Decreased opsonization for Streptococcus pneumoniae in sickle cell disease: Studies on selected complement components and immunoglobulins

Bjornson, Ann B.; Gaston, Marilyn H.; Zellner, Constance L.

doi:10.1016/s0022-3476(77)81303-6

Cited by 53 publications

(25 citation statements)

References 21 publications

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“…Em crianças e adolescentes sem doença de base, a prevalência para a hipertrofia de tonsilas palatinas levando a restrição de vias aéreas superiores tem sido relatada entre 11 e 12,6% 4,5 , ao passo que para tonsilas faríngeas, entre 30 e 37,6% 5,6 . Um dos mecanismos que podem justificar a elevada prevalência encontrada no nosso estudo corresponde a maior susceptibilidade a contrair infecções graves, a qual é devido a asplenia, diminuição da capacidade de opsonização, alterações do sistema reticuloendotelial e da função fagocítica [7][8][9][10] .…”

Section: Discussionunclassified

Association between adenotonsillar hypertrophy, tonsillitis and painful crises in sickle cell disease

Salles¹,

Ramos²,

Daltro³

et al. 2009

J Pediatr (Rio J)

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Objectives: To determine the prevalence of obstructive adenotonsillar hypertrophy in children and adolescents with sickle cell anemia; to investigate possible associations between the presence of more than five episodes of tonsillitis in the last 12 months and episodes of painful crises in the same period; and to compare the mean annual hemoglobin level in children and adolescents with and without obstructive adenotonsillar hypertrophy. Methods:Prospective, observational, cross-sectional study involving 85 children and adolescents with sickle cell anemia. All patients answered a questionnaire and underwent a standard otolaryngology examination, including endoscopic endonasal approach. The diagnosis of obstructive adenotonsillar hypertrophy was made according to the Brodsky scale. Results:The prevalence of obstructive adenotonsillar hypertrophy was 55.3%. Obstructive adenotonsillar hypertrophy was associated with history of difficulty in eating (76.7 vs. 23.5%, p = 0.003), presence of more than five episodes of tonsillitis in the last 12 months (70.6 vs. 29.4%, p = 0.021), loud snoring (73.0 vs. 27.0%, p = 0.004), and sleep apnea (71.8 vs. 28.2%, p = 0.005). Patients with obstructive adenotonsillar hypertrophy had more episodes of recurrent upper airway tract infection (62.5 vs. 37.5; p = 0.010). The presence of more than five episodes of tonsillitis in the last 12 months was associated with episodes of painful crises (median = 12 vs. 2, p = 0.017). There was no significant difference between mean annual hemoglobin levels of patients with obstructive adenotonsilar hypertrophy vs. nonobstructive adenotonsillar hypertrophy: 7.6 vs. 8.2 g/dL, p = 0.199. Conclusion:The prevalence of obstructive adenotonsillar hypertrophy was 55.3% in children and adolescents with sickle cell anemia; the presence of more than five episodes of tonsillitis in the last 12 months was associated with episodes of painful crises in the same period; there was no difference in the mean annual hemoglobin value among those with or without obstructive adenotonsillar hypertrophy. J Pediatr (Rio J). 2009;85(3):249-253:Tonsil, tonsillitis, hemoglobin, children, adolescents, sickle cell disease. ResumoObjetivos: Determinar a prevalência da hipertrofia adenotonsilar obstrutiva em crianças e adolescentes portadores de anemia falciforme; investigar possível associação entre presença de mais de cinco episódios de tonsilite nos últimos 12 meses e episódios de crise álgica no mesmo período; e comparar a hemoglobina anual média entre os que apresentam e os que não apresentam hipertrofia adenotonsilar obstrutiva.Métodos: Trata-se de estudo prospectivo, observacional do tipo corte transversal, com 85 crianças e adolescentes com anemia falciforme. Todos responderam questionário e avaliação otorrinolaringológica, incluindo endoscopia nasossinusal. Para o diagnóstico da hipertrofia adenotonsilar obstrutiva foram adotados os critérios de Brodsky.Resultados: A prevalência da hipertrofia adenotonsilar obstrutiva foi de 55,3%. A hipertrofia adenotonsilar obs...

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Section: Discussionunclassified

Association between adenotonsillar hypertrophy, tonsillitis and painful crises in sickle cell disease

Salles¹,

Ramos²,

Daltro³

et al. 2009

J Pediatr (Rio J)

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“…The higher propensity for bacterial infections has been attributed to decreased splenic function (11). Abnormal opsonic activity (12)(13)(14) and evidence ofalternative complement pathway activation (15)(16)(17)(18) have been observed in serum from patients with SCA, suggesting that decreased serum complement may also contribute to the higher risk of bacterial infections. The source of this complement activation has not been determined.…”

Section: Introductionmentioning

confidence: 99%

Activation of the alternative complement pathway by exposure of phosphatidylethanolamine and phosphatidylserine on erythrocytes from sickle cell disease patients.

Wang¹,

Phillips²,

Medof³

et al. 1993

J. Clin. Invest.

118

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Deoxygenation of erythrocytes from sickle cell anemia (SCA) patients alters membrane phospholipid distribution with increased exposure of phosphatidylethanolamine (PE) and phosphatidylserine (PS) on the outer leaflet. This study investigated whether altered membrane phospholipid exposure on sickle erythrocytes results in complement activation. In vitro deoxygenation of sickle but not normal erythrocytes resulted in complement activation measured by C3 binding. Additional evidence indicated that this activation was the result of the alterations in membrane phospholipids. First, complement was activated by normal erythrocytes after incubation with sodium tetrathionate, which produces similar phospholipid changes. Second, antibody was not required for complement activation by sickle or tetrathionate-treated erythrocytes. Third, the membrane regulatory proteins, decay-accelerating factor (CD55) and the C3b/C4b receptor (CD35), were normal on sickle and tetrathionate-treated erythrocytes. Finally, insertion of PE or PS into normal erythrocytes induced alternative pathway activation. SCA patients in crisis exhibited increased plasma factor Bb levels compared with baseline, and erythrocytes isolated from hospitalized SCA patients had increased levels of bound C3, indicating that alternative pathway activation occurs in vivo. Activation of complement may be a contributing factor in sickle crisis episodes, shortening the life span of erythrocytes, and decreasing host defense against infections. (J. Clin. Invest. 1993. 92:1326-1335

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“…A second, less well characterized alteration of host defense occurring in a subpopulation ofchildren and adults with sickle cell disease is reduction in serum opsonization ofStreptococcus pneumoniae (7)(8)(9)(10)(11)(12)(13)(14). Initial studies attempting to characterize this alteration examined the relationship between serum opsonization of S. pneumoniae and various functional measurements ofcomplement, i.e., total hemolytic complement and C3 conversion by activators of the alternative complement pathway (zymosan, inulin, and cobra venon factor) (7)(8)(9)(10). Total hemolytic complement was found to be below normal in certain sera, but not consistently in opsonically deficient sera (7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

“…Initial studies attempting to characterize this alteration examined the relationship between serum opsonization of S. pneumoniae and various functional measurements ofcomplement, i.e., total hemolytic complement and C3 conversion by activators of the alternative complement pathway (zymosan, inulin, and cobra venon factor) (7)(8)(9)(10). Total hemolytic complement was found to be below normal in certain sera, but not consistently in opsonically deficient sera (7)(8)(9)(10). Johnston et al demonstrated that C3 conversion by zymosan was reduced in these sera (8).…”

Section: Introductionmentioning

confidence: 99%

Direct evidence that decreased serum opsonization of Streptococcus pneumoniae via the alternative complement pathway in sickle cell disease is related to antibody deficiency.

Bjornson¹,

Lobel²

1987

J. Clin. Invest.

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Two approaches were used to demonstrate that reduction in serum opsonization of Streptococcus pneumoniae via the alternative complement pathway in children with sickle cell disease is related to a deficiency of antibodies to pneumococcal capsular polysaccharide. First, opsonization of S. pneumoniae mediated by the alternative pathway in patients' sera was restored to normal by addition of the purified IgG or IgM fraction of goat antiserum to capsular polysaccharide of the homologous serotype. Secondly, IgG antibody titers to capsular polysaccharide in patients' sera correlated significantly with alternative pathwaymediated opsonization; the correlation between titers of IgM anticapsular antibodies and opsonization approached statistical significance. The sum of the IgG and IgM anticapsular antibody titers correlated most significantly with opsonization. Our results suggest that reduction in alternative pathway-mediated opsonization in sera from children with sickle cell disease is related to low levels of both IgG and IgM anticapsular antibodies.

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Decreased opsonization for Streptococcus pneumoniae in sickle cell disease: Studies on selected complement components and immunoglobulins

Cited by 53 publications

References 21 publications

Association between adenotonsillar hypertrophy, tonsillitis and painful crises in sickle cell disease

Association between adenotonsillar hypertrophy, tonsillitis and painful crises in sickle cell disease

Activation of the alternative complement pathway by exposure of phosphatidylethanolamine and phosphatidylserine on erythrocytes from sickle cell disease patients.

Direct evidence that decreased serum opsonization of Streptococcus pneumoniae via the alternative complement pathway in sickle cell disease is related to antibody deficiency.

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