• Users Online: 2148
  • Print this page
  • Email this page


 
  Table of Contents  
LETTER TO THE EDITOR
Year : 2016  |  Volume : 7  |  Issue : 4  |  Page : 340-342  

Annular atrophic plaque over the arm


1 Department of Dermatology and STD, Dr. Dhawan's Skin, Cosmetology and Laser Clinic, Delhi, India
2 Department of Dermatology and STD, University College of Medical Sciences, Guru Tegh Bahadur Hospital, Delhi, India
3 Department of Pathology, University College of Medical Sciences, Guru Tegh Bahadur Hospital, Delhi, India

Date of Web Publication5-Jul-2016

Correspondence Address:
Amit Kumar Dhawan
Dr. Dhawan's Skin, Cosmetology and Laser Clinic, House No. 436, 2nd Floor, Indra Vihar - 110 009, Delhi
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2229-5178.185486

Rights and Permissions

How to cite this article:
Dhawan AK, Bisherwal K, Grover C, Diwaker P. Annular atrophic plaque over the arm. Indian Dermatol Online J 2016;7:340-2

How to cite this URL:
Dhawan AK, Bisherwal K, Grover C, Diwaker P. Annular atrophic plaque over the arm. Indian Dermatol Online J [serial online] 2016 [cited 2020 Feb 20];7:340-2. Available from: http://www.idoj.in/text.asp?2016/7/4/340/185486

Sir,

A 60-year-old male farmer, a resident of eastern Uttar Pradesh, India presented with a complaint of gradually increasing skin lesion over his right arm of six months duration. He had a history of blunt trauma over that site, 3 months prior to the onset of the lesion. The lesion initially started as a skin-colored papule, which gradually progressed to the present size. There was no significant past medical history and the patient had not taken any prior topical or systemic treatment. His examination revealed a single erythematous annular plaque measuring 6 × 5 cm over flexor aspect of his right forearm. The plaque had well-defined, irregular margins with atrophy and hair loss in the centre without any evidence of black dots on its surface [Figure 1]. Diascopy was negative for apple jelly nodules. The sensory, motor, neural, and systemic examination were not contributory. Skin biopsy was performed with borderline tuberculoid leprosy, lupus vulgaris, and subcutaneous mycosis as differential diagnoses. Histopathological examination from infiltrated margin of plaque showed hyperkeratosis and irregular acanthosis. The reticular dermis had numerous microabscesses and a granulomatous infiltrate. A fair number of brown, rounds, thick-walled fungal spores were seen in the microabscesses and within the giant cells of neutrophilic granulomas [Figure 2]. In view of these biopsy findings a diagnosis of chromoblastomycosis was concluded. Fungal culture on Sabouraud media was performed on two occasions; however it did not yield any growth and further identification of the causative agent could not be performed due to financial constraints. His hematological, biochemical, and serological examination for Human Immunodeficiency Virus (1 and 2) did not yield any abnormality. The patient was treated with tablet terbinafine 250 mg twice daily for 3 months with complete resolution of the lesion and no recurrence at two year follow up [Figure 3]. The patient did not consent for a post-treatment histopathological examination.
Figure 1: Erythematous annular plaque measuring 6 × 5 cm over flexor aspect of right forearm with well-defined irregular margins, atrophy, and hair loss in the center

Click here to view
Figure 2: Histopathological examination (hematoxylin and eosin staining) showing hyperkeratosis, irregular acanthosis, and numerous microabscesses and granulomatous infiltrate in reticular dermis (H and E, ×100). Brown, round, thick--walled structures (sclerotic/medlar bodies) seen in the microabscesses and within the giant cells of neutrophilic granulomas in inset. (H and E, ×200)

Click here to view
Figure 3: Complete resolution of lesion after 3 months of treatment

Click here to view


Chromoblastomycosis is a chronic granulomatous fungal infection affecting skin and subcutaneous tissue.[1],[2] Majority of cases are from tropical and subtropical regions. In India, it is mainly reported from sub-Himalayan belt, eastern and western coastal regions.[2],[3] Most of the affected patients are agriculturist males (70%) of age between 30 and 50 years.[1] The lesions are commonly seen over lower extremities, with a history of preceding trauma with vegetating matter, leading to inoculation of dematiaceous moulds in tissue. It can occur in both immunocompetent and immunocompromised individuals (renal, pancreatic transplant patients, patients receiving corticosteroids/cyclosporine, diabetics).[1] The most common agent is Fonsecaea pedrosoi. Other less common ones include Fonsecaea compacta, Phialophora verrucosa, Cladphialophora carrionii, and Rhinocladiella aquaspersa.[1] Clinical presentation is variable and the lesions are classified into five different types: Nodular, plaque, tumoral, cicatricial, and verrucous.[2] Out of these nodular, tumoral, and verrucous types are more frequent than the cicatricial and plaque-type.[2] However, ulceronodular or nodular lesions in sporotrichoid fashion and rarely fistulous lesion may be seen.[1],[2] Cicatricial type is characterized by non-elevated lesions that enlarge by peripheral extension, atrophic scarring with central healing and annular, arciform, or serpiginous outline.[2] Cutaneous lesion in our patient also had similar features. The important differential diagnoses include subcutaneous mycoses, bacterial infections (leprosy, nocardiosis), mycobacterial infections (tuberculosis verrucosa cutis, lupus vulgaris), and parasitic infections (leishmaniasis and rhinosporidiosis). It should also be differentiated from noninfectious diseases such as planoepithelial carcinoma, psoriasis, sarcoidosis, or lupus erythematous.[2],[3],[4],[5] The diagnosis of chromoblastomycosis is done with the help of microscopy, culture, histopathology/cytological, and molecular techniques.[1],[2],[3],[4] Direct microscopic examination of skin scraping/crust with 10% KOH, especially calcofluor and other fluorochromes stains demonstrate thick-walled round fungal sclerotic bodies. The confirmation of diagnosis and further speciation can be done by culture on Sabouraud's dextrose agar containing antimicrobials incubated at 25°C, which produces colony of melanized fungus over 2–4 weeks.[1],[2],[3] On histopathology, pseudoepitheliomatous hyperplasia, intraepidermal microabscesses, and lichenoid granulomatous inflammation are seen throughout dermis. The inflammatory infiltrate comprises of lymphocytes, plasma cells, histiocytes, eosinophils, and giant cells. Fungal elements are seen as pigmented sclerotic bodies with vertical and horizontal cross walls (5–12 µm) known as medlar or copper penny bodies, diagnostic of chromoblastomycosis,[1],[2],[3] as seen in our case also. Fontana–Masson stain specific to melanin is also helpful in visualization of fungal elements in tissue specimens. Enzyme linked immunosorbent assay for detection of F. pedrosoi and Cladophialophora carrionii have limited usefulness due to low sensitivity and specificity. Molecular techniques using ribosomal RNA polymerase chain reaction have been used in speciation and identification of new species and research purposes.[1] The treatment requires an individualized approach. The various treatment modalities used are medical, surgical excision/debridement, and physical destructive modalities. The firstline drugs are triazoles, allylamines, potassium iodide, amphotericin B, photodynamic therapy, and imiquimod.[1],[2],[3] Combination therapy using itraconazole (200–400 mg) and terbinafine (500–1000 mg) has been used synergistically for 3–6 months with good success. Newer antifungals such as posaconazole and voriconazole are also being used. Cryotherapy, thermal therapy, and surgical excision can be combined with medical modalities.[1],[2],[3] Patient should be kept under follow up to detect any recurrence or failure of treatment. Thus our case represents an uncommon morphological presentation of chromoblastomycosis and importance of an astute histopathology examination to clinch the diagnosis in culture-negative and resource-constrained scenarios.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Krzyściak PM, Pindycka-Piaszczyńska M, Piaszczyński M. Chromoblastomycosis. Postepy Dermatol Alergol 2014;31:310-21.  Back to cited text no. 1
    
2.
Queiroz-Telles F, Esterre P, Perez-Blanco M, Vitale RG, Salgado CG, Bonifaz A. Chromoblastomycosis: An overview of clinical manifestations, diagnosis and treatment. Med Mycol 2009;47:3-15.  Back to cited text no. 2
    
3.
Mittal A, Agarwal N, Gupta LK, Khare AK. Chromoblastomycosis from a non-endemic area and response to itraconazole. Indian J Dermatol 2014;59:606-8  Back to cited text no. 3
    
4.
Gomes NM, Bastos TC, Cruz KS, Francesconi F. Chromoblastomycosis: An exuberant case. An Bras Dermatol 2014;89:351-2.  Back to cited text no. 4
    
5.
Roy AD, Das D, Deka M. Chromoblastomycosis-A clinical mimic of squamous carcinoma. Australas Med J 2013;6:458-60.  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

Top
 
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    References
    Article Figures

 Article Access Statistics
    Viewed989    
    Printed4    
    Emailed0    
    PDF Downloaded123    
    Comments [Add]    

Recommend this journal