|Year : 2017 | Volume
| Issue : 2 | Page : 76-78
Leprosy: a mimicker of psoriasis
Rita V Vora MD , Rahul Krishna S Kota, Kira A Pariath
Department of Skin and V.d., Shree Krishna Hospital, Karamsad, Gujarat, India
|Date of Submission||17-Mar-2017|
|Date of Acceptance||23-Feb-2017|
|Date of Web Publication||4-Aug-2017|
Rita V Vora
(Dermatology, Venerology and Leprosy), Department of Skin and V.d., Shree Krishna Hospital, Karamsad, Anand, - 388 325 Gujarat
Source of Support: None, Conflict of Interest: None
Leprosy is a slowly progressive mutilating and stigmatizing disease. As the spectrum of disease is varied, various dermatological conditions may lead to diagnostic dilemma. Early diagnosis will help in the initiation of its treatment to avoid complications and morbidity due to the disease. The diagnosis of leprosy is made from the clinical picture, but must be complimented by biopsy and slit skin smear. Here, we report a case of leprosy that was mimicking psoriasis – a papulosqaumous disease clinically.
Keywords: leprosy, papulosquamous, psoriasis
|How to cite this article:|
Vora RV, Kota RS, Pariath KA. Leprosy: a mimicker of psoriasis. Egypt J Dermatol Venerol 2017;37:76-8
| Introduction|| |
Leprosy presents as a spectrum of clinical manifestations, which have bacteriologic, pathologic, and immunologic characteristics. The spectrum from tuberculoid to borderline tuberculoid, to mid-borderline (which is rare) to borderline lepromatous to polar lepromatous disease is associated with an evolution from asymmetric localized macules and plaques to nodular, indurated symmetric generalized cutaneous involvement, an increased bacterial load, and loss of cellular immunity . Because of varied presentation of leprosy, early diagnosis along with appropriate treatment is essential to prevent morbidity associated with it. A great social stigma is associated with leprosy. Leprosy has varied presentations and can cause disability and complications if not diagnosed and treated in right time. The clinical presentation of leprosy is highly variable, and in all its stages it can mimic a great variety of other dermatological conditions. The differential diagnosis is so wide that one has to exclude a wide variety of dermatological diseases before stamping it to be leprosy, as the stigma of leprosy is very high. We hereby present a case of leprosy that was clinically mimicking chronic plaque psoriasis, but histopathology showed features of borderline lepromatous leprosy.
| Case report|| |
A 20-year-old male patient presented to skin OPD with complains of red raised lesions over the body since 6 months. On thorough dermatological examinations, multiple (>15) well-defined plaques with silvery scaling over the lower back, abdomen, and lower legs were present ([Figure 1]a and [Figure 1]b). He also had swelling over extremities and loss of sensation in a glove and stocking pattern. Nerves were not palpable. Sensations, both temperature and touch, were lost in a glove and stocking pattern. Auspitz sign was negative. Our differential diagnoses were psoriasis vulgaris and borderline lepromatous leprosy. All patients gave their formal consent. The protocol was approved the Ethical Committee of the hospital.
|Figure 1 (a) Well-defined plaques with silvery scaling over lower back. (b) Well-defined plaques with silvery scaling over lower legs|
Click here to view
Slit skin smears were positive for acid-fast bacilli. Biopsy showed clear grenz zone and multiple granulomas in the dermis with foamy macrophages ([Figure 2]a and [Figure 2]b), which confirmed the diagnosis of borderline lepromatous leprosy. The patient was started on antileprosy treatment (multibacillary packs), and there was resolution of lesions ([Figure 3]a and [Figure 3]b).
|Figure 2 (a) Clear grenz zone. (b) Multiple granulomas in the dermis with foamy macrophages|
Click here to view
|Figure 3 (a) Resolution of lesions over back after antileprosy treatment. (b) Resolution of lesions over legs after antileprosy treatment|
Click here to view
| Discussion|| |
Leprosy is a slowly progressive infectious disease caused by the bacillus Mycobacterium leprae. It is a mutilating and stigmatizing disease and early diagnosis and therapy is the most important strategy for its control. The diagnosis of leprosy is made from the clinical picture, but must be complimented by biopsy and slit skin smear. Psoriasis is characterized by an abnormally excessive and rapid growth of the epidermal layer of the skin. A diagnosis of psoriasis is usually based on the clinical appearance of lesions, which generally present as well-defined erythematous plaques with silvery scales and itching.
Controversies about the relationship between leprosy and psoriasis have existed since the time when people considered psoriasis to be a form of leprosy. The biblical term ‘lepra’ included what is now called psoriasis . This confusion between leprosy and psoriasis lasted for almost 19 centuries when it was realized that the two diseases are entirely different and have nothing in common.
M. leprae has the special characteristic of invading nerves, resulting in neuritis and nerve damage. However, in the pathogenesis of psoriasis, an increasing number of biochemical and clinical studies also provide strong evidence for the functional role of cutaneous nerves and their neuropeptides. Psoriatic lesions have a significantly larger number of nerves with increased content of neuropeptides. It has been documented that the damage to sensory nerves results in clearance of psoriatic lesions in anesthetic areas, and that neuropeptide-modulating drugs such as capsaicin, peptide T, somatostatin, spantide, etc. have some beneficial role in psoriasis . Recently, apoptosis has been implicated to play an important role in the lymphocytic alterations in leprosy because a highly significant increase in the level of spontaneous apoptosis in leprosy patients as compared with controls has been reported . Apoptosis is a regular phenomenon in leprosy; however, in psoriasis, the keratinocytes acquire an apoptosis-resistant phenotype attributed to the overexpression of Bcl-X, cell survival gene products, and other growth-regulatory or cell cycle changes .
Leprosy has a number of distinct clinical presentations, and hence it can be confused with many conditions such as granuloma annulare, leishmaniasis, neurofibromatosis, psoriasis, plaque, sarcoidosis, syphilis, tinea versicolor, vitiligo and xanthomas. Clinical diagnosis depends on the history and pathology. The immunity of an individual also plays a role ,. In our case, the patient presented with multiple scaly plaques, which simulated lesions of psoriasis with no nerve enlargement or tenderness, and thus lead to a misdiagnosis. Hence, if the clinical diagnosis is uncertain, a skin biopsy or slit skin smear may be performed to rule out other disorders and to confirm the diagnosis. When the diagnosis of Hansen’s disease is suspected, the physician should request a special acid-fast stain (Fite’s method) to identify the bacillus because the bacteria may lose its acid-fast characteristic when fixed and stained with Ziehl–Neelsen stain.
Hence, proper history taking and examination with strong suspicion is required to diagnose atypical presentations of leprosy. The time of appearance, the fact whether they are inherited or have been acquired in the course of life, the duration, and the distribution are all important.
The absence of typical dermatological features greatly decreases clinical diagnostic accuracy and necessitates histological confirmation . Only when doctors, other health workers, and the population in endemic countries become fully aware of, and be able to recognize, the disease in its initial phase, it will be possible for therapy to be instituted at the very beginning. Leprosy is a great imitator due to its varied clinical presentation, and hence physicians should have keen eyes to suspect Hansen’s from common dermatological conditions.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Gelber RH Leprosy. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J et al.
, editors. Harrison’s principles of internal medicine. 18th ed. New York, NY: McGraw Hill; 2012. pp. 1359–1367.
Shai A, Vardy D, Zvulunov A. Psoriasis, biblical afflictions and patients’ dignity. Harefuah 2002; 141:479–482.
Dewing SB. Remission of psoriasis associated with cutaneous nerve section. Arch Dermatol 1971; 104:220–221
Niang MN, Balde AT, Perraut R, Mane I, Cartel JL. Apoptosis in leprosy patients. Int J Lepr Other Mycobact Dis 1999; 67:473–474.
Nickoloff BJ. The immunologic and genetic basis of psoriasis. Arch Dermatol 1999; 135:1104–1109.
Wathen PI. Hansen’s disease. South Med J 1996; 89:647–652.
Sowell JK, Baker GF, Dinehart SM. Widespread annular erythematous plaques. Multibacillary leprosy. Arch Dermatol 1996; 132:965–968.
Vijaikumar M, D’Souza M, Kumar S, Badhe B. Fine needle aspiration cytology (FNAC) of nerves in leprosy. Lepr Rev 2001; 72:171–178.
[Figure 1], [Figure 2], [Figure 3]