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A rare case report of apixaban-induced lichenoid eruption.

ABSTRACT: With recent increase in the use of direct oral anticoagulants (DOACs), several new cases of adverse drug reactions (ADRs) have been identified in pharmacovigilance surveys. These ADRs can result in significant mortality and morbidity if not identified and treated promptly. It is important for physicians to recognize that immunologically mediated delayed hypersensitivity reactions, although rare in occurrence, can have significant impact on patient's quality of life. To the best of our knowledge, we report the first case of lichenoid eruption associated with apixaban. We further provide evidence of tolerance to rivaroxaban in the same patient. Plain language summary:Apixaban-induced lichenoid eruption Well documented case reports, although providing evidence of probable causal relationship between a drug and specific adverse drug reactions (ADRs), can increase awareness amongst clinicians treating patients with direct oral anticoagulants (DOACs), especially with its rapid utilization. Rare ADRs are difficult to detect as clinical trials of DOACs lacked enough patient sample, making post-marketing reporting of such events important so both patients and clinicians can be vigilant to help with prompt recognition of such symptoms. We report the first case of lichenoid eruption hypersensitivity reaction associated with apixaban in patient with tolerance to rivaroxaban.

SUBMITTER: Patil T

PROVIDER: S-EPMC7436782 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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A rare case report of apixaban-induced lichenoid eruption.

Patil Tanvi T Hanna Suzanne S Torre Wayne W

Therapeutic advances in drug safety 20200817

With recent increase in the use of direct oral anticoagulants (DOACs), several new cases of adverse drug reactions (ADRs) have been identified in pharmacovigilance surveys. These ADRs can result in significant mortality and morbidity if not identified and treated promptly. It is important for physicians to recognize that immunologically mediated delayed hypersensitivity reactions, although rare in occurrence, can have significant impact on patient's quality of life. To the best of our knowledge, ...[more]

PMID: 32874531

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Project description:Introduction and importance Subarachnoid hemorrhage (SAH) is mostly associated with head trauma. Non-traumatic subarachnoid hemorrhage is mostly due to vascular abnormalities: either hemorrhage from ruptured aneurysm or bleeding from arteriovenous malformation. Aneurysmal hemorrhage is the biggest cause in non-traumatic cases. Warfarin is associated with cerebral intraparenchymal hemorrhage, but it is rarely associated with SAH. Case presentation Here, we report the case of a 45-year-old male patient who was admitted to the neurology ward of our hospital due to acute ischemic stroke. The patient was treated with a vitamin K antagonist (warfarin). However, on the third day, his condition deteriorated (his GCS regressed from 11/15 to 5/15). His pupils were anisocoric. Brain CT showed extensive subarachnoid hemorrhage without intraparenchymal involvement. Cerebral magnetic resonance angiography ruled out aneurysmal rupture. The patient was intubated and transferred to the intensive care unit. Due to his poor condition, neurosurgical intervention could not be done. The patient was managed conservatively, but the patient passed away 4 days later in the intensive care unit. Clinical discussion Non-traumatic SAH is mostly caused by aneurysmal rupture. Warfarin increases the risk of intracranial hemorrhage and mostly causes intraparenchymal hemorrhage. Isolated warfarin-related SAH without parenchymal involvement is a rare event. Here we present a young male patient with an isolated warfarin-induced SAH. Conclusion Warfarin is rarely associated with isolated subarachnoid hemorrhage. This case highlights a young male patient with spontaneous SAH after warfarin therapy for acute ischemic stroke. Aneurysmal rupture and trauma should be excluded before a diagnosis of warfarin-induced SAH is made. Highlights • Non-traumatic subarachnoid hemorrhage (SAH) is mostly caused by aneurysmal rupture.• Warfarin increases the risk of intracranial hemorrhage and mostly causes intraparenchymal hemorrhage. Isolated warfarin-related SAH without parenchymal involvement is a rare event.• Here we present a young male patient with isolated SAH due to warfarin treatment for acute ischemic stroke.

Project description:BACKGROUND:Apixaban effectively lowers the risk of ischemic stroke and systemic embolism in patients with non-valvular atrial fibrillation. Systemic exposure to a given apixaban dose depends on multiple clearance pathways. Though routine quantification of direct oral anticoagulants (DOACs) in neurological emergency situations has not been widely established, suspected associations of DOAC peak concentrations with bleeding events and DOAC trough concentrations with efficacy and safety suggest that such information might support clinical decision making. CASE PRESENTATION:We describe the case of a 75?year-old woman with atrial fibrillation maintained on apixaban who was admitted due to suspected acute stroke. Clinical work-up did not confirm ischemic or hemorrhagic stroke but routine quantification of apixaban revealed an excessively high apixaban plasma concentration (~?3?h after the last drug intake: 1100?ng/ml (expected range: 91-321?ng/ml); ~?12?h after drug intake: 900?ng/ml (expected range: 41-230?ng/ml)) and a substantially prolonged elimination half-life (~?31?h). The corresponding apixaban concentration-to-dose ratio was 9900 (ng/ml)/(mg/kg/d) and 8100 (ng/ml)/(mg/kg/d), respectively (expected range: 249-463 (ng/ml)/(mg/kg/d)). Renal function was only moderately impaired (creatinine 1.36?mg/dl (0.5-1.1?mg/dl), creatinine clearance 40?ml/min). Genotype analyses revealed that the patient was a CYP3A5*3/*3 non-expressor, a heterozygous carrier of the ABCG2 c.421C/A alleles, and a homozygous carrier of ABCB1 c.2677?T/T and ABCB1 c.3435?T/T. In the absence of known drug interactions explaining apixaban clearance impairment, excessive apixaban concentrations were most probably caused by moderate renal impairment combined with multiple functional polymorphisms of apixaban clearance pathways. CONCLUSIONS:This case suggests that concurrent genetic polymorphisms can impair multiple apixaban elimination pathways and thus substantially increase its exposure.

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A rare case report of apixaban-induced lichenoid eruption.

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A rare case report of apixaban-induced lichenoid eruption.

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