Reye's Syndrome Associated With Adenovirus Infections in Infants

Edwards, Kathryn M.; Bennett, Steven R.; Garner, William Lance; Bratton, Donna L.; Glick, Alan D.; Greene, Harry L.; Wright, Peter F.

doi:10.1001/archpedi.1985.02140060025019

Cited by 8 publications

(4 citation statements)

References 8 publications

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“…22 The most important are: Influenza A and B, Varicella-Zoster, followed by Parainfluenza, Measles, Adenoviruses, Coxsackie viruses, Parechovirus, Cytomegalovirus, Epstein-Barr virus, HIV and Hepatitis A and B viruses. [23][24][25][26][27][28][29][30][31] Recently also Rotaviruses have been involved in this syndrome, prevalently by means of inflammatory cytokine induction. 32,33 Other than viral infections, especially of the upper respiratory tract, some intracellular bacteria such as Mycoplasma and Chlamydia have been considered in the syndrome initiation events.…”

Section: Infective Agents Involved In Reye's Syndromementioning

confidence: 99%

Reye's and Reye's‐like syndromes

Pugliese

Beltramo

Torre³

2008

Cell Biochemistry & Function

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The review reports various questions about Reye's syndrome and Reye's-like syndromes. Although there is a significant decrease in the classic Reye's syndrome cases, because of the reduced employment of salicylates in children (salicylate seems to be the most important inducing factor of the syndrome in paediatric subjects affected by viral infection), the problem is still of interest considering the presence of different Reye's-like forms. All these pathological situations are associated with various aetiologic or predisposing causes that are examined in the text. Particular attention is placed on metabolic disorders, especially of fatty acid metabolism, and also of one amino acid. In fact, a latent form can also be the basis of possible biochemical disturbances induced by various exogenous factors such as viral infections, particularly of the respiratory tract (more rarely of bacterial aetiology), or produced by microbial toxins, or by chemical substances, including some therapeutic drugs. A full discussion of biochemical mechanisms of salicylate-induced Reye's syndrome is reported. Finally a possible diagnostic differentiation from classic Reye's syndrome and Reye's-like syndromes plus therapeutic prospects are briefly examined.

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Section: Infective Agents Involved In Reye's Syndromementioning

confidence: 99%

Reye's and Reye's‐like syndromes

Pugliese

Beltramo

Torre³

2008

Cell Biochemistry & Function

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“…The acute onset of generalized seizures, the marked increase in serum aminotransferase level, and prothrombin time in an infant infected with adenovirus suggested Reye's syndrome. Liver dysfunction with fatty degeneration of hepatocytes was also present, in the absence of cerebral edema, hypoglycemia, and hyperammoniemia [Edwards et al, 1985]. These findings fail to meet the diagnostic criteria of Reye's syndrome, but are consistent with the pseudo-Reye's syndrome described by Ladisch et al [1979] in adenoviral infection.…”

Section: Discussionmentioning

confidence: 64%

Fatal adenovirus infection associated with new genome type

et al. 1998

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The first fatal case caused by the new genome type 7i is described in an 8-month-old boy requiring long-term respiratory support who developed Reye's syndrome, acute respiratory distress, and bronchiolitis obliterans with fatal evolution. Adenovirus was detected in nasopharyngeal secretions and was persistently positive during hospitalization. IgM and IgG adenovirus antibody titers measured in serum by enzyme-linked immunoassay (EIA) were 1:32 and 1:800, respectively. Serum interleukins (IL) and interferons (IFN) measured by EIA were as follows: IL-2, 110 pg/ml; IL-6, 300 pg/ml; IL-8, 7,000 pg/ml; TNF-alpha, 35 pg/ml, IL-1 and IL-4 undetectable, IFN-alpha 2,200 pg/ml, and IFN-gamma 700 pg/ml. Virologic studies showed that adenovirus isolated belonged to subgenus B, and digestion of viral DNA with Bam HI, Sma I, Bgl II, and Hind III identified the isolate as belonging to genome type 7i. Autopsy showed bronchiolitis obliterans with diffuse alveolar damage and perivenular fatty degeneration with polymorphonuclear infiltrates in the periportal spaces. The difficulty in obtaining adequate oxygenation with minimization of iatrogenic oxygen injury is discussed.

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“…17 that patients with postoperative infections had higher mean perioperative blood glucose. 18 All in all, patients with lower BMI and albumin, which implies a worse state of nutrition, may experience poor healing of the surgical site. Moreover, a higher blood glucose level may result in poor wound healing and more microbial reproduction.…”

Section: Discussionmentioning

confidence: 99%

Predictive nomogram for deep brain stimulation–related infections

Chen

Meng

et al. 2022

Neurosurgical Focus

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OBJECTIVE Infection is one of the important and frequent complications following implantable pulse generator and deep brain stimulation (DBS) electrode insertion. The goal of this study was to retrospectively evaluate and identify potential risk factors for DBS infections. METHODS From January 2015 to January 2021 in Qingdao municipal hospital (training cohort) and The First Affiliated Hospital of the University of Science and Technology of China (validation cohort), the authors enrolled patients with Parkinson disease who had undergone primary DBS placement or implantable pulse generator replacement. The cases were divided into infection or no-infection groups according to the 6-month follow-up. The authors used the logistic regression models to determine the association between the variables and DBS infection. Depending on the results of logistic regression, the authors established a nomogram. The calibration curves, receiver operating characteristic curve analysis, and decision curves were used to evaluate the reliability of the nomogram. RESULTS There were 191 cases enrolled in the no-infection group and 20 cases in the infection group in the training cohort. The univariate logistic regression showed that BMI, blood glucose, and albumin were all significant predictors of infection after DBS surgery (OR 0.832 [p = 0.009], OR 1.735 [p < 0.001], and OR 0.823 [p = 0.001], respectively). In the crude, adjust I, and adjust II models, the three variables stated above were all considered to be significant predictors of infection after DBS surgery. The calibration curves in both training and validation cohorts showed that the predicted outcome fitted well to the observed outcome (p > 0.05). The decision curves showed that the nomogram had more benefits than the "All or None" scheme. The areas under the curve were 0.93 and 0.83 in the training and validation cohorts, respectively. CONCLUSIONS The nomogram included BMI, blood glucose, and albumin, which were significant predictors of infection in patients with DBS surgery. The nomogram was reliable for clinical application.

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Reye's Syndrome Associated With Adenovirus Infections in Infants

Cited by 8 publications

References 8 publications

Reye's and Reye's‐like syndromes

Reye's and Reye's‐like syndromes

Fatal adenovirus infection associated with new genome type

Predictive nomogram for deep brain stimulation–related infections

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