Clostridioides difficile infection in a patient with immunoglobulin A vasculitis: a triggering factor or a rare complication of the disease? A case-based review

IgA vasculitis, formerly known as Henoch–Schonlein purpura (HSP), is the most common form of systemic vasculitis in children and is characterized by inflammation of the small vessels with typical deposition of IgA immune complexes. It is a leukocytoclastic type of vasculitis and is characterized by a tetrad of clinical manifestations: non-thrombocytopenia or coagulopathy-induced palpable purpura, arthritis, or arthralgia, gastrointestinal, and renal involvement. The exact cause of IgA vasculitis is not known yet, although infections, vaccinations and insect bites have been implicated in the appearance of the disease. The main risk factors for Clostridioides difficile infection (CDI) are previous CDI, age > 65 years old, pharmacologic agents (antibiotics, PPIs, histamine-2 receptor antagonists, glucocorticoids, and chemotherapy), prior hospitalization, the presence of co-morbidities, especially inflammatory bowel diseases and chronic kidney disease (CKD) and immunosuppression. Oral vancomycin or fidaxomicin are the gold standard of the therapy, with metronidazole being an alternative choice. The purpose of this study was to describe a case of IgA vasculitis and Clostridioides difficile infection to see whether there is any association between the two distinct clinical entities. Herein, we describe a 17-year old patient with IgA vasculitis and bloody diarrhea due to Clostridioides difficile infection and we discuss the co-existence of these two pathological conditions. The patient presented to the hospital with diffuse abdominal pain, nausea, vomiting, and two episodes of bloody diarrhea. Stools tested positive for Clostridioides difficile toxins, while he remained afebrile with hs-CRP = 1.5 mg/dL (normal range < 0.5 mg/dL). Direct immunofluorescence from the extremities’ purplish eruption showed leukocytoclastic vasculitis with IgA deposition. Whether co-existence of the two above-mentioned distinct clinical entities is just a co-incidence or CDI is a triggering factor for IgA vasculitis remains to be elucidated in future large-scale studies.