ABSTRACT
Chronic symptomatic dermographism is a challenging dermatologic condition characterized by recurrent wheals triggered by nonspecific physical stimuli, and management typically begins with H1‐antihistamines, escalating as needed, with anti‐IgE therapy such as omalizumab reserved for refractory cases based on clinical response rather than serum IgE levels. We report a 20‐year‐old male with a long‐standing history of symptomatic dermographism and childhood atopy, provoked by minimal mechanical stimuli such as friction from clothing or light stroking of the skin, which significantly impaired his daily activities and academic performance. Diagnosis was made clinically and by exclusion of systemic disease, with laboratory investigations revealing fluctuating serum IgE levels over multiple measurements, ranging from markedly elevated to near‐normal, without correlation to disease severity, highlighting the limitations of using IgE to guide therapy. Standard management included up‐dosed second‐generation H1‐antihistamines (up to fourfold the standard dose) and intermittent short courses of oral corticosteroids resulting in partial disease control. Omalizumab was considered but not initiated, as partial clinical improvement was achieved without meeting criteria for refractory urticaria. Despite ongoing therapy, the patient continued to experience recurrent urticarial episodes during follow‐up, although with reduced frequency and severity. The case emphasizes phenotype‐driven management in chronic symptomatic dermographism and the limited role of IgE in therapeutic decision‐making.
Keywords: fluctuating IgE, monoclonal antibody therapy, omalizumab, refractory urticaria
Urticarial flare showing multiple erythematous, raised, edematous and coalescing wheals characteristic of symptomatic dermographism.

Abbreviations
- DLQI
Dermatology Life Quality Index
- FcεRI
High‐affinity receptor for the Fc region of immunoglobulin E (IgE)
- IgE
Immunoglobulin E
- UAS7
Urticaria Activity Score 7
Key Clinical Message.
In symptomatic dermographism among atopic individuals, total serum IgE may not reliably reflect disease severity and can be influenced by assay‐related variability. Clinical decision‐making should prioritize phenotype and symptom burden rather than relying solely on IgE levels. A tailored, patient‐centered approach is essential for optimal outcomes.
1. Introduction
Chronic symptomatic dermographism is a heterogeneous disorder characterized by the development of transient wheals in response to nonspecific environmental or physical stimuli [1]. Among the various subtypes, urticaria is defined by the appearance of erythematous, pruritic wheals after minimal mechanical stimulation, such as stroking the skin, friction from clothing, or pressure from surfaces [1]. These lesions typically arise within minutes and resolve spontaneously within a few hours [1]; however, recurrent episodes can significantly impair quality of life and disrupt daily activities, particularly in young adults and students [2].
Management of symptomatic dermographism is challenging due to its variable response to standard therapy [3]. H1‐antihistamines constitute the first‐line treatment, with doses escalated up to fourfold in refractory cases [1, 4]. Short courses of systemic corticosteroids may be added when H1‐antihistamines fail to control symptoms [1]. Despite these interventions, a subset of patients continues to experience severe disease manifestations, underscoring the need for alternative treatment strategies, including biologic therapy [1].
Omalizumab, a monoclonal antibody targeting IgE, has demonstrated efficacy in chronic symptomatic dermographism and select cases of urticaria that are refractory to H1‐antihistamines [5]. Although serum IgE levels have been investigated as potential biomarkers of treatment response, their clinical utility remains uncertain, as some patients with normal or fluctuating IgE levels may also respond favorably to anti‐IgE therapy [6]. These observations raise important questions regarding the pathophysiological role of IgE in symptomatic dermographism and suggest that the therapeutic effects of omalizumab may extend beyond simple IgE neutralization, potentially involving modulation of mast cell and basophil activity, as well as downstream inflammatory pathways [7].
In this report, we describe a 20‐year‐old male with chronic symptomatic dermographism and a history of childhood atopy, whose serum IgE levels fluctuated over time and whose disease severity remained consistently high. The case illustrates the limitations of relying solely on IgE to guide therapy and emphasizes the importance of phenotype‐driven management strategies.
2. Case Presentation/Examination
A 20‐year‐old male college student presented with a three‐year history of recurrent, progressively worsening urticaria, predominantly triggered by nonspecific stimuli such as light touch, friction from clothing, or contact with surfaces such as study tables. The wheals were erythematous, raised, and intensely pruritic, appearing within minutes of the stimulus and typically resolving spontaneously within a few hours. The patient reported that even minor mechanical stimulation, such as stroking the forearm, elicited wheals consistent with dermographism. There was no history of angioedema or systemic involvement. The patient had a long‐standing history of atopy since childhood, with known hypersensitivity to foods such as peanuts. He had no personal or family history of asthma, autoimmune disorders, or chronic systemic illness. Clinical examination during symptomatic periods confirmed widespread erythematous wheals predominantly on the trunk and extremities.
3. Differential Diagnosis, Investigations and Treatment
Laboratory investigations, including complete blood count, liver and renal function tests, thyroid profile, autoimmune markers, and inflammatory markers such as erythrocyte sedimentation rate (ESR) and C‐reactive protein (CRP), were all within normal limits. These results effectively ruled out secondary causes of urticaria related to systemic inflammatory, autoimmune, or metabolic disorders and supported the diagnosis of a primary urticaria phenotype rather than a systemic disease manifestation. Skin prick testing confirmed selective sensitivities for common allergens. Serial total serum IgE measurements over a period of nearly 3 years demonstrated marked fluctuation without a consistent trend or correlation to disease severity. The results varied widely between elevated and normal ranges across different time points, yet no corresponding change in clinical disease activity was observed. The patient continued to experience persistent symptomatic dermographism throughout the follow‐up period. This clear dissociation between total serum IgE levels and clinical severity highlights the limited utility of IgE as a standalone biomarker in chronic symptomatic dermographism.
For clarity and completeness, all four serial total serum IgE values obtained during the patient's disease course are summarized in Table 1, which provides a consolidated view of the laboratory findings.
TABLE 1.
Serial total serum IgE measurements in the patient.
| Date | IgE value (IU/mL) | Laboratory reference range (IU/mL) a |
|---|---|---|
| 08 Jan 2023 | 550.0 | < 200.0 |
| 08 Jan 2024 | 42.45 | < 150.0 |
| 19 Oct 2024 | 50.8 | < 100–200 |
| 21 Aug 2025 | 140.0 | < 100.0 |
Total serum IgE was measured using a standardized automated immunoassay (chemiluminescent immunoassay) in the laboratory. Reference ranges varied according to laboratory‐specific methodologies.
Disease monitoring in chronic symptomatic dermographism is better guided by validated clinical assessment tools such as the Urticaria Activity Score over 7 days (UAS7) and the Dermatology Life Quality Index (DLQI). However, these standardized instruments were not formally applied in this case, limiting objective longitudinal assessment. Despite this limitation, clinical evaluation and patient‐reported outcomes consistently indicated persistent symptomatic disease with significant impairment in daily functioning. Representative urticarial lesions during flare episodes are shown in Figures 1 and 2.
FIGURE 1.

Multiple erythematous, raised, and edematous wheals of varying sizes involving the extensor aspect of the forearm, with ill‐defined borders and blanching on pressure.
FIGURE 2.

Multiple erythematous, raised, edematous and coalescing urticarial wheals involving the trunk, with ill‐defined borders and variable sizes.
The patient was managed with second‐generation H1 antihistamines, with dose escalation according to clinical response during active disease periods. In addition, a short course of oral corticosteroids was administered during exacerbations to achieve rapid symptomatic relief. The patient was also counseled regarding avoidance of potential triggering factors which were identified as consistent precipitants of symptoms. Environmental and behavioral modifications were advised to minimize disease provocation. This treatment strategy resulted in partial but clinically acceptable improvement, with a reduction in both frequency and intensity of wheals, although complete remission was not achieved. Omalizumab was considered as a potential escalation therapy in view of persistent symptoms; however, it was not initiated as the patient demonstrated partial but stable disease control with optimized H1‐antihistamine therapy, and the overall symptom burden was considered manageable without requiring biologic intervention.
4. Conclusion and Results
The urticaria episodes also interfered with daily activities, including academic performance, because even minor physical contact, such as writing, carrying books, or wearing certain clothes, could provoke symptoms, making it difficult for the patient to concentrate, complete tasks efficiently, or maintain academic performance. Beyond the physical manifestations, the disease had a substantial impact on quality of life, as reported by the patient. He described difficulties in social interactions, including avoiding close contact with peers or family members for fear of triggering lesions, and experienced disturbances in sleep, likely due to nocturnal itching or anxiety about flare‐ups. Routine activities, such as bathing, dressing, or performing daily chores, were also affected because of the unpredictability of symptom onset and the need to avoid triggers. Overall, these findings indicate a moderate but clinically significant disease burden with both physical and psychosocial impact. In the absence of formal scoring systems, patient‐reported outcomes provided meaningful insight into disease activity and helped guide management decisions.
During follow‐up, the patient remained on second‐generation H1‐antihistamine therapy with intermittent dose adjustment and continued avoidance of triggering factors. He experienced persistent but reduced episodes of symptomatic dermographism compared to baseline, with overall improvement in daily functioning and quality of life. At last follow‐up, the disease remained partially controlled without progression to refractory disease or requiring biologic therapy.
5. Discussion
The pathophysiology of symptomatic dermographism, specifically urticaria, is multifactorial [8]. While IgE‐mediated activation of mast cells and basophils is a known mechanism in urticaria, it is increasingly recognized that mast cells can also be activated by IgE‐independent pathways, including IgG‐mediated mechanisms, complement activation, and direct physical stimulation [9]. These alternative pathways may explain why some patients continue to exhibit severe disease despite normal or fluctuating IgE levels [10].
In our patient with a strong atopic background, serum IgE measurements demonstrated marked fluctuations over time, ranging from elevated to near‐normal, and did not correlate with the frequency or severity of urticarial episodes. This observation underscores the limitations of using IgE as a sole biomarker to guide therapeutic decisions. Although omalizumab has shown efficacy in H1‐antihistamine‐refractory urticaria, its benefit cannot be predicted solely based on IgE levels, particularly in patients with chronic symptomatic dermographism [11]. The patient was managed with up‐dosed second‐generation H1‐antihistamines (up to fourfold the standard dose) and intermittent short courses of oral corticosteroids, resulting in partial clinical improvement with reduced frequency and severity of urticarial episodes. Complete remission was not achieved, and intermittent symptoms persisted throughout follow‐up. Omalizumab was considered as a potential therapeutic option; however, it was not initiated because the patient demonstrated partial but stable disease control with conventional therapy and did not meet criteria for refractory chronic urticaria. Clinical assessment remains the cornerstone of chronic symptomatic dermographism management [12]. The severity, frequency, and impact on daily activities should guide therapeutic decisions, rather than laboratory markers alone [13]. In our patient, symptoms improved with conventional therapy despite persistent fluctuations in serum IgE levels, emphasizing the importance of phenotype‐driven management. This case highlights the limited utility of serum IgE as a standalone biomarker and underscores the need for further research to clarify its role in guiding treatment decisions in chronic symptomatic dermographism.
The absence of standardized disease activity and quality‐of‐life scoring systems, such as UAS7 and DLQI, represents an important limitation in the objective assessment of disease burden in this case. Although chronic urticaria guidelines recommend these validated tools for monitoring disease severity and treatment response [1], their use was not implemented during follow‐up, limiting quantitative evaluation of longitudinal changes. Despite this, consistent clinical assessments and patient‐reported outcomes suggested ongoing symptomatic disease with variable intensity. This highlights the importance of incorporating standardized outcome measures in routine practice to improve comparability across studies and to better evaluate therapeutic response in chronic symptomatic dermographism.
Additionally, the complex immune mechanisms underlying symptomatic dermographism and urticaria suggest that therapeutic interventions may exert effects beyond IgE neutralization [14]. Clinical experience demonstrates that omalizumab's effects may extend beyond IgE neutralization, supporting personalized, phenotype‐driven therapy for patients with recurrent chronic spontaneous urticaria [15]. These mechanisms may contribute to the clinical benefit observed in some patients with normal or borderline IgE, highlighting the need for further mechanistic studies. Further studies are needed to refine patient selection for anti‐IgE therapy, particularly among patients with severe symptoms despite low or fluctuating serum IgE levels.
Interpretation of serial total IgE measurements should be undertaken with caution, as assay methodologies and upper reference limits may vary between laboratories [16]. In the present case, IgE measurements were obtained over several years, and differences in laboratory‐specific reference ranges may have influenced the classification of individual results as normal or elevated. This highlights an important limitation in the longitudinal assessment of total IgE and underscores the challenges associated with comparing values across different analytical platforms. Nevertheless, despite these methodological considerations, no consistent relationship was observed between total IgE levels and clinical disease activity, supporting the conclusion that serum IgE alone may have limited utility as a biomarker for disease severity or treatment decision‐making in chronic symptomatic dermographism.
This case highlights the need for larger studies to better define the role of IgE in the pathophysiology of chronic urticaria and to clarify its utility as a biomarker for treatment decision‐making. Personalized management strategies based on clinical phenotype and treatment response, rather than serum IgE levels alone, are likely to provide the most effective outcomes for patients with chronic symptomatic dermographism [12].
6. Limitations
This report describes the clinical course of a single patient with chronic symptomatic dermographism, which inherently limits the generalizability of the observations to a broader population. The fluctuating serum IgE levels and absence of correlation with symptom severity in this case highlight the complexity of disease mechanisms but cannot be extrapolated to all patients with symptomatic dermographism. Interpretation of serial IgE measurements is further limited by potential inter‐laboratory variability, differences in assay methodologies, and nonuniform reference intervals, which may affect comparability of results over time. Additionally, confirmatory testing for autoantibodies, such as anti‐FcεRI or anti‐IgE, was not performed, preventing definitive classification of the underlying immunopathology. The lack of long‐term follow‐up data also restricts evaluation of natural disease progression, potential spontaneous remission, or risk of exacerbations over time. A further limitation is the absence of formal UAS7 and DLQI assessments during the patient's course, which are validated tools for objectively assessing disease activity and quality of life in chronic urticaria. Consequently, disease burden could not be quantified using standardized measures, although clinical evaluation suggested persistent symptomatic dermographism with significant functional impact. Future studies involving larger patient cohorts, comprehensive immunologic profiling, and extended observation periods are needed to elucidate the pathophysiological role of IgE fluctuations and to guide personalized, phenotype‐driven management strategies.
Author Contributions
Ali Ahmed Shaju: conceptualization, data curation, investigation, writing – original draft. Samin Sadaf: resources. Md Hasanuzzaman: supervision. Noushin Nawal: writing – review and editing.
Funding
The authors have nothing to report.
Ethics Statement
All procedures in this case report were conducted in accordance with the ethical standards of the institutional research committee and the Declaration of Helsinki.
Consent
Written informed consent for publication of this case report, including clinical images, was obtained from the patient, who confirmed understanding of the purpose, details, and potential implications of the publication.
Conflicts of Interest
The authors declare no conflicts of interest.
Acknowledgments
We sincerely thank the patient for providing informed consent and cooperating throughout the evaluation and follow‐up. We also extend our gratitude to the clinical staff and nursing team for their dedicated support in patient care and data collection.
Data Availability Statement
The data underlying this study are accessible from the corresponding author upon reasonable request.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The data underlying this study are accessible from the corresponding author upon reasonable request.
