Oxacillin-Induced Granulocytopenia

Fallon, John; Tall, Alan R.; Janis, Mark G.; Brauer, Mark J.

doi:10.1159/000207758

Cited by 7 publications

(11 citation statements)

References 9 publications

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“…I cannot agree with Fallon et al [1] that there is no published literature reporting the occurrence of granulocytopenia secondary to oxacillin therapy. Probably, the first case of oxacillin-induced neutropenia was reported by Freedman [2] in January 1965 in a 33-year-old woman following 272 months of therapy with oral oxacillin, 3 g/day.…”

contrasting

confidence: 66%

Oxacillin-induced Granulocytopenia

1979

Acta Haematol

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contrasting

confidence: 66%

Oxacillin-induced Granulocytopenia

1979

Acta Haematol

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“…Mechanisms on the pathophysiology of β-lactam-induced neutropenia have been proposed and like other causes of drug-induced neutropenia involve both a direct toxic effect inhibiting granulopoiesis and an immunologic reaction involving drug-induced or drug-dependent antibodies. 3,4,8,[10][11][12][13][14][15][16][17][18][19]68,69 Genetic variation causing predisposition to drug-induced neutropenia has been described and may play a role by increasing risk of a reaction to a specific agent. 70,71 A recent review of drug-induced agranulocytosis concluded that the available evidence supports an immunemediated mechanism as the primary pathogenesis.…”

Section: Pathogenesismentioning

confidence: 99%

“…Bone marrow studies generally reveal granulopoietic hypoplasia, secondary to the presence of immature granulocyte precursors, and apparent myeloid maturation arrest, presumably as a result of antibody-mediated destruction of mature myeloid cells. 1,8,10,12,20,68 Drug-induced neutropenia with a more rapid onset and resolution (<2 days) suggests peripheral neutrophil destruction by antineutrophil antibodies, whereas delayed resolution (2-7 days or longer) may indicate the presence of marrow toxicity and maturation arrest. Protracted recovery (14 days) may represent depletion of myeloid precursors.…”

Section: Pathogenesismentioning

confidence: 99%

“…Cumulative β-lactam dose appears to be an important factor, suggesting that the reaction may be triggered by accumulation of toxic metabolites. 3,4,[10][11][12][13][14][15][16][17][18][19][20] Primary management of β-lactam-induced neutropenia involves discontinuation of the offending agent. To expedite Annals of Pharmacotherapy 55 (8) resolution of neutropenia, the use of granulocyte-colony stimulating factor (G-CSF) has been advocated, particularly for those with poor prognosis.…”

Section: Introductionmentioning

confidence: 99%

“…When additional antimicrobial therapy is indicated, controversy exists over the safety of a direct substitution to an alternative β-lactam in the setting of this reaction. Although several early reports indicate success with this strategy, 10,12,[25][26][27][28] it has been discouraged in other cases describing relapse of neutropenia following rechallenge. 7,[29][30][31] The present report reviews the incidence, management, and current understanding of the mechanism of β-lactam-induced neutropenia and discusses the practicality and evidence for a direct switch to an alternative β-lactam class with low cross-reactivity.…”

Section: Introductionmentioning

confidence: 99%

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A Review of β-Lactam–Associated Neutropenia and Implications for Cross-reactivity

2020

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Objective: To review the incidence, management, and current understanding of the pathophysiology of β-lactam–induced neutropenia and to critically evaluate the practicality and safety of direct substitution to an alternative β-lactam in the setting of this reaction. Data Sources: A literature analysis using the PubMed and Ovid search engines (July 1968 to October 2020) was performed using the search terms neutropenia, leukopenia, β-lactam, nonchemotherapy, agranulocytosis, and G-CSF (granulocyte colony-stimulating factor). Study Selection and Data Extraction: The included English-language studies evaluated the incidence, mechanism, and/or management of β-lactam–induced neutropenia in pediatric or adult patients. Data Synthesis: Drug-induced neutropenia is a well-documented adverse reaction of β-lactam antibiotics, with an incidence of approximately 10% following at least 2 weeks of intravenous therapy. However, multiple gaps in knowledge remain in the mechanism of pathophysiology and optimal management of this reaction. Both direct toxic and immune-mediated mechanisms have been implicated. Although the cornerstone of management includes cessation of the offending agent, controversy exists on the appropriateness of direct substitution or future use of an alternative β-lactam. Relevance to Patient Care and Clinical Practice: Given the frequency of use and superiority of β-lactams over alternative therapy for several infectious disease states, practical recommendations are needed on the management and safe use of β-lactams following β-lactam–induced neutropenia. Conclusion: Future use of β-lactams with differing R1 side chains, particularly those from a separate class, should not be deemed contraindicated following β-lactam–induced neutropenia and may be considered when indicated, with close laboratory monitoring.

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Agranulocytosis associated with semisynthetic penicillins and cephalosporines

Schmid

Heit

Flury

1984

Blut

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Within one year we observed in the same intensive care unit seven severely polytraumatized patients with agranulocytosis (AG) associated with treatment by semisynthetic penicillins or cephalosporins combined with aminoglycosides. Antibiotics were given because of severe bacterial respiratory or generalised infections. Five patients died, four of them without haematological remission. Bone marrow aspirates showed hypoplasia of granulopoiesis due to a lack of mature cells. Leukocyte and granulocyte counts in the blood declined continuously over a period of 8 to 11 days. In average, minimal granulocyte counts occurred after 21 days of hospitalisation and 14 days of antibiotic drug exposure. Beside the incriminated antibiotics all patients were treated sporadically with other agents of which may cause AG. Granulocyte kinetics and serial bone marrow examinations of one patient suggest a phenothiazine type of AG, which is caused by a toxic damage of granulopoiesis. Declining absolute granulocyte counts in the blood together with persisting high temperatures during antibiotic treatment should give rise to the suspicion of a beginning AG.

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Oxacillin-Induced Granulocytopenia

Cited by 7 publications

References 9 publications

Oxacillin-induced Granulocytopenia

Oxacillin-induced Granulocytopenia

A Review of β-Lactam–Associated Neutropenia and Implications for Cross-reactivity

Agranulocytosis associated with semisynthetic penicillins and cephalosporines

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