Vulnerable populations

2016

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Letters to the editor

Volume 45, No.10, 2016 Pages 699-699

The opinions expressed by correspondents in this column are in no way endorsed by the Editors or The Royal Australian College of General Practitioners.

Chronic rhinosinusitis and immunodeficiency

We write with regards to the recent article on sinusitis by Morcom et al (AFP June 2016).1 We wish to highlight that recurrent or chronic rhinosinusitis (CRS) may be a sign of an underlying immunodeficiency, which is an important consideration for general practitioners (GPs) and other clinicians in the assessment of patients with rhinosinusitis. Immunodeficiency is more likely if rhinosinusitis persists or recurs despite adequate medical and/or surgical management,2 and it is of the ‘without nasal polyposis’ subtype.3

CRS may indicate dysfunctional humoral immunity, as this part of the adaptive immune system is particularly important in the control of bacterial infections. Any humoral immunodeficiency, for example, common variable immunodeficiency (CVID), may predispose to chronic or recurrent acute rhinosinusitis. Patients with a humoral deficiency are also more susceptible to other sinopulmonary infections, such as otitis media and pneumonia. Retrospective studies found approximately one-fifth of patients with CRS have evidence of low/deficient antibody levels4 and two-thirds had a depressed antibody titre response to vaccine challenge, indicative of a specific antibody defect.5

Consequently, we believe GPs should consider testing patients with CRS for immunodeficiency, including serum immunoglobulins, lymphocyte subset analysis and vaccine antibody responses, particularly if there are other clinical red flags such as recurrent, deep-seated, unusual or prolonged infections, or a suggestive family history. Consideration must also be given to secondary causes of immunodeficiencies (eg human immunodeficiency virus (HIV), immunosuppressive drugs) and, where possible, managed accordingly. A referral to a clinical immunologist or other specialist may be in order as appropriate.

Adrian YS Lee, MBBS, BMedSc (Hons), Basic Physician Trainee, Western Health, Vic. adrian.lee@wh.org.au

Katie Frith, FRACP, MRCPCH, Paediatric Immunologist/Allergist, Sydney Children’s Hospital, Randwick, NSW;
University of New South Wales, Randwick, NSW

References

  1. Morcom S, Phillips N, Pastuszek A, Timperley D. Sinusitis. Aust Fam Physician 2016;45(6):374–77.
  2. Dykewicz MS, Hamilos DL. Rhinitis and sinusitis. J Allergy Clin Immunol 2010;125(2 Suppl 2):S103–15.
  3. Hamilos DL. Chronic rhinosinusitis patterns of illness. Clin Allergy Immunol 2007;20:1–13.
  4. Vanlerberghe L, Joniau S, Jorissen M. The prevalence of humoral immunodeficiency in refractory rhinosinusitis: a retrospective analysis. B-ENT 2006;2(4):161–66.
  5. Alqudah M, Graham SM, Ballas ZK. High prevalence of humoral immunodeficiency patients with refractory chronic rhinosinusitis. Am J Rhinol Allergy 2010;24(6):409–12.

Reply

Individuals with pre-existing or acquired immunodeficiencies are at risk of developing CRS. In a study by Chee et al1 of 79 patients with CRS (with or without nasal polyps) refractory to medical treatment, 30% had decreased T-cell function and 20% had an immunoglobulin deficiency. Common variable immunodeficiency was present in 10%.

A meta-analysis by Schwitzguébel et al2 revealed immunoglobulin deficiencies in 13% of patients with refractory CRS, and 23% of patients with difficult to treat CRS (persistent symptoms despite surgery and ongoing medical therapy). As such, investigation of possible immunodeficiencies should be considered if adequate medical treatment has failed, or for individuals with multiple infections (otitis media, bronchitis, pneumonia).

The benefits of surgery in individuals with a non-acquired immunodeficiency are similar to that experienced by individuals with normal immune function3 and, as such, treatment should be approached in a similar fashion.

The presence of a sinus mycetoma (fungal ball) is not suggestive of an underlying immunodeficiency, with no difference in immunoglobulin levels detected compared to CRS.4 Acquired immunodeficiencies (HIV infection, haematpoetic stem cell transplants) may predispose to acute invasive fungal rhinosinusitis, with a significant risk of mortality. Treatment in this setting should be multimodal, with surgical debridement and antifungal treatment, along with management of the underlying immunodeficiency state.

Samuel Morcom BSc, MBBS, ENT Principal House Officer, Nambour General Hospital, Nambour, Qld

References

  1. Chee L, Graham SM, Carothers DG, Ballas ZK. Immune dysfunction in refractory sinusitis in a tertiary care setting. The Laryngoscope 2001 Feb;111(2):233–35.
  2. Schwitzguébel AJ, Jandus P, Lacroix JS, Seebach JD, Harr T. Immunoglobulin deficiency in patients with chronic rhinosinusitis: Systematic review of the literature and meta-analysis. J Allergy Clin Immunol 2015;136(6):1523–31.
  3. Khalid AN, Mace JC, Smith TL. Outcomes of sinus surgery in ambulatory patients with immune dysfunction. Am J Rhinol Allergy 2010;24(3):230–33.
  4. Jiang RS, Hsu CY. Serum immunoglobulins and IgG subclass levels in sinus mycetoma. Otolaryngol Head Neck Surg 2004;130(5):563–66

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Letters to the editor

2016