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| ORIGINAL ARTICLE |
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| Year : 2016 | Volume
: 4
| Issue : 2 | Page : 189-195 |
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A study of spectrum of histopathological features in patients presenting with hyperpigmented skin lesions
Smitha Mruthyunjayappa, Hemalata Mahantappa, MG Gopal, Suguna Belur Venugopal
Department of Pathology, Kempegowda Institute of Medical Sciences, Bengaluru, Karnataka, India
| Date of Web Publication | 20-Dec-2016 |
Correspondence Address:
Hemalata Mahantappa
Kempegowda Institute of Medical Sciences, BSK II Stage, Bengaluru - 560 070, Karnataka
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2321-4848.196195
Background: Pigmentary problems are one of the most frequent causes for dermatologic consultation. For accurate diagnosis, histopathological examination is useful. Pathologic examination often serves as a complementary or a confirmative part of the clinical diagnosis. Objective: To study the pattern of hyperpigmented skin lesions and their histopathological features. Materials and Methods: We prospectively studied histopathological features of hyperpigmented skin lesions in all age groups attending the dermatology department of a teaching hospital over a 2-year period. The skin lesions included inflammatory, genetic, metabolic, and endocrine lesions but excluded neoplastic, infectious, and developmental lesions. Results: Of the 980 skin biopsies, 200 (20.4%) were hyperpigmented lesions. Lesions were most common in the second and third decades. Clinically, itching was the most common presentation. Most common biopsy confirmed hyperpigmented lesions included classical lichen planus and its variants (55%). Histopathologically, most lesions showed lichenoid/interface dermatitis. Most hyperpigmented skin lesions were epidermal (75%) with lichen planus pigmentosus being the only dermal hyperpigmented lesion. Conclusion: Classical lichen planus was the most common hyperpigmented lesion seen in our study. Histopathological examination is useful in accurate diagnosis of hyperpigmented skin lesions, particularly in those with unclear or overlapping clinical features. Keywords: Hyperpigmented skin lesions, lichen planus, lichen planus pigmentosus
How to cite this article:
Mruthyunjayappa S, Mahantappa H, Gopal M G, Venugopal SB. A study of spectrum of histopathological features in patients presenting with hyperpigmented skin lesions. Arch Med Health Sci 2016;4:189-95 |
How to cite this URL:
Mruthyunjayappa S, Mahantappa H, Gopal M G, Venugopal SB. A study of spectrum of histopathological features in patients presenting with hyperpigmented skin lesions. Arch Med Health Sci [serial online] 2016 [cited 2023 Mar 29];4:189-95. Available from: https://www.amhsjournal.org/text.asp?2016/4/2/189/196195 |
| Introduction | |  |
Pigmentary problems are one of the most frequent causes for dermatologic consultation. In India, they are a major concern with great psychological impact on quality of life.[1] Hyperpigmentary skin disorders comprise a group of diseases of extreme heterogeneity of epidermal and dermal hyperpigmentation subdivided into various types according to etiology, underlying pathology, and the nature of the pigment.[2]
When the patient seeks medical attention for skin lesions, particularly in those with nonclassical clinical presentation, histopathology is a useful aid in arriving at a definitive diagnosis. Evidence for a correct diagnosis may be lacking in some instances without histopathologic examination of skin biopsies. It is well known that the histologic diagnosis of inflammatory and other skin diseases requires clinicopathologic correlation, and there is evolution of skin lesions into different stages as the disease progresses. Pathologic examination often serves as a complementary or a confirmative part of the diagnosis.[3]
The aim was to study the pattern of hyperpigmented skin lesions and their histopathological features in patients attending dermatology clinical services of a tertiary care center.
| Materials and Methods | | |
This prospective study was undertaken after Institute Ethics Committee approval in patients of all age groups clinically diagnosed with hyperpigmented skin lesions attending the Dermatology Department of a teaching hospital attached to a medical college in Bengaluru from August 2012 to August 2014. These included inflammatory, genetic, metabolic, and endocrine lesions but excluded neoplastic, infectious, and developmental lesions. After informed consent, two punch biopsies of 4 mm were performed for histopathological examination.
In histopathology, biopsy tissue was prepared for light microscopic examination after fixation in 10% formalin. The sections were cut and stained using routine hematoxylin and eosin stain. Special stains were used when needed. Detail examination of epidermal and dermal features was noted.
| Results | | |
Of the 980 skin biopsies received during the study period, 200 (20.4%) were hyperpigmented lesions. Out of 200 patients, 110 (55%) were female, and the remaining 90 (45%) were male. Lesions were more common in the second and third decades. Clinically, itching was the most common presentation. Clinical features of various common biopsy confirmed hyperpigmented lesions are shown in [Table 1]. The less common lesions included prurigo simplex (n = 2) presented with multiple itchy papules on trunk and extremities, discoid lupus erythmatosus (n = 3) presented with macules and papules over face and neck, lichen amyloidosis (n = 3) presented with papules and macules over limbs and trunk, and two cases of freckles presented with macular lesions on the face and neck.
The skin lesions were typed based on the classification suggested by Mosher et al.[2] into epidermal and dermal hyperpigmentation. Epidermal pigmentation was more common accounting for 75% of the lesions, and 25% showed dermal pigmentation. All dermal hyperpigmented lesions were lichen planus pigmentosus (LPP). Histopathological features of hyperpigmented lesions showing interphase dermatitis is shown in [Table 2]. [Table 3] shows histopathology of other common lesions. The less common lesions were prurigo simplex (n = 2), discoid lupus erythematosus (DLE) (n = 3), lichen amyloidosis (n = 3), and freckles (n = 2). In this study, positive correlation between clinical diagnosis and histopathological diagnosis was seen in 95% of cases and negative correlation in 5% of cases. Discordance between clinical and histopathological diagnosis is shown in [Table 4]. Discordance was essentially sorted out by identifying key histopathological features that were not in agreement with the clinical diagnoses by consensus of two pathologists and the referring clinician. | Table 2: Histopathological features of hyperpigmented lesions with lichenoid/interface dermatitis
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| Discussion | | |
Our study examined, clinicopathological correlation in a diverse set of pigmentary skin lesions confirming findings of the previous studies. Our study showed a positive correlation between clinical diagnosis and histopathological diagnosis in 95% of cases. A higher percentage of clinical concordance can be attributed to many differential diagnoses given by the dermatologist. A high positive correlation emphasizes the need for a good clinical diagnosis and detailed histopathology in arriving at a conclusive diagnosis.
Histopathologically, most lesions showed lichenoid tissue reaction/interface dermatitis. Persistent interface reactions often result in the loss of pigment from basal cells and their ingestion by melanophages. Hence, postinflammatory pigmentary changes may result from long-standing lesions of interface dermatitis.[4],[5]
Lichen planus and its variants were the most common hyperpigmented lesions seen in our study [Table 1]. Among these, classical lichen planus was most frequent (26%). D'Costa and Bharambe studied the different lichenoid reactions and found out that lichen planus was the most frequent (57%) in their study, followed by hypertrophic lichen planus (HLP) (19%), LPP (12%), and all other variants (12%).[6]
Lichen planus
The term “lichen” is derived from the Greek verb “to lick.”[7] It is a self-limited eruption most commonly affecting middle-aged adults with a female preponderance.[6],[8] Lichen planus is known to present in a variety of clinical forms. The different clinical patterns may reflect the differences in ethnicity, genetics, various eliciting factors, and extent of skin response to immunological stimuli.[9]
Clinically, lesions are characterized by purple, papular eruptions on the skin that can also involve the mucous membranes, and the nails.[7] A network of fine white lines is present in many papules known as Wickhams striae.[8] The predilection sites of lichen planus include the upper and lower limbs, particularly the extensor surfaces of the lower legs and the volar aspect of the wrists and forearms as well as on the trunk and the lumbar region.[10]
Lichen planus is a classic example of the lichenoid interface dermatitis and is characterized by the basal cell damage in the form of multiple Civatte bodies, and a band-like infiltrate of lymphocytes hugging the epidermis (hence the Greek verb “to lick” meaning lichen) along with wedge-shaped hypergranulosis with saw-toothed rete-ridges [Figure 1].[11] | Figure 1: Classical lichen planus: Multiple hyperpigmented papules over the leg; photomicrograph shows hyperkeratosis, basal cell degeneration, band-like inflammatory infiltrate, and melanin incontinence (H and E, ×100); inset shows Civatte body (H and E, ×400).
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Our clinical and histopathological features correlated well with other studies.[6],[11],[12] Our study showed less hyperkeratosis compared to that in Ellis et al.[11] which could be due to categorizing the lesions showing moderate to marked hyperkeratosis separately under HLP, which has not been done in their study. Lower incidence of Civatte bodies and Max Joseph spaces in our study may be due to lesser number of cases studied.
Lichen planus pigmentosus
LPP was the second most common pigmentary disorder seen in our study accounting for 23% of total cases. Bhutani et al. studied LPP in 40 Indian patients and found an association with lichen planus clinically and histologically in one-third of their cases. Hence, this entity was termed LPP, and it was considered a macular variant of lichen planus.[13]
LPP is characterized clinically as asymptomatic, diffuse, mottled, reticulated or perifollicular hyperpigmented dark brown to slate gray to black macules present mostly overexposed areas and flexures.[14]
The histopathological changes consisted of vacuolar cell degeneration of the basal layer in the epidermis. All the cases showed pigment incontinence and perivascular lymphocytic infiltrate in the dermis with thinning of the epidermis in the majority of the cases [Figure 2]. Most of the changes noted in the biopsies were identical to those reported in the previous studies.[15],[16] LPP thus follows the typical changes seen in lichen palnus, but with thinning of the epidermis. | Figure 2: Lichen planus pigmentosus: Slate Gray hyperpigmentation axilla; photomicrograph showing orthokeratosis, thinning of the epidermis, basal cell degeneration, and dermal pigment incontinence (H and E, ×100).
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Hypertrophic lichen planus
HLP is a variant of Lichen planus which is generally confined to the shins and is rarely generalized. Most striking feature is raised extensive hypertrophic hyperpigmented pruritic plaques. Histopathologically, HLP showed moderate to marked hyperkeratosis and basal cell degeneration in epidermis with band-like infiltrate of lymphoplasmacytic at the dermoepidermal junction. Clinical and histopathological features correlated with other studies.[17],[18],[19] Although it is a benign disorder, malignant changes have been reported in long-standing cases of HLP of the legs of long duration. Ulcerative HLP of the soles may develop into squamous cell carcinoma.[19] The underlying mechanism of this malignant conversion is not exactly known, but speculatively, chronic inflammatory processes show an overdrive of growth factors that constantly stimulate epithelial cell proliferation into neoplastic conditions.[20]
Lichen amyloidosis
Lichen amyloidosis was diagnosed in only three cases. Lichen amyloidosis is a primary localized cutaneous amyloidosis. Clinically, lesions consist of pruritic, small discrete, hyperkeratotic, hyperpigmented, waxy papules in rippled pattern, usually on the extensor surface of the lower limbs, pretibial areas (shin) being the most common site of involvement with a female preponderance.[21],[22] Cutaneous amyloidosis can be papular or lichenoid, macular, and nodular or tumefactive types. Chronic irritation to the skin (e.g. friction due to physical objects such as bath sponges, nylon brushes, towels, plant sticks, etc.,) has been proposed as an etiological factor.[21]
Histopathologically, papillary dermis showed eosinophilic amorphous material of amyloid. Amyloid deposits were restricted to papillary dermis. Special stain with Congo red showed “salmon pink color” which is considered the key diagnostic feature of lichen amyloidosis.[21],[22]
Lichen simplex chronicus
Lichen simplex chronicus (LSC) is characterized by central lichenified plaque and is often hyperpigmented as a result of primary excessive scratching. Most common sites are the neck, ankles, scalp, vulva, pubis, scrotum, and extensor aspect of forearms. The peak incidence is between 35 and 50 years of age and women are more affected than men.[23] LSC can be associated with anxiety, depression, and obsessive-compulsive disorder. Severe intractable pruritus is the hallmark of LSC in almost all patients.[24]
LSC showed irregular elongation of rete ridges with vertically oriented collagen and in addition, the majority of the cases showed mild perivascular lymphocytic infiltration and acanthosis. The histopathological features are similar to those mentioned in other studies.[23],[25]
Lichenoid drug eruptions
Lichenoid drug eruptions are reactions encountered in response to heterogeneous group of ingested drugs, clinically mimicking lichen planus. Histopathologically, differentiating features of lichenoid eruptions include focal parakeratosis and mild basal vacuolar changes with a few eosinophils and plasma cells [Figure 3]. The degree of melanin incontinence is higher, and dermal infiltrate is less dense and less band like than that of lichen planus.[5],[26] | Figure 3: Lichenoid drug reaction: Hyperpigmented scaly raised lesions over forearms; photomicrograph shows hyperkeratosis, parakeratosis, orthokeratosis, and heavy inflammatory infiltrate with prominent interstitial pattern, perivascular inflammation (H and E, ×100).
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Postinflammatory hyperpigmentation
Postinflammatory hyperpigmentation (PIH) was the third most common hyperpigmentary skin lesion found in our study accounting for 9% of the total lesions. Skin insults that result in inflammation can induce PIH, particularly in people with dark skin, such insults are acne lesions, ingrown hairs, scratches, and insect bites.[27] It presents as discrete, hyperpigmented macules with hazy feathered margins, which may involve epidermis or dermis.
Histologically, the sun exposed skin has elevated inflammatory cell count. Epidermal PIH involves increased melanin pigment in the basal cell layer of the epidermis. Dermal PIH involves the upper dermis, with pigment incontinence due to increased numbers of melanophages in the papillary dermis.[28]
Histopathologically, all the cases showed perivascular lymphocytic inflammatory cell infiltrate with 83% showing pigment incontinence [Figure 4] which is similar to histopathological features described by Stulberg et al.[28] Other histological features were increased basal cell pigmentation, hyperkeratosis, and basal cell degeneration. Another study by Ortonne and Bissett found similar results comparable to our present study.[27] | Figure 4: Postinflammatory hyperpigmentation: Hyperpigmented papules over chin; photomicrograph showing pigmented melanophages in superficial dermis and lymphohistiocytic infiltrate around superficial blood vessel (H and E, ×100).
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Prurigo nodules
Prurigo nodular is a dermatologic condition which can occur at all ages and equally in both sexes. It presents with hard nodule (s) 1–5 cm in diameter, with a warty, excoriated, pigmented dark red surface with central crusts, usually surrounded by an irregular hyperpigmented ring. The extensor area of the limbs, face, and trunk are usually affected by the lesions, which may leave scars.[23],[29] Prurigo nodularis has been associated with psychological disorders such as depression and anxiety.[30] Histologically, prurigo nodularis is characterized by marked hyperkeratosis, often focal parakeratosis, and marked irregular acanthosis that is often of pseudoepitheliomatous proportions. The characteristic neurological changes include hypertrophy and proliferation of dermal nerves.[30] Our cases also showed above features [Figure 5], but the closest differential diagnosis is LSC, which has a similar histologic picture although less circumscribed and less exuberant.[29] | Figure 5: Prurigo nodularis: Multiple nodules on both legs; photomicrograph shows hyperkeratosis, parakeratosis, irregular acanthosis, lymphocytic infiltrate in dermis, and vertical collagen bundles (H and E, ×100).
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Polymorphic light eruption
PLE is thought to be caused by an immune reaction to a compound in the skin, which is altered by exposure to ultraviolet (UV) radiation resulting in an inflammatory rash. It is usually provoked not only by short wavelength UV-B but also by longer wavelength UV-A.[31],[32] It is more common in females and associated with autoimmune thyroiditis.[33] The cutaneous response has been described as nonscarring, pruritic, erythematous papules, vesicles, or plaques on light-exposed skin.[31],[32]
The histologic findings vary according to the age of the lesion sampled. Very early lesions show either a normal epidermis or mild spongiosis with focal lymphocyte exocytosis and mild to moderate lymphohistiocytic perivascular or periadnexal infiltration.[31],[34] As lesions progress, there is marked edema of the papillary dermis and more prominent dermal inflammation. Histologically, PLE must be differentiated from lupus erythematosus, the porphyrias, actinic prurigo, and Jessners lymphocytic infiltrate.[35]
PLE showed perivascular lymphocytic infiltrate in all cases along with 87% of cases showing edema and 73% cases showing spongiosis [Figure 6]. Histopathological features are similar to those reported by others.[31],[36] | Figure 6: Polymorphic light eruption: Hyperpigmented lesions on the neck; photomicrograph shows acanthosis, spongiosis, edema in the papillary dermis, and perivascular lymphocytic infiltration (H and E, ×100).
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Morphea
Morphea are characterized by purplish or mauve color with lilac border. On Fontana-Masson stained sections, there is increased melanocytic activity in the form of prominent melanocytes in the basal cell layer. There is no basal cell degeneration and melanin incontinence.[37] Morphea is divided on the basis of the distribution of the lesions as guttate, plaque, linear, segmental, subcutaneous, and generalized. Histopathology of morphea is termed early inflammatory, intermediate, and late sclerotic stages. Early lesion shows interstitial lymphoplasmacytic infiltrates with or without eosinophils among slightly thickened collagen bundles. Late sclerotic stage shows more thickened collagen bundles with almost normal epidermis and complete disappearance of inflammatory infiltrate.[38] Histopathologically, sclerotic collagen bundles with pulled up adnexal structures were seen in 75% of cases and perivascular lymphocytic infiltration in 83% of the cases which correlates with other studies [Figure 7].[37] | Figure 7: Morphea over the dorsum of the hand: Photomicrograph reticular dermis showing mild lymphocytic infiltrate and thickened collagen bundles (H and E, ×100).
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Discoid lupus erythematosus
DLE is the most common form of chronic cutaneous lupus erythematosus. They present as well-defined erythematous plaques showing thick adherent scales and follicular plugging, and old lesions atrophic scarring with verrucous hyperkeratosis may be seen. DLE usually affects sun-exposed skin, most often on the face. UV light induces apoptosis of keratinocytes, autoantigen translocation, and the release of pro-inflammatory cytokines which trigger DLE.[39]
Histopathology of DLE showed orthokeratotic hyperkeratosis, follicular plugging, mild exocytosis, basal cell degeneration, and lymphocytic infiltration at dermoepidermal junction. Dense mononuclear infiltrates around perivascular and periadnexal areas were noted. These findings are comparable to those reported in other studies.[39],[40]
Prurigo simplex and freckles
Prurigo simplex is characterized by intensely pruritic, erythematous urticarial papules that are seen in symmetric distribution, especially on the trunk and extensor surfaces of the extremities of middle-aged patients. Prurigo simplex can lead to prurigo nodularis. It is the most common type of pruritic eruption in HIV-infected individuals.[41]
The histological feature of early papule shows mild acanthosis, spongiosis with an occasional small spongiotic vesicle, and parakeratosis. The superficial dermis shows perivascular lymphocytic infiltrate.[42] Similar findings were seen in our study. Histopathology in freckles showed increased pigmentation in the basal layer of the epidermis.[27]
| Conclusion | | |
Classical lichen planus was the most common hyperpigmented lesion seen in our study. Most hyperpigmented skin lesions were epidermal with LPP being the only dermal hyperpigmented lesion. Recognition of these commonly encountered cutaneous conditions depend on the familiarity of clinical presentation, and the diagnosis can be confirmed by histopathology. The pathologist's ability to render an accurate diagnosis also depends on the availability of clinical information provided. Although lichenoid lesions, classical lichen planus, in particular, are often easily diagnosed clinically, in many instances, histopathology aids in clarifying diagnosis in conditions which have atypical or overlapping clinical features. For example, lichen planus can be confused clinically for lichenoid drug eruptions, psoriasis punctata, cutaneous sarcoidosis, and lichenoid eruptions due to graft versus host disease.[43] Rarely, squamous cell carcinoma can arise in long-standing hyertrophic lichen planus.[44] To conclude, histopathology is a useful aid in diagnosing hyper pigmentary skin lesions.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Shenoi SD, Prabhu S. Role of cultural factors in the biopsychosocial model of psychosomatic skin diseases: An Indian perspective. Clin Dermatol 2013;31:62-5.  |
| 2. | Moscher DB, Fitzpatrick TB, Hori Y, Ortonne JP. Disorders of pigmentation. In: Fitzpatick TB, Isen AZ, Wolff K, Freedberg IM, Austen KF , editors. Dermatology in General Medicine. 4 th ed., New York: McGraw-Hill; 1993. p. 903-5. |
| 3. | McGrath JA, Uitto J. Anatomy and organization of skin. In: Burns DA, editor. Rooks Text Book of Dermatology. 8 th ed., Vol. 1. London: Blackwell Publishers; 2010. p. 3.1-3.5. |
| 4. | Ackerman AB. Supplement to the Fourth Printing of Histologic Diagnosis of Inflammatory Skin Diseases. Philadelphia: Lea and Febiger; 1988. |
| 5. | Sontheimer RD. Lichenoid tissue reaction/interface dermatitis: Clinical and histological perspectives. J Invest Dermatol 2009;129:1088-99. |
| 6. | D'Costa G, Bharambe BM. Spectrum of non-infectious erythematous, papular and squamous lesions of the skin. Indian J Dermatol 2010;55:225-8. |
| 7. | Kanwar AJ, De D. Lichen planus in children. Indian J Dermatol Venereol Leprol 2010;76:366-72. [ PUBMED]  |
| 8. | Boyd AS, Neldner KH. Lichen planus. J Am Acad Dermatol 1991;25:593-619. |
| 9. | Lin MY, Chen LJ, Ma L, Wu WY, Xiang LH. Generalized reticulated hyperpigmentation induced by lichen planus. Clin Exp Dermatol 2009;34:e636-9. |
| 10. | Bhattacharya M, Kaur I, Kumar B. Lichen planus: A clinical and epidemiological study. J Dermatol 2000;27:576-82. |
| 11. | Ellis FA. Histopathology of lichen planus based on analysis of one hundred biopsy specimens. J Invest Dermatol 1967;48:143-8. |
| 12. | Kachhawa D, Kachhawa V, Kalla G, Gupta LP. A clinico-aetiological profile of 375 cases of lichen planus. Indian J Dermatol Venereol Leprol 1995;61:276-9. [ PUBMED] |
| 13. | Bhutani LK, Bedi TR, Pandhi RK, Nayak NC. Lichen planus pigmentosus. Dermatologica 1974;149:43-50. |
| 14. | Khanna N, Rasool S. Facial melanoses: Indian perspective. Indian J Dermatol Venereol Leprol 2011;77:552-63. [ PUBMED] |
| 15. | Kanwar AJ, Dogra S, Handa S, Parsad D, Radotra BD. A study of 124 Indian patients with lichen planus pigmentosus. Clin Exp Dermatol 2003;28:481-5. |
| 16. | Vega ME, Waxtein L, Arenas R, Hojyo T, Dominguez-Soto L. Ashy dermatosis versus lichen planus pigmentosus: A controversial matter. Int J Dermatol 1992;31:87-8. |
| 17. | Dhar S. Fountain sign in lichen planus hypertrophicus. Indian J Dermatol Venereol Leprol 1997;63:210. |
| 18. | Kumari R, Singh N, Thappa DM. Hypertrophic lichen planus as a presenting feature of HIV infection. Indian J Dermatol 2009;54:8-10. |
| 19. | Dogra D, Sharma N, Khanna N. Squamous cell carcinoma arising in lichen planus hypertrophicus. Indian J Dermatol 1997;42:30-1. |
| 20. | Sengupta S, Das JK, Gangopadhyay A. Malignant transformation of hypertrophic lichen planus. Indian J Dermatol Venereol Leprol 2006;72:470. |
| 21. | Salim T, Shenoi SD, Balachandran C, Mehta VR. Lichen amyloidosus: A study of clinical, histopathologic and immunofluorescence findings in 30 cases. Indian J Dermatol Venereol Leprol 2005;71:166-9. [ PUBMED] |
| 22. | Das J, Gogoi RK. Treatment of primary localised cutaneous amyloidosis with cyclophosphamide. Indian J Dermatol Venereol Leprol 2003;69:163-4. [ PUBMED] |
| 23. | Lotti T, Buggiani G, Prignano F. Prurigo nodularis and lichen simplex chronicus. Dermatol Ther 2008;21:42-6. |
| 24. | Rajalakshmi R, Thappa DM, Jaisankar TJ, Nath AK. Lichen simplex chronicus of anogenital region: A clinico-etiological study. Indian J Dermatol Venereol Leprol 2011;77:28-36. [ PUBMED] |
| 25. | Kouskoukis CE, Scher RK, Ackerman AB. The problem of features of lichen simplex chronicus complicating the histology of diseases of the nail. Am J Dermatopathol 1984;6:45-9. |
| 26. | Lakshmi C, Srinivas CR, Ramachandran B, Pillai SB, Nirmala V. Perforating lichenoid reaction to amlodipine. Indian J Dermatol 2008;53:98-9. [ PUBMED] |
| 27. | Ortonne JP, Bissett DL. Latest insights into skin hyperpigmentation. J Investig Dermatol Symp Proc 2008;13:10-4. |
| 28. | Stulberg DL, Clark N, Tovey D. Common hyperpigmentation disorders in adults: Part II. Melanoma, seborrheic keratoses, acanthosis nigricans, melasma, diabetic dermopathy, tinea versicolor, and postinflammatory hyperpigmentation. Am Fam Physician 2003 15;68:1963-8. |
| 29. | Thadeus J, Thappa DM, Ratnakar C. Prurigo nodularis with cutaneous horn. Indian J Dermatol 1997;42:188-90. |
| 30. | Lee MR, Shumack S. Prurigo nodularis: A review. Australas J Dermatol 2005;46:211-8. |
| 31. | Pareek A, Khopkar U, Sacchidanand S, Chandurkar N, Naik GS. Comparative study of efficacy and safety of hydroxychloroquine and chloroquine in polymorphic light eruption: A randomized, double-blind, multicentric study. Indian J Dermatol Venereol Leprol 2008;74:18-22. [ PUBMED] |
| 32. | Sharma L, Basnet A. A clinicoepidemiological study of polymorphic light eruption. Indian J Dermatol Venereol Leprol 2008;74:15-7. [ PUBMED] |
| 33. | Seetharam KA, Sridevi K. Association of polymorphic light eruption and autoimmune thyroiditis. Indian J Dermatol Venereol Leprol 2010;76:704-5. [ PUBMED] |
| 34. | Dhar S, Jain S. High incidence of polymorphic light eruption in Kota. Indian J Dermatol Venereol Leprol 1996;62:265-6. [ PUBMED] |
| 35. | Epstein JH. Polymorphous light eruption. J Am Acad Dermatol 1980;3:329-43. |
| 36. | Hood AF, Elpern DJ, Morison WL. Histopathologic findings in papulovesicular light eruption. J Cutan Pathol 1986;13:13-21. |
| 37. | Dhar S, Dhar S. Why lesions of morphoea are often hyperpigmented? Indian J Dermatol Venereol Leprol 1996;62:131. [ PUBMED] |
| 38. | Jaworsky C, Winfield H. Connective tissue diseases. In: Elders DE, editor. Lever's Histopathology of Skin. 10 th ed. Philadelphia, USA: Wolters Kluwer/Lippincott Williams & Williams; 2008. p. 296-8. |
| 39. | Vukicevic JS, Milobratovic DJ. Discoid lupus erythematosus of the eyelid. Indian J Dermatol Venereol Leprol 2010;76:418-20. [ PUBMED] |
| 40. | Dhar S, Kanwar AJ. Discoid lupus erythematosus in Northern India: A study of 102 patients. Indian J Dermatol 1996;41:118-21. |
| 41. | Annam V, Yelikar BR, Inamadar AC, Palit A. Histopathological study of pruritic papular eruptions in HIV-infected patients in relationship with CD4, CD8 counts. Indian J Pathol Microbiol 2009;52:321-4. [ PUBMED] |
| 42. | Uehara M, Ofuji S. Primary eruption of prurigo simplex subacuta. Dermatologica 1976;153:49-56. |
| 43. | Staubach P. Lichen planus. CME Dermatol 2009;4:68-79. |
| 44. | Weedon D. The lichenoid reaction pattern (interface dermatitis). In: Weedon D, editor. Weedon's Skin Pathology. 3 rd ed. China: Churchill Livingstone Elsevier; 2010. p. 38-42. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
[Table 1], [Table 2], [Table 3], [Table 4]
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