Precision Medicine Paradigms in Allergic Rhinitis: Navigating Immunotherapy and Digital Healthcare

Figures & data

Figure 1. Pathophysiology of Allergic Rhinitis.

Figure 2. Immunotherapy tailored to allergens, processes, and cellular responses.

Table 1. Different routes of administration for Allergen Specific Immunotherapy.

Sr. No.	Route of Administration	Advantages	Disadvantages	References
1.	Oral Immunotherapy (OIT)	Food allergy treatment that may be curative	Concerns regarding efficacy and safety	[83–85]
2.	Subcutaneous Immunotherapy (SCIT)	Immunotherapy with venom: potential applications Verified efficiency and safety Head-to-head comparisons revealed improved efficacy	Time-consuming Repetition of injections The need for injections in the healthcare unit Extreme hypersensitivity risk	[86,87]
3.	Epicutaneous Immunotherapy (EPIT)	Safe product profile Significance in aero and food allergens Research produced encouraging findings.	Harmful adverse reaction	[88,89]
4.	Sublingual Immunotherapy (SLIT)	Essential for children Verified safety and effectiveness Possibility of usage at home No parenteral administration Reduced reliance on the medical facility	Possibly less effective than subcutaneous immunotherapy	[90,91]
5.	Intralymphatic Immunotherapy (ILIT)	Shorter length of treatment Fewer doses administered	Hazard of adverse reactions as a result of allergens leaking via injected lymph nodes Need for skilled personnel to administer injections while using ultrasound therapy	[92–95]

Table 2. Case studies related to pharmacogenomic practices in precision medicines for AR.

Sr No.	Case study	Background	Description	Intervention	References
1.	Corticosteroid Sensitivity and Nasal Steroids	A 30-year-old female with allergic rhinitis experiences recurrent episodes of nasal congestion and sneezing. She has been using an intranasal corticosteroid spray (e.g. fluticasone) as per her physician’s recommendation but notices only partial relief.	Pharmacogenomic testing reveals genetic variants in the glucocorticoid receptor (GR) gene associated with reduced sensitivity to corticosteroids. This genetic profile may explain the patient’s suboptimal response to intranasal corticosteroid therapy.	In light of the pharmacogenomic findings, the healthcare provider adjusts the dosage of the intranasal corticosteroid or switches to an alternative formulation (e.g. mometasone) with potentially greater efficacy in individuals with reduced corticosteroid sensitivity. The patient experiences improved symptom control and quality of life.	[96]
2.	Corticosteroids and Glucocorticoid Receptor Variants.	Intranasal corticosteroids (INCS) are recommended as first-line therapy for moderate to severe AR. However, individual responses to INCS can vary, partly due to genetic variations in glucocorticoid receptor (GR) genes.	A patient with persistent AR fails to achieve adequate symptom control despite treatment with a standard dose of an INCS. The patient also experiences nasal irritation, a common side effect of INCS therapy. Pharmacogenomic testing reveals genetic variants in the GR gene associated with reduced sensitivity to corticosteroids.	In light of the pharmacogenomic findings, the healthcare provider switches the patient to an alternative INCS formulation or adjusts the dosage to achieve optimal therapeutic effects. Additionally, the provider may recommend adjunctive therapies to manage nasal irritation while maintaining AR control.	[97]
3.	Antihistamines and CYP2D6 Variants.	Antihistamines are commonly used for AR treatment, but individual responses to these drugs can vary due to genetic differences in drug metabolism enzymes like CYP2D6.	A patient with AR is prescribed a standard dose of a second-generation antihistamine. Despite adherence to the treatment regimen, the patient reports inadequate symptom relief and experiences drowsiness, a common side effect of antihistamines. Pharmacogenomic testing reveals that the patient carries genetic variants associated with reduced CYP2D6 activity, leading to slower metabolism of the antihistamine and increased susceptibility to side effects.	Based on the pharmacogenomic results, the healthcare provider adjusts the dosage or selects an alternative antihistamine that is less dependent on CYP2D6 metabolism. Subsequent treatment with the adjusted regimen leads to improved symptom control with fewer adverse effects.	[98]
4.	Genetic Variants and Antihistamine Response.	A 45-year-old male presents with persistent allergic rhinitis symptoms despite regular use of a second-generation antihistamine (e.g. cetirizine). He reports moderate relief but complains of ongoing nasal congestion and occasional breakthrough symptoms.	Genetic testing reveals that the patient carries variants in the CYP2C19 gene associated with reduced metabolism of cetirizine. As a result, the patient may experience slower clearance of the drug, leading to suboptimal symptom control.	Based on the pharmacogenomic findings, the healthcare provider switches the patient to an alternative second-generation antihistamine with a different metabolic pathway (e.g. fexofenadine). Subsequent treatment leads to improved symptom control and patient satisfaction.	[99]

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