Suspected Mast Cell Activation Mimicking Heart Failure Exacerbation and Abdominal-Wall Cellulitis in a...

Mast cell activation syndrome (MCAS) is a mediator-driven disorder characterized by episodic, multisystem symptoms that can resemble common cardiopulmonary and infectious conditions. Diagnostic confirmation often relies on demonstration of mast cell mediator release (eg, event-related serum tryptase rise) and clinical response to anti-mediator therapy; however, access to specialized testing may be limited in low-resource settings.

A 75-year-old woman with recently diagnosed heart failure with reduced ejection fraction (HFrEF) presented with seven days of diffuse edema, severe pruritus with abdominal-wall erythema and thickening, wheezing and dyspnea, and nausea with vomiting. Symptoms began one day after ingestion of an unspecified herbal preparation. She was afebrile and hemodynamically stable Laboratory evaluation showed elevated total IgE (634 IU/mL) with normal C-reactive protein and no leukocytosis. Imaging demonstrated cardiomegaly with a small right pleural effusion and diffuse abdominal-wall edema without abscess. Although cellulitis and heart failure exacerbation were initially considered, the combination of multisystem involvement, lack of infectious features, and recent trigger exposure supported a suspected mast-cell-mediated reaction, with MCAS considered in the differential diagnosis. Because detailed long-term symptom history and confirmatory mediator testing were unavailable, definitive diagnosis of MCAS could not be established. Serum tryptase and urinary mediator assays were unavailable. She was treated with cetirizine, famotidine, and montelukast while continuing guideline-directed heart failure therapy and receiving low-dose diuresis; antibiotics were withheld. Symptoms resolved rapidly, and she remained asymptomatic at four-week follow-up.

This case highlights that acute mast-cell-mediated reactions may mimic heart failure exacerbation and cellulitis, particularly when cutaneous, respiratory, and gastrointestinal manifestations occur together after a potential trigger. In low-resource settings, careful exclusion of infection and true cardiogenic worsening, combined with close assessment of therapeutic response, may help guide management. However, in the absence of recurrent episodes and confirmatory mediator testing, a definitive diagnosis of MCAS should be made cautiously.