Case Presentation: A 77 y/o man with Parkinson’s and BPH presented for acute onset of a pruritic morbilliform rash on the torso and extremities and odynophagia. He took sulfamethoxazole-trimethoprim two days prior to presentation. He received methylprednisolone 125mg IV x1 and was transferred for urgent dermatology consultation.Upon transfer, dermatology recommended no additional systemic steroids as the rash was more consistent with morbilliform drug eruption. He was noted to have an isolated alkaline phosphatase level of 329 U/L with no signs of acute cholecystitis or ductal dilation on ultrasound. His CBC obtained after steroids showed WBC 9.8 K/uL and eosinophils 0.2 K/uL. He received topical steroids and cetirizine. On day 2, he developed sepsis with Tmax of 39°C. He was treated for aspiration pneumonia. Despite clinical improvement in respiratory status and no leukocytosis, he continued to fever. His rash worsened, becoming more erythematous and migrating to his palms. Antibiotics were stopped on day 4, and CBC with differential on day 5 demonstrated peripheral eosinophilia (1 K/uL). Given the fevers, eosinophilia, possible liver involvement, and rash, concern for DRESS was raised. He had an elevated high-sensitivity troponin (74 ng/L) and NT-proBNP (2380 pg/mL), prompting workup for myocarditis. Echocardiogram revealed new ventricular wall motion abnormalities and a reduced EF of 40%, confirming concern for myocarditis vs. ischemia. He started oral prednisone with resolution of fevers and improvement in rash. Cardiology consult recommended initiation of metoprolol for frequent ectopy and sacubitril-valsartan for new HFrEF. Cardiac MRI on day 7 confirmed the diagnosis of myocarditis. He was placed on a prednisone taper and discharged home with close follow-up. Since discharge, his rash resolved, and he is off steroids. An ePatch showed periods of atrial and ventricular tachycardia. He was counseled to limit exercise due to an ongoing increased risk of cardiac events.
Discussion: Classically, drug reaction with eosinophilia and systemic symptoms (DRESS) is a delayed T-cell-mediated adverse drug reaction, noted 2-8 weeks after taking the offending agent. Several known agents are associated with DRESS, including antibiotics like sulfamethoxazole-trimethoprim. RegiSCAR diagnostic criteria for DRESS include acute rash, hospitalization, suspected relation to a drug, and optionally fever, atypical lymphocytosis or eosinophilia, involvement of ≥ 1 internal organ, or ≥2 enlarged lymph nodes. One review showed that mortality worsens in cases of DRESS with myocarditis when the latency period between taking the offending drug and onset of cardiovascular symptoms is shorter. In this case, the unique timing and initial steroid treatment made it difficult to differentiate the patient’s condition from a morbilliform drug eruption, hypersensitivity myocarditis, or DRESS. As a result, additional systemic steroids were delayed. This case argues for considering DRESS even in acute cases to avoid potential organ damage and to consider how early interventions can alter the presentation.
Conclusions: Our patient developed myocarditis and new HFrEF as a result of a hypersensitivity reaction to sulfamethoxazole-trimethoprim. Due to the presentation timeline, treatment was delayed, resulting in increased length of stay and unnecessary antibiotics. We suggest a work-up for systemic inflammatory responses in any case of a morbilliform drug eruption to a known offender to ensure timely intervention.