Altered surface marker expression and function of G‐CSF‐induced neutrophils from test subjects and patients under chemotherapy

Spiekermann, Karsten; Emmendoerffer, Andreas; Elsner, J.; Raeder, Evelin; Lohmann‐Matthes, Marie‐Luise; Prahst, A; Link, Hartmut; Freund, Mathias; Welte, Karl; Roesler, Joachim

doi:10.1111/j.1365-2141.1994.tb04866.x

Cited by 44 publications

(36 citation statements)

References 28 publications

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“…In addition, these neutrophils have decreased FcgRIII expression as compared with baseline. These changes were similar in magnitude when compared with both effects seen in healthy volunteers (Kerst et al, 1993a) and in non-HIV-infected individuals treated with chemotherapy and G-CSF (Spiekermann et al, 1994). In contrast to a previous report by Capsoni et al (1992), we could not demonstrate expression of FcgRI on neutrophils before start of treatment.…”

Section: Discussionsupporting

confidence: 66%

Addition of granulocyte colony‐stimulating factor to chemotherapy in patients with AIDS‐related lymphoma: effects on neutrophil Fcγ receptor expression and soluble FcγRIII plasma levels

et al. 1997

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Summary. AIDS-related neutropenia and neutrophil dysfunction can (partly) be reversed by granulocyte-colony stimulating factor (G-CSF). We studied the effect of G-CSF on neutrophil increment and levels of soluble Fcg receptor type III in 15 patients with AIDS-related lymphoma (ARL) undergoing chemotherapy. In six of these patients we performed a detailed kinetic analysis of the membrane expression of the functionally important Fcg-receptors type I, II and III. In all these patients G-CSF induced FcgRI positive neutrophils with a decreased expression of the FcgRIII receptor. These changes were similar to those seen both in healthy volunteers and in non-HIV-infected individuals treated with chemotherapy. Interestingly, the mean neutrophil and sFcgRIII increment were significantly lower and more patients had a nadir granulocyte count < 0 . 5 × 10 9 /l after the first cycle than after the second cycle of chemotherapy. This may be related to a therapy-associated decrease in HIV-1 viral load.The conclusion is that patients treated with chemotherapy for ARL have a qualitatively normal response to G-CSF.

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Section: Discussionsupporting

confidence: 66%

Addition of granulocyte colony‐stimulating factor to chemotherapy in patients with AIDS‐related lymphoma: effects on neutrophil Fcγ receptor expression and soluble FcγRIII plasma levels

et al. 1997

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“…In addition to the amelioration of severe and long-lasting neutropenia, systemic G-CSF or GM-CSF activates neutrophil migration, chemotaxis, phagocytosis and cytotoxicity. 127 In addition, G-/GM-CSF may exert an effect on epithelial cell proliferation of the oral mucosa via the paracrine mechanisms of fibroblasts. However the precise mechanisms are unknown.…”

Section: G-/gm-csfmentioning

confidence: 99%

Prophylaxis and treatment of chemo- and radiotherapy-induced oral mucositis – are there new strategies?

Karthaus

Rosenthal

Ganser

1999

Bone Marrow Transplant

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Summary:Oral mucositis is a major dose-limiting toxic effect of intensive cancer chemotherapy. Oral complications may lead to dose reduction or delay in further cancer treatment. Mucositis can be caused directly by cytotoxic effects and indirectly by sustained neutropenia after cytostatic therapy. An impaired mucosal barrier predisposes to life-threatening septic complications during aplasia. The prevalence of an oral focus in febrile neutropenia has been reported in up to 30% of cases and also reduces quality of life. The basic strategies aim at pain relief and prevention of bacterial and fungal infectious complications. However, no effective causal prophylaxis or treatment of oral mucositis is widely accepted. The introduction of cytokines, eg granulocytemacrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) for oral mucositis may be particularly effective and offer a new and hopeful approach. At present, the optimal growth factor, best schedule, effective dosage and best mode of application is not known.

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“…In only four out of 16 episodes with G-CSF, was WHO grade IV mucos- Table 4 Effects of oral mucositis on the incidence and duration of fever, need and days of opioids therapy, and days in hospital In addition, the G-CSF patients recovered earlier from mucositis (100% vs 80% at day 20, P = 0.22). This effect is possibly due to local activation of neutrophils by G-CSF, since it is well known that G-CSF stimulates migration, phagocytosis, and cytotoxicity of neutrophils, 18 the precise mechanism, however, being unknown.…”

Section: Discussionmentioning

confidence: 99%

“…14-17 G-CSF is known to stimulate migration, phagocytosis and cytotoxicity of neutrophils. 18 We postulated an effect of topical oral G-CSF on neutrophils in the oral cavity as a rationale for this study.…”

mentioning

confidence: 99%

Effect of topical oral G-CSF on oral mucositis: a randomised placebo-controlled trial

Karthaus

Rosenthal

Huebner

et al. 1998

Bone Marrow Transplant

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Summary:Oral mucositis is a dose-limiting toxicity of intensive chemotherapy. It is caused directly by the cytotoxic effect of chemotherapeutic agents and indirectly by sustained neutropenia. Severe oral mucositis is an important predisposing factor for life-threatening septic complications during aplasia. It also reduces quality of life. At present, no effective causal prophylaxis or treatment against oral mucositis is established. We performed a prospective randomised placebo-controlled trial using topical oral r-metHuG-CSF (filgrastim) in highgrade lymphoma patients treated according to the B-NHL protocol, which contains high-dose methotrexate and causes severe oral mucositis (WHO grades I-IV) in Ͼ50% of patients. Between August 1996 and July 1997, a total of 32 chemotherapy cycles were documented in eight patients (four male, four female). Mucosal erythema and ulceration were recorded. All patients assessed their oral pain and impact on swallowing daily, using a subjective scale from no to maximal discomfort (1-10). In addition, oral mucositis was assessed according to the WHO score. Filgrastim was administered in 16 cycles as a viscous mouthrinse (carboxymethylcellulose 2%, oleum citrii) 4 × 120 g/day from days 10 to 16. Sixteen cycles were given to control patients, of these 14 with placebo, and another two cycles with no treatment. Severe mucositis (WHO grade III/IV) was documented in 21 of 32 cycles (65.5%). A difference of borderline significance was observed for the reduction of maximum severity of oral mucositis between G-CSF vs placebo (P = 0.058), with a reduction of WHO grade IV of 50% (four G-CSF vs eight control). The number of days in hospital was reduced significantly in the G-CSF group (P = 0.02). In conclusion, topical oral G-CSF mouthrinses may be beneficial to reduce oral mucositis. Keywords: oral mucositis; topical G-CSF; high-grade lymphoma; randomised trial Oral mucositis is a major side-effect of chemotherapy. It occurs with an incidence of about 40%. 1,2 The causes of

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Altered surface marker expression and function of G‐CSF‐induced neutrophils from test subjects and patients under chemotherapy

Cited by 44 publications

References 28 publications

Addition of granulocyte colony‐stimulating factor to chemotherapy in patients with AIDS‐related lymphoma: effects on neutrophil Fcγ receptor expression and soluble FcγRIII plasma levels

Addition of granulocyte colony‐stimulating factor to chemotherapy in patients with AIDS‐related lymphoma: effects on neutrophil Fcγ receptor expression and soluble FcγRIII plasma levels

Prophylaxis and treatment of chemo- and radiotherapy-induced oral mucositis – are there new strategies?

Effect of topical oral G-CSF on oral mucositis: a randomised placebo-controlled trial

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