Indian Journal of Dermatology
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CASE REPORT
Year : 2009  |  Volume : 54  |  Issue : 5  |  Page : 8-10
Hypertrophic lichen planus as a presenting feature of human immunodeficiency virus infection


Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry - 605 006, India

Correspondence Address:
Devinder Mohan Thappa
Department of Dermatology and STD, JIPMER, Pondicherry - 605 006
India
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Source of Support: None, Conflict of Interest: None


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   Abstract 

Lichen planus (LP) is a chronic papulosquamous dermatosis in which both skin and mucous membranes may be involved. To date, there have been only five reports of human immunodeficiency virus (HIV)-positive patients with hypertrophic LP. In the present report, we describe a 37-year-old female who presented with widely distributed, hyperpigmented, pruritic scaly lesions involving the face, trunk, and upper and lower extremities for one month. She also had swelling of both lower legs with low grade fever for past one week. She was diagnosed to be a HIV-positive patient who had severe, widespread hypertrophic LP lesions along with acute eruptive lesions of LP. These LP lesions were a presenting feature of HIV infection in our case.


Keywords: Acitretin, human immunodeficiency virus (HIV), hypertrophic lichen planus


How to cite this article:
Kumari R, Singh N, Thappa DM. Hypertrophic lichen planus as a presenting feature of human immunodeficiency virus infection. Indian J Dermatol 2009;54, Suppl S1:8-10

How to cite this URL:
Kumari R, Singh N, Thappa DM. Hypertrophic lichen planus as a presenting feature of human immunodeficiency virus infection. Indian J Dermatol [serial online] 2009 [cited 2019 May 19];54, Suppl S1:8-10. Available from: http://www.e-ijd.org/text.asp?2009/54/5/8/45431



   Introduction Top


It is well known that. patients with human immunodeficiency virus (HIV) infection suffer from a variety of skin diseases, including those which are relatively specific for HIV-positive patients, like bacillary angiomatosis, Kaposi's sarcoma, and eosinophilic folliculitis, and more common dermatoses which manifest in a more severe form in HIV infected such as psoriasis vulgaris, seborrheic dermatitis, and molluscum contagiosum. [1] These dermatoses are sometimes a presenting feature of HIV infection.

Lichen planus (LP) is a chronic papulosquamous dermatosis in which both skin and mucous membranes may be involved. To date, there have been only five reports of HIV-positive patients with hypertrophic LP. [2],[3],[4] In the present report; we describe a HIV-positive patient who presented with severe, widespread hypertrophic LP lesions along with acute eruptive lesions of LP. In our case, these LP lesions were a presenting feature of HIV infection.


   Case History Top


A 37-year-old female presented with widely distributed, hyperpigmented, pruritic scaly lesions involving the face, trunk, and upper and lower extremities for one month. She also had swelling of both lower legs with low grade fever for the past one week. These lesions started first over the forehead followed by the palms, lower legs, upper limbs and trunk. Burning sensation was present in oral cavity with similar lesions over the lips. She had used some topical antibiotics but there was no prior history of taking any oral medications. She also had non productive cough for the past one week and some degree of breathlessness. There was no history of similar lesions in the past. Her husband had died one year back of pulmonary tuberculosis.

On general physical examination, the patient was toxic, febrile and had generalized lymphadenopathy. Systemic examination was normal except for tachypnoea. Both lower legs were edematous and tender suggestive of cellulitis. Cutaneous examination revealed violaceous, flat-topped, polygonal, papules and plaques widely distributed over the lips, face, forearms, dorsum of hands, trunk, inner aspect of thighs, lower legs [Figure 1] and feet. Palms and soles were extensively involved with erythematous plaques, scaling and fissuring. Both oral and genital mucosae were involved with violaceous papules and plaques.

The most striking feature in our case was the presence of raised extensive hypertrophic hyperpigmented plaques predominantly on lower legs, with largest plaque measuring 20x13cm. Similar raised hypertrophic plaques with a distinct violaceous hue were present over dorsum of feet, extensor aspect of arms, medial aspect of thighs and vulva. Nails were yellowish, dystrophic, thinned out with increased longitudinal striations.

A clinical diagnosis of acute eruptive and hypertrophic lichen planus was made and was confirmed by biopsy of the representative skin lesion from the left leg. Histopathological examination showed typical features of hypertrophic LP. There was compact hyperkeratosis and marked acanthosis of the epidermis with hypergranulosis, vacuolar degeneration of basal keratinocytes and a bandlike lymphocytic infiltrate at the dermoepidermal junction. The papillary dermis contained abundant melanophages and numerous Civatte bodies.

Initial investigations included hemogram, blood urea, electrolytes, liver function tests, ECG, chest skiagram, pus and blood culture and sensitivity. Lymphocyte count was 3700/mm 3 , hemoglobin 10.5 gm%, peripheral smear showed shift towards left. Chest X-ray was normal. Serology for VDRL, HCV and HBsAg was negative. Short course of systemic steroid of small dose is not absolutely contraindicated in a setting of cellulitis under antibiotic cover. Hence oral prednisolone 30mg daily was started under the cover of systemic antibiotics.

In view of the extensive, atypical and aggressive presentation of acute eruptive lichen planus with hypertrophic plaques, ELISA for HIV antibodies was done which came positive. Subsequently her CD4+count was found to be 250/mm 3 . Hence, it was decided to taper systemic steroids over next two weeks. Oral acitretin at a dose of 25mg twice daily was initiated with topical steroids and tretinoin applied locally over the hypertrophic plaques. During the period of tapering steroids, her breathlessness increased. Investigations revealed hypoxia and respiratory alkalosis on arterial blood gas analysis. She also had hyponatraemia, and raised LDH possibly due to Pneumocystis carinii (jerovecii) infection. A course of oral cotrimoxazole for 21 days gave her relief. She was subsequently initiated on HAART regimen with 3 drugs including zidovudine, lamivudine and nevirapine.

The acute LP lesions responded well to prednisolone with resolution of all lesions except for the hypertrophic LP lesions. But these hypertrophied plaques responded well to acitretin with almost complete subsidence of lesions within six weeks of starting treatment [Figure 2]. The patient was discharged following recovery but she defaulted for two months and came with recurrence of hypertrophic plaques over bilateral lower legs.


   Discussion Top


Lichen planus has been reported to occur in immunocompromised hosts such as patients with graft versus host disease and abnormal humoral immunity, however, there are only 5 case reports of hypertrophic lichen planus occurring in AIDS patient. [2],[3],[4] Our case is atypical due to extensive involvement with hypertrophic LP plaques not restricted to lower legs but also involving inner thighs, trunk and genital mucosa. This presentation is in contrast with immunocompetent host with hypertrophic LP, whose lesions are generally confined to the lower extremities. [5] The more widespread and severe nature of the lesions in our case is similar to the reports of other dermatoses (such as psoriasis vulgaris and seborrheic dermatitis) which manifest in a more severe form in a patient with HIV infection. The presence of hypertrophic lesions in our patient may simply reflect the abnormal immunological host response in the presence of HIV infection, which may result in epidermal acanthosis and hyperkeratosis.

There have been several studies examining the immunophenotype of the lymphocytic infiltrate in LP. Most have shown that the dermal lymphocytic infiltrate of LP is predominantly composed of T helper cells whereas in the epidermis the cytotoxic reaction towards the basal keratinocytes is mediated by CD8-positive suppressor T cells. In one report in which the immunophenotype of epidermal lymphocytes was studied, it was found that the infiltrate, which initially was predominantly CD4-positive in early lesions, later changed to a CD8-positive infiltrate in older lesions. This suggests that the age of the lesion may determine, in part, whether the predominant T lymphocyte is helper or suppressor. [6] Probably, secondary to the systemic depression of circulating T-helper lymphocytes in HIV-positive patients, or differences in antigenic presentation and altered response by these immumocompromised patients to immune stimuli, there is appearance of LP lesions in this patient. There are many case reports that have shown an association between HIV and lichen planus. [7],[8],[9]

The association of LP lesions with hepatitis C virus is well known. A clinical report that the keratotic forms (reticular and plaque) of oral LP occurs in anti-HCV seropositive patients more frequently than in seronegative patients is available. [10] The persistent HCV antigenemia may result in a repeated LP reaction and thus the resultant keratotic forms of LP in those infected with HCV. The same may hold true in case of hypertrophic LP which present with HIV infection where persistent antigenemia from HIV virus results in keratotic forms of LP.

 
   References Top

1.Sadick NS, McNutt NS, Kaplan MH. Papulosquamous dermatoses of AIDS. J Am Acad Dermatol 1990;22:1270-5.  Back to cited text no. 1  [PUBMED]  
2.Rippis GE, Becker B, Scott G. Hypertrophic lichen planus in three HIV-positive patients: A histologic and immunological study. Cutan Pathol 1994;21:52-8.  Back to cited text no. 2    
3.Fitzgerald E, Purcell SM, Goldman HM. Photodistributed hypertrophic lichen planus in association with acquired immunodeficiency syndrome: A distinct entity. Cutis 1995;55:109-11.  Back to cited text no. 3  [PUBMED]  
4.Pardo RJ, Kerdel FA. Hypertrophic lichen planus and light sensitivity in an HIV-positive patient. Int J Dermatol 1988;27:642-4.  Back to cited text no. 4  [PUBMED]  
5.Daoud MS, Pittelkow MR. Lichen planus. In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, editors, Fitzpatrick's dermatology in general medicine, 6th ed. New York: McGraw Hill; 2003. p. 463-77.   Back to cited text no. 5    
6.De Panfilis G, Manara G, Sansoni P, Allegra F. T-cell infiltrate in lichen planus: Demonstration of activated lymphocytes using monoclonal antibodies. J Cutan Palhol 1983;10:52-8.  Back to cited text no. 6    
7.Berger TG, Dhar A. Lichenoid photoeruptions in human immunodeficiency virus infection. Arch Dermatol 1994;130:609-13.  Back to cited text no. 7  [PUBMED]  
8.Bessinger GT, Conologue TD, Krivda SJ, Turiansky GW. Violaceous plaques in a patient with acquired immunodeficiency syndrome. Arch Dermatol 2003;139:215-20.  Back to cited text no. 8    
9.Ruiz Villaverde R, Blasco Melguizo J, Naranjo Sintes R. Multiple linear lichen planus in HIV patient. J Eur Acad Dermatol Venereol 2002;16:412-4.  Back to cited text no. 9    
10.Daramola OM, Ogunbiyi AO, George AO. Evaluation of clinical types of cutaneous lichen planus in antihepatitis C virus seronegative and seropositive Nigerian patient. Int J Dermatol 2003;42:933-5.  Back to cited text no. 10    


    Figures

  [Figure 1], [Figure 2]



 

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    Abstract
    Introduction
    Case History
    Discussion
    References
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