A case series on cutaneous reactions to ivig Free

Intravenous immunoglobulin (IVIg) is increasingly utilised to treat a wide spectrum of indications. While generally well-tolerated, IVIg has been associated with a range of dermatological adverse effects, including eczematous eruptions, diffuse exanthematous reactions, and rare but severe presentations such as toxic epidermal necrolysis (TEN). The mechanisms underpinning these reactions remain poorly defined. This abstract discusses two distinct cases of rare, severe, recurrent cutaneous adverse reactions to IVIg.

Case 1 depicts a 61-year-old female with chronic, severe eosinophilic asthma and atopy who developed a recurrent, erythematous, desquamating rash following initiation of IVIg (Octogam) for corticosteroid-induced secondary immunodeficiency. The rash lacked mucosal involvement and was disseminated beyond sun-exposed areas, first appeared two months after commencing IVIg in November 2022. Despite ongoing systemic corticosteroids and withdrawal of other, potential culprit drugs including voriconazole and benralizumab, the rash persisted with cyclical flares over 15 months with some corticosteroid responsiveness. Notable clinical improvement occurred by May 2025, approximately three months after discontinuation of IVIg. Rechallenge with IVIg (Octogam) later in 2025 resulted in rapid recurrence of the exanthema, suggesting a likely causative role.

Case 2 depicts an 88-year-old male with chronic lymphocytic leukaemia (CLL), receiving zanubrutinib since October 2023, with significant hypogammaglobulinaemia for which he was initiated on IVIg. After three uneventful infusions of IVIg (Privigen AU) in 2023, he developed a severe, desquamating erythrodermic rash following the fourth dose. The rash was initially thought to be IVIg related, however a second flare in the rash without re-exposure raised concern about paraneoplastic pemphigus, and he improved with prolonged corticosteroid wean. Over a year later, the patient was re-challenged with an alternative IVIg product (Octagam). This once again precipitated erythroderma within days, necessitating hospitalisation for steroids and wet dressings.

Delayed, severe, recurrent cutaneous adverse reactions to IVIg, as illustrated in these cases, underscore diagnostic and management challenges that are increasingly relevant given widespread IVIg use. Unlike the more common eczematous eruptions after initial infusions, these hypersensitivity reactions are not product-specific and represent a distinct phenomenon. Diagnostically, differentiating IVIg-induced skin reactions from other drug-related or disease-associated causes, such as paraneoplastic syndromes, is complex. In both cases, clinical resolution occurred after discontinuation of IVIg and glucocorticoid therapy, pointing to underlying immune dysregulation. Notably, initial infusions were initially well tolerated for several months, and peripheral eosinophil counts, total IgA, and IgE levels remained within normal limits. This delayed onset suggests a more complex immune mechanism than traditional type I–IV hypersensitivity. Potential pathophysiological mechanisms described include complement activation, dysregulated IgE/IgG responses, and T cell abnormalities. Nonetheless, further research is crucial to uncover the underlying pathological mechanisms of these reactions, which will help inform future management strategies for hypogammaglobulinemia. It remains to be determined whether more frequent administration of lower doses, as with subcutaneous immunoglobulin (SCIg), might mitigate these risks.