency, anatomic or functional asplenia, or HIV infection; recipients of hematopoietic stem cell transplant; and recipients of chemotherapy or radiation therapy for malignant neoplasms). This report summarizes current information on Hib epidemiology in the United States and describes Hib vaccines licensed for use in the United States. Guidelines for antimicrobial chemoprophylaxis of contacts of persons with Hib disease also are provided.
