Vitiligo is an acquired depigmentary disorder characterized by selective loss of functional melanocytes, resulting in well defined achromic macules. Although the disease manifests cutaneously, substantial evidence indicates that vitiligo represents a systemic disorder with a strong genetic basis [1][2]. Familial clustering, twin concordance, and variable penetrance strongly support inherited susceptibility [3][4]. The embryologic origin of melanocytes and epidermal ridges is ectodermal, with both structures developing during a critical intrauterine period between the thirteenth and twenty fourth weeks of gestation [5][6]. Dermatoglyphics, the study of epidermal ridge patterns of fingers and palms, therefore offers a stable phenotypic window into early developmental events and genetic influences [7][8]. Classical dermatoglyphic studies have demonstrated that deviations in ridge pattern frequency ridge counts and palmar configurations are associated with several genetically mediated disorders [9][10]. In vitiligo, earlier investigations have reported increased loop patterns reduced whorl frequency altered ridge counts and displacement of palmar triradii, though findings have varied across populations [11][12][13]. Methodological inconsistencies and limited statistical stratification have been cited as major causes for this heterogeneity [14][15]. Given these considerations, the present study was undertaken to conduct a comprehensive qualitative and quantitative digito palmar dermatoglyphic evaluation in vitiligo patients using standardized recording techniques and rigorous statistical analysis, while accounting for sex and side specific variation [16][17]. AIMS AND OBJECTIVES • To conduct a comprehensive qualitative analysis of fingertip dermatoglyphic patterns, specifically evaluating the distribution and relative frequencies of loop, whorl, and arch configurations in individuals with vitiligo, and to systematically compare these findings with age and sex matched healthy control subjects in order to identify characteristic pattern deviations associated with the disease. • To perform a detailed quantitative assessment of digital ridge architecture by measuring Total Finger Ridge Count as an index of overall ridge density and Absolute Finger Ridge Count as a measure of cumulative ridge complexity, and to compare these parameters between vitiligo patients and controls with additional stratification based on sex to elucidate developmental and genetic influences. • To evaluate palmar ridge metrics with precision by analyzing the a b ridge count as an indicator of transverse palmar growth and measuring the atd angle to assess axial triradial position and palmar morphogenesis, thereby determining whether vitiligo is associated with altered palmar ridge development during early fetal life. • To analyze the presence, frequency, and regional distribution of true palmar dermatoglyphic patterns within the hypothenar, thenar, and interdigital areas of the palm, and to compare these distributions between vitiligo subjects and controls in order to identify region specific palmar pattern alterations that may reflect underlying developmental instability.

 Study design A hospital-based observational case control study was conducted in accordance with established dermatoglyphic research protocols.  Study population Clinically diagnosed vitiligo patients attending the dermatology outpatient department were enrolled as cases. Healthy age and sex matched individuals without vitiligo or family history of pigmentary disorders served as controls.  Sample size The sample size for the present case control study was determined using the standard formula for comparison of two independent means, expressed as n=2(Zα/2+Zβ)2σ2d2n = \frac{2 (Z_{\alpha/2} + Z_{\beta})^2 \sigma^2}{d^2}n=d22(Zα/2 +Zβ )2σ2 , where nnn represents the minimum required number of subjects in each group, Zα/2Z_{\alpha/2}Zα/2 is the standard normal deviate corresponding to the two sided level of significance set at 5 percent with a value of 1.96, ZβZ_{\beta}Zβ is the standard normal deviate corresponding to a statistical power of 80 percent with a value of 0.84, σ\sigmaσ denotes the pooled standard deviation of the primary quantitative dermatoglyphic parameters derived from previously published vitiligo studies, and ddd represents the minimum expected difference in mean values between vitiligo patients and controls considered to be clinically meaningful. Substitution of these values, assuming a moderate effect size consistent with earlier dermatoglyphic research, yielded a minimum sample size requirement of approximately 180 subjects per group. To ensure adequate power for sex wise subgroup analysis, to accommodate multiple qualitative and quantitative dermatoglyphic variables, and to account for potential exclusion due to poor print quality or incomplete ridge visualization, the calculated sample size was increased. Accordingly, a total of 424 subjects were included in the study, comprising 212 vitiligo patients and 212 age and sex matched controls, providing sufficient statistical power and methodological robustness for all planned analyses.  Inclusion criteria • Confirmed diagnosis of vitiligo • Age above 10 years • Absence of congenital anomalies  Exclusion criteria • Chromosomal disorders known to affect dermatoglyphics • Palmar dermatologic conditions or trauma • History of hand surgery  Dermatoglyphic recording technique Finger and palmar prints were obtained using the ink and roller method originally described by Cummins and Midlo and subsequently standardized for medical genetics research [7][8]. Rolled impressions of all ten digits were recorded, followed by complete palmar prints of both hands.  Parameters studied  Qualitative fingertip patterns • Loops • Whorls • Arches  Quantitative fingertip parameters • Total Finger Ridge Count calculated as the sum of the highest ridge count on each finger [7][18] • Absolute Finger Ridge Count calculated as the total of all ridge counts from all triradii [18][21]  Quantitative palmar parameters • a b ridge count measured between triradii a and b [19][22] • atd angle measured between triradii a t and d [9][10]  Qualitative palmar parameters • Presence of true palmar patterns in hypothenar thenar and interdigital regions [10][20]  Statistical analysis • Normality testing using Kolmogorov Smirnov test [23] • Comparison of means using Student t test for normally distributed data • Mann Whitney U test for non parametric variables • Chi square test for categorical variables • Statistical significance defined as p less than 0.05

 Fingertip dermatoglyphic pattern distribution • Increased frequency of loop patterns in vitiligo subjects Vitiligo subjects demonstrated a significantly higher frequency of loop patterns across both hands when compared with controls. Loops represent a relatively simpler fingerprint configuration characterized by a single triradius and unidirectional ridge flow. Clinically, an excess of loop patterns is widely interpreted as an indicator of reduced ridge complexity during fetal development. This finding suggests that individuals with vitiligo may have experienced subtle disturbances in epidermal ridge differentiation during early gestation. Since ridge formation and melanocyte migration occur concurrently in fetal life, increased loop frequency supports the concept of a shared developmental vulnerability affecting both systems. From a clinical perspective, this reinforces the view that vitiligo susceptibility is constitutionally determined rather than purely acquired. • Reduced frequency of whorl patterns in vitiligo subjects Whorl patterns, which are the most complex fingerprint configurations and typically associated with higher ridge counts, were significantly less frequent in vitiligo patients compared to controls. Clinically, a reduction in whorls implies diminished ridge proliferation and reduced morphogenetic activity during the critical period of ridge formation. Whorls are considered markers of developmental stability, and their reduced presence suggests increased developmental noise or instability. In the context of vitiligo, this finding aligns with the hypothesis that genetic or epigenetic disruptions during embryogenesis may predispose individuals to later melanocyte vulnerability. Figure 1: This bubble plot demonstrates a marked increase in loop pattern frequency in vitiligo subjects compared with controls, with bubble size proportionally reflecting prevalence. Statistically, the larger bubble associated with the vitiligo group indicates a significant shift in qualitative fingerprint pattern distribution. Clinically, this predominance of loops suggests simplification of ridge architecture during fetal development, a finding consistent with reduced morphogenetic complexity. The visual separation between groups reinforces the concept of developmental instability in vitiligo rather than random variation. • Increased arch patterns in female vitiligo subjects Arch patterns, the simplest of all fingerprint types and often regarded as indicators of disturbed ridge formation when present in excess, were significantly increased in female vitiligo subjects. This sex specific finding is clinically meaningful, as arches are associated with delayed ridge initiation and reduced ridge differentiation. The higher prevalence in females suggests that female fetuses may exhibit greater sensitivity to genetic or hormonal influences during ridge development. Clinically, this may partially explain observed sex differences in disease expression and progression in vitiligo, highlighting the importance of considering sex specific developmental pathways. Figure 2: The treemap demonstrates a statistically meaningful over-representation of arch fingerprint patterns among female vitiligo subjects, with arches occupying a disproportionately larger area compared to loops and whorls, directly reflecting their increased percentage frequency. Since arches are the simplest ridge configuration and are embryologically associated with delayed volar pad regression and reduced ridge differentiation, their excess suggests early developmental instability during the critical period of epidermal ridge formation. The sex-specific predominance indicates that female fetuses may be more sensitive to genetic, hormonal, or intrauterine environmental influences affecting ectodermal development. Clinically, this supports the concept that vitiligo has a constitutional developmental component, not merely an acquired autoimmune process. Statistically, the clear segregation and emphasis of arches against more complex patterns strengthens their value as a discriminative dermatoglyphic marker in female vitiligo. This finding provides objective, non-invasive evidence linking altered ridge morphogenesis with sex-dependent disease expression and progression.  Quantitative fingertip dermatoglyphic parameters • Reduced Total Finger Ridge Count in vitiligo subjects Total Finger Ridge Count was consistently lower in vitiligo subjects across both sexes when compared with controls. TFRC reflects the overall ridge density and is determined by the timing and rate of ridge formation during fetal life. A reduced TFRC indicates fewer epidermal ridges, suggesting delayed ridge initiation or reduced cellular proliferation. Clinically, this reduction supports the concept that vitiligo patients may have experienced subtle delays or disruptions in ectodermal development. Such developmental alterations may not produce overt congenital anomalies but can manifest later as increased susceptibility to disorders involving ectodermal derivatives, including melanocytes. Figure 3: The violin plot illustrates a clear downward shift in the distribution of Total Finger Ridge Count among vitiligo subjects, accompanied by reduced density and narrower spread. Statistically, this reflects a consistent reduction in ridge number across the cohort rather than isolated outliers. Clinically, lower ridge counts indicate delayed or diminished epidermal ridge proliferation during embryogenesis, supporting the hypothesis of early developmental alteration in individuals predisposed to vitiligo. • Significantly reduced Absolute Finger Ridge Count in male vitiligo subjects AFRC was significantly lower in male vitiligo subjects, indicating a reduction in total ridge complexity across all digits. Unlike TFRC, AFRC captures the cumulative ridge contribution from all triradii and is considered a more sensitive measure of ridge architecture. Clinically, this finding suggests that male vitiligo patients may have experienced a more pronounced global reduction in ridge formation. This sex specific effect may reflect differential genetic expression or hormonal influences during fetal development. From a clinical standpoint, it emphasizes that male and female vitiligo patients may not share identical developmental pathways, which may have implications for disease susceptibility and progression. Figure 4: This box plot demonstrates a lower median and reduced interquartile range of Absolute Finger Ridge Count in male vitiligo subjects. Statistically, the downward shift indicates a significant reduction in overall ridge complexity. Clinically, lower AFRC reflects diminished global ridge formation and supports the notion that male vitiligo patients may experience more pronounced developmental perturbations at the ectodermal level.  Quantitative palmar dermatoglyphic parameters • Altered a b ridge count with sex specific divergence Male vitiligo subjects exhibited a significant reduction in a b ridge count, whereas female vitiligo subjects showed a significant increase. The a b ridge count reflects the transverse growth of palmar ridges between the index and middle fingers and is a sensitive indicator of palmar growth dynamics. A reduced count in males suggests constricted palmar ridge expansion, while an increased count in females may indicate compensatory or altered growth patterns. Clinically, this divergence highlights sex dependent modulation of palmar development and supports the notion that vitiligo susceptibility may arise from different developmental trajectories in males and females. Figure 5: The area chart reveals a reduced mean a b ridge count in male vitiligo subjects, visualized as a compressed area relative to controls. Statistically, this reduction signifies constrained transverse palmar ridge growth. Clinically, diminished a b ridge count suggests altered palmar morphogenesis during early fetal life, supporting the presence of sex specific developmental pathways influencing vitiligo susceptibility. • Increased atd angle in vitiligo subjects Vitiligo subjects demonstrated increased atd angles, with the change being more pronounced and statistically significant in females. The atd angle reflects the spatial position of the axial triradius and is influenced by the overall growth and shape of the palm during fetal life. An increased atd angle indicates outward displacement of the axial triradius, which is considered a marker of altered palmar morphogenesis. Clinically, this finding provides strong evidence of disturbed ridge growth during early gestation and reinforces the developmental origin of vitiligo susceptibility. Figure 6: The candlestick chart illustrates an upward displacement of the median and interquartile range of atd angle values in female vitiligo subjects. Statistically, this shift reflects significant alteration in palmar triradial geometry. Clinically, increased atd angle indicates outward movement of the axial triradius, a recognized marker of disturbed palmar growth during embryogenesis, further strengthening the developmental origin of vitiligo.  Qualitative palmar dermatoglyphic patterns • Increased true palmar patterns in hypothenar region Vitiligo subjects exhibited a higher frequency of true palmar patterns in the hypothenar region. The hypothenar area is particularly sensitive to developmental disturbances and is often involved in genetically influenced disorders. Increased patterning in this region suggests localized instability in ridge formation. Clinically, this supports the idea that vitiligo is associated with region specific alterations in palmar development rather than uniform changes across the palm. • Increased patterns in first interdigital area in vitiligo subjects The first interdigital region showed a higher frequency of true palmar patterns in vitiligo patients. This area is closely related to digital ridge development and its alteration suggests coordinated disturbance between finger and palmar ridge systems. Clinically, this reinforces the observation that vitiligo related developmental changes are not confined to isolated regions but reflect broader alterations in ridge morphogenesis. • Higher pattern frequency in third interdigital area in controls Controls demonstrated a higher frequency of patterns in the third interdigital region, indicating that normal ridge development favors balanced and regionally distributed palmar patterning. The relative absence of such patterns in vitiligo subjects suggests redistribution of ridge complexity rather than absolute loss. Clinically, this finding underscores that vitiligo related dermatoglyphic changes represent reorganization of ridge architecture rather than random variation. Figure : This donut chart provides a proportional overview of fingerprint pattern composition in vitiligo subjects, highlighting the dominance of loop patterns and the relative reduction of whorls. Statistically, the unequal distribution underscores a non random deviation from expected population norms. Clinically, this pattern profile reflects reduced ridge complexity and altered differentiation, reinforcing the concept of constitutional susceptibility rather than postnatal causation. • Integrated clinical interpretation Taken collectively, the dermatoglyphic findings reveal a coherent pattern of simplified ridge architecture reduced ridge counts altered palmar geometry and region specific pattern redistribution in vitiligo subjects. These features are consistent with subtle disturbances in ectodermal development during early fetal life. Clinically, this supports the understanding of vitiligo as a disorder with deep developmental roots rather than a purely postnatal autoimmune phenomenon. Dermatoglyphics thus provides valuable phenotypic evidence of constitutional susceptibility and strengthens the developmental biology framework for vitiligo pathogenesis.

Vitiligo is increasingly understood as a complex disorder arising from an interplay of genetic developmental and immunological factors rather than a purely localized skin condition. The present study contributes to this understanding by demonstrating consistent and statistically meaningful dermatoglyphic deviations in individuals with vitiligo. Since dermatoglyphic patterns are established early in intrauterine life and remain unchanged thereafter, the observed alterations strongly suggest that events occurring during embryogenesis may predispose individuals to vitiligo later in life [5][6][7]. One of the most striking findings of this study is the predominance of loop patterns and the concomitant reduction of whorl patterns in vitiligo patients. This shift in qualitative fingerprint pattern distribution has been reported previously by several investigators across different populations [11][12][13][14]. Whorl patterns are generally associated with higher ridge counts and greater pattern complexity, whereas loop patterns reflect relatively simpler ridge configurations [7][18]. The increased frequency of loops in vitiligo patients therefore suggests a relative simplification of epidermal ridge development. This simplification may reflect reduced cellular proliferation or altered ridge differentiation during the critical period of ectodermal development [5][8]. The increase in arch patterns particularly among female vitiligo subjects further supports the concept of developmental instability. Arches represent the simplest fingerprint pattern and are considered markers of disturbed ridge formation when present in excess [9][21]. The sex specific increase in arches observed in this study is consistent with earlier reports indicating that females may exhibit greater dermatoglyphic sensitivity to genetic or hormonal influences during fetal life [16][17]. Such findings lend support to the hypothesis that sex related factors may modulate susceptibility to vitiligo through early developmental mechanisms. Quantitative dermatoglyphic parameters provide additional insight into the nature of ridge development in vitiligo. The reduction in Total Finger Ridge Count observed consistently across vitiligo subjects suggests a global decrease in ridge number. Ridge counts are known to be determined by both genetic factors and the timing of ridge differentiation during fetal growth [7][18]. A lower ridge count implies either delayed ridge initiation or reduced ridge proliferation, both of which may reflect subtle disturbances in ectodermal maturation. Similar reductions in ridge counts have been documented in other genetically mediated conditions, further reinforcing the validity of this observation [9][21]. The finding of a significantly reduced Absolute Finger Ridge Count in male vitiligo subjects is particularly noteworthy. AFRC is considered a more sensitive indicator of total ridge complexity because it accounts for all triradii rather than only the highest count per finger [18][21]. A reduction in AFRC therefore suggests a more pronounced alteration in overall ridge architecture. The male specific significance observed in this study may reflect differential genetic expression or hormonal influences affecting ridge development in males and females [16][17]. This sex divergence underscores the importance of stratified analysis in dermatoglyphic research. Palmar dermatoglyphic variables further strengthen the evidence for altered embryologic development in vitiligo. The a b ridge count reflects the breadth of palmar ridge growth between the digital triradii a and b and is considered a sensitive indicator of palmar growth dynamics [19][22]. The reduced a b ridge count observed in male vitiligo subjects suggests constricted ridge growth in this region, whereas the increased count in females may indicate compensatory or differential growth patterns. Similar sex specific variations have been reported in previous dermatoglyphic studies of genetically influenced disorders [10][19]. The atd angle is another important palmar parameter that reflects the spatial relationship between digital and axial triradii. An increased atd angle indicates outward displacement of the axial triradius, which is thought to result from altered palmar growth during early fetal life [9][10]. In the present study, vitiligo subjects exhibited increased atd angles, with statistical significance particularly evident in females. This finding is consistent with earlier studies in vitiligo and other multifactorial disorders and supports the concept of disturbed palmar ridge growth and triradial positioning [11][13][20]. The analysis of true palmar patterns provides further evidence of dermatoglyphic deviation in vitiligo. Increased pattern frequency in the hypothenar and first interdigital regions among vitiligo subjects suggests localized alterations in ridge formation in these areas. The hypothenar region is known to be particularly sensitive to developmental disturbances, and increased patterning in this area has been reported in several congenital and genetically influenced conditions [10][20]. Conversely, the higher frequency of patterns in the third interdigital region among controls indicates that normal ridge development favors more balanced palmar pattern distribution. Taken together, these findings strongly support the hypothesis that vitiligo is associated with genetically mediated disturbances in ectodermal development. Since melanocytes and epidermal ridges originate from the same embryologic layer and develop during overlapping time periods, it is biologically plausible that factors affecting melanocyte survival or migration may simultaneously influence ridge formation [5][6][8]. Dermatoglyphic deviations thus serve as indirect markers of these early developmental events. The consistency of the present findings with multiple earlier studies conducted across different ethnic and geographic populations enhances their validity [11][12][13][14][15][20]. While individual parameters may vary in magnitude or direction across studies, the overall pattern of increased loops reduced whorls altered ridge counts and modified palmar angles remains remarkably stable. This convergence of evidence strengthens the argument that dermatoglyphic analysis can provide meaningful insights into the constitutional background of vitiligo. From a clinical perspective, dermatoglyphic assessment offers several advantages. It is noninvasive inexpensive and easily reproducible. Although it cannot be used as a diagnostic tool for vitiligo, it may serve as an adjunctive method for identifying individuals with increased genetic susceptibility, particularly in familial or high risk populations [3][4][9]. In research settings, dermatoglyphics may also help stratify patients into subgroups based on underlying developmental profiles. Nevertheless, it is important to interpret these findings within their limitations. Dermatoglyphic patterns reflect probabilistic associations rather than deterministic outcomes. Not all individuals with altered dermatoglyphics will develop vitiligo, and not all vitiligo patients will exhibit marked dermatoglyphic deviations. These patterns should therefore be viewed as markers of susceptibility rather than causation [14][23]. In conclusion, the expanded dermatoglyphic analysis presented in this study reinforces the concept that vitiligo has a strong developmental and genetic component. The observed alterations in fingertip and palmar ridge patterns reflect disturbances occurring during early fetal life and provide stable phenotypic evidence of underlying susceptibility. Future studies incorporating familial analysis molecular genetics and longitudinal follow up may further clarify the relationship between dermatoglyphic markers and the pathogenesis of vitiligo [15][17][18]. LIMITATIONS Despite the strengths of this study, including a reasonably large sample size and the use of standardized dermatoglyphic techniques, several limitations must be acknowledged to ensure balanced interpretation of the findings. Recognizing these limitations is essential not only for scientific transparency but also for guiding future research in this domain. First, the study employed a hospital-based case control design. Participants were recruited from a tertiary care center, which may not fully represent the broader population of individuals with vitiligo. Patients attending tertiary hospitals often have more extensive diseases for longer duration or greater health seeking behavior. As a result, the dermatoglyphic patterns observed in this cohort may not accurately reflect those present in individuals with milder or early-stage vitiligo in the community. A population based design would have provided greater external validity and generalizability. Second, the cross-sectional nature of the study limits the ability to draw conclusions regarding causality or temporal relationships. Dermatoglyphic patterns are fixed at birth, while vitiligo typically manifests later in life. Although this temporal separation supports the concept of dermatoglyphics as markers of susceptibility, the study design cannot establish a direct developmental pathway linking ridge formation to disease onset. Longitudinal studies following individuals from birth or early childhood would be required to clarify whether specific dermatoglyphic patterns are predictive of future vitiligo development. Third, familial and genetic correlation analyses were not incorporated into the study design. While vitiligo is known to exhibit familial aggregation, the absence of first-degree relative evaluation limits insight into inherited dermatoglyphic traits. Including parents and siblings could have strengthened the argument that the observed ridge variations are genetically transmitted rather than sporadic developmental deviations. Such familial studies would also help differentiate between shared genetic influences and shared environmental factors acting during gestation. Fourth, the study did not include plantar dermatoglyphic analysis. Sole patterns are formed during the same embryologic period as palmar and digital ridges and may provide complementary information regarding developmental stability. The exclusion of plantar dermatoglyphics may therefore represent a missed opportunity to capture a more comprehensive picture of ectodermal ridge development. Future studies incorporating both palmar and plantar analyses could yield a more holistic understanding of dermatoglyphic alterations in vitiligo. Another limitation relates to potential observer variability. Although standardized methods were used for recording and analyzing dermatoglyphic prints, subtle differences in ridge counting and pattern interpretation can occur, particularly in borderline cases. While every effort was made to maintain consistency, the study did not formally assess inter observer or intra observer reliability. Including such reliability testing would enhance confidence in the precision and reproducibility of the measurements. The study also did not stratify vitiligo patients based on clinical subtype disease duration or extent of involvement. Vitiligo is a heterogeneous condition, and it is possible that different clinical forms may have distinct developmental or genetic backgrounds. By analyzing vitiligo as a single group, potentially meaningful subgroup differences may have been obscured. Future research could benefit from stratifying patients into localized generalized segmental and non-segmental forms to explore whether dermatoglyphic variations correlate with clinical phenotypes. Environmental and prenatal influences were not assessed in this study. Maternal health nutrition stress exposure to toxins and intrauterine conditions can influence both melanocyte development and epidermal ridge formation. Without data on prenatal exposures, it is difficult to disentangle genetic influences from environmental factors acting during fetal life. Incorporating maternal history and prenatal data would allow a more nuanced interpretation of dermatoglyphic findings. Finally, while statistical significance was demonstrated for several parameters, the clinical relevance of some differences remains uncertain. Dermatoglyphic variations often reflect subtle shifts in probability rather than dramatic deviations. As such, their utility lies more in population level research than in individual level prediction. Overinterpretation of small statistical differences should therefore be avoided, and findings should be viewed as contributory rather than definitive.

This study provides meaningful insight into the developmental background of vitiligo by demonstrating consistent and reproducible dermatoglyphic alterations in affected individuals. By examining both qualitative and quantitative parameters of fingertip and palmar ridge patterns, the study reinforces the concept that vitiligo is not merely a localized skin disorder but rather a condition rooted in early developmental and genetic processes. The observed predominance of simpler fingerprint patterns, reduction in ridge counts, and alteration in palmar indices collectively point toward subtle disturbances in ectodermal maturation during fetal life. Because dermatoglyphic patterns are established early and remain unchanged thereafter, they serve as stable biological records of intrauterine events. Their association with vitiligo suggests that susceptibility to the disease may be determined long before clinical manifestations appear. Importantly, the study highlights the value of dermatoglyphics as a noninvasive and cost effective research tool. While dermatoglyphic analysis is not intended for diagnostic or prognostic use in individual patients, it offers a unique window into constitutional vulnerability at the population level. In settings where advanced genetic testing may not be readily available, dermatoglyphics can complement other epidemiological and clinical approaches to understanding disease predisposition. The findings also underscore the importance of considering sex specific differences in developmental biology. The differential patterns observed between male and female subjects suggest that genetic and hormonal influences may interact during ridge formation, contributing to variability in disease susceptibility. Recognizing such differences is essential for advancing personalized and biologically informed models of disease risk. Beyond vitiligo, this study contributes to a broader understanding of how early developmental processes influence later health outcomes. It supports the growing recognition that many adult onset conditions have roots in prenatal life and that subtle developmental markers can provide valuable clues to disease mechanisms. Dermatoglyphics, in this context, represents a bridge between embryology genetics and clinical medicine. Future research building on these findings could integrate dermatoglyphic analysis with molecular genetic studies immunological profiling and longitudinal follow up. Such multidisciplinary approaches would help clarify how genetic susceptibility interacts with environmental triggers to produce the clinical spectrum of vitiligo. Familial studies in particular could elucidate inheritance patterns and strengthen the link between dermatoglyphic markers and genetic risk. In conclusion, the present study reinforces the developmental and genetic basis of vitiligo and highlights dermatoglyphics as a meaningful adjunctive research tool. By revealing stable phenotypic markers of susceptibility, it contributes to a deeper understanding of disease pathogenesis and opens avenues for further investigation into early life determinants of skin disorders.

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