Indian Journal of Dermatology
: 2009  |  Volume : 54  |  Issue : 5  |  Page : 41--42

Parthenium dermatitis in a HIV patient

Sekar C Shanmuga, Sundaram V Shanmuga, CR Srinivas 
 Department of Dermatology, PSG Hospitals, Peelamedu, Coimbatore, India

Correspondence Address:
C R Srinivas
Department of Dermatology, PSG Hospitals, Peelamedu, Coimbatore - 641 004, Tamil Nadu


Parthenium dermatitis is a distressing problem in India. Both type 1 (immediate and late phase reaction) and type 4 hypersensitivity phenomenon play a role in pathogenesis. We prick tested the patient after administering various drugs to assess the best agent to prevent late phase reaction.

How to cite this article:
Shanmuga SC, Shanmuga SV, Srinivas C R. Parthenium dermatitis in a HIV patient.Indian J Dermatol 2009;54:41-42

How to cite this URL:
Shanmuga SC, Shanmuga SV, Srinivas C R. Parthenium dermatitis in a HIV patient. Indian J Dermatol [serial online] 2009 [cited 2020 Aug 6 ];54:41-42
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Full Text


Parthenium dermatitis is a widespread dermatosis caused by Parthenium hysterophorus. [1] The disease is mediated by delayed hypersensitivity to parthenium antigen but type 1 hypersensitivity also plays a role in the pathogenesis. [2] We report a case of parthenium dermatitis in a HIV patient.

 Case History

A 35-year-old man presented with recurrent dermatitis over the face, extensor aspect of forearms and lower legs since five years. He gave history of exposure to parthenium since seven years. He was diagnosed as a case of retroviral disease one year ago and is currently on ART.

Patch testing with parthenium leaf and antigen confirmed the diagnosis of parthenium dermatitis. Prick testing was done with parthenium leaf, parthenium antigen extract, glycerinated saline as negative control and histamine 0.1% W/V as positive control [Figure 1]. Flexor surface of forearm and arm were selected as the test sites. On day1 rupatadine 20mg was given and prick tested on day 2. On day 3 montelukast 20mg was given and prick testing done on day 4. Colchicine 0.5mg was given on day 5 and prick tested on day 6 and the results were tabulated [Table 1]. Halobetasol, mometasone and tacrolimus 0.1% were applied under occlusion on day 7 [Figure 2] and prick testing with parthenium leaf was done over these sites on day 8 and the results were tabulated [Table 2].


Allergic contact dermatitis is a prototype of delayed-type hypersensitivity (DTH) reaction, which should be depressed by cellular immunodeficiency as occurs in HIV-1 infection. However contact sensitization, unlike other DTH reactions, is apparently driven predominantly by CD8 lymphocytes, which are normal or increased in HIV-1 infection. [3] In our patient there was continuous exposure to parthenium antigen even before the onset of HIV infection. However the patient did not notice any aggravation or subsidence of dermatitis after contracting HIV infection and the patch tests with parthenium were positive.

We prick tested the patient after administering rupatadine, montelukast and colchicine to assess its ability to prevent LPR. Rupatadine is a novel antihistaminic with H1 and PAF antagonistic activity. [4] It also inhibits antigen induced histamine release from mast cells and prevents degranulation of eosinophils and neutrophils. Montelukast is a leukotriene antagonist and leukotriene is one of the secondary inflammatory mediators in LPR. Colchicine inhibits the migration of neutrophils and since the histopathology of LPR usually shows a leukocytoclastic vasculitis pattern with neutrophils [5] we also prick tested the patient after giving colchicine, but LPR remained positive suggesting that all these drugs when administered singly do not inhibit LPR. We prick tested with parthenium leaf after applying topical halobetasol, mometasone and tacrolimus under occlusion for 24 h and LPR was negative. It is a well known fact that steroids inhibit LPR. Tacrolimus is an immunomodulator drug that inhibits T-cell-receptor-mediated exocytosis of cytotoxins from killer T cells and inhibition of IgE Fce receptor-mediated exocytosis and cytokine transcription in mast cells and basophils. Cyclosporin, which was proved to be effective in parthenium dermatitis [5] was not administered since it may aggravate immunosuppression. We discharged the patient with alternate day application of mometasone and tacrolimus and the patient was symptom free on follow-up.

We conclude that antihistaminics and colchicine are not much effective in preventing LPR. Since steroids and tacrolimus block the immune mediated reactions mediated by mast cells and T-lymphocytes they were more effective in preventing LPR. This case also proves that the incidence of contact dermatitis and patch test results are not much affected by HIV infection since CD 8 cells play a major part in its pathogenesis.


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