# Paradoxical Worsening of Chronic Spontaneous Urticaria Following Omalizumab Administration: The Missing Link

**Authors:** George N Konstantinou, Indrashis Podder

PMC · DOI: 10.7759/cureus.61453 · Cureus · 2024-05-31

## TL;DR

A patient with chronic hives worsened after omalizumab treatment, revealing a hidden parasitic infection, highlighting the need for screening in similar cases.

## Contribution

Identifies a potential link between omalizumab use and undetected parasitic infections in chronic urticaria patients.

## Key findings

- A patient's worsening hives after omalizumab was linked to a parasitic infection.
- Normal eosinophil and IgE levels did not indicate the infection, emphasizing the need for additional screening.
- Discontinuing omalizumab and treating the infection resolved the patient's symptoms.

## Abstract

Omalizumab, a humanized anti-IgE monoclonal antibody, is commonly employed in the treatment of antihistamine-refractory chronic spontaneous urticaria (CSU), where it significantly reduces free IgE levels, minimizing histamine release from basophils and mast cells. Despite its efficacy, there are concerns regarding its effect on parasitic defense due to IgE's role in combating parasitic infestations. We present a case of a 28-year-old female agriculturist with a six-month history of CSU who experienced a paradoxical exacerbation of her symptoms following an increase in the omalizumab treatment dose. This deterioration coincided with a serologically confirmed parasitic infection with Echinococcus granulosus and Toxocara canis. Despite normal eosinophil counts and IgE levels, which are typically used to identify parasitic infections, the patient's clinical worsening prompted further investigation that led to the identification of the parasitic infection. Treatment with albendazole and omalizumab discontinuation led to the resolution of her CSU, suggesting that the parasitic infection was contributing to the symptom exacerbation. This case highlights the need for careful screening for parasitic infections before initiating omalizumab in antihistamine-refractory CSU patients from endemic regions, or patients who deteriorate clinically on omalizumab, especially when other indicators such as eosinophil count and IgE levels might not suggest infection. It also underscores the importance of considering a tailored approach to managing CSU that balances effective treatment with the potential for adverse effects related to immunomodulation.

## Linked entities

- **Chemicals:** albendazole (PubChem CID 2082)

## Full-text entities

- **Genes:** IGHE (immunoglobulin heavy constant epsilon) [NCBI Gene 3497] {aka IgE}
- **Diseases:** parasitic infection (MESH:D010272), infection (MESH:D007239), CSU (MESH:D000080223)
- **Chemicals:** albendazole (MESH:D015766), histamine (MESH:D006632), Omalizumab (MESH:D000069444)
- **Species:** Echinococcus granulosus (species) [taxon 6210], Homo sapiens (human, species) [taxon 9606], Toxocara canis (dog roundworm, species) [taxon 6265]

## Full text

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## References

11 references — full list in the complete paper: https://tomesphere.com/paper/PMC11214840/full.md

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Source: https://tomesphere.com/paper/PMC11214840