|
 
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| CASE REPORT |
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| Year : 2017 | Volume
: 4
| Issue : 1 | Page : 45-47 |
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Deck chair sign in lichen aureus
Chitralekha Keisham MD 1, Yumnam Lokendra1, Rashmi Sarkar2, Zamzachin Guite1
1 Department of Dermatology, Jawahar Lal Nehru Institute of Medical Science, Porompat, Imphal East, Manipur, India
2 Department of Dermatology, Maulana Azad Medical College, New Delhi, India
| Date of Web Publication | 19-Jun-2017 |
Correspondence Address:
Chitralekha Keisham
Keishamthong Thangjam Leirak, Imphal West, Manipur - 795 001
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2349-5847.208299
Lichen aureus is a localized variant of pigmented purpuric dermatosis and is rarely reported. The “deck chair sign” (DCS) defines a peculiar clinical pattern that was initially described in patients with Papuloerythroderma of Ofuji and has been considered the clinical hallmark of this controversial entity. However, DCS has been reported in other cutaneous disorders as well. We report a case of lichen aureus seen in a 22-year-old male patient which showed DCS.
Keywords: Deck chair sign, lichen aureus, pigmented purpuric dermatosis
How to cite this article:
Keisham C, Lokendra Y, Sarkar R, Guite Z. Deck chair sign in lichen aureus. Pigment Int 2017;4:45-7 |
| Introduction | |  |
Lichen aureus is a rare variant of pigmented purpuric dermatosis (PPD) characterized by asymptomatic orange-brown colored closely grouped papules which have a purpuric center.[1] The eruption is usually asymptomatic, highly chronic, and therapy-resistant.
A 22-year-old male presented to the skin department with complaints of asymptomatic reddish to brownish patches over bilateral lower limbs and left buttock since 2 months. There was no history of use of any topical medications for it. These lesions were sometimes itchy. There was no significant drug history. The systemic examination did not reveal any abnormality. On local examination, there were closely aggregated, superficial, orange-brown flat papules of size 3 cm × 4 cm to 3.5 cm × 4.5 cm. They were a total of five such lesions. In two such lesions, there were petechiae at the center and a yellow or golden hue at the periphery [Figure 1]. These lesions were distributed over bilateral popliteal fossae and one over the left buttock. They were neither segmental nor in a dermatomal pattern. Neither did they follow the course of veins. Besides this, those lesions over the popliteal fossa had sparing at the site of skin creases, that is, deck chair sign (DCS) [Figure 2]. The biopsy revealed a narrow grenz zone in the upper dermis, a band-like infiltrate of lymphocytes beneath it and interspersed with extravasated erythrocytes [[Figure 3]a and [Figure 3]b]. Routine blood investigations were also normal. Therefore, based on the clinical presentation and histology, a diagnosis of lichen aureus was made. The patient was given topical tacrolimus ointment 0.1% to be applied twice daily. He came for follow-up after 1 month with slight improvement in the pigmentation and erythema. Later, he was lost to follow-up. DCS, though seen in few other dermatoses, has not been reported in lichen aureus. This case highlights the presence of DCS which has not been seen earlier in lichen aureus. It also emphasizes that DCS is not specific to a particular cutaneous disorder. | Figure 1: Lesions of lichen aureus with petechiae at the center and a yellow or golden hue at the periphery
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 | Figure 2: Lesions of lichen aureus over the popliteal fossa with sparing at the site of skin creases, that is, deck chair sign
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 | Figure 3: (a) A band-like infiltrate of lymphocytes beneath a narrow grenz zone of normal tissue was observed in the upper dermis, interspersed with extravasated erythrocytes (hematoxylin and eosin, ×100). (b) Extravasated erythrocytes with lymphocytic infiltrate in the dermis in lichen aureus (hematoxylin and eosin, ×400)
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| Discussion | | |
Lichen aureus, also known as lichen purpuricus, is a localized uncommon variant of PPD. Lichen aureus was originally reported in 1958 by Martin.[1] It is clinically characterized by closely aggregated purpuric papules. The lesions have a distinctive gold, rust, or orange-brown color and show a predilection for men and lower extremities, most commonly the lower legs.
The etiology of lichen aureus is unknown. There are three different views regarding the pathogenesis of pigmented purpuric eruptions. The first theory is that they are due to a disturbance or weakness of the cutaneous blood vessels leading to capillary fragility and erythrocyte extravasation. But this does not explain the inflammatory components in lichen aureus. The second proposed mechanism is humoral immunity, which is supported by direct mmunofluorescence studies showing vascular deposition of complements and immunoglobulins. However, several cases have not shown these deposits. The third proposed mechanism is cellular immunity. The infiltrate in PPD consists of lymphocytes, macrophages, and Langerhans cells.[2],[3] This inflammatory infiltrate leads to vascular fragility and subsequent leakage of erythrocytes. Gravity and increased venous pressure may account for the lesions localizing to lower extremities. Shelley et al.[4] reported an obvious varicose perforator vein in patients with lichen aureus. This hypothesis, however, cannot explain the appearance of the eruption on the trunk and upper extremities or the eruptions appearing in a young age group. Other investigators have suggested drugs or infection as causative factors of PPD and lichen aureus. However, no conclusive evidence has been obtained.[5],[6]
DCS is a clinical pattern initially observed in patients of Papuloerythroderma of Ofuji (PEO) characterized by a selective sparing of skin folds like axillary, inguinal, submammary, and the flexures. There is sparing of natural skin folds resembling the slats of deck chair.[7] Besides PEO, DCS has also been observed in angio-immunoblastic lymphoma, cutaneous Waldenstrom’s macroglobulinemia, acanthosis nigricans, erysipelas, discoid lupus erythematosus, acute contact dermatitis, and parthenium dermatitis.[7],[8],[9],[10],[11] In a study of 90 patients with erythroderma, Pal and Haroon[12] observed DCS in 5.5% of the cases. It is still inconclusive whether PEO is a distinct clinical entity or merely a manifestation pattern of several underlying diseases.[7],[13] This observation opens the interesting question of how the compression of a skin area can save it from inflammation. DCS has also been reported in cases of lepromatous leprosy.[14],[15] The presence of DCS in such a case of leprosy could possibly be due to compression in the folds that increases the temperature that has led to sparing in these areas. Clinical evidence suggests that the DCS is typical but not pathognomonic of PEO. The mechanism by which the DCS appears still remains unclear. It is likely that some “occlusive dressing effect” of topical corticosteroids used in inflammatory dermatosis may have something to do with this phenomenon because, in skin folds, topical corticosteroids stay longer and penetrate deeper, hence leading to a stronger clinical effect in interrupting formation of the rash. In our patient, as there was no history of use of any medications either topical or oral, the most likely explanation would be the pressure effect that has led to sparing the area of any inflammation.Though it has been reported that PPD progressed to mycosis fungoides, classic lesions of lichen aureus do not show progression to mycosis fungoides.[16],[17],[18] Treatment modalities for lichen aureus are topical steroids, topical tacrolimus, PUVA, oral pentoxyphylline and prostacyclin combination, and pulsed dye laser.[19],[20],[21],[22],[23]
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Martin RH. Case for diagnosis. Trans Rep St John’s Hosp Dermatol Soc Lond 1958;40:93.  |
| 2. | von den Driesch P, Simon M Jr. Cellular adhesion antigen modulation in purpura pigmentosa chronica. J Am Acad Dermatol 1994;30:193-200. |
| 3. | Ghersetich I, Lotti T, Bacci S, Comacchi C, Campanile G, Romagnoli P. Cell infiltrate in progressive pigmented purpura (Schamberg’s disease): Immunophenotype, adhesion receptors, and intercellular relationships. Int J Dermatol 1995;34:846-50. [ PUBMED] |
| 4. | Shelley WB, Swaminathan R, Shelley ED. Lichen aureus: A hemosiderin tattoo associated with perforator vein incompetence. J Am Acad Dermatol 1984;11:260-4. |
| 5. | Nishioka K, Katayama I, Masuzawa M, Yokozeki H, Nishiyama S. Drug induced chronic pigmented purpura. J Dermatol 1989;16:220-2. |
| 6. | Reinhardt L, Wilkin JK, Tausend R. Vascular abnormalities in lichen aureus. J Am Acad Dermatol 1983;8:417-20. |
| 7. | Bettoli V, Pizzigoni S, Borghi A, Virgili A. Ofuji papuloerythroderma: A reappraisal of the deck-chair sign. Dermatology 2004;209:1-4. |
| 8. | Ferran M, Gallardo F, Baena V, Ferrer A, Florensa L, Pujol RM. The ‘deck chair sign’ in specific cutaneous involvement by angioimmunoblastic T cell lymphoma. Dermatology 2006;213:50-2. |
| 9. | Autier J, Buffet M, Pinquier L, Merlat-Guitard AI, Carlotti A, Franck N et al. Cutaneous Waldenstrom’s macroglobulinemia with “deck-chair” sign treated with cyclophosphamide. J Am Acad Dermatol 2005;52:45-7. |
| 10. | Murao K, Sadamoto Y, Kubo Y, Arase S. Generalized malignant acanthosis nigricans with deck-chair sign. Int J Dermatol 2013;52:377-8. |
| 11. | Pai S, Shetty S, Rao R. Parthenium dermatitis with deck chair sign. JAMA Dermatol 2015;151:906-7. |
| 12. | Pal S, Haroon TS. Erythroderma: A clinico-etiologic study of 90 cases. Int J Dermatol 1998;37:104-7. |
| 13. | Ofuji S. Papulo-erythroderma. J Am Acad Dermatol 1990;22:697. |
| 14. | Prashar A, Narang T, Saikia UN, Dogra S. Deck chair sign in lepromatous leprosy. Lepr Rev 2013;84:252-4. |
| 15. | Shenoy MM, Bendigeri MA, Kamath PR, Vishal B. Diffuse leprosy with “deck chair” sign. Indian Dermatol Online J 2015;6:204-6. [ PUBMED] [Full text] |
| 16. | Barnhill RL, Braverman IM. Progression of pigmented purpura like eruptions to mycosis fungoides. Report of three cases. J Am Acad Dermatol 1988;19:25-31. |
| 17. | Lipsker D. The pigmented and purpuric dermatitis and many faces of mycosis fungoides. Dermatology 2003;207:246-7. |
| 18. | Fink-Puches R, Wolf P, Kerl H, Cerroni L. Lichen aureus: Clinicopathological features, natural history, and relationship to mycosis fungoides. Arch Dermatol 2008;144:1169-73. |
| 19. | Moche J, Glassman S, Modi D, Grayson W. Segmental lichen aureus: A report of two cases treated with methylprednisolone aceponate. Australas J Dermatol 2011;52:e15-8. |
| 20. | Murota H, Katayama I. Lichen aureus responding to topical tacrolimus treatment. J Dermatol 2011;38:823-5. |
| 21. | Ling TC, Goulden V, Goodfield MJ. PUVA therapy in lichen aureus. J Am Acad Dermatol 2001;45:145-6. |
| 22. | Lee HW, Lee DK, Chang SE, Lee MW, Choi JH, Moon KC et al. Segmental lichen aureus: Combination therapy with pentoxyphylline and prostacyclin. J Eur Acad Dermatol Venereol 2006;20:1378-80. |
| 23. | Hong DK, Chang IK, Lee Y, Seo YJ, Kim CD, Lee JH et al. Treatment of segmental lichen aureus with a pulsed-dye laser: New treatment options for lichen aureus. Eur J Dermatol 2013;23:891-2. |
[Figure 1], [Figure 2], [Figure 3]
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