A clinical and pathological study of resistance to infection in chronic lymphatic leukemia

Miller, Daniel G.; Budinger, John M.; Karnofsky, David A.

doi:10.1002/1097-0142(196203/04)15:2<307::aid-cncr2820150214>3.0.co;2-8

Cited by 22 publications

(3 citation statements)

References 8 publications

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“…Not all investigators have noted a correlation between serum immunoglobulin levels and the frequency of repeated infections [ 1,4,23,25,29]. While hypogammaglobulinemia may correlate with the extent of the leukemia [25,27,28], serum levels of immunoglobulins often do not normalize with disease control despite a reduction in the frequency of infections [ 17,231. In addition, the use of gammaglobulin injections, without concurrent antibiotics, may not be effective in either preventing or treating infections [2]. It has also been suggested that patients with CLL are at a greater risk for bacterial infections at higher levels of immunoglobulins than are children with hypogammaglobulinemia [ 171.…”

Section: Discussionmentioning

confidence: 99%

“…All six patients with a history of a bacterial infection were receiving therapy at the time they became infected. Ultmann et a1 [7], Twomey [5], and others [2,17,24], however, failed to observe a close correlation between therapy and the occurrence of infections in patients with CLL. A larger number of patients will have to be evaluated to resolve this discrepancy.…”

Section: Discussionmentioning

confidence: 99%

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Defective complement activity in chronic lymphocytic leukemia

Heath

Cheson

1985

American J Hematol

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Patients with chronic lymphocytic leukemia (CLL) are at an increased risk for infections with bacteria which require complement for osponization. We explored the possibility that patients with CLL have a defect in binding the potent opsonin C3b to bacteria. Bacteria selected for these experiments included Streptococcus pneumoniae type 3, which binds C3 by activating the classical complement pathway (CCP), type 25, which can bind normal amounts of C3b by the alternative complement pathway (ACP), type 14, which can activate both the CCP and ACP, and Staphylococcus aureus and Escherichia coli, both of which activate the CCP. Bacteria were treated with normal serum or serum from 15 patients with CLL, and the bound C3b was quantified spectrophotofluorometrically. Despite normal serum concentrations of C3, C4, Factor B, C-reactive protein, and total hemolytic complement activity, all 15 CLL sera bound reduced amounts of C3b to at least one bacterial species; 9 to S pneumoniae type 3, 8 to types 14 and 25, 11 to S aureus, and 13 to E coli. Mixing normal serum with CLL serum restored C3b binding to all bacteria, suggesting a deficiency rather than an inhibitor of activity. Serum from ten hypogammaglobulinemic CLL patients bound less C3b (62.7 +/- 5% of normal) (means +/- SEM) than those with normal immunoglobulin levels (81.9 +/- 5%) (p less than .005). Nevertheless, the addition of specific antibacterial antibodies to CLL serum did not enhance C3b binding to any of the bacteria. Serum from patients with a history of a bacterial infection bound less C3b (62.3 +/- 5%) than those without a history of infections (76.1 +/- 6%) (p less than .05). Thus, there is a defect in either the activation or activity of C3 in CLL serum which may contribute to the increased incidence of infections in these patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Defective complement activity in chronic lymphocytic leukemia

Heath

Cheson

1985

American J Hematol

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“…Figure 2 shows that the gradients derived from each plot correlated well with each other and conclusions were interchangeable providing comparisons were made in kind-that is, the gradients from the linear plot should not be compared with those from the logarithmic plot. Table 4 Incidence ofinhibition ofchemotaxis in paraproteinaemia IgA myeloma (9) Non-myeloma with IgG myeloma (6) Lymphoma with IgA * (2) IgG* (2) a cells y cells IgA excess (2) IgM in excess (4) 56% (5) 100% (2) 33% (2) 0 -100%-0 1'00%-(0 IgA* = purified IgA paraprotein. IgG* = purified IgG paraprotein.…”

Section: Indicator Cellsmentioning

confidence: 99%

Impairment of neutrophil chemotaxis by serum from patients with chronic lymphoproliferative disease.

Jayaswal¹,

Roper²,

Roath³

1983

Journal of Clinical Pathology

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SUMMARY The sera of 74 individuals with chronic lymphoproliferative disease were screened for the presence of inhibitory activity against neutrophil chemotaxis. This was present in more than half the patients with IgA myeloma and Hodgkin's disease but was less common in chronic lymphocytic leukaemia, lymphocytic lymphoma and non-IgA paraproteinaemia. Heating the sera prior to testing frequently enhanced inhibitory activity particularly in myeloma and lymphoma.

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Engulfment and bactericidal capabilities of peripheral blood leukocytes in chronic leukemias

Kalinske

Hoeprich

1969

Cancer

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The phagocytic function of peripheral blood leukocytes from 7 patients with chronic myelocytic leukemia (CML; 10 studies) and 7 patients with chronic lymphocytic leukemia (CLL; 11 studies) was assessed using noncapsulated Diplococcus pneumoniae. Evaluation was based on the simultaneous use of normal controls, the exact equilibration of the phagocytic potential of suspensions of patients' and controls' phagocytes in each other's, as well as autologous serum, and the maintenance of reasonable and constant ratios of bacteria to phagocytes. Neither CML nor CLL phagocytes displayed a consistent depression of either engulfment or of bactericidal functions, compared with phagocytes from normal controls.

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A clinical and pathological study of resistance to infection in chronic lymphatic leukemia

Cited by 22 publications

References 8 publications

Defective complement activity in chronic lymphocytic leukemia

Defective complement activity in chronic lymphocytic leukemia

Impairment of neutrophil chemotaxis by serum from patients with chronic lymphoproliferative disease.

Engulfment and bactericidal capabilities of peripheral blood leukocytes in chronic leukemias

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