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Nail changes as clinical markers of disease spectrum and reactional states in Hansen’s disease: A retrospective record-based cross-sectional study
*Corresponding author: Rishav Sanghai, Department of Dermatology, All India Institute of Medical Sciences, Patna, Bihar, India. rishav.sanghai21@gmail.com
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Received: ,
Accepted: ,
How to cite this article: Pradhan S, Sanghai R, Shahid R. Nail changes as clinical markers of disease spectrum and reactional states in Hansen’s disease: A retrospective record-based cross-sectional study. J Onychol Nail Surg. 2026;3:11-7. doi: 10.25259/JONS_2_2026
Abstract
Background:
Nails are an integral component of the integumentary system and serve as a useful window to systemic and dermatological diseases. Hansen’s disease is a chronic infectious condition caused by Mycobacterium leprae, primarily affecting the skin and peripheral nerves. Nail changes in leprosy result from a combination of peripheral neuropathy, repeated micro-trauma, vascular compromise, secondary infections and immunological reactional states. Despite their clinical relevance, nail changes are frequently overlooked, and real-world Indian data on nail involvement in Hansen’s disease remain limited.
Objectives:
The objectives of the study were to determine the frequency and spectrum of nail changes in Hansen’s disease and to assess their association with various types of leprosy as per the Ridley–Jopling spectrum, or with lepra reactions.
Material and Methods:
A retrospective, record-based cross-sectional study was conducted over 14 months (November 2020–January 2022) in a tertiary care hospital in Eastern India. Clinical records of 106 patients with Hansen’s disease were analysed. Nail findings were documented and categorised. Data were analysed using descriptive statistics, and associations were tested using Chi-square or Fisher’s exact test, as applicable with a p < 0.05 being considered statistically significant.
Results:
The mean age of patients was 36.4 ± 15.2 years. Nail changes were observed in 93.4% of cases. Of the 106 patients, 49 (56.6%) belonged to the tuberculoid pole, 11 patients had pure neuritic hansen and 46 (43.4%) belonged to the lepromatous pole. Tuberculoid disease predominantly showed brittle and infective nail changes such as onychorrhexis, onychomycosis and paronychia, whereas lepromatous disease demonstrated advanced dystrophic changes including subungual hyperkeratosis, onychomadesis, brachyonychia, anonychia and trachyonychia. Trachyonychia (p = 0.033) and subungual hyperkeratosis (p=0.031) were found to be significantly associated with the lepromatous spectrum. Longitudinal ridging, Beau’s lines and onychomadesis were significantly more common in patients with lepra reactions (p < 0.05); onychomadesis was strongly associated with type 2 reactions.
Conclusion:
Nail involvement was very common in our cohort and appeared to reflect the disease spectrum, duration and immunological activity. Routine nail examination is a simple, non-invasive assessment that may provide useful clinical clues and can be incorporated into the standard evaluation of patients with Hansen’s disease.
Keywords
Hansen
Lepra reaction
Nails
Onychomycosis
Subungual hyperkeratosis
INTRODUCTION
Hansen’s disease is a chronic granulomatous infection caused by Mycobacterium leprae that primarily affects the skin and peripheral nerves. Despite sustained global control efforts, leprosy remains a public health concern in endemic countries such as India, which continues to report a significant proportion of new cases.[1] Not only does it involve the skin and peripheral nerves but also affects the appendages such as hair, sweat glands and nails.
Nails are sensitive indicators of chronic systemic disease, inflammation, vascular compromise and neurological dysfunction. In leprosy, nail changes arise due to a combination of neuropathy, vascular insult, secondary infection as well as adverse drug effects.[2,3] Despite their clinical relevance, nail changes are often under-recognised during routine examination.
The clinical spectrum of Hansen’s disease, as described by the Ridley-Jopling classification, ranges from tuberculoid to lepromatous forms. Tuberculoid disease is characterised by strong cell-mediated immunity and localised involvement, whereas lepromatous disease is associated with diffuse infiltration, widespread neuropathy, vascular involvement and chronic disease progression.[4] Consequently, the frequency and pattern of nail involvement are expected to vary across the disease spectrum. Previous studies have documented a wide range of nail abnormalities in leprosy, including onychorrhexis, paronychia, onychomycosis, Beau’s lines, subungual hyperkeratosis, brachyonychia, anonychia, pterygium, onychomadesis and trachyonychia.[5] Mild and infective nail changes are more commonly reported in tuberculoid disease, whereas severe dystrophic and destructive changes are typically associated with lepromatous leprosy (LL). Nail changes such as brachyonychia and anonychia have been linked to acro-osteolysis and loss of distal phalangeal support, emphasising the close relationship between the nail unit and underlying bone.[6]
Lepra reactions represent acute immunological episodes superimposed on the chronic disease process and are a major cause of morbidty in these patients. Type 1 reaction reflects fluctuations in cell-mediated immunity, while Type 2 reaction, including erythema nodosum leprosum (ENL), is immune-complex-mediated hypersensitivity reaction.[7] These states may disrupt nail matrix activity, resulting in growth-arrest phenomena such as Beau’s lines and onychomadesis, though systematic data correlating nail changes with reactions remain limited.
Given that nail involvement is often overlooked during routine clinical assessment, and that spectrum-wise analyses remain limited, the present study was undertaken to evaluate nail changes in patients with leprosy, and to correlate these findings with the clinical spectrum and lepra reactions. By systematically documenting nail abnormalities across different disease types, this study aims to provide a comprehensive overview of nail involvement in Hansen’s disease and to highlight its potential value as a simple, non-invasive clinical indicator of disease chronicity and immunological activity.
MATERIAL AND METHODS
This was a retrospective, record-based, cross-sectional analytical study, conducted in the Department of Dermatology at All India Institute of Medical Sciences (AIIMS), Patna. Clinical records of leprosy patients seen over a 14-month period, from November 2020 to January 2022, were reviewed. All patients diagnosed with Hansen’s disease during the study period and having comprehensive clinical documentation, including nail examination findings, were eligible for inclusion. A total of 106 patients fulfilling the inclusion criteria were included in the final analysis. These included patients aged >12 years with leprosy as per the World Health Organization diagnostic criteria (clinical features with peripheral nerve thickening, with or without supportive slit-skin smear and/or histopathological findings). Patients with co-existing dermatological conditions known to cause nail changes (psoriasis, lichen planus, alopecia areata); those with systemic illnesses associated with peripheral neuropathy or nail abnormalities (diabetes mellitus and vitamin B12 deficiency); or incomplete medical records were excluded.
Data were extracted using a structured proforma and included demographic (age, gender, occupation, residence, education and contact/family history) and clinical variables (clinical spectrum of Hansen’s disease categorised according to the Ridley–Jopling classification). Patients with pure neuritic leprosy (PNL) (absence of skin lesions with peripheral nerve involvement) were classified separately as PNL and analysed independently. The presence and type of lepra reaction (type 1 or type 2), presence of deformity, bacteriological index (where available) and nail features were recorded. It was based on a detailed examination of the finger and toe nails for dystrophic, infective, pigmentary and growth-related abnormalities. All twenty nails were examined sequentially, assessing the nail plate, nail bed, proximal and lateral nail folds and periungual tissues. Nail examination was performed under adequate illumination by trained senior dermatologists in the department and was cross-verified by another dermatologist to minimise inter-observer variability. Parameters evaluated included nail colour changes, surface abnormalities (ridging, pitting), nail dystrophy, onycholysis, subungual hyperkeratosis and periungual changes. The changes were categorised as brittle changes (onychorrhexis), infective changes (onychomycosis, paronychia), dystrophic changes (brachyonychia, anonychia, twenty-nail dystrophy), growth arrest phenomena (Beau’s lines, onychomadesis) and surface changes (longitudinal ridging). Findings were recorded in a structured proforma to ensure consistent documentation.
Statistical analysis
Data were entered into Microsoft Excel and analysed using Jamovi statistical software (version 2.6.44). Continuous variables were assessed for normality using visual inspection of histograms and the Shapiro–Wilk test. Normally distributed continuous data were expressed as mean ± standard deviation, while non-normally distributed data were expressed as median with interquartile range. Categorical variables were summarised as frequencies and percentages. Associations between categorical variables (nail changes vs. disease spectrum; nail changes vs. lepra reaction status) were analysed using the Chi-square test. Fisher’s exact test was applied wherever expected cell counts were <5. Post hoc pairwise comparisons were performed where applicable using adjusted p-values. All statistical tests were two-tailed, and a p < 0.05 was considered statistically significant.
RESULTS
Demographic profile
A total of 106 patients with Hansen’s disease were included in the study. The age of the patients ranged from 14 to 72 years, with a mean age of 36.4 ± 15.2 years. The majority of patients were in the third and fourth decades of life [Figure 1]. There was a male predominance (73.5%), with 26.5% being females. The mean age was comparable for both sexes, being 36.6±6.8 years and 35.9±7.5 years, respectively. A definite family or household contact history of Hansen’s disease was elicited in 12 patients (11.3%). Overall, 66% of the subjects resided in the rural area. Majority of our patients were daily wagers (48.11%) and housewives (22.6%). Around 46% patients had secondary level of education with 21.3% being graduates. However, 26.2% of the population were illiterate.
Clinical profile of Hansen’s disease
Based on the Ridley–Jopling classification, 49 patients (46.2%) had tuberculoid disease (TT, BT), while 46 patients (43.4%) had lepromatous disease (BL and LL) and 11 patients (10.4%) had pure neuritic leprosy. Borderline forms constituted the majority of cases, reflecting the immunologically unstable nature of Hansen’s disease [Figure 2]. Among the patients, 66.1% patients were treatment naïve, 11.3% were treatment defaulter and 7.5% had been released from treatment. Lepra reactions were documented in a substantial proportion of patients. Type 1 reaction was observed predominantly among patients with BT and BL disease (18 patients); whereas Type 2 reaction (ENL) was seen almost exclusively in patients with lepromatous disease (17 patients). Reactional states were more frequent in patients with multibacillary disease and those with longer disease duration.
No deformities were seen in 74.6% patients. Deformities of hands (15.3% patients) were most commonly seen as ulnar clawing, thenar or hypothenar atrophy, and acral osteolysis; while deformities of feet (3.8%) were seen as trophic ulcer; foot drop or osteolysis. Both hand/feet deformities were seen in 5.7% patients. Patients with higher grades of deformity frequently exhibited severe nail dystrophy.
Nail changes
Nail changes were observed in 99 patients (93.4%). Only seven patients (6.6%) did not exhibit any nail abnormality. Both finger and toenails were affected. These were not analysed separately. Distinct and characteristic patterns of nail involvement were observed across the disease spectrum [Table 1]. Onychomycosis was a common finding in 26 patients, subungual hyperkeratosis in 25 patients, and longitudinal ridging (onychorrhexis) in 21 patients. Paronychia and brachyonychia were seen in 13 patients each and koilonychia in 12 patients. Nail abnormalities were not mutually exclusive, with a single patient often exhibiting more than one nail change.
| Nail changes | TT (n=1) | BT (n=48) | PNL (n=11) | BL (n=11) | LL (n=35) | Frequency of nail changes (n=101) |
|---|---|---|---|---|---|---|
| Onychomycosis | 0 | 10 | 6 | 2 | 8 | 26 |
| Longitudinal ridging (onychorrhexis) | 0 | 11 | 1 | 2 | 7 | 21 |
| Subungual hyperkeratosis | 0 | 7 | 3 | 3 | 12 | 25 |
| Koilonychia | 0 | 5 | 0 | 2 | 5 | 12 |
| Brachyonychia | 0 | 7 | 0 | 1 | 5 | 13 |
| Onycholysis | 0 | 6 | 0 | 2 | 4 | 12 |
| Pterygium | 0 | 7 | 0 | 0 | 4 | 11 |
| Twenty nail dystrophy | 0 | 0 | 0 | 0 | 4 | 4 |
| Melanonychia | 0 | 3 | 0 | 0 | 4 | 7 |
| Onychomadesis | 0 | 3 | 0 | 2 | 4 | 9 |
| Paronychia | 1 | 8 | 0 | 1 | 3 | 13 |
| Beau’s lines | 0 | 4 | 1 | 0 | 3 | 8 |
| Leuconychia | 0 | 5 | 0 | 2 | 3 | 10 |
| Pincer nails | 0 | 4 | 0 | 2 | 3 | 9 |
| Anonychia | 0 | 0 | 1 | 0 | 2 | 3 |
| Onychogryphosis | 0 | 3 | 0 | 0 | 2 | 5 |
| No change | 0 | 3 | 2 | 1 | 1 | 7 |
Patients had multiple nail changes simultaneously; therefore, row totals do not correspond to the total number of patients in each spectrum category. TT: Tuberculoid, BT: Borderline tuberculoid, PNL: Pure neuritic leprosy, BL: Borderline lepromatous, LL: Lepromatous leprosy
In tuberculoid disease, nail changes were generally mild to moderate, localised and asymmetric. The most common nail abnormalities observed were onychorrhexis (28%), onychomycosis (20%) and paronychia (18%). These reflected brittle and infective nail pathology and were frequently associated with localised sensory loss, repeated unnoticed trauma and secondary infections. In contrast, patients with lepromatous dsiease exhibited extensive, bilateral and severe nail involvement. Subungual hyperkeratosis was the most frequent finding (21%), followed by onychomadesis (17%), brachyonychia (15%), anonychia and trachyonychia (9%). These changes reflected chronic disease, widespread neuropathy, vascular compromise and acro-osteolysis. Patients with trachyonychia (4) had lepromatous disease. A comparative analysis of nail changes in the tuberculoid and lepromatous disease is depicted in Figure 3.
Statistical analysis showed trachyonychia to be significantly associated with lepromatous disease (p = 0.033) (Fisher’s exact test). Similarly, subungual hyperkeratosis was also significantly associated with lepromatous disease (p = 0.031). Other nail changes, although more frequently seen with lepromatous disease, did not reach statistical significance. Some changes, like onychomycosis and paronychia, were seen with higher frequency with tuberculoid disease, though the association was not statistically significant [Figure 4].
Nail abnormalities were significantly more frequent and more severe among patients who experienced reactional episodes. Fisher’s exact test demonstrated statistically significant associations between lepra reactions and specific nail changes including longitudinal ridging (p = 0.046), and Beau’s lines (p = 0.014), reflecting transient disturbances of nail matrix activity, with episodic growth arrest. Onychomadesis demonstrated the strongest association with lepra reactions (p = 0.005), signifying profound nail matrix arrest secondary to severe systemic inflammation and immune-complex-mediated vasculitis. Conversely, brachyonychia (p = 0.010) and pterygium (p = 0.018) were observed exclusively in patients without active lepra reactions, suggesting their association with chronic structural damage rather than acute inflammatory activity.
Comparison of nail changes between patients with Type 1 and Type 2 lepra reactions [Table 2] revealed that Type 1 lepra reaction was more commonly associated with longitudinal ridging, Beau’s lines and onycholysis, suggesting transient nail matrix stress related to acute cell-mediated immune responses. In contrast, onychomadesis showed a strong and exclusive association with type 2 lepra reactions (p < 0.001), indicating severe systemic involvement and immune-complex-mediated vascular injury. Other nail changes did not demonstrate statistically significant discriminatory value between the two types of reactions.
| Nail changes | Type 1 reaction (n) | Type 2 reaction (n) | p-value |
|---|---|---|---|
| Longitudinal ridging | 8 | 3 | >0.05 |
| Onycholysis | 5 | 2 | >0.05 |
| Beau’s lines | 5 | 1 | >0.05 |
| Koilonychia | 2 | 1 | >0.05 |
| Leuconychia | 2 | 1 | >0.05 |
| Onychomadesis | 1 | 6 | <0.001 |
| Twenty-nail dystrophy | 0 | 2 | 0.08 |
| Onychomycosis | 4 | 4 | >0.05 |
| Subungual hyperkeratosis | 2 | 2 | >0.05 |
| Paronychia | 1 | 1 | >0.05 |
| Melanonychia | 1 | 0 | >0.05 |
| No nail change | 2 | 3 | >0.05 |
Significant p value is 0.05
DISCUSSION
The present study provides a detailed and comprehensive evaluation of nail changes in Hansen’s disease and demonstrates that nail involvement closely reflects disease spectrum, chronicity, neuropathic damage and immunological activity. This study reinforces the concept that nail changes are not merely incidental findings but represent important clinical markers of disease behaviour, stratifying with the disease spectrum.
In the present study, nail changes were observed in 93.4% of patients with Hansen’s disease, indicating that nail involvement is almost universal. This prevalence is higher than that reported in earlier studies, where nail changes were documented in 64–86% of cases. Patki and Baran reported nail involvement in 64% of their cohort, while Kaur et al. observed nail changes in 77.3% of patients with leprosy.[2,5] Rajput et al., in a large Indian study, documented nail abnormalities in approximately 80% of cases.[8] The higher prevalence in our study may be attributed to the inclusion of subtle abnormalities such as longitudinal ridging and Beau’s lines, and analysis across the entire Ridley-Jopling spectrum rather than the conventional paucibacillarymultibacillary categorisation. These findings highlight the importance of routine and systematic nail examination in all patients with Hansen’s disease.
A distinct spectrum-wise pattern of nail involvement was evident in our study. Patients with tuberculoid disease predominantly exhibited mild to moderate nail changes, such as onychorrhexis, onychomycosis and paronychia. Similar findings have been reported by Kaur et al. and El-Darouti et al., who attributed these changes to localised sensory loss, repeated unnoticed trauma and secondary infections.[5,9] The asymmetric and localised nature of nail involvement in tuberculoid disease observed in our study further supports a focal neuropathic mechanism. In contrast, patients with lepromatous disease had extensive, bilateral and severe dystrophic nail changes, including subungual hyperkeratosis, brachyonychia, anonychia, onychomadesis and trachyonychia. Rajput et al. similarly reported that advanced dystrophic and mutilating nail changes were predominantly seen in BL and LL.[8] The statistically significant association of trachyonychia and subungual hyperkeratosis with lepromatous disease emphasises their value as markers of advanced disease with widespread neuropathy, vascular compromise and prolonged disease duration. Brachyonychia and anonychia are believed to result from acro-osteolysis and loss of distal phalangeal support. Patki and Baran emphasised the dependence of nail morphology on the integrity of the distal phalanx, proposing that destruction of bone leads to shortening and dystrophy of the nail plate.[2] The predominance of these changes in patients with longstanding lepromatous disease and deformities in our study strongly supports this pathogenic mechanism.
An important observation in this study was the association between nail changes and lepra reactions. Longitudinal ridging and Beau’s lines were significantly more frequent among patients experiencing reactional episodes, reflecting transient nail matrix stress during periods of acute inflammation. Similar observations have been reported in earlier studies, where growth-arrest phenomena were noted during reactional states, particularly ENL.[7,8]
Onychomadesis showed the strongest association with lepra reactions in the present study, particularly with type 2 lepra reactions. This finding is clinically significant, as onychomadesis represents severe nail matrix arrest. Rajput et al. described onychomadesis as a striking but uncommon finding following severe ENL episodes.[8] The strong association observed in our study reinforces the concept that onychomadesis may serve as a marker of severe systemic inflammation, immune-complex-mediated vasculitis and abrupt interruption of nail matrix activity. Interestingly, brachyonychia and pterygium were observed exclusively in patients without active lepra reactions, suggesting that these nail changes are more closely related to chronic structural damage rather than acute immunological activity. Patki and Baran previously proposed that pterygium formation in leprosy may result from chronic ischemia and fibrosis involving the nail matrix and proximal nail fold.[2]
Nail changes in Hansen’s disease are multifactorial in origin. Peripheral neuropathy leads to repeated unnoticed trauma and trophic alterations, while autonomic dysfunction contributes to anhidrosis and impaired local defence mechanisms. Vascular involvement results in ischemia and growth disturbances of the nail matrix. Secondary infections, particularly dermatophytosis, contribute to brittle and infective nail changes. In addition, drug-related factors, such as clofazimine-induced pigmentation and subungual hyperkeratosis, may further influence nail morphology.[3] The frequency of nail involvement observed in our study, especially in lepromatous disease, may be explained by greater mechanical stress, footwear-related trauma and more severe sensory loss in the lower limbs. Similar observations have been consistently reported in earlier studies.[5,8]
The findings of the present study underscore the clinical relevance of nail examination in Hansen’s disease. Nail changes serve as easily accessible, non-invasive markers of disease spectrum, chronicity and immunological activity. Certain nail abnormalities, such as trachyonychia, brachyonychia and onychomadesis, may alert clinicians to advanced disease or ongoing reactional states, thereby facilitating closer monitoring and timely intervention. Routine nail examination should therefore be incorporated as an integral component of the clinical assessment of patients with leprosy.
Limitations
A retrospective design makes the results dependent on the accuracy and completeness of medical records. Being a single-centre study, the findings may not be generalisable to other settings. The sample size, although adequate for descriptive analysis, limits extensive multivariate modelling. Long-term outcomes and evolution of nail changes could not be assessed due to a lack of followup.
CONCLUSION
Nail involvement was very common in our cohort and appeared to reflect the disease spectrum, duration and immunological activity. Certain nail abnormalities show significant associations with parts of disease spectrum and type of lepra reactions. Routine nail examination is a simple, cost-effective and non-invasive tool that can aid in the comprehensive assessment of patients with leprosy and should be incorporated into standard clinical evaluation.
Authors’ contributions:
Dr. Swetalina Pradhan: Involved in the clinical care of the patient, including diagnosis and management, and contributed to the conception of the study. She performed the initial literature review and had core conception of the entire. She critically reviewed the manuscript for scientific accuracy and clarity. She is responsible for overall supervision of the project, contributed to the conception and design, and provided critical revisions for intellectual content. She acts as the guarantor of the study and is also responsible for the integrity of the work as a whole. Dr. Rishav Sanghai: Contributed to an extensive review of the literature, statistical analysis and interpretation of results and provided critical inputs in structuring the discussion section and revised the manuscript for important intellectual content. Dr. Rashid Shahid: Helped in framing of the introduction and discussion segment. He also helped us in acquiring great clinical images and identification of specific nail changes and deformities as well as structuring of the manuscript. All authors meet the ICMJE criteria for authorship. All authors have read and approved the final manuscript and agree to be accountable for all aspects of the work, ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
Ethical approval:
The Institutional Review Board approval is not required as it is a retrospective study.
Declaration of patient consent:
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given consent for their images and other clinical information to be reported in the journal. The patient understands that the patient’s names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Conflicts of interest:
There are no conflicts of interest.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.
Financial support and sponsorship: Nil.
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