Data from 2,482 patients were included in the analysis. The study population showed a clear female predominance, with 1,679 females (67.6%) and 803 males (32.4%). The largest age group was 21–40 years (1,294 patients; 52.1%), followed by 41–60 years (927 patients; 37.3%), ≥61 years (132 patients; 5.3%), and 0–20 years (129 patients; 5.2%).

762 patients (30.7%) tested positive for at least one ANA antibody, whereas 1,720 patients (69.3%) tested negative. Among ANA-positive individuals, the maximum number of antibodies detected in a single patient was nine. Anti-Ro52 had the highest positivity rate (7.9%, n = 195), followed by anti-SSA/Ro (7.2%, n = 178) and anti-RNP/Sm (4.3%, n = 107). The least frequently detected antibodies were anti-ribosomal P (1.4%, n = 35) and anti-PCNA (1.5%, n = 38) ( Figure 1).

ANA positivity differed significantly across age groups (p = 0.03), with the highest rate observed in individuals aged ≥61 years ( Table 1). Individual antibodies showed some variation across age groups; however, anti-RNP/Sm, anti-Ro52, and anti-SSA/Ro did not reach statistical significance (p ≥ 0.05). The remaining antibodies also did not achieve statistical significance across age categories ( Table 2).

The prevalence of ANA positivity was higher among females (33.1%) compared with males (23.1%), and this difference was statistically significant (p < 0.001) ( Table 3).

Specific antibodies in females showed a higher prevalence of anti-Ro52 (4.7%), anti-SSA/Ro (8.7%), anti-SSB/La (2.7%), and anti-histone (3.5%). These gender differences were statistically significant (Pearson’s chi-square test, p < 0.05).

For the remaining antibodies AMA-M2, anti-Jo-1, anti-Ku, anti-Mi-2, anti-PCNA, anti-PM-Scl, anti-RNP/Sm, anti-Scl-70, anti-Sm, anti-centromere B, anti-dsDNA, anti-nucleosome/chromatin, and anti-ribosomal P, no statistically significant gender differences were observed ( Table 4).

Binary logistic regression showed that gender was also an independent predictor of the presence of specific autoantibodies, including anti-Ro52, anti-SSA/Ro, anti-SSB/La, and anti-histone. In contrast, age group did not serve as an independent predictor for ANA positivity or any of the antibodies tested.

Female gender was significantly associated with ANA positivity (OR = 1.42; 95% CI: 1.18–1.72; p < 0.001). For specific antibodies, females had higher odds of testing positive for: Anti-Ro52: OR = 2.08 (95% CI: 1.44–2.99; p < 0.001), Anti-SSA/Ro: OR = 2.30 (95% CI: 1.55–3.40; p < 0.001), Anti-SSB/La: OR = 3.74 (95% CI: 1.59–8.80; p = 0.002), Anti-histone: OR = 1.88 (95% CI: 1.06–3.34; p = 0.03), Age group was not statistically significant for overall ANA positivity nor for any individual autoantibody category ( Table 5, Figure 2).

This 10-year analysis provides a systematic description of ANA profiles in Ajman. It reveals a moderate serological ANA positivity rate, a predominance of Ro52/SSA reactivity, and a consistent gender gradient. Rather than representing a descriptive prevalence report, these findings contribute to an emerging understanding of ANA as a population-level marker of systemic immune activation.

Growing evidence suggests that ANA positivity, even in the absence of overt rheumatologic disease, reflects underlying immune perturbations influenced by demographic and environmental factors. ^{7, 10, 16} Increasing attention to ANA as a preclinical biomarker underscores the public health significance of mapping serological patterns within diverse populations. ^{17, 18} In this context, the Ajman data offer an immuno-epidemiological baseline for a region undergoing rapid demographic and healthcare expansion.

ANA screening was performed using HEp-2 IIFA, the ICAP-endorsed reference method, which remains the global standard for detecting a broad spectrum of nuclear and cytoplasmic autoantibodies. ¹⁹ ICAP emphasizes the interpretive value of recognizing distinct fluorescence patterns, particularly fine speckled categories (AC-4/AC-4a), that frequently correspond to Ro52/SSA and RNP/Sm reactivity. ²⁰ Although pattern data were not available in our dataset, the observed antibody distribution is compatible with such patterns. It corresponds to serological profiles commonly associated with early immune activation or broad, non-disease-specific autoimmunity.

The prominence of Ro52 and SSA/Ro reinforces the importance of reflex testing strategies, as recommended by EFLM/ICAP, to improve diagnostic accuracy in both rheumatic and non-rheumatic conditions. ^{5, 21} By situating the dataset within these international interpretive frameworks, the study provides insights that extend beyond frequency reporting toward understanding the laboratory and clinical relevance of ANA patterns in a high-volume diagnostic environment.

The strongest demographic predictor of ANA positivity in this cohort was gender, with females exhibiting significantly higher odds of both overall ANA positivity and specific antibody reactivities. This finding aligns with global epidemiological research demonstrating a consistent female predominance in ANA expression and autoimmune susceptibility. ^{8, 16} Large-scale mechanistic reviews attribute these differences to several intersecting pathways, including X-chromosome–encoded immune response genes, incomplete X-inactivation, and estrogen-driven B-cell activation, though these mechanisms remain proposed explanations rather than determinants demonstrated within our dataset. ^{22– 24}

The observed gender gradient in Ajman reinforces a broader immunological paradigm of sex-differentiated humoral responsiveness. ²⁵ The fact that gender remained an independent predictor in regression analysis further underscores the robustness of this association. From a clinical standpoint, these findings parallel extensive population-based analyses showing differential outcomes and immune phenotypes in ANA-positive individuals across genders. ^{15, 26, 27}

One of the most distinctive features of our dataset is the dominant expression of anti-Ro52 and anti-SSA/Ro antibodies. Mechanistically, Ro52 (TRIM21) functions as an intracellular Fc receptor that regulates innate immune signaling; experimental loss or dysregulation of Ro52 accelerates tissue inflammation and promotes systemic autoimmunity. ^{28, 29} Clinically, SSA/Ro and Ro52 are recognized as early and cross-disease biomarkers, detectable years before the onset of primary Sjögren’s syndrome and associated with diverse autoimmune phenotypes, including SLE, autoimmune thyroid disease, mixed connective tissue disease, and interstitial lung disease. ^{30– 32}

The high frequency of these antibodies in this laboratory-based population likely reflects underlying immunological activation rather than established rheumatic disease, and it mirrors trends reported in heterogeneous urban populations where autoimmune risk factors and health-seeking behaviors vary widely. Conversely, the lower rates of antibodies such as PCNA and ribosomal P are consistent with their more specific clinical associations. ¹⁵ Collectively, these patterns form a coherent serological profile that may offer predictive value for future longitudinal studies in the region.

ANA positivity varied significantly by age, with the highest rates observed in those aged ≥61 years; however, specific autoantibodies did not show significant age-related differences. This divergence aligns with the concept of “inflammaging,” in which aging is associated with chronic, low-grade immune activation that increases the likelihood of autoantibody production without substantially altering specificity profiles. ^{33, 34} Earlier work similarly documented ANA positivity in otherwise healthy older adults, reinforcing the notion that autoimmunity is a graded rather than binary state. ³⁵

The stability of Ro52, SSA/Ro, and RNP/Sm frequencies across age groups in this study, thus, may reflect age-associated immune remodeling rather than disease-specific serological pathways. This pattern may additionally reflect clinical ordering practices or differential health-care utilization among age strata within the Ajman population.

From a clinical and laboratory perspective, our dataset offers essential insights into ANA testing and interpretation within the UAE. The predominance of Ro52/SSA reactivity suggests that many ANA-positive individuals may require targeted follow-up, even in the absence of classic rheumatologic symptoms. Gender-associated differences further emphasize the importance of contextualizing ANA results within established demographic patterns to avoid both over- and under-diagnosis.

The integration of ICAP-compliant reporting, reflex ENA testing, and standardized laboratory pathways could significantly enhance ANA interpretation and improve patient stratification. At the public health level, these findings provide baseline data to underpin future autoimmune surveillance initiatives across the region. Given global evidence that ANA may serve as a preclinical biomarker for autoimmune risk, the identification of consistent serological signatures within Ajman has implications for early detection, prevention, and longitudinal clinical research.

Limitations include its retrospective nature, absence of clinical diagnostic information, potential referral bias, and the lack of fluorescence pattern data, an essential interpretive layer within the ICAP framework. Future studies incorporating clinical phenotypes, environmental exposure data, and pattern-specific analyses will be necessary to fully contextualize these findings.