RESUMO
Infectious tenosynovitis can involve both flexor and extensor tendons of the extremities. If left untreated, it can lead to high morbidity and mortality. Most emergency providers recognize the signs and symptoms of flexor and extensor tenosynovitis of the hand. However, extensor tenosynovitis of the hallucis longus tendon is a rare condition with a risk of complications similar to infectious tenosynovitis of the hand. This case report describes a presentation of extensor tenosynovitis of the hallucis longus tendon. Clinical suspicion is essential to help the provider not miss this rare condition, which can lead to significant morbidity if not treated promptly or appropriately.
RESUMO
Nimodipine, an L-type cerebroselective calcium channel antagonist, is the only drug approved by the US Food and Drug Administration for the neuroprotection of patients with aneurysmal subarachnoid hemorrhage (aSAH). Four randomized, placebo-controlled trials of nimodipine demonstrated clinical improvement over placebo; however, these occurred before precision medicine with pharmacogenomics was readily available. The standard enteral dose of nimodipine recommended after aSAH is 60 mg every 4 h. However, up to 78% of patients with aSAH develop systemic arterial hypotension after taking the drug at the recommended dose, which could theoretically limit its neuroprotective role and worsen cerebral perfusion pressure and cerebral blood flow, particularly when concomitant vasospasm is present. We investigated the association between nimodipine dose changes and clinical outcomes in a consecutive series of 150 patients (mean age, 56 years; 70.7% women) with acute aSAH. We describe the pharmacogenomic relationship of nimodipine dose reduction with clinical outcomes. These results have major implications for future individualized dosing of nimodipine in the era of precision medicine.
Assuntos
Bloqueadores dos Canais de Cálcio , Nimodipina , Farmacogenética , Hemorragia Subaracnóidea , Humanos , Nimodipina/administração & dosagem , Nimodipina/efeitos adversos , Hemorragia Subaracnóidea/tratamento farmacológico , Hemorragia Subaracnóidea/genética , Hemorragia Subaracnóidea/complicações , Pessoa de Meia-Idade , Feminino , Masculino , Bloqueadores dos Canais de Cálcio/administração & dosagem , Bloqueadores dos Canais de Cálcio/efeitos adversos , Bloqueadores dos Canais de Cálcio/uso terapêutico , Idoso , Farmacogenética/métodos , Resultado do Tratamento , Relação Dose-Resposta a Droga , Adulto , Medicina de Precisão/métodos , Vasoespasmo Intracraniano/tratamento farmacológicoRESUMO
Subarachnoid hemorrhage is a devastating form of stroke with often detrimental outcomes for patients. Here we describe a patient with subarachnoid hemorrhage treated with nimodipine, which resulted in marked bradycardia with junctional atrioventricular heart block. Nimodipine is metabolized predominantly by the cytochrome P450 3A subfamily, and its use is often associated with adverse events, such as hypotension and bradycardia, which can be exacerbated by advanced age. Our patient had the CYP3A5*3/*3 genotype, possibly predisposing her to poor metabolism of this drug. Our case report demonstrates the potential for pharmacogenomics in patients with subarachnoid hemorrhage to help predict their response to nimodipine, minimize adverse drug reactions, and potentially individualize dosing to improve future clinical outcomes.
