Polyvalent Immunoglobulin as a Potential Treatment Option for Patients with Recurrent COPD Exacerbations

Figures & data

Table 1 Summary of Study Characteristics and Study Outcomes

Study	Study Design	Number of Patients	IG Dosage	Observation Period	Outcomes
Barth 2001 (abstract only)^Citation11	Randomized control trial	28 – IG 28 - Albumin	5 mL of 16% Intravenous Immunoglobulin (IVIg) monthly	1 year	No significant difference in Number and duration of exacerbations Change of airway resistance Time to first exacerbation Duration of hospitalization due to exacerbation Number of proven infections But a trend in less prednisolone use in the Ig group (p=0.1)
Cowan 2015^Citation7	Retrospective longitudinal cohort	14	Did not specify but standard dosing as a replacement therapy for immunodeficiency - ~30 g/month.	1 year	The incidence of AECOPD was consistently and significantly reduced in frequency from mean 4.7 (± 3.1) per patient-year before, to 0.6 (±1.0) after immunoglobulin (Ig) treatment (p=0.0001). There were twelve episodes of severe AECOPD (in seven cases) in the year prior, and one in the year of Ig treatment (p=0.016).
McCullagh 2017^Citation8	Retrospective case series	Total = 29 (9 Ig treatment, 13 prophylactic antibiotics, 7 no treatment)	300–600 mg/kg/4-week period every 3–4 weeks for IVIg or every 1–2 weeks for SCIg. Antibiotic regimens: trimethoprim/sulfamethoxazole 1 double strength tablet twice daily alternating with doxycycline 100 mg twice daily every two weeks, or azithromycin 250–500 mg three times/week	At least one and up to 10 years before and after diagnosis and treatment initiation	In those receiving Ig, there was a reduction in annual courses of steroid from 12 (4.5–12) to 0.5 (0–1.5) (p=0.031) and annual courses of rescue antibiotic from 9 (5.5–12) to 0 (0–1.5) (p=0.016). Annual acute exacerbations in this group decreased from 4 (3–5.5) to 0.5 (0–1.5) (p=0.016). Numbers were too small to see a difference in annual rates of hospital admission for AECOPD pre-treatment 1.5 (1–3) and post-treatment 0 (0–1.5) (p=0.25).

Figure 1 Author’s proposed hypothesis. Humoral immunodeficiency is more prevalent in COPD patients with “high-risk of exacerbations phenotype” than those with a “low-risk of exacerbations phenotype”.

Novaretti M, Dinardo C. Immunoglobulin: production, mechanisms of action and formulations. Rev Bras Hematol Hemoter. 2011;33(5):377–382. doi:10.5581/1516-8484.20110102

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Cowan J, Gaudet L, Mulpuru S, et al. A retrospective longitudinal within-subject risk interval analysis of immunoglobulin treatment for recurrent acute exacerbation of chronic obstructive pulmonary disease. PLoS One. 2015;10(11):e0142205. doi:10.1371/journal.pone.0142205

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McCullagh BN, Comellas AP, Ballas ZK, Newell JD, Zimmerman MB, Azar AE. Antibody deficiency in patients with frequent exacerbations of Chronic Obstructive Pulmonary Disease (COPD). PLoS One. 2017;12(2):e0172437. doi:10.1371/journal.pone.0172437

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