Haematopoiesis in drug-induced agranulocytosis

Ruvidic, R

doi:10.1016/0753-3322(96)84825-6

Cited by 2 publications

(7 citation statements)

References 22 publications

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“…Drug-induced agranulocytosis (DIA) is defined as severe neutropenia (granulocyte count < 0.5 x 10 3 /mm 3 ) due to an unpredictable adverse drug reaction in hypersensitive individuals. 1,2 Patients generally have normal erythrocyte and platelet levels. 2 The incidence of DIA is estimated to be approximately 2.6-10 cases/million drug exposures/year.…”

Section: (Pharmacotherapy 1999;19(3):299-305)mentioning

confidence: 99%

“…1,2 Patients generally have normal erythrocyte and platelet levels. 2 The incidence of DIA is estimated to be approximately 2.6-10 cases/million drug exposures/year. 3 The precise incidence, however, is difficult to determine since reliable information regarding drug use is often unavailable, 4 and thus DIA is probably underreported.…”

Section: (Pharmacotherapy 1999;19(3):299-305)mentioning

confidence: 99%

“…1 In vitro studies indicated that insignificant numbers of colony-forming unit granulocyte-macrophages (CFU-GMs) are present in the agranulocytic phase. 2 Aplasia in bone marrow is followed by a regenerative phase in which the number of CFU-GM approaches normal to increased levels, with successive appearance of myeloid precursors (myeloblasts, promyelocytes, myelocytes). 2 The appearance of these precursors precedes granulocyte count recovery by approximately 7 days.…”

Section: (Pharmacotherapy 1999;19(3):299-305)mentioning

confidence: 99%

“…2 Aplasia in bone marrow is followed by a regenerative phase in which the number of CFU-GM approaches normal to increased levels, with successive appearance of myeloid precursors (myeloblasts, promyelocytes, myelocytes). 2 The appearance of these precursors precedes granulocyte count recovery by approximately 7 days. 2,6 The presence of earliest forms of the granulocytic series may be characterized as maturation arrest.…”

Section: (Pharmacotherapy 1999;19(3):299-305)mentioning

confidence: 99%

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Nonchemotherapy Drug‐Induced Agranulocytosis: A Review of 118 Patients Treated with Colony‐Stimulating Factors

Beauchesne

Shalansky

1999

Pharmacotherapy

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To determine the role of growth factors in nonchemotherapy drug-induced agranulocytosis, we reviewed 118 published reports of administration of colony-stimulating factors for the disorder. Main outcomes were total duration of neutropenia and mortality. The mean time to neutrophil recovery was 4.6 +/- 3.2 days and 7.7 +/- 5.1 days in patients with a granulocyte count at diagnosis of 0.1-0.5 x 10(3)/mm3 and less than 0.1 x 103/mm3, respectively. The mortality rate was 4.2%. Without therapy with growth factors, the mean time to neutrophil recovery after discontinuation of the offending agent was reported to be 10 +/- 8 days. The mortality rate was 16% in one study. We conclude that hematopoietic growth factors may shorten the duration of neutropenia and reduce mortality in patients with severe drug-induced agranulocytosis.

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Section: (Pharmacotherapy 1999;19(3):299-305)mentioning

confidence: 99%

Section: (Pharmacotherapy 1999;19(3):299-305)mentioning

confidence: 99%

Section: (Pharmacotherapy 1999;19(3):299-305)mentioning

confidence: 99%

Section: (Pharmacotherapy 1999;19(3):299-305)mentioning

confidence: 99%

See 2 more Smart Citations

Nonchemotherapy Drug‐Induced Agranulocytosis: A Review of 118 Patients Treated with Colony‐Stimulating Factors

Beauchesne

Shalansky

1999

Pharmacotherapy

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“…In general, agranulocytosis is thought to be caused by direct drug-induced toxicity or immune-mediated reaction against hematopoietic stem cells (Meyer-Gessner et al, 1994;Ruvidic, 1996). Vesnarinone was reported to suppress the colony formation of blasts obtained from leukemia patients and the proliferation of several leukemia cell lines (Fujiwara et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Vesnarinone Causes Oxidative Damage by Inhibiting Catalase Function through Ceramide Action in Myeloid Cell Apoptosis

Kondo

Suzuki²,

Kitano³

et al. 2002

Mol Pharmacol

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Vesnarinone is an effective inotropic agent for treating congestive heart failure, but its clinical usage is restricted because of the severe side effect of agranulocytosis. In myeloid HL-60 cells, vesnarinone increased the intracellular content of a proapoptotic lipid mediator, ceramide, in a time-and dose-dependent manner. Vesnarinone-induced apoptosis was significantly enhanced by simultaneous treatment with a cell-permeable N-acetyl sphingosine (C2-ceramide). Treatment with neither vesnarinone, C2-ceramide, nor simultaneously with vesnarinone and C2-ceramide caused a marked increase of reactive oxygen intermediates (ROI) generation measured by the 2Ј,7Ј-dichlorofluorescin method. However, oxidative damage judged by the production of lipid peroxidates and the nitroblue tetrazolium-reducing ability were enhanced more significantly by simultaneous treatment with vesnarinone and C2-ceramide than by vesnarinone alone. Moreover, vesnarinone inhibited catalase function both at the protein and activity level, and this inhibition was synergistically enhanced by C2-ceramide, and vesnarinone-induced oxidative damage and apoptosis were significantly suppressed by treatment of HL-60 cells with purified catalase. C2-ceramide enhanced vesnarinone-induced inhibition of the ROI-scavenging enzyme catalase at the levels of protein and activity in HL-60 cells; in contrast, however, vesnarinone did not induce ceramide generation, oxidative damage, or catalase depletion in HL-60/ves cells, where vesnarinone could not induce apoptosis. Taken together, the results suggest that vesnarinone induces myeloid cell apoptosis by increasing oxidative damage via ceramide-induced inhibition of catalase function.

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Haematopoiesis in drug-induced agranulocytosis

Cited by 2 publications

References 22 publications

Nonchemotherapy Drug‐Induced Agranulocytosis: A Review of 118 Patients Treated with Colony‐Stimulating Factors

Nonchemotherapy Drug‐Induced Agranulocytosis: A Review of 118 Patients Treated with Colony‐Stimulating Factors

Vesnarinone Causes Oxidative Damage by Inhibiting Catalase Function through Ceramide Action in Myeloid Cell Apoptosis

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