Gastrointestinal (GI) involvements are important clinical signs in children with immunoglobulin A (IgA) vasculitis. In this context, we read with a great interest a paper by Uehara et al. in… Click to show full abstract
Gastrointestinal (GI) involvements are important clinical signs in children with immunoglobulin A (IgA) vasculitis. In this context, we read with a great interest a paper by Uehara et al. in this journal. We experienced two patients with IgA vasculitis who developed severe sequela of GI involvements. The intestinal tract not only serves as an organ for digestion and absorption, but also has an important barrier function. Notably, some patients with inflammatory bowel diseases (IBD) reportedly experienced bacterial translocation, which is defined as the passage of viable indigenous bacteria from the GI tract to extraintestinal sites. However, as far as we are aware, children with IgA vasculitis who subsequently developed bacterial translocation-associated septicemia have not been reported in the English literature so far. Case 1: A 5-year-old girl was admitted to hospital because of purpura, ankle joint pain and severe abdominal pain. She was treated with 2 mg/kg/day of prednisolone (PSL). However, repeated abdominal pain occurred. Twenty three days after admission, she developed high body temperature of 39 °C with hypotension (60/20 mmHg) and was diagnosed as having septic shock. Her serum endotoxin concentration value was markedly increased to 85.8 pg/mL (normal, <4.9 pg/mL) and C-reactive protein was 11.05 mg/dL. Serratia liquefaciens was detected from her blood culture. The patient was successfully treated with meropenem for 14 days, intravenous immunoglobulin (IVIG) for 5 days under a continuous hemodiafiltration. Case 2: A 7-year-old girl was admitted to hospital because of purpura, severe abdominal pain, and mild ankle joint pain. She was treated with 1 mg/kg/day of PSL and parenteral nutrition. However, repeated abdominal pain occurred. Twenty two days after admission, she developed a high body temperature of 40 °C with severe chills. Although her serum endotoxin concentration value was not increased, C-reactive protein was 16.06 mg/dL and Enterobacter agglomerans was detected from her blood culture. The patient was successfully treated with meropenem for 14 days and IVIG for 5 days. Table 1 shows clinical characteristics of these patients with subsequently development of septicemia. In both cases, serology for immunologic evaluation revealed hypogammmaglobulinemia and hypoproteinemia / hypoalbuminemia, suggesting that these conditions might be risk factors for subsequent septicemia. Proteinuria was not detected before onset of septicemia. The major mechanisms promoting bacterial translocation are disruption of the ecologic equilibrium to allow intestinal bacterial overgrowth, deficiencies in host immune defenses, and increased permeability of the intestinal mucosal barrier. These mechanisms could act in concert to promote synergistically the systemic spread of indigenous translocating bacteria to cause lethal sepsis. We did not perform endoscopic examination at the onset of septicemia in our patients due to ill condition, so the precise etiology of their septicemia, which was probably due to bacterial translocation, remains speculative.
               
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