|Year : 2016 | Volume
| Issue : 1 | Page : 70-72
Psoriasis and leprosy: A rare co-occurence
Mayur R Bhobe, Shylaja Someshwar, Neha Bhalla, Hemangi R Jerajani
Department of Skin and VD, Mahatma Gandhi Memorial Medical College, Navi Mumbai, Maharashtra, India
|Date of Web Publication||21-Jan-2016|
Mayur R Bhobe
SRIRAM, House No. 613/e/d/c, Plot No. 16, SPARC, Behind Chowgule College, Cupangale, Fatorda, Salcete - 403 602, Goa
Source of Support: None, Conflict of Interest: None
Occurence of psoriasis and leprosy in a single patient is extremely rare with very few cases reported. Better knowledge of the pathogenesis of these two diseases has led to some understanding of this rare association. We report such an association in one of our patients. We also report the therapeutic dilemma faced in treating lepra reaction with steroids while preventing the acute flare-up of psoriasis.
Keywords: Co-occurrence, leprosy, psoriasis
|How to cite this article:|
Bhobe MR, Someshwar S, Bhalla N, Jerajani HR. Psoriasis and leprosy: A rare co-occurence. Muller J Med Sci Res 2016;7:70-2
|How to cite this URL:|
Bhobe MR, Someshwar S, Bhalla N, Jerajani HR. Psoriasis and leprosy: A rare co-occurence. Muller J Med Sci Res [serial online] 2016 [cited 2022 Oct 2];7:70-2. Available from: https://www.mjmsr.net/text.asp?2016/7/1/70/174655
| Introduction|| |
Coexistence of leprosy with psoriasis is rare. Bhushan Kumar et al. found 1.4 cases of concurrent psoriasis among a population of 10,000 leprosy patients,  indicating that patients with leprosy may be protected against psoriasis and vice versa. We hereby report such a rare case of concurrent occurrence.
| Case Report|| |
A 53-year-old male presented with a history of multiple light colored lesions over the body since 5 years and numbness over the extremities since 3 years. He was diagnosed clinically with leprosy at the primary health center and had completed multibacillary multidrug therapy 2 years ago.
A year later, reddish lesions with flaking and itching appeared. With the diagnosis of psoriasis, he was administered weekly oral methotrexate for 2 months 2 years ago, along with topical medications, which gave a partial improvement.
Cutaneous examination revealed lesions of two distinct morphologies. First, multiple erythematous scaly plaques were seen on the body in a generalized and symmetric distribution, mainly on the extensor aspects of the elbows, knees, abdomen, and back [Figure 1]. Secondly, hypopigmented ill-defined patches with a shiny surface were seen bilaterally symmetrically distributed over the trunk, extremities, and left shoulder. The sensation of pain, touch, and temperature was normal over the patches. Similar erythematous scaly plaques were also found superimposed over the hypopigmented patches [Figure 2]. Left infraorbital, right radial cutaneous and bilateral ulnar, common peroneal, and posterior tibial nerves were enlarged. The ulnar nerves were tender. Glove and stocking anesthesia were noted.
|Figure 1: Erythematous scaly plaques in a generalized and symmetric distribution on the back with positive Koebner phenomenon|
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|Figure 2: Hypopigmented ill-defined plaques over the left side of the chest and left arm with superimposed erythematous plaques|
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A provisional diagnosis of borderline lepromatous leprosy with Type 1 lepra reaction coexistent with psoriasis vulgaris was made. Biopsy was taken from a psoriatic plaque and a hypopigmented patch, which confirmed our diagnosis of both [Figure 3]a, b and [Figure 4]a, b. Slit skin smear for leprosy was also negative.
|Figure 3: (a) (H and E 4×) Section from erythematous scaly plaque showing psoriasiform epidermal hyperplasia. Dermis shows superficial perivascular lymphocytic infi ltrate (b) (H and E 10×) Section from psoriatic plaque with the epidermis showing parakeratosis and hypogranulosis in addition to psoriasiform epidermal hyperplasia|
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|Figure 4: (a) (H and E 4×) Section from the hypopigmented patch showing perineural and periappendageal infiltrate of lymphocytes and epitheloid cells (b) (H and E 10×) Section from the hypopigmented patch showing periappendageal infiltrate (c) (H and E 40×) Section from the hypopigmented patch showing perineural infiltrate under high power|
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Since there was clinical evidence of neuritis, the patient was started on 40 mg prednisolone for 2 weeks and gradually tapered off over a course of 4 weeks. Nerve tenderness subsided completely within 1 week. He was administered topical steroids and emollients for psoriasis. Plaques showed partial improvement. The patient was therefore, started on 7.5 mg of methotrexate weekly dose and his psoriatic lesions responded well leaving postinflammatory hypopigmentation [Figure 5].
|Figure 5: Clinical photograph showing psoriasis plaques subsiding with postinflammatory hypopigmentation following 1 month of weekly therapy with methotrexate|
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| Conclusion|| |
Leprosy and psoriasis were both included under the term lepra until the 19th century when these two diseases began to be recognized as distinct entities.
There have been sporadic reports of co-occurrence of leprosy and psoriasis. ,,,, Many theories have been suggested to explain the rarity of their association. Neuropeptides such as substance P (SP), vasoactive intestinal peptide (VIP), and calcitonin gene-related peptide (CGRP) are of great significance in the inflammatory and proliferative process and symmetrical distribution of lesions in psoriasis. ,, It has been postulated that destruction of cutaneous nerves in leprosy and the consequent decrease in neuropeptides is the reason for psoriatic lesions not developing in skin affected by leprosy. 
One hypothesis suggests that the prevalence of psoriasis in different populations mainly results from differences in natural selection for gene polymorphisms associated with more vigorous immunity against infectious agents. Therefore, resisting infection by lepra bacilli may have been the evolutionary advantage that favored the expansion of some psoriasis-associated genotypes. 
Genetic factors may play a role in protecting psoriatic patients from leprosy. Studies have associated human leukocyte antigen (HLA)-DR2 and HLA DQW1 with leprosy. However, in psoriasis there is a higher frequency of HLA-A1, B13, B16, B17, B38, CW6, and DR7. 
It has been found that a markedly thickened epidermis in psoriatic lesions is likely the result of both hyperproliferation and decreased cell death (apoptosis),  rather than an increase in the level of spontaneous apoptosis seen in leprosy patients,  This may contribute to the rarity of coexixtence of the two disorders.
The appearance of psoriatic lesions even on leprosy patches as in our patient was reported by Dogra et al., which may be explained by partial regeneration of nerves in treated leprosy patients. 
In our case, we preferred to treat the lepra reaction first with oral steroids in view of the neuritis and impending neurological deficit. This was gradually tapered while methotrexate was introduced in order to prevent the flare-up of psoriasis during withdrawal of steroids. A similar therapeutic dilemma has been reported by Pai et al. where a flare-up of psoriasis following the withdrawal of oral steroids was used for treatment of concurrent leprosy with type I lepra reaction. 
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Conflicts of Interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]