Recognition and Management of Medication Excipient Reactivity in Patients With Mast Cell Activation Syndrome.

Mast cell activation syndrome (MCAS) is a complex disorder hallmarked by chronic multisystem inflammatory, allergic and growth dystrophic phenomena caused by inappropriate mast cell activation. MCAS has been estimated to affect as many as 17% of the population with a severity ranging from mild to life-threatening. MCAS patients are more sensitive than the average person to chemicals in the environment, including the nondrug ("inactive") ingredients (excipients) in medications and supplements. Excipient reactivity may explain unusual side effects to medications health professionals often find puzzling, such as the patient who appears intolerant of prednisone, acetaminophen, levothyroxine, or a vitamin. We present a series of patients with MCAS to illustrate important points regarding excipient reactivity which may be useful in everyday practice.

Fatal copper deficiency from excessive use of zinc-based denture adhesive.

INTRODUCTION: Human stores of zinc and copper exist in dynamic equilibrium; an increase in one causes a fall in the other, and clinical consequences of toxicity or deficiency of one or the other may result. Some of the most widely used denture adhesives are zinc based, creating a potential for zinc toxicity and corresponding copper deficiency. A case of denture adhesive-based zinc toxicity with corresponding copper deficiency leading to fatal ascending sensorimotor polyneuropathy was identified. The objectives of this study were to illustrate the evolution, and disparate response to treatment, of neurologic and hematologic abnormalities resulting from copper deficiency, and to discuss opportunities to mitigate denture adhesive-related zinc toxicity. METHODS: Detailed clinical and laboratory data for the subject patient were compiled. The patient received copper supplementation. Copper and zinc levels were obtained posttreatment at varying intervals. RESULTS: Hematologic and neurologic abnormalities progressed, as excessive use of zinc-based denture adhesive persisted. Hematologic and neurologic consultants were initially considered purely hematologic or neurologic diagnoses. Eventual consideration of unifying hypotheses led to definitive diagnosis 10 months after presentation. Hematologic abnormalities responded to copper supplementation, but neurologic abnormalities did not. The patient died of aspiration likely due to severe sensorimotor polyneuropathy. CONCLUSIONS: Early recognition of copper deficiency and improved warnings regarding excessive use of zinc-based denture adhesives may be the routes to improved outcomes.