Opportunistic infections in pediatrics: when to suspect and how to approach

Moraes-Pinto, Maria Isabel de; Ferrarini, Maria Aparecida Gadiani

doi:10.1016/j.jped.2019.09.008

Cited by 4 publications

(1 citation statement)

References 29 publications

(30 reference statements)

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“…Thus, our results suggest that PD patients should be considered a population at risk for opportunistic infections. Opportunistic infections are pathogens that take advantage of the host’s weakened immune system [ 29 , 30 ]. The conditions of a host that predisposes him or her to an opportunistic infection are well known and include profound and prolonged neutropenia, clinical instability or significant medical comorbidities, cancer and chemotherapy, primary immunodeficiency, cystic fibrosis, catheters, prolonged use of steroids or immunosuppressive drugs, HIV infection, prolonged hospitalizations, and malnutrition, among others [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Hypogammaglobulinemia Class G Is Present in Compensated and Decompensated Patients with Propionate Defects, Independent of Their Nutritional Status

López-Mejía,

Vela-Amieva,

Guillén-López

et al. 2024

Nutrients

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Propionate defects (PDs) mainly include methylmalonic (MMA) and propionic acidemia (PA) defects. Lifelong PD patients progress from the compensated to the decompensated stages, the latter of which are characterized by life-threatening acidemia and hyperammonemia crises. PD patients can suffer immunocompromise, especially during the decompensation stage. There is a significant gap in the research regarding the humoral immune response in PD patients. Here, we analyzed serum immunoglobulin concentrations and hemograms across compensated and decompensated stages in PD patients. Nutritional status and crisis triggers of decompensation were also explored. Twenty patients were studied, and 25 decompensation events (DE) and 8 compensation events (CE) were recorded. Compared with those in the CE group, the IgG levels in the DE group (513.4 ± 244.5 mg/dL) were significantly lower than those in the CE group (860.8 ± 456.5 mg/dL) (p < 0.0087). The mean hemoglobin concentration was significantly lower in the DE group (11.8 g/dL) than in the CE group (13.4 g/dL) (p < 0.05). The most frequent (48%) possible decompensation trigger factor was infection. Most of the events were registered in eutrophic patients (87.9%), despite which 65.2% and 50% of patients who experienced decompensated and compensated events, respectively, presented with hypogammaglobulinemia G. These findings provide evidence of the immunodeficiency of PD patients, independent of their nutritional status. We suggest that PD patients be managed as immunocompromised independently of their nutritional status or metabolic state (compensated or decompensated).

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Section: Discussionmentioning

confidence: 99%