Flecanide-Induced Immune Neutropenia

Samlowski, Wolfram E.

doi:10.1001/archinte.1987.00370020201066

Cited by 20 publications

(1 citation statement)

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“…Drugs commonly leading to transient neutropenia include, but are not limited to anticonvulsants (carbamazepine, valproate), antimicrobials (sulfonamides, penicillins, trimethoprim/sulfamethoxazole), antipsychotics (clozapine, olanzapine, phenothiazines), and antithyroidals (methimazole, propylthiouracil) [4]. Furthermore, antiarrhythmic agents such as tocainide, procainamide, and flecainide are generally known to cause agranulocytosis [5,6]. Drug-induced agranulocytosis is also characterized into two groups based on the mechanism of agranulocytosis.…”

Section: Discussionmentioning

confidence: 99%

Amiodarone-Induced Neutropenia: An Uncommon Side Effect of a Common Drug

Kohli

Sharma

2020

Cureus

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Amiodarone is widely used as an antiarrhythmic agent for the treatment of both supraventricular and ventricular arrhythmias in various inpatient as well as outpatient settings. Classified as a class III antiarrhythmic agent, it acts mainly by inhibition of potassium channels in the cardiac muscle. Adverse effects are quite common and usually involve pulmonary, gastrointestinal, endocrine, dermatologic, or neuromuscular systems. Although hematologic side effects including thrombocytopenia have also been reported, amiodarone-induced neutropenia is quite rare. We present a case of amiodarone-induced neutropenia in a 66-year-old Caucasian gentleman. He presented to our hospital with cardiac arrest due to ventricular-fibrillation and had received amiodarone as a part of his therapy. His hospital course was complicated by neutropenia which was found to have a clear temporal relation with amiodarone. His initial white blood cell count was 6400/mm3 with an absolute neutrophil count (ANC) of 4800/mm3. His ANC started to downtrend and reached a nadir of 400/mm3 at day six of therapy. This improved significantly after stopping amiodarone, without any change in other medications. Given the rapid improvement of his neutropenia with the discontinuation of amiodarone, further workup with a bone marrow biopsy was not performed. Severe selective neutropenia, also known as agranulocytosis, is a life-threatening condition due to increased risk of severe infections. Antiarrhythmic agents such as tocainamide, procainamide, and flecainide are generally known to cause agranulocytosis. The mechanism of agranulocytosis or neutropenia is thought to be mediated by either immune-mediated destruction or direct and indirect toxicity to myeloid precursors. Although amiodarone has been in use for over 20 years in the management of tachyarrhythmias, agranulocytosis as a direct side effect of amiodarone therapy has been rarely reported. It is important to keep in mind this rare but potentially life-threatening adverse effect of amiodarone when initiating therapy.

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Section: Discussionmentioning

confidence: 99%

Amiodarone-Induced Neutropenia: An Uncommon Side Effect of a Common Drug

Kohli

Sharma

2020

Cureus

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Idiosyncratic drug‐induced agranulocytosis: Possible mechanisms and management

2009

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The incidence of drug‐induced neutropenia has not changed in the western hemisphere over the last 30 years. Yet, the drug panorama has changed considerably. This implies that host factors may play an intriguing role for this idiosyncratic reaction. The knowledge as to mechanisms for the reaction has advanced with emerging understanding of neutropoiesis and immune regulation. Nonetheless, it is still remarkably difficult to pinpoint why and how a drug causes this unexpected, severe adverse event in a patient. Patient characteristics, e.g. genetics, appear to be keys for better understanding, predictions and prevention. Am. J. Hematol. 2009. © 2009 Wiley‐Liss, Inc.

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Immune neutropenia mediated by micafungin

2019

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| CASE PRESENTATIONA 70-year-old male with diabetes mellitus and coronary artery disease was found unresponsive at his home. Upon arrival to the hospital, he was confused and was noted to have a right-sided visual field deficit.Given the patient's cardiovascular risk factors, the patient's presentation with right-sided visual field deficit was most consistent with acute stroke. Other etiologies include an intracranial mass of malignant or infectious etiology, especially in the setting of underlying diabetes mellitus and resultant immunosuppression. The patient unfortunately presented outside the window for rtPA therapy. MRI of the brain demonstrated severe stenosis of the left internal carotid artery and a focus of decreased attenuation in the left occipital area, consistent with an acute ischemic stroke. He was started on atorvastatin and continued on aspirin. Also noted on the MRI was a nasopharyngeal mass with direct skull base invasion and external compression of the left proximal internal carotid artery. His chest radiograph was unremarkable. Testing for HIV was negative. Blood cultures grew S. pneumoniae. The differential for this nasopharyngeal mass included malignant and infectious etiologies. The patient's history of diabetes mellitus placed him at risk for the development of severe infection with microbes, such as Mucorales, Streptococcus pyogenes, Alternaria, Candida, and metastatic infection, among others. Given the suspicion of an underlying malignancy, the nasopharyngeal mass was biopsied and found to represent a fungal mass (Alternaria species). As the fungal mass involved critical vasculature, surgical resection was considered excessively risky and the patient was started on multiple antibiotic and antifungal therapies including cefepime, metronidazole, vancomycin, meropenem, amphotericin, micafungin, and caspofungin (Figure 1). The patient initially received cefepime, metronidazole, and vancomycin, and once blood cultures grew Streptococcus pneumoniae, he was narrowed to vancomycin. Multiple antifungal therapies were administered simultaneously given the patient's life-threatening infection with Alternaria. The patient's absolute neutrophil count (ANC) began to trend down to a nadir of 80 (Figure 1). His hemoglobin (9.3 g/dL) and platelet count (266 000/μL), as well as his absolute lymphocyte, monocyte, eosinophil and basophils counts, remained stable. The peripheral blood smear was unremarkable. Filgrastim was administered and the patient's ANC recovered. Drug induced neutropenia was suspected as the most likely etiology for this patient's decline in neutrophil count. Systemic infection was also considered but was felt to be less likely given the absence of other cytopenias. The stability of the patient's hemoglobin and platelet count argued against a process of general bone marrow suppression. A sample of the patient's serum was submitted to the Blood Center of Wisconsin to evaluate for immune neutropenia. Flow cytometric analysis revealed the presence of micafungin-dependent, neutrophilreactiv...

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Flecanide-Induced Immune Neutropenia

Cited by 20 publications

References 1 publication

Amiodarone-Induced Neutropenia: An Uncommon Side Effect of a Common Drug

Amiodarone-Induced Neutropenia: An Uncommon Side Effect of a Common Drug

Idiosyncratic drug‐induced agranulocytosis: Possible mechanisms and management

Immune neutropenia mediated by micafungin

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