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CASE REPORT
Year : 2018  |  Volume : 7  |  Issue : 1  |  Page : 63-65

Tuberculoid leprosy presenting with multiple skin lesions


1 Department of Skin and VD, Pramukhswami Medical College, Karamsad, Gujarat, India
2 Department of Pathology, Pramukhswami Medical College, Karamsad, Gujarat, India

Date of Web Publication22-Mar-2018

Correspondence Address:
Dr. Rita V Vora
Department of Skin and VD, Pramukhswami Medical College, Karamsad, Gujarat
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JDRNTRUHS.JDRNTRUHS_21_17

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  Abstract 


Leprosy is a chronic infectious disease caused by Mycobacterium leprae. The most commonly accepted classification is that of Ridley and Jopling, which is primarily based on immunity but has been correlated with clinical, histopathological, and bacteriological findings. In majority of cases, there is concordance between clinical findings and histopathological findings. But in few cases, there is discordance between them. Categorizing leprosy in a particular spectrum is necessary to decide the plan of management where histopathology plays a major role. Here we present a case where there was an extreme degree of discordance and patient presented with clinical features of lepromatous leprosy but turned out to have tuberculoid leprosy on histopathology.

Keywords: Discordance, lepromatous leprosy, tuberculoid leprosy


How to cite this article:
Kota RK, Vora RV, Sheth NK, Ranapurwala MF. Tuberculoid leprosy presenting with multiple skin lesions. J NTR Univ Health Sci 2018;7:63-5

How to cite this URL:
Kota RK, Vora RV, Sheth NK, Ranapurwala MF. Tuberculoid leprosy presenting with multiple skin lesions. J NTR Univ Health Sci [serial online] 2018 [cited 2019 Aug 22];7:63-5. Available from: http://www.jdrntruhs.org/text.asp?2018/7/1/63/228145




  Introduction Top


Leprosy is a chronic infectious disease caused by Mycobacterium leprae. It expresses itself in different clinicopathological forms depending on the immune status of the host.[1] Although large majority of patients are readily identified on clinical grounds, there is increasing number of cases leading to diagnostic dilemma. In such cases, histopathology is the gold standard for diagnosis of leprosy. Here we present a case where there was extreme degree of discordance and patient presented with clinical features of lepromatous leprosy but turned out to have tuberculoid leprosy on histopathology.


  Case Report Top


A 53-year-old male presented to skin outpatient department with multiple red raised asymptomatic lesions over body since 15 days. There was no history of any other complaint. There were no other associated comorbidities. He was not on any drug. There was no history of epistaxis, nasal stuffiness, loss of chappals, redness or watering of eyes, swelling of legs, hoarseness of voice, and anosmia. There was no associated fever, weakness of hands and foot, or of similar complaints in the past. Clinical examination revealed multiple asymptomatic erythematous plaques and well-circumscribed nodules of size 1.5–2 cm, tending toward symmetry over the forehead [Figure 1]a, ala of nose and cheek [Figure 1]b, ear lobes [Figure 1]c, chest, back [Figure 1]d, and both upper and lower limbs. A total of 24 nodules and 30 plaques were seen. Bilateral ulnar nerves were thickened, uniform, and nontender. There was no night pain. Other nerve trunks such as median nerve, radial nerve, common peroneal nerve, posterior tibial nerve, facial nerve, and its zygomatic branch were not palpable. Superficial cutaneous nerves such as great auricular nerve, supratrochlear nerve, supraorbital, infraorbital nerve, supraclavicular nerves, cutaneous nerves of forearm and thigh were not palpable. Nerves on or around the lesions were not palpable. Hot and cold, touch sensations were lost on the lesions. There were infiltrative nodules present over the ear lobes. There was no lymphadenopathy. Our clinical diagnosis was lepromatous leprosy. Serology for HIV was negative. Slit skin smears for acid fast bacilli taken from six sites, i.e., both eyebrows, both ear lobules, and two lesions were negative. Biopsy from a nodule was showing epidermal thinning with the presence of numerous granulomas in the superficial and deep dermis [Figure 2]a, which are primarily around neurovascular and adnexal structures [Figure 2]b and c]. The granulomas consisted of epithelioid cells, multinucleated Langhan's giant cells, lymphocytes, and occasional polymorphonuclear cells suggestive of tuberculoid leprosy. Fite Faraco staining of the biopsy specimen was negative and the patient was treated by antileprosy treatment.
Figure 1: (a) Well-circumscribed nodular lesions over the forehead. (b) Erythematous plaque over left ala of the nose and left cheek. (c) Nodular lesions over the right ear. (d) Multiple erythematous plaques over back

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Figure 2: (a) Epidermal thinning with the presence of numerous granulomas in the superficial and deep dermis (hematoxylin and eosin stain, 4×). (b) Granuloma present around adnexal structures (hematoxylin and eosin stain, 10×). (c) Granuloma present around neural bundles (hematoxylin and eosin stain, 40×)

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  Discussion Top


Leprosy is a chronic disease which may present with various morphological patterns clinically. A disease such as leprosy needs an appropriate classification because of its varied manifestations as well as to decide on the plan of management. The most commonly accepted classification by research workers is that of Ridley and Jopling, which is primarily based on immunity but has been correlated with clinical, histopathological, and bacteriological findings.[2] They first suggested a subdivision of leprosy on an immunological basis into five types: tuberculoid (TT), borderline tuberculoid (BT), mid-borderline (BB), borderline lepromatous (BL), and lepromatous (LL).[3] Later they further developed this idea and correlated clinical and bacteriological findings in each group with respective immunological and histological findings.[4] When M. leprae enters a person with sufficient cell-mediated immunity (CMI) against it, the bacilli will be destroyed. If the CMI is slightly impaired, some bacilli will multiply and a lesion will develop. Depending upon the degree of the immunity, more apparent clinical and histopathological features of the various types of leprosy may gradually develop. The clinicopathological picture is determined by the equilibrium between the agent and the host resistance. Skin has different pathophysiological subunits wherein there is some local modulation of the central host response as a result of which there are different grades of resistance and hence different clinicopathological responses.

On histopathological study, the type of the granuloma cell serves to provide the spectrum of leprosy in two, with epithelioid cells extending from TT to BB and macrophages occurring in BL and LL.

Histopathological examination helps to confirm a presumptive clinical diagnosis and also helps for exact typing.[5],[6] Histology also gives indication of progression and regression of disease under treatment.[7] Various factors also influence the histopathological diagnosis such as differences in sample size, choosing the biopsy site, age of the lesion, immunological, and treatment status of the patient at the time of biopsy.[8],[9]

According to Ridley and Jopling classification, if patient is having more than 30 lesions, he is placed under borderline lepromatous leprosy. According to World Health Organization classification of leprosy, if patient is having more than or equal to six lesions, he is placed under multibacillary spectrum.[10] But in our patient, though he is having more than 50 lesions, histopathological features were suggestive of tuberculoid leprosy, which comes under paucibacillary spectrum.

Ridley and Jopling in their study found complete agreement between clinical and histological types in 68.3% patients. Kalla et al. in a study of 736 patients observed highest parity in LL and TT group (76.7 and 75.6%), respectively, followed by BT (44.2%), BL (43.7%), and BB (37.0%) groups.[10] Despite having such an accurate classification, leprosy cases showed so many diversities between the clinical and histopathological features. Clinicopathological concordance is highest in polar forms of disease, which are usually stable. But in our case there was extreme discordance where patient was clinically at lepromatous pole and histologically at tuberculoid pole.

The disparity between clinical and histological observations is anticipated because the parameters used for the histopathologic classification are well-defined, precise, and also take into account the immunologic response of the tissue, while the clinical classification gives recognition only to the gross appearances of the lesions which is due to the underlying pathological change.[11] Moreover, a sizable proportion of leprosy cases are in a continuously changing immunological spectrum, and histological classification gives a better indication for any recent shift of a case position in the spectrum. In some early cases, clinical signs and symptoms may precede the presently known characteristic tissue changes or vice versa. If a biopsy is taken at an early stage, there is likely to be discordance between the clinical and histopathologic observations. As disparity depends upon the lesion biopsied at the time of study, biopsy from the lesion which is morphologically suggestive of clinical diagnosis, serial biopsies from the same lesion or from paired lesions should be studied for a better clinicohistopathological correlation. Categorizing leprosy in a particular spectrum is necessary to decide the plan of management, where histopathology plays a major role.


  Conclusion Top


The reporting of this case is important as it shows utmost clinicopathological discordance. We conclude that histopathological examination should be carried out in all cases of leprosy to arrive at a definite diagnosis of leprosy and to classify the type of disease.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Tan SY, Graham C. Armauer Hansen (1841-1912): Discoverer of the cause of leprosy. Singapore Med J 2008;49:520-1.  Back to cited text no. 1
[PUBMED]    
2.
Moreira MV, Waldman EA, Martins CL. Leprosy in Espinto santo-state Brazil; a growing endemic. Cad Saude Publ 2008;24:1619-30.  Back to cited text no. 2
    
3.
Ridley DS, Jopling WH. A classification for research purposes. Lepr Rev 1962;33:119.  Back to cited text no. 3
[PUBMED]    
4.
Ridley DS, Jopling WH. WHO classification of leprosy according to immunity: A five group system. Int J Lepr 1966;34:255-73.  Back to cited text no. 4
    
5.
Chacko CJG. Leprosy: Pathology. In: Valia RG, Valia AR, editors. Textbook and Atlas of Dermatology. 1st edition. Bombay: Bhalani Publishing House; 1994. pp 1340-9.  Back to cited text no. 5
    
6.
Lucus SB, Ridley DS. The use of histopathology in leprosy diagnosis and research. Lepr Rev 1989;60:257-62.  Back to cited text no. 6
    
7.
Ridley DS, Charles SK. The pathology of leprosy. In: Leprosy (Hastings). Churchill Livingstone; 1985. pp. 111.  Back to cited text no. 7
    
8.
Bhatia AS, Katoch K, Narayanan RB, Ramu G, Mukherjee A, Lavania RK. Clinical and histopathological correlation in the classification of leprosy. Int J Lepr 1993;61:433-8.  Back to cited text no. 8
    
9.
Nadkarni NS, Rege VL. Significance of histopathological classification in leprosy. Indian J Lepr 1982;71:325-32.  Back to cited text no. 9
    
10.
Kumar B, Dogra S. Case Definition and clinical types of leprosy. In: Kumar B, Kumar KH, editors. IAL textbook of leprosy. 2nd ed. Jaypee Brothers Medical Publishers (P) Ltd; 2016. pp 236-53.  Back to cited text no. 10
    
11.
Kalla G, Salodkar A, Kachhawa D. Clinical and histopathological correlation in leprosy. Int J Lepr 2000;68:184-5.  Back to cited text no. 11
    


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