Interface dermatitis includes a heterogeneous group of dermatoses with overlapping microscopic features, often requiring clinicopathological correlation for accurate diagnosis. It is a histological pattern in which the main site of injury lies at the dermoepidermal junction. The lymphocytic inflammation targets the basal keratinocytes and leads to their vacuolar degeneration. Our series of eight cases illustrated this broad spectrum, encompassing classic lichenoid disorders, connective tissue disease-associated lesions, and drug-induced eruptions. This diversity highlights that pattern recognition alone is inadequate; accurate diagnosis requires integrating histopathological findings with clinical correlation.[1] We categorised the inflammatory infiltrate into three distinct presentations: a vacuolar, lichenoid pattern and mixed pattern.

In our tropical setting, drug‑induced eruptions are particularly common among patients with interface dermatitis, likely reflecting polypharmacy in those with diabetes or chronic infections.[2]

Disorders such as lichen planus, lupus erythematosus, drug-related eruptions, and erythema multiforme may show overlapping clinical and microscopic features. Beyond the standard biopsy findings, we focused on diagnostic clues like dermal mucin, eosinophilic infiltration, and evidence of vascular or follicular injury which proved vital in resolving ambiguous cases. In resource-limited settings, where extensive immunological investigations may not always be available, recognition of these subtle features gains further importance.

This case series includes eight histopathologically confirmed cases and provides a practical histopathological approach to interface dermatitis, emphasising pattern recognition and clinicopathological correlation to aid accurate diagnosis in routine practice.

Clinicopathological Profile of Patients with Interface Dermatitis

Case 1: A 22-year-old male presented with recurrent pruritic erythematous scaly papules and plaques over bilateral lower limbs for one month. A prior similar episode had resolved with corticosteroid therapy. There was no relevant drug intake or family history. Cutaneous examination revealed polygonal scaly papules and plaques. Clinical diagnosis was lichen planus. Histopathological examination showed wedge-shaped hypergranulosis, irregular acanthosis with saw-toothed rete ridges, basal vacuolar degeneration, civatte bodies, and a dense band-like lymphocytic infiltrate obscuring the dermoepidermal junction. No special stains were required. Findings were consistent with lichen planus. [Table/Fig-1,2] Case 2: A 54-year-old female with breast carcinoma presented with progressive hyperpigmented bluish-grey macules over the trunk and upper limbs for six months, associated with mild pruritus. Cutaneous examination showed irregularly bordered macules coalescing into patches. Clinical differential diagnosis included lichen planus pigmentosus, lupus erythematosus, and lichenoid drug eruption. Histopathological examination revealed epidermal atrophy, basal vacuolar degeneration, focal hypergranulosis, pigment incontinence, numerous dermal melanophages, and sparse superficial lymphocytic infiltrate. Alcian blue stain did not demonstrate dermal mucin. Findings were in favor of lichen planus pigmentosus. [Table/Fig-1,3] Case 3: A 65-year-old female presented with a long-standing hypopigmented alopecic patch over the scalp without history of photosensitivity. Clinical differential diagnoses included lichen sclerosus, discoid lupus erythematosus, and scalp psoriasis. Histopathological examination revealed epidermal atrophy, follicular plugging, basal vacuolar degeneration, and increased dermal mucin. Alcian blue stain highlighted dermal mucin deposition. Findings were in favor of discoid lupus erythematosus. [Table/Fig-1,4] Case 4: A 64-year-old male presented with proximal muscle weakness and elevated serum aldolase levels. Autoimmune work-up showed a borderline myositis panel, negative antinuclear antibody, and creatine kinase (CK) levels were mildly elevated (45 U/L) with a relatively increased CK-MB fraction (15 U/L). The patient had inadequate response to corticosteroid tapering. Clinical diagnosis was dermatomyositis. Histopathological examination of skin biopsy revealed epidermal atrophy, basal vacuolar degeneration, and increased dermal mucin without a dense lichenoid infiltrate. Alcian blue stain highlighted dermal mucin deposition. Findings were in favor of dermatomyositis-associated interface dermatitis, representing a cell-poor vacuolar pattern. [Table/Fig-1,4] A 79-year-old female receiving prednisolone and hydroxychloroquine for recently diagnosed Sjögren syndrome presented with acute onset pruritic erythematous papules and plaques involving the lips, scalp, trunk, and extremities of four days duration, beginning one day after hair dye application. Clinical differential diagnoses included allergic contact dermatitis to hair dye, drug eruption, urticarial vasculitis, subacute cutaneous lupus erythematosus, and erythema multiforme. Histopathological examination showed basal vacuolar degeneration, lymphocyte exocytosis, scattered necrotic keratinocytes, and mixed superficial perivascular inflammatory infiltrate composed of lymphocytes, eosinophils, and neutrophils. No special stains were performed. Findings were in favor of erythema multiforme. [Table/Fig-1,5] Case 6: A 70-year-old male with diabetes mellitus and hypertension, receiving dapagliflozin, presented with generalised pruritic scaly papules and plaques of 30 days duration, initially involving the lower limbs with subsequent proximal spread. He was also hepatitis C seropositive. Cutaneous examination showed erythematous scaly plaques with focal erosions and excoriations. Clinical differential diagnoses included lichenoid drug eruption, adult atopic dermatitis, and lichenoid psoriasis. Histopathological examination revealed parakeratosis, focal basal vacuolar degeneration, band-like lymphohistiocytic infiltrate, pigment incontinence, and occasional eosinophils. No special stains were performed. Findings were in favor of lichenoid drug eruption. [Table/Fig-1,6] Case 7: A 48-year-old female presented with asymptomatic hyperpigmented macules over the hips and inframammary regions of one month duration, developing after intake of paracetamol for fever with pruritus. Cutaneous examination showed multiple brownish macules. Clinical differential diagnoses included fixed drug eruption and lichen planus. Histopathological examination revealed mild acanthosis, basal vacuolar degeneration, focal follicular plugging, marked pigment incontinence, and numerous dermal melanophages. No special stains were performed. Findings were in favor of fixed drug eruption. [Table/Fig-1,7] Case 8: A 63-year-old female developed multiple erythematous papules and vesicular lesions with crusting over the upper limbs, axillae, abdomen, and thighs while receiving cefuroxime. There was no associated pruritus, fever, or prior history suggestive of varicella. Clinical differential diagnoses included atypical varicella, pityriasis lichenoides et varioliformis acuta, leukocytoclastic vasculitis, drug-induced eruption, and miliaria. Histopathological examination revealed spongiosis, lymphocyte exocytosis, parakeratosis with focal ulceration, basal vacuolar degeneration, superficial perivascular lymphocytic and neutrophilic infiltrate, mild fibrinoid vascular change, and erythrocyte extravasation. No special stains were performed. Findings were in favor of pityriasis lichenoides et varioliformis acuta. [Table/Fig-1,8]

In our study, the age range varied from 22 to 79 years. Elderly patients predominated, mirroring trends in recent studies which likely stems from lifelong UV damage, declining immunity, and coexisting illnesses[3]. Such findings highlight the importance of screening for interface-related skin changes in older adults with ongoing or unusual eruptions. The present study revealed a female predominance, with five of the eight patients being women. This is in agreement with several clinicopathological studies of interface dermatitis, particularly those encompassing autoimmune conditions such as lupus erythematosus and pigmentary interface disorders, where female‑to‑male ratios frequently exceed 2:1[4].

This retrospective series highlighted the wide clinical spectrum of the pattern of interface dermatitis. Studies note discrepancies between initial clinical diagnoses and histopathology in such cases. In our cohort, drug reactions, pityriasis lichenoides et varioliformis acuta, and lichen planus pigmentosus showed broad clinical differentials; histopathology confirmed the final diagnoses.

In the present series, histological overlap was evident, as basal vacuolar degeneration, lichenoid band and civatte bodies were observed across multiple entities, supporting the diagnostic challenge by Fleming et al. that these are diagnostic clues rather than disease-specific markers[5]. Accurate diagnosis thus requires evaluating epidermal architecture, inflammatory infiltrate characteristics, dermal changes, and clinical correlation. [Table/Fig-9]

[Table/Fig-9]:

Pattern-based Histopathological Diagnostic Approach to Interface Dermatitis

Recent classification systems broadly divide interface dermatitis into three patterns: cell-rich (lichenoid), cell-poor (vacuolar), and mixed types. In the present series, the lichenoid and vacuolar patterns were equal in number, indicating a balanced representation of the major interface reaction patterns described in literature. Lichenoid pattern included cases of lichen planus, lichen planus pigmentosus, lichenoid drug eruption. In contrast, the vacuolar pattern in our series was identified in autoimmune connective tissue disease-related lesions, namely discoid lupus erythematosus and dermatomyositis . The dermatomyositis case in the present series showed a pauci-inflammatory vacuolar interface pattern with minimal inflammation, consistent with the characteristic histopathological findings reported in cutaneous dermatomyositis[6].

Mixed-pattern lesions were also seen in our series which showed overlapping lichenoid and vacuolar features. The biopsy diagnosed as pityriasis lichenoides et varioliformis acuta was a good example of this mixed morphology. A clinicopathological review by Khachemoune et al. [7] reported that pleva commonly shows mixed interface changes with necrotic keratinocytes and vascular damage, which closely matches our findings.

Drug-related interface dermatitis emerged as a key subgroup in this series, with several cases linked to medications. Prior studies by Singh J et al, [8] confirm drugs as a frequent cause, especially in elderly patients on polypharmacy. Biopsies from suspected cases revealed eosinophils, parakeratosis, mixed infiltrates, and scattered necrotic keratinocytes which are recognized but nonspecific clues for drug-induced lichenoid or vacuolar reactions. Drug-induced lichenoid eruptions are known to demonstrate eosinophils and focal parakeratosis more frequently than idiopathic lichen planus, aiding histopathological differentiation[9].

In two cases, alcian blue staining highlighted prominent dermal mucin accumulation, strongly favouring connective tissue disease‑associated interface dermatitis and aiding differentiation from lichenoid mimics. Alcian blue effectively reveals subtle mucin deposits that may be overlooked on routine H&E sections and serves as a useful ancillary tool in everyday practice and is cost effective. This aligns with Kuhn A, et al.,[10]who reported high specificity (85.7%) of reticular dermal mucin for lupus versus other dermatoses using combined H&E/Alcian blue scoring.

One patient with pre-existing Sjögren syndrome developed erythema multiforme. This case illustrated interface dermatitis as an overlap between underlying autoimmune disease and medication trigger. Such presentations often complicate diagnostic efforts, as the features of the drug-induced reaction may obscure or mimic the patient’s primary autoimmune pathology[11].

This series of eight cases shows that interface dermatitis is often encountered not as a single disease, but as a common tissue reaction shared by autoimmune, pigmentary, idiopathic, and drug-related dermatoses. In routine practice, the challenge lies less in identifying interface change and more in distinguishing close mimics through subtle histological clues and clinical correlation. A pattern-based approach can improve diagnostic confidence and remains especially useful in settings where ancillary investigations are limited.

FIGURE LEGENDS

[Table/Fig-1]:

Clinicopathological Profile of Patients with Interface Dermatitis

[Table/Fig-2]:

(a) Lichen planus shows epidermis with wedge-shaped hypergranulosis and irregular acanthosis (H&E, 10X);

 (b) Saw-toothed rete ridges with basal cell vacuolation and dense band-like lymphocytic infiltrate obscuring the dermoepidermal junction (H&E, 10X).

[Table/Fig-3]:Lichen planus pigmentosus shows atrophic epidermis with basal cell vacuolation, pigment incontinence, dermal melanophages and sparse lymphocytic infiltrate (H&E, 10X);

[Table/Fig-4]:

 (a) Discoid lupus erythematosus shows epidermal atrophy with follicular plugging and basal cell vacuolation with sparse inflammatory infiltrate (H&E, 10X);

 (b) Discoid lupus erythematosus shows increased dermal mucin highlighted by Alcian blue stain (Alcian blue, 10X);

(c) Dermatomyositis shows epidermal atrophy with subtle basal cell vacuolation (H&E, 10X);

(d) Dermatomyositis shows increased dermal mucin deposition (Alcian blue, 10X).

[Table/Fig-5]:

(a) Drug-induced interface dermatitis shows epidermis with spongiosis, basal cell vacuolation, and lymphocyte exocytosis (H&E, 10X);

(b) Mixed inflammatory infiltrate with eosinophils in the dermis (H&E, 40X).

[Table/Fig-6]:

(a) Lichenoid drug eruption shows epidermis with parakeratosis, irregular acanthosis, and basal cell vacuolation with a moderate lymphohistiocytic band at the dermoepidermal junction (H&E, 10X);

 (b) Dermal melanophages with mild lymphocytic infiltrate and occasional eosinophils (H&E, 40X).

[Table/Fig-7]:

(a) Lichen planus pigmentosus shows mild epidermal acanthosis with follicular plugging and basal cell vacuolation (H&E, 10X);

(b) Prominent pigment incontinence with dermal melanophages (H&E, 10X).

[Table/Fig-8]:

(a) Pityriasis lichenoides et varioliformis acuta shows epidermis with spongiosis and basal cell vacuolation (H&E, 10X);

(b) Pityriasis lichenoides et varioliformis acuta shows lymphocyte exocytosis (H&E, 40X);

(c) Dermal inflammation with RBC extravasation (H&E, 40X).

[Table/Fig-9]:

Pattern-based Histopathological Diagnostic Approach to Interface Dermatitis

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