Lindsey Finklea, MD

Targeted laboratory testing and an understanding of the type I and type IIb immune pathways help clinicians characterize CIndU and explain to patients why their skin reacts the way it does.

Laboratory Workup and Mast Cell Pathophysiology in CIndU

In "Laboratory Workup and Mast Cell Pathophysiology in CIndU," the panel moves from the history to the bloodwork and the biology beneath it.

Dr. Cotter asks which laboratory tests help distinguish CIndU subtypes. Dr. Finklea explains that when CSU and CIndU overlap, she orders a complete blood count with differential, total IgE, anti-thyroid peroxidase antibodies, and an erythrocyte sedimentation rate or C-reactive protein. Updated guidelines suggest similar testing for certain CIndU subtypes, including cold urticaria and symptomatic dermographism. In these patients she typically expects elevated IgE, normal basophils, normal CRP, and negative anti-TPO antibodies.

Dr. Trotter notes that overlap between subtypes may reach 35% in the literature. She adds the CSU workup when an overlap is suspected and extends it for cold urticaria. Without formal provocation tools, her clinic uses ice cube testing and even a small treadmill to reproduce cholinergic symptoms. Dr. Cotter jokes that this amounts to a dermatology stress test.

Dr. Finklea then turns to pathophysiology. CIndU is not fully elucidated, but it is considered primarily mast cell driven. Basophils, neutrophils, B cells, T cells, and sensory nerves also contribute. Two immune pathways activate the mast cell. Type I autoallergy is IgE mediated, with IgE binding autoallergens such as double-stranded DNA, IL-24, or thyroid peroxidase. Type IIb autoimmunity is IgG mediated. Both converge on Bruton tyrosine kinase, triggering histamine and cytokine release.

She believes type I is dominant in CIndU, supported by response to anti-IgE therapy and typical laboratory findings. Subtype nuances exist, including neutrophil involvement in delayed pressure urticaria, MRGPRX2 and gut microbiome links in dermographism, and adrenergic features in cholinergic urticaria. Dr. Trotter closes by describing how patients want to know why, and how she explains autoreactivity and the skin-gut axis.

"The Hidden Quality-of-Life and Mental Health Burden of CIndU,"

 turns to the toll CIndU takes on sleep, work, school, and mental health.Welcome back to another HCPLive Peer Exchange series. In "CIndU Subtypes, Overlap With CSU, and Practical Provocation Testing," moderator David Cotter, MD, PhD is joined by Shannon Trotter, DO, FAOCD, FAAD and Lindsey Finklea, MD to open the series on chronic inducible urticaria.

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Chronic inducible urticaria spans many subtypes and frequently overlaps with chronic spontaneous urticaria, making careful history taking and pragmatic provocation testing central to an accurate diagnosis.

CIndU Subtypes, Overlap With CSU, and Practical Provocation Testing

Welcome back to another HCPLive Peer Exchange series. In "CIndU Subtypes, Overlap With CSU, and Practical Provocation Testing," moderator David Cotter, MD, PhD is joined by Shannon Trotter, DO, FAOCD, FAAD and Lindsey Finklea, MD to open the series on chronic inducible urticaria.

Dr. Cotter opens by asking Dr. Trotter to outline the principal CIndU subtypes. She identifies symptomatic dermographism, cholinergic urticaria, and cold urticaria as the three most common forms seen in practice. Symptomatic dermographism is more common than many clinicians assume, affecting an estimated 2% to 5% of the population. Beyond these three, she notes heat, solar, delayed pressure, aquagenic, vibratory, and contact urticaria as less common subtypes. Dr. Cotter adds that symptomatic dermographism often surfaces incidentally during routine skin examinations, in patients who never realized they had it.

Dr. Finklea then addresses overlap between CIndU and chronic spontaneous urticaria (CSU). She estimates that 20% to 30% of patients have symptoms of both conditions, which makes the clinical picture harder to untangle. A standardized history and physical examination is therefore essential. When patients are strong historians, the trigger is usually obvious, but vague histories demand more detective work.

She illustrates the challenge with a patient who reports hives at the beach. That reaction could reflect dermographism from sand, solar urticaria, cholinergic urticaria from sweating, or even delayed pressure urticaria from being buried in sand. In such cases, clinicians rely on provocation testing to confirm the trigger.

Dr. Finklea acknowledges that most dermatology clinics lack formal provocation equipment. Clinicians often improvise with the back of a pen or a tongue depressor, an ice cube test, or hot running water. When standardized tools are available, options include the FricTest 4.0 for dermographism, TempTest for cold and heat urticaria, and pulse-controlled ergometry for cholinergic urticaria. These standardized approaches produce reproducible, predictable responses. Dr. Cotter agrees that provocation testing becomes especially valuable when overlapping features obscure the trigger.

"Laboratory Workup and Mast Cell Pathophysiology in CIndU,"

 features Dr. Finklea walking through laboratory evaluation and the immune pathways that converge on the mast cell.

Lindsey Finklea, MD

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