A study of 42 episodes of overwhelming post-splenectomy infection: Is current guidance for asplenic individuals being followed?

Waghorn, D J; Mayon-White, R.T.

doi:10.1016/s0163-4453(97)93232-1

Cited by 92 publications

(70 citation statements)

References 23 publications

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“…5 A recent study in England showed that the coverage of pneumococcal, meningococcal, and Hib vaccine was 79%, 51%, and 40%, respectively. 8 However, in our present study, it is possible that vaccine coverage was lower among splenectomy patients who had died, and that our results are biased.…”

Section: Resultsmentioning

confidence: 99%

A survey of vaccine coverage and antibiotic prophylaxis in splenectomised patients in Scotland

Kyaw

Holmes²,

Chalmers³

et al. 2002

Journal of Clinical Pathology

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Aims: To determine the coverage of vaccine and antibiotic prophylaxis in splenectomised patients in Scotland. Methods: Patients who had undergone splenectomy between 1 January 1988 and 31 December 1998 were identified. A questionnaire was sent to general practitioners to validate vaccine and antibiotic status for these patients.Results: A total of 974 living splenectomised patients were identified during the study period. Information on vaccine and antibiotic status was available for 708 (73%) and 770 (79%) of living patients, respectively. Coverage of pneumococcal vaccine (88%) was higher than that of Haemophilus influenza type b (Hib) conjugate vaccine (70%) or meningococcal vaccine (51%). Only 47% of patients received all three vaccines. A higher coverage was also documented for pneumococcal vaccine (28%) than Hib (19%) and meningococcal vaccine (14%) before elective splenectomy. Only 13% received all three vaccines before splenectomy. Coverage of influenza vaccine increased significantly, from 76% in the 1997/ 1998 season to 96% in the 2000/2001 season. Antibiotic prophylaxis was received by 67% of all patients. The current recommendation, comprising pneumococcal and Hib vaccination and antibiotic prophylaxis, was received by only 52% of the patients. There was no association between the coverage of vaccine and socioeconomic status. Conclusion: Further improvement in coverage of recommended vaccines and antibiotic prophylaxis is still needed to reduce the risk of serious infection in this high risk group. P atients without spleens are at a significantly increased risk of serious infection with encapsulated bacteria, especially Streptococcus pneumoniae, Haemophilus influenzae type b (Hib), and Neisseria meningitidis. 1 Antibiotics and polysaccharide pneumococcal, meningococcal, influenza, and Hib conjugate vaccines are available for the prevention of postsplenectomy infection and are recommended for all splenectomised patients by the Department of Health (DoH) and the British Committee for Standards in Haematology (BCSH), with the exception of meningococcal polysaccharide vaccine. 2 3 Because the adherence to preventive measures has been reported to be low, 4 5 we conducted this study to determine the coverage of appropriate vaccination and antibiotic prophylaxis in splenectomised patients in Scotland during an 11 year period from 1988 to 1998. "Patients without spleens are at a significantly increased risk of serious infection with encapsulated bacteria" METHODSPatients who underwent splenectomy from 1 January 1988 to 31 December 1998 were identified using the Scottish Morbidity Record (SMR01), which is collected at discharge from all episodes of hospital inpatient or day case care. It records information on demography, number of hospital admissions, and the clinical nature of the patient treatment episode. SMR01 records were linked to General Register Office (Scotland) death registrations using probability matching to exclude patients who had died because their medical records would not be available to gene...

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Section: Resultsmentioning

confidence: 99%

A survey of vaccine coverage and antibiotic prophylaxis in splenectomised patients in Scotland

Kyaw

Holmes²,

Chalmers³

et al. 2002

Journal of Clinical Pathology

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“…[66][67][68] Thus, splenectomy should be avoided unless it is the only remaining measure to control chronic, refractory, life-threatening cytopenias in ALPS patients. Even under those circumstances, feasibility and efficacy of a partial splenectomy or splenic embolization should be explored.…”

Section: Org Frommentioning

confidence: 99%

“…64,65 Recently, there has been an increased awareness of some associated morbidity and mortality, including overwhelming postsplenectomy infection, on long-term follow-up of patients after splenectomy for other indications as well. [66][67][68] Thus, splenectomy should be avoided unless it is the only remaining measure to control chronic, refractory, life-threatening cytopenias in ALPS patients. Even under those circumstances, feasibility and efficacy of a partial splenectomy or splenic embolization should be explored.…”

Section: Splenectomy and Care Of Its Aftermathmentioning

confidence: 99%

How I treat autoimmune lymphoproliferative syndrome

Rao

Oliveira²

2011

Blood

165

153

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Autoimmune lymphoproliferative syndrome (ALPS) represents a failure of apoptotic mechanisms to maintain lymphocyte homeostasis, permitting accumulation of lymphoid mass and persistence of autoreactive cells that often manifest in childhood with chronic nonmalignant lymphadenopathy, hepatosplenomegaly, and recurring multilineage cytopenias. Cytopenias in these patients can be the result of splenic sequestration as well as autoimmune complications manifesting as autoimmune hemolytic anemia, immune-mediated thrombocytopenia, and autoimmune neutropenia. More than 300 families with hereditary ALPS have now been described; nearly 500 patients from these families have been studied and followed worldwide over the last 20 years by our colleagues and ourselves. Some of these patients with FAS mutations affecting the intracellular portion of the FAS protein also have an increased risk of B-cell lymphoma. The best approaches to diagnosis, followup, and management of ALPS, its associated cytopenias, and other complications resulting from infiltrative lymphoproliferation and autoimmunity are presented. This trial was registered at www.clinicaltrial.gov as #NCT00001350. (Blood. 2011;118(22): 5741-5751) IntroductionAutoimmunity results from failure of self-tolerance, which can be further divided into central and peripheral tolerance. Central tolerance is fostered by apoptosis through elimination of autoreactive lymphocytes in generative lymphoid organs (the bone marrow and thymus), whereas mechanisms of peripheral tolerance include anergy, deletion by apoptosis, and suppression by regulatory T cells to avoid autoimmunity and tissue damage. 1 Apoptosis, the intrinsic program of cell death, is triggered by receptor-ligand interactions at the cell surface (the extrinsic pathway) or by the activation of mitochondrial proteins (the intrinsic pathway), leading to processing and activation of caspases and their downstream targets. Lymphocyte apoptosis mediated by the cell surface receptor FAS plays a pivotal role in lymphocyte homeostasis. FAS (also termed CD95/APO1) is a member of the tumor necrosis factor receptor superfamily of proteins that directly trigger apoptosis to maintain lymphocyte homeostasis and peripheral immune tolerance and prevent autoimmunity. 2,3 It is a membrane-bound molecule that is highly expressed, not only on activated B and T lymphocytes but also present in other cells, such as hepatocytes. FAS is present on the cell surface as a preformed trimer. 4 Its binding with FAS ligand leads to conformational changes on the intracellular portion of FAS protein triggering rapid recruitment of the death domain of the adaptor protein FADD (Fas-associated death domain) to the homologous death domain in the cytoplasmic tail of FAS. This is followed by the recruitment of procaspases 8 or 10 through the interaction of their death-effecter domains with the amino termini of FADD. The resulting Fas/FADD/caspase complex is termed the death-inducing signaling complex that incites a further cascade of caspase activation culminati...

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“…Asplenic patients are therefore at increased risk for invasive infections with S. pneumoniae (13). Although most infections occur within the first few years after splenectomy, the risk of overwhelming postsplenectomy infections is lifelong (9,36). Therefore, vaccination against S. pneumoniae is indicated for this group.…”

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confidence: 99%

Pneumococcal Conjugate Vaccines Overcome Splenic Dependency of Antibody Response to Pneumococcal Polysaccharides

Breukels

Zandvoort²,

Dobbelsteen

et al. 2001

Infect Immun

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Protection against infections with Streptococcus pneumoniae depends on the presence of antibodies against capsular polysaccharides that facilitate phagocytosis. Asplenic patients are at increased risk for pneumococcal infections, since both phagocytosis and the initiation of the antibody response to polysaccharides take place in the spleen. Therefore, vaccination with pneumococcal polysaccharide vaccines is recommended prior to splenectomy, which, as in the case of trauma, is not always feasible. We show that in rats, vaccination with a pneumococcal conjugate vaccine can induce good antibody responses even after splenectomy, particularly after a second dose. The spleen remains necessary for a fast, primary response to (blood-borne) polysaccharides, even when they are presented in a conjugated form. Coadministration of a conjugate vaccine with additional nonconjugated polysaccharides of other serotypes did not improve the response to the nonconjugated polysaccharides. We conclude that pneumococcal conjugate vaccines can be of value in protecting asplenic or hyposplenic patients against pneumococcal infections.Protection against infections with encapsulated bacteria such as Streptococcus pneumoniae depends on the presence of antibodies against capsular polysaccharides. These serotypespecific antibodies facilitate phagocytosis, the main mode of host defense against S. pneumoniae. The spleen is an important organ in the immune response to S. pneumoniae, since it contains both antibody-producing B cells and phagocytes (4, 26). Asplenic patients are therefore at increased risk for invasive infections with S. pneumoniae (13). Although most infections occur within the first few years after splenectomy, the risk of overwhelming postsplenectomy infections is lifelong (9, 36). Therefore, vaccination against S. pneumoniae is indicated for this group. At present, the vaccine available for this aim is the 23-valent pneumococcal polysaccharide (PPS) vaccine (1). The immunogenicity of PPS vaccine in splenectomized patients has been assessed in a number of trials. Some studies have shown the effectiveness of vaccination in inducing protective concentrations of specific antibodies (5, 10, 24, 33), while others have shown limited serological responses (15). As the initiation of the antibody response to polysaccharides seems to depend on the presence of splenic tissue, and in particular on a functional marginal-zone B-cell compartment (3,14,18,34), it may be expected that polysaccharide vaccines are of limited use in asplenic patients.The physical coupling of a polysaccharide to a carrier protein greatly improves the immunogenicity of the polysaccharide, a principle first described in 1929 (11). Conjugated polysaccharides overcome the antipolysaccharide unresponsiveness in early life (2, 8), which is thought to be due to a still immature splenic marginal-zone B-cell compartment (2). The induction of antipolysaccharide antibodies by conjugate vaccines at a young age suggests that conjugates might initiate the antipolysaccharide anti...

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A study of 42 episodes of overwhelming post-splenectomy infection: Is current guidance for asplenic individuals being followed?

Cited by 92 publications

References 23 publications

A survey of vaccine coverage and antibiotic prophylaxis in splenectomised patients in Scotland

A survey of vaccine coverage and antibiotic prophylaxis in splenectomised patients in Scotland

How I treat autoimmune lymphoproliferative syndrome

Pneumococcal Conjugate Vaccines Overcome Splenic Dependency of Antibody Response to Pneumococcal Polysaccharides

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