Acute infective dermatoses constitute an important proportion of pediatric dermatological disorders and include bacterial, viral, fungal, and parasitic infections. Children are particularly vulnerable because of their developing immune system, immature skin barrier, frequent exposure to infectious agents, and close interpersonal contact. Pediatric skin infections may range from localized superficial lesions to extensive skin and soft-tissue infections associated with systemic inflammatory responses and complications. Recent pediatric studies have demonstrated substantial clinical and microbiological diversity among skin and soft-tissue infections, with Staphylococcus aureus being an important pathogen and disease severity influencing clinical outcomes.¹˒² In a Pakistani pediatric dermatology population, infectious and infestational conditions have also been reported among the most frequently encountered dermatoses, highlighting their continuing clinical and public-health relevance.³

The pathophysiology of acute infection involves activation of both innate and adaptive immune mechanisms. Recognition of microbial components by immune cells stimulates the release of pro-inflammatory mediators and recruitment of neutrophils and other leukocytes to the site of infection. Although these mechanisms are essential for pathogen elimination, excessive inflammatory activation can result in increased production of reactive oxygen species (ROS). Oxidative stress develops when ROS generation exceeds the capacity of endogenous antioxidant systems to neutralize them, resulting in oxidative modification of lipids, proteins, and nucleic acids.⁴˒⁵ Recent evidence indicates that oxidative stress is particularly relevant during childhood because physiological growth and high metabolic demands may influence redox homeostasis, while infectious diseases can further increase oxidative burden.⁵

The skin is both a target and a source of oxidative processes. Reactive oxygen species participate in host defense, cellular signaling, and inflammatory responses; however, excessive ROS generation may damage keratinocytes and other cellular components and amplify local tissue inflammation. Studies examining oxidative pathways in dermatological diseases have demonstrated alterations in antioxidant systems and redox homeostasis, including changes in thiol-disulfide balance.⁴ Similarly, oxidative stress has been recognized as an important component of inflammatory skin pathology, with oxidative damage potentially contributing to impaired cellular integrity and disruption of normal skin barrier function.⁶ Although oxidative stress has been investigated in several inflammatory and infectious disorders of the skin, comparatively limited information is available regarding its systemic biochemical expression in children with acute infective dermatoses.

Several biomarkers may be used to characterize oxidative imbalance. Malondialdehyde (MDA), a product of lipid peroxidation, is commonly used as an indicator of oxidative damage, whereas total antioxidant capacity (TAC), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase reflect different components of antioxidant defense.⁴˒⁵ Evidence from pediatric infectious diseases demonstrates that infection can disturb the oxidant-antioxidant equilibrium, with increased oxidative products and altered antioxidant activity.⁵˒⁷ Experimental and clinical evidence from viral infections further suggests that excessive ROS production may contribute to inflammatory tissue injury and disease severity.⁷ These observations provide a physiological basis for investigating oxidative stress as a potential marker of systemic response in children with acute infective dermatoses.

Serum ferritin represents another potentially important biomarker in acute infection. Although ferritin is traditionally regarded as an indicator of body iron stores, it is also an acute-phase protein whose concentration increases in response to inflammation. Inflammatory signaling promotes alterations in iron homeostasis and increases intracellular iron sequestration, thereby contributing to elevated circulating ferritin.⁸ Marked hyperferritinemia has been documented in several pediatric infectious and inflammatory conditions and may reflect the intensity of systemic immune activation. In children hospitalized with scrub typhus, for example, hyperferritinemia was common and was associated with severe disease characteristics, demonstrating the potential clinical relevance of ferritin as an indicator of inflammatory burden.⁸ Similarly, elevated ferritin has been reported in severe pediatric inflammatory syndromes, where its concentration may parallel disease severity and systemic involvement.⁹

The complete blood count (CBC) provides readily available information regarding the hematological response to infection. Leukocytosis, neutrophilia, lymphocyte alterations, anemia, and platelet abnormalities may occur depending on the type and severity of infection. In hospitalized children with skin and soft-tissue infections, clinical and laboratory parameters have been investigated for their ability to distinguish different infection patterns and predict disease characteristics.¹⁰ Inflammatory markers and hematological indices may therefore provide useful complementary information when interpreted alongside biochemical indicators of oxidative stress and inflammation.

Despite growing evidence linking infection, inflammation, oxidative stress, and ferritin metabolism, most available studies have focused on systemic infections, critical illness, or chronic inflammatory skin diseases rather than acute infective dermatoses in otherwise healthy children.⁴˒⁵˒⁷–⁹ Consequently, the relationship between oxidative stress markers, serum ferritin, hematological changes, and the clinical severity of acute pediatric skin infections remains insufficiently characterized. A combined assessment of these parameters may provide insight into the systemic pathophysiological response accompanying apparently localized dermatological infection.

Therefore, the present study was designed to evaluate the association of oxidative stress markers, serum ferritin, and CBC parameters with pathophysiological changes in children with acute infective dermatoses. It also aimed to determine whether alterations in these biochemical and hematological parameters are associated with clinical disease severity. Understanding these relationships may help identify accessible biomarkers of disease burden and provide a better physiological and biochemical understanding of acute infective dermatoses during childhood.

A comparative cross-sectional study was conducted in the Departments of Dermatology and Pediatrics in collaboration with the Departments of Physiology, Biochemistry and Pathology at a tertiary care teaching hospital. The study included 120 children aged 2–12 years, comprising 80 patients presenting with acute infective dermatoses and 40 age- and sex-matched apparently healthy children serving as controls. Participants were enrolled through non-probability consecutive sampling after obtaining informed written consent from their parents or legal guardians. Children presenting with clinically diagnosed acute bacterial, viral, fungal, or parasitic dermatoses of less than four weeks duration were considered eligible for inclusion. The diagnosis was established by a consultant dermatologist on the basis of clinical history and dermatological examination and was supported, where required, by appropriate microbiological investigations. Children with chronic inflammatory or autoimmune skin diseases, chronic systemic illness, hematological disorders, known iron-storage disorders, malnutrition requiring therapeutic intervention, recent major surgery or trauma, or those receiving iron supplementation, systemic corticosteroids, immunosuppressive therapy, or antioxidant supplements were excluded. Children with evidence of concurrent systemic infection unrelated to the primary dermatological condition were also excluded to minimize potential confounding effects on inflammatory and oxidative stress parameters.

Demographic and clinical information, including age, sex, residence, socioeconomic status, duration of illness, presenting symptoms, type and distribution of skin lesions, associated fever, previous treatment, and relevant medical history, was recorded on a structured data collection proforma. A detailed general physical and dermatological examination was performed for each participant. Acute infective dermatoses were categorized as bacterial, viral, fungal, or parasitic according to clinical and laboratory findings. Disease severity was assessed according to the extent of body surface involvement, number and distribution of lesions, intensity of local inflammatory changes, presence of systemic manifestations, and complications. Patients were subsequently classified into mild, moderate, and severe disease categories using a predefined clinical severity assessment protocol. Height and weight were recorded using standardized procedures, and body mass index was calculated to evaluate the nutritional status of the participants.

Approximately 5–7 mL of venous blood was collected from each participant under aseptic conditions before initiation of systemic antimicrobial treatment wherever feasible. A portion of the sample was transferred into an EDTA-containing tube for complete blood count, while the remaining blood was collected in a plain serum-separator tube, allowed to clot, and centrifuged at approximately 3000 rpm for 10–15 minutes. The separated serum was aliquoted and stored at −80°C until biochemical analysis. Complete blood count was performed using an automated hematology analyzer and included hemoglobin concentration, red blood cell count, total leukocyte count, differential leukocyte count, platelet count, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration. Serum ferritin concentration was measured using a commercially available chemiluminescent immunoassay or enzyme-linked immunosorbent assay according to the manufacturer's instructions.

Oxidative stress was evaluated by measuring serum malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD), and glutathione peroxidase (GPx). MDA, representing lipid peroxidation, was determined using the thiobarbituric acid reactive substances method or a commercially available colorimetric assay kit. TAC was determined by a standardized colorimetric method reflecting the cumulative antioxidant capacity of the serum. SOD activity was measured on the basis of inhibition of superoxide-mediated reactions, while GPx activity was determined through an enzyme-based spectrophotometric assay. All biochemical analyses were performed according to the manufacturers' protocols, and samples from patients and controls were analyzed under similar laboratory conditions. Appropriate standards, controls, and duplicate measurements were used where applicable to maintain analytical accuracy and minimize inter-assay variability.

Data were entered and analyzed using IBM SPSS Statistics. Continuous variables were expressed as mean ± standard deviation for normally distributed data and median with interquartile range for non-normally distributed data, whereas categorical variables were presented as frequencies and percentages. Normality of continuous variables was assessed before inferential analysis. The independent-samples t-test or Mann–Whitney U test was used to compare biochemical and hematological parameters between children with infective dermatoses and healthy controls. Comparisons among mild, moderate, and severe disease categories were performed using one-way analysis of variance with an appropriate post-hoc test or the Kruskal–Wallis test, as applicable. Categorical variables were compared using the chi-square or Fisher's exact test. Pearson or Spearman correlation analysis was performed to determine relationships between disease severity, serum ferritin, CBC parameters, and oxidative stress markers. Multivariable regression analysis was performed to identify independent biochemical and hematological predictors of greater disease severity after adjustment for potential confounding variables such as age, sex, and duration of illness. A two-tailed p-value of <0.05 was considered statistically significant. The study was conducted in accordance with the principles of the Declaration of Helsinki, and ethical approval was obtained from the Institutional Review Board/Ethical Review Committee of the participating institution before commencement of data collection.

A total of 120 children were included in the study, comprising 80 children with acute infective dermatoses and 40 healthy controls. The mean age of children in the patient group was 7.4±2.9 years compared with 7.2±2.8 years in the control group, with no statistically significant difference (p=0.721). Males constituted 55.0% of the patient group and 52.5% of the control group. The mean duration of illness among affected children was 11.6±6.4 days. Among the 80 patients, bacterial dermatoses were the most frequent (35.0%), followed by fungal (27.5%), viral (22.5%), and parasitic (15.0%) infections.

Table 1. Demographic and clinical characteristics of study participants

The distribution of infective dermatoses is presented in Table 2. Bacterial infections were the predominant category, accounting for 28 cases (35.0%), followed by fungal infections in 22 cases (27.5%), viral infections in 18 cases (22.5%), and parasitic infections in 12 cases (15.0%). Regarding clinical severity, 35 (43.8%) patients had mild disease, 29 (36.3%) had moderate disease, and 16 (20.0%) had severe disease.

Table 2. Distribution and clinical severity of acute infective dermatoses

Significant differences were observed in several hematological parameters between patients and controls. The mean total leukocyte count and neutrophil percentage were significantly higher among children with infective dermatoses, whereas hemoglobin concentration and lymphocyte percentage were significantly lower. Platelet count was also significantly increased in the patient group. No significant difference was observed in MCV between the two groups.

Table 3. Comparison of CBC parameters between patients and healthy controls

Marked differences were observed in oxidative stress parameters. Serum MDA was significantly elevated in children with acute infective dermatoses compared with controls (4.82±1.21 vs. 2.91±0.74 nmol/mL, p<0.001). Conversely, TAC, SOD, and GPx were significantly lower in the patient group, indicating a disturbed oxidant-antioxidant balance.

Table 4. Comparison of oxidative stress markers between patients and controls

Serum ferritin was significantly higher among affected children than healthy controls (86.4±34.7 vs. 51.8±22.6 ng/mL, p<0.001). The increase in ferritin was progressively greater with increasing disease severity. Mean ferritin levels were 64.8±19.7 ng/mL in mild disease, 91.6±25.8 ng/mL in moderate disease, and 121.4±38.6 ng/mL in severe disease (p<0.001).

Table 5. Serum ferritin according to disease severity

A progressive increase in oxidative stress was also observed with increasing clinical severity. MDA concentrations were lowest among children with mild disease and highest among those with severe disease. In contrast, TAC, SOD, and GPx demonstrated a progressive decline with increasing severity.

Table 6. Oxidative stress markers according to clinical severity

Significant correlations were identified between biochemical markers and clinical disease severity. MDA showed a strong positive correlation with disease severity (r=0.61, p<0.001), while ferritin demonstrated a moderate positive correlation (r=0.48, p<0.001). Conversely, TAC showed a significant inverse correlation with severity (r=-0.56, p<0.001). SOD and GPx also demonstrated significant inverse correlations with disease severity.

Table 7. Correlation of biochemical parameters with disease severity

MDA also demonstrated a significant positive correlation with serum ferritin (r=0.48, p<0.001), whereas TAC was inversely correlated with ferritin (r=-0.39, p<0.001). Higher total leukocyte and neutrophil counts were associated with increased MDA and ferritin levels. These findings indicate that greater clinical severity was accompanied by increased oxidative damage, reduced antioxidant defense, elevated ferritin, and more pronounced hematological alterations.

Table 8. Correlation between oxidative stress markers and serum ferritin

In multivariable regression analysis, elevated MDA and ferritin and reduced TAC remained significantly associated with greater disease severity after adjustment for age, sex, and duration of illness. MDA demonstrated the strongest independent association with severe clinical disease, suggesting that oxidative imbalance may represent an important component of the systemic pathophysiological response in children with acute infective dermatoses.

The present study demonstrated a clear association between acute infective dermatoses and systemic biochemical and hematological alterations in children. The affected group showed significantly higher MDA and ferritin concentrations together with reduced TAC, SOD, and GPx activity compared with healthy controls. In addition, increased total leukocyte and neutrophil counts, reduced lymphocyte percentage, and lower hemoglobin concentrations were observed. These findings suggest that acute infection of the skin is accompanied not only by local inflammatory activity but also by measurable systemic alterations in redox balance and hematological homeostasis. Contemporary pediatric dermatology literature recognizes bacterial, viral, and superficial fungal infections as important causes of childhood morbidity, with clinical severity and systemic manifestations varying according to the infective process.¹⁰

The significantly elevated MDA observed in the present study indicates increased lipid peroxidation in children with acute infective dermatoses. MDA is generated during oxidative degradation of polyunsaturated fatty acids and therefore provides an indirect measure of oxidative cellular injury. The simultaneous reduction in TAC, SOD, and GPx suggests that increased oxidant generation was accompanied by depletion or inadequate compensation of antioxidant defenses. This pattern is consistent with findings from pediatric infectious conditions in which infection has been associated with increased oxidative damage and altered antioxidant activity. Bennemann et al. demonstrated increased TBARS, a marker of lipid peroxidation, together with reduced catalase and GPx activity in children with systemic bacterial infection associated with cystic fibrosis.¹¹ Similarly, pediatric COVID-19 studies have demonstrated increased total oxidant status and oxidative stress index with reduced total antioxidant status, supporting the concept that infectious inflammation can disturb redox homeostasis in children.¹²

The progressive increase in MDA from mild to severe disease in our study is particularly noteworthy. Children with severe dermatoses had substantially higher MDA concentrations than those with mild disease, while TAC, SOD, and GPx progressively decreased. This graded relationship suggests that oxidative imbalance may increase in parallel with the intensity of the inflammatory response rather than representing merely a nonspecific consequence of infection. Evidence from other pediatric infectious diseases supports this interpretation. In children with Mycoplasma pneumoniae pneumonia, higher MDA and advanced oxidation protein products and lower SOD and glutathione peroxidase were associated with more severe disease manifestations.¹³ Likewise, oxidative stress has been associated with disease severity and adverse outcomes in severe childhood malaria, indicating that oxidative injury may contribute to systemic disease progression.¹⁴

The positive correlation between MDA and clinical severity in the present study (r=0.61, p<0.001) further strengthens the potential value of oxidative stress markers as indicators of disease burden. The inverse association between TAC and severity (r=-0.56, p<0.001), along with significant negative correlations for SOD and GPx, suggests that deterioration in antioxidant capacity accompanies increasing clinical severity. These relationships are physiologically plausible because activated neutrophils and other immune cells generate reactive oxygen species during microbial killing. Excessive or sustained ROS production may subsequently cause lipid, protein, and cellular membrane damage. Recent work on respiratory viral infection has similarly emphasized the interaction between ROS generation, inflammatory signaling, cellular injury, and disease severity.¹⁵

Serum ferritin was also significantly elevated in the affected children and showed a progressive increase from mild to severe disease. Ferritin should therefore be interpreted in this setting not simply as an indicator of iron storage but also as an inflammation-responsive biomarker. Infection-induced cytokine signaling alters iron metabolism and promotes sequestration of iron within cells, while inflammatory activation can increase ferritin synthesis. Studies in children have demonstrated that ferritin concentrations are strongly influenced by inflammatory status, emphasizing the importance of considering inflammation when interpreting ferritin as an indicator of iron status.¹⁶ In pediatric sepsis, higher serum ferritin has been associated with increasing disease severity, supporting the observation in our study that ferritin increased progressively across clinical severity categories.¹⁷

The moderate positive correlation between ferritin and MDA (r=0.48, p<0.001) is another important finding. This relationship may indicate an interaction between inflammatory iron metabolism and oxidative injury. Iron is capable of participating in redox reactions that facilitate formation of highly reactive oxygen species, while inflammation simultaneously stimulates ferritin production as part of the acute-phase response. Thus, elevated ferritin in the present cohort may reflect both inflammatory activation and altered iron handling accompanying oxidative stress. Importantly, however, ferritin should not be interpreted as a direct measure of iron stores during acute infection without complementary iron-status and inflammatory biomarkers. Recent pediatric studies have emphasized that inflammation can substantially alter ferritin-based assessment of iron status.¹⁶

The CBC findings provide additional evidence of systemic inflammatory activation. The significantly higher total leukocyte and neutrophil counts in affected children are compatible with an acute innate immune response, particularly in children with bacterial or more extensive infections. Conversely, the reduction in lymphocyte percentage may reflect the relative neutrophilia accompanying acute inflammation. Contemporary research on biomarkers of pediatric infection emphasizes that leukocyte profiles and combinations of inflammatory biomarkers can provide useful information regarding the underlying infectious and inflammatory process.¹⁸ The positive correlations observed between total leukocyte count, neutrophils, ferritin, and MDA in our study suggest that hematological activation and oxidative stress may be interconnected components of the host response.

The reduction in mean hemoglobin concentration among affected children also deserves consideration. Acute infection may influence erythropoiesis and iron availability through inflammatory pathways, although the relatively short duration of illness in the present cohort makes chronic disease-related anemia less likely as the sole explanation. Ferritin elevation in the presence of lower hemoglobin may represent inflammation-associated alterations in iron utilization rather than necessarily indicating adequate functional iron availability. Consequently, interpretation of hemoglobin and ferritin together may provide more meaningful information than either parameter alone.

From a clinical perspective, the findings suggest that a combination of readily available hematological parameters with selected biochemical markers may provide a broader picture of disease severity in pediatric infective dermatoses. MDA and TAC demonstrated particularly strong relationships with clinical severity, while ferritin and CBC parameters provided complementary information regarding inflammatory and hematological responses. Nevertheless, these markers should currently be considered supportive rather than diagnostic biomarkers because oxidative stress and ferritin elevations are not specific to skin infection. The present findings therefore provide a rationale for future longitudinal studies evaluating whether these parameters normalize with successful treatment and whether their baseline values can predict complications, treatment response, or duration of illness.

An important strength of the present study is the simultaneous assessment of oxidative stress, antioxidant defense, ferritin, and hematological parameters in the same pediatric population. This multidisciplinary approach allows the inflammatory, biochemical, and physiological components of acute infective dermatoses to be considered together. However, the cross-sectional design limits conclusions regarding causality, and the relatively modest sample size may limit generalizability. In addition, different types of infective dermatoses may produce distinct inflammatory and oxidative responses. Future studies with larger cohorts, pathogen-specific analysis, inflammatory markers such as CRP and IL-6, and longitudinal follow-up before and after treatment would help clarify the temporal relationship between infection, oxidative stress, ferritin elevation, and clinical recovery.

Overall, the present findings support the concept that acute infective dermatoses in children are associated with a measurable systemic oxidative and inflammatory response. The simultaneous elevation of MDA and ferritin, reduction of antioxidant defenses, and alteration of CBC parameters; particularly their relationship with clinical severity; suggest that these variables may provide complementary insight into the pathophysiological burden of pediatric infective dermatoses.

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