Abstract
ObjectiveTo determine the relationship between plasma zinc values and the severity of dengue viral infection (DVI) and DVI-caused hepatitis.MethodsA prospective cohort study was conducted during 2008–2010 in hospitalized children aged <15 years confirmed with DVI. Complete blood count, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and zinc values (mcg/dL) were determined twice: first during the toxic phase (Zn1) and secondly two weeks after recovery (Zn2).Results39 patients were enrolled with a mean age of 9.7±3.7 years, and 15/39 diagnosed with dengue shock syndrome (DSS). Zn1 values were lower than Zn2 values [median (IQR): 46.0 (37.0, 58.0) vs 65.0 (58.0, 81.0) mcg/dL, respectively, p <0.01]. Zn1 but not Zn2 values had a negative correlation with AST and ALT (rs = −0.33, p = 0.04 and rs = −0.31, p = 0.05, respectively). Patients with DSS had lower Zn1 but not Zn2 values compared with non-DSS patients [median (IQR) Zn1, 38.0 (30.0, 48.0) vs 52.5 (41.2, 58.7), p = 0.02; Zn2, 61.0 (56.0, 88.0) vs 65.0 (59.5, 77.5), respectively, p = 0.76]. Zn1 values showed a decreasing trend across increasing dengue severity groups (p = 0.02). Age <5 years and DVI-associated diarrhea were associated with low Zn1.ConclusionChildren who had a higher grade of dengue disease severity and liver cell injury had lower Zn1 values. Low Zn1 values were probably caused by loss from diarrhea and from zinc translocating to liver cells.
Highlights
The immunopathogenesis of dengue viral infection (DVI) is not well understood, and the level of disease severity is multifactorial, depending on various factors such as viral virulence, secondary DVI, immune response to DVI, and host factors including genetic and nutritional status [1,2,3]
Age,5 years and DVI-associated diarrhea were associated with low Zn1
Children who had a higher grade of dengue disease severity and liver cell injury had lower Zn1 values
Summary
The immunopathogenesis of dengue viral infection (DVI) is not well understood, and the level of disease severity is multifactorial, depending on various factors such as viral virulence, secondary DVI, immune response to DVI, and host factors including genetic and nutritional status [1,2,3]. Other studies have found that obese or malnourished children with DVI had higher morbidity and mortality rates than those with normal body weight, suggesting that nutritional status might play an important role in the immunopathogenesis of DVI [3,4], and that obese and malnourished children had higher proportions of zinc deficiency than normal body weight children [10,11,12,13]. In Thailand, more than half of school children tested had zinc deficiency [14,15]
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