Generic selectors
Exact matches only
Search in title
Search in content
Post Type Selectors
Filter by Categories
15th National Conference of the IAOMFP, Chennai, 2006
Abstracts from current literature
Acne in India: Guidelines for management - IAA Consensus Document
Art & Psychiatry
Association Activities
Association Notes
Award Article
Book Review
Brief Report
Case Analysis
Case Letter
Case Letters
Case Notes
Case Report
Case Reports
Clinical and Laboratory Investigations
Clinical Article
Clinical Studies
Clinical Study
Conference Oration
Conference Summary
Continuing Medical Education
Cosmetic Dermatology
Current Best Evidence
Current Issue
Current View
Derma Quest
Dermato Surgery
Dermatosurgery Specials
Dispensing Pearl
Do you know?
Drug Dialogues
Editor Speaks
Editorial Remarks
Editorial Report
Editorial Report - 2007
Editorial report for 2004-2005
Fourth All India Conference Programme
From Our Book Shelf
From the Desk of Chief Editor
Get Set for Net
Get set for the net
Guest Article
Guest Editorial
How I Manage?
IADVL Announcement
IADVL Announcements
IJDVL Awards
IJDVL Awards 2018
IJDVL Awards 2019
IJDVL Awards 2020
IJDVL International Awards 2018
Images in Clinical Practice
In Memorium
Inaugural Address
Knowledge From World Contemporaries
Leprosy Section
Letter in Response to Previous Publication
Letter to Editor
Letter to the Editor
Letter to the Editor - Case Letter
Letter to the Editor - Letter in Response to Published Article
Letter to the Editor - Observation Letter
Letter to the Editor - Study Letter
Letter to the Editor - Therapy Letter
Letter to the Editor: Articles in Response to Previously Published Articles
Letters in Response to Previous Publication
Letters to the Editor
Letters to the Editor - Letter in Response to Previously Published Articles
Letters to the Editor: Case Letters
Letters to the Editor: Letters in Response to Previously Published Articles
Medicolegal Window
Miscellaneous Letter
Net Case
Net case report
Net Image
Net Letter
Net Quiz
Net Study
New Preparations
News & Views
Observation Letter
Observation Letters
Original Article
Original Contributions
Pattern of Skin Diseases
Pediatric Dermatology
Pediatric Rounds
Presedential Address
Presidential Address
Presidents Remarks
Report of chief editor
Report of Hon : Treasurer IADVL
Report of Hon. General Secretary IADVL
Research Methdology
Research Methodology
Resident page
Resident's Page
Resident’s Page
Residents' Corner
Residents' Corner
Residents' Page
Review Article
Review Articles
Revision Corner
Self Assessment Programme
Seminar: Chronic Arsenicosis in India
Seminar: HIV Infection
Short Communication
Short Communications
Short Report
Special Article
Specialty Interface
Study Letter
Study Letters
Symposium - Contact Dermatitis
Symposium - Lasers
Symposium - Pediatric Dermatoses
Symposium - Psoriasis
Symposium - Vesicobullous Disorders
Symposium Aesthetic Surgery
Symposium Dermatopathology
Symposium-Hair Disorders
Symposium-Nails Part I
Symposium-Nails-Part II
Systematic Review and Meta-Analysis
Systematic Reviews and Meta-analyses
Systematic Reviews and Meta-analysis
Therapeutic Guideline-IADVL
Therapeutic Guidelines
Therapeutic Guidelines - IADVL
Therapy Letter
Therapy Letters
View Point
What’s new in Dermatology
View/Download PDF

Translate this page into:

Residents Corner
doi: 10.4103/0378-6323.172911

Viva questions from the IJDVL

Vishalakshi Viswanath1 , Resham Vasani2
1 Department of Dermatology, Rajiv Gandhi Medical College, Thane, India
2 Department of Dermatology, K J Somaiya Medical College and Research Centre, Sion, Mumbai, Maharashtra, India

Correspondence Address:
Vishalakshi Viswanath
Department of Dermatology, Rajiv Gandhi Medical College, Thane, Maharashtra
How to cite this article:
Viswanath V, Vasani R. Viva questions from the IJDVL. Indian J Dermatol Venereol Leprol 2016;82:114-119
Copyright: (C)2016 Indian Journal of Dermatology, Venereology, and Leprology

Spotter[Figure - 1]

Figure 1: Enumerate the differential diagnosis in this case. Courtesy: Rajiv Gandhi Medical College, Thane

The differentials in this case include lupus miliaris disseminatus faciei, acne, granulomatous rosacea and sarcoidosis.

What are the synonyms for lupus miliaris disseminatus faciei?

The other terminologies are acne agminata, acnitis, Lewandowsky's rosaceiform eruption and facial idiopathic granulomas with regressive evolution.

How does lupus miliaris disseminatus faciei differ from its clinical mimickers?

  • Lupus miliaris disseminatus faciei is characterized by the presence of reddish-brown symmetrical papulo-nodules which may show evidence of central necrosis. The lesions characteristically involve the eyelids, especially the lower eyelid
  • In contrast to acne, there are no comedones and the lesions are not consistently related to the hair follicles. In contrast to lupus miliaris disseminatus faciei, acne has polymorphous lesions with comedones, inflammatory lesions, scars and pigmentary disturbances
  • In lupus vulgaris, there is cutaneous hypersensitivity to tuberculin and isolation of mycobacterial DNA through polymerase chain reaction is possible, unlike lupus miliaris disseminatus faciei. Lupus vulgaris responds to antituberculous treatment while lupus miliaris disseminatus faciei does not
  • Granulomatous rosacea has a background of erythema and telangiectasia and can have extra-facial lesions; these are uncommon in lupus miliaris disseminatus faciei
  • Sarcoidosis can have associated systemic involvement while lupus miliaris disseminatus faciei does not
  • Sudden eruption of dome-shaped papules and nodules in a leprosy patient with resistance to dapsone having characteristic epidermal Grenz zone and dermal spindle-shaped histiocytes characterizes histoid leprosy, whereas lupus miliaris disseminatus faciei shows perifollicular epithelioid cell granulomas with Langhans giant cells and occasionally caseation necrosis.

What are the idiopathic facial granulomatous eruptions and what are their differentiating features?

The salient differentiating features of idiopathic facial granulomatous eruptions are outlined in [Table - 1].

Table 1: Salient features of idiopathic facial granulomatous eruptions

Therapeutic Paradox

What is a “therapeutic paradox?”

A “paradox” is defined as a “seemingly absurd or contradictory statement or proposition which when investigated may prove to be well founded or true.”

When a drug is given for the treatment of a particular condition, paradoxically, it is also responsible for the causation/exacerbation of the condition; this is called as a “therapeutic paradox.”

Enumerate some “therapeutic paradoxes” in dermatology

  • Tumor necrosis factor alpha inhibitor-induced psoriasis
  • Isotretinoin-induced acne fulminans
  • Cetirizine-induced urticaria
  • Chloroquine-induced lichenoid drug eruption
  • Chloroquine-induced photosensitivity
  • Topical calcineurin inhibitor-induced rosacea
  • D-penicillamine-induced pseudoscleroderma
  • Potassium iodide for erythema nodosum
  • Clofazimine in erythema dyschromicum perstans
  • Allergic contact dermatitis due to steroid moiety
  • Antileprosy treatment as a trigger for reactions in leprosy
  • Antiretroviral therapy and the immunological boost responsible for immune reconstitution inflammatory syndrome
  • Intense pulsed light or laser-induced hypertrichosis
  • Q-switched laser-induced darkening of tattoos.

Enumerate some paradoxes in clinical dermatology

  • Allergic contact dermatitis due to toslyamide and formaldehyde induced resins in nail lacquer may occur on any part accessible to the nails, but dermatitis is not seen in the periungual area
  • Oral exposure to nickel (through tap water/dental braces) may induce tolerance and reduced severity of the disease
  • The “photo-hardening” effect of psoralen and ultraviolet A is utilized in treatment of photosensitive dermatoses
  • Paraben and lanolin responsible for contact dermatitis produce false negative results on patch tests
  • Vitamin B12 deficiency causes cutaneous hyperpigmentation but depigmentation of hair
  • Development of leukoderma in melanoma may be seen in advanced stage of the disease with metastasis. Leukoderma indicates T-cell mediated immunological response against the target antigens present on both melanoma cells as well as normal melanocytes resulting in melanoma regression and vitiligo
  • Itching is a consistent symptom in lichen planus, but paradoxically excoriations are conspicuously absent as the patient rubs rather than scratches to gain relief and hence the pathognomonic lesion morphology and Wickham's striae are preserved (Brocq's phenomenon)
  • In cases of co-infection of leprosy and human immunodeficiency virus, the clinical, immunological and pathological features are same even in progressive human immunodeficiency virus disease and granuloma formation remains well preserved even with declining T-cell mediated immunity – the so-called “granuloma paradox.”

Adapted from and for further reading: Adya KA, Inamdar AC, Palit A. Paradoxes in dermatology. Indian Dermatol Online J 2013;4:133-42.

Trichoscopy Crossword

Identify the condition and solve the crossword puzzle [Figure - 2] based on the trichoscopic clues [Box 1]. Answers to the crossword puzzle are provided in [Figure - 3] on page 118.

Figure 2: Crossword puzzle (identify the condition based on the trichoscopic clues)
Figure 3: Answer key to crossword puzzle

Leser-Trelat Sign

What is sign of Leser-Trelat?

The sign of Leser-Trelat is characterized by the sudden eruption of numerous seborrheic keratoses, often with associated pruritus, or a rapid increase in their size within weeks or months. It is considered a marker of internal malignancy.

Enumerate the conditions wherein the sign of Leser-Trelat is found.

This sign has been described with various malignancies such as stomach cancer, gastrointestinal adenocarcinoma, lymphoma, leukemia, mycosis fungoides, Sezary syndrome, breast carcinoma, lung carcinoma, prostate carcinoma, laryngeal carcinoma and sarcomas (neurofibrosarcoma). The sign has been also reported in non-malignant situations as in heart transplant recipients, erythrodermic pityriasis rubra pilaris and human immunodeficiency virus infection; it can also occur in normal persons.

Kasabach–merritt Syndrome

What is Kasabach–Merritt syndrome or Kasabach–Merritt phenomenon?

Kasabach–Merritt phenomenon is characterized by a rapidly enlarging vascular tumor associated with thrombocytopenia, microangiopathic hemolytic anemia and a consumptive coagulopathy.

Which are the tumors associated with Kasabach–Merritt phenomenon?

Infantile hemangiomas, tufted angiomas, kaposiform hemangioendotheliomas, hemangiopericytomas and angiosarcomas can be associated with Kasabach–Merritt phenomenon. The location of these vascular tumors may be cutaneous, intrathoracic (mediastinal), abdominal (retroperitoneal or intrahepatic), pelvic or skeletal.

When should one suspect Kasabach–Merritt phenomenon?

Kasabach–Merritt phenomenon should be suspected in case of a rapidly enlarging vascular tumor associated with sudden appearance of ecchymoses which may extend beyond the margins of the tumor. There is a woody texture and the overlying inflammation may appear cellulitic. There is a bleeding diathesis that may manifest with hematuria, epistaxis and prolonged bleeding at sites of trauma. There is thrombocytopenia and activation of the fibrinolytic system. Due to the disseminated intravascular coagulation, there is consumption of clotting factors, low fibrinogen levels, elevated D-dimers, elevated prothrombin time and activated partial thromboplastin time.

What are the treatment options in Kasabach–Merritt phenomenon?

The treatment options depend on the severity of the coagulation defect, the site of tumor and the presence or absence of the physical effects of compression of surrounding tissues.

Initial conservative management with regular monitoring of platelets, clotting studies, fibrinogen and D-dimers should be done. Platelet transfusions and systemic corticosteroids should initially be used. Tumor reduction can be done with cytotoxic therapy, interferons. Surgical treatment (with pre-embolization) and radiotherapy can be considered in difficult cases.

Eosinophilic Fasciitis

What is the synonym of eosinophilic fasciitis?

This scleroderma-like syndrome is also termed as Shulman's syndrome. It is an uncommon connective tissue disease that may mimic and overlap with other sclerosing disorders such as morphea and lichen sclerosus.

Enumerate the trigger factors in eosinophilic fasciitis?

Eosinophilic fasciitis is triggered by various factors:

  • Strenuous exercise and trauma are responsible in at least 66% of cases which are hypothesized to induce the antigenicity of the fascia and subcutis
  • Arthropod bites, borreliosis and Mycoplasma arginini infection may be other triggers
  • Drugs such as simvastatin, atorvastatin, ramipril and phenytoin may be responsible; ingestion of L-tryptophan may contribute to the eosinophilia -myalgia syndrome
  • Neoplasia, autoimmune thyroiditis, eosinophilic colitis, hypercalcemia and amegakaryocytic thrombocytopenic purpura may be other factors associated with disease onset.

Describe the salient features of eosinophilic fasciitis

The characteristic clinical, histological and investigative findings include:


Sudden-onset erythema, edema in the early phase and symmetrical woody induration of the distal extremities later are characteristic. There is a limitation of movement of the feet and hands. Occasionally, the face or abdomen can be affected and there may be superficial blistering and hemorrhage.


There is dermal sclerosis with inflammation and fibrosis extending to the subcutaneous tissue and deep fascia. The fascia is thickened and infiltrated with lymphocytes, plasma cells, histiocytes and eosinophils. Immunoglobulin G and C3 deposits can be demonstrated in the deep fascia. The inflammatory infiltrate consists of macrophages and predominantly CD8+ T-cells with eosinophils.


Blood eosinophilia (up to 30%) is the predominant feature in most patients. Erythrocyte sedimentation rate may be elevated. There may be hyperglobulinemia, rarely, aplastic anemia and thrombocytopenia may be seen. Magnetic resonance imaging shows thickened deep fasciae on T1-weighted sequences and relatively increased signal intensity greater than that of muscle on fat-suppressed or fat-saturated T2-weighted sequences.

What are the overlapping and differentiating features of eosinophilic fasciitis and scleroderma?

The differentiation of eosinophilic fasciitis from deep morphea or overlapping cases with morphea or scleroderma may be problematic. Overlapping features of eosinophilic fasciitis and deep morphea are involvement of subcutaneous tissue, fascia, muscles, eosinophilia and positive antinuclear antibody and association with systemic sclerosis.

The features favoring the diagnosis of eosinophilic fasciitis are venous furrowing, prayer sign, the absence of sclerodactyly and Raynaud's phenomenon, prominent eosinophilia, hypergammaglobulinemia and the absence of nailfold capillary changes.

What are the treatment options?

Corticosteroids are the mainstay of treatment. Adjuvant modalities include hydroxychloroquine, methotrexate, cyclosporine and psoralen and ultraviolet A.

Photodynamic Therapy

What is the mechanism of photodynamic therapy?

Photodynamic therapy involves treatment with 5-aminolevulenic acid and various sources of light. There is absorption of 5-aminolevulenic acid by the rapidly proliferating epidermal and dermal cells and it is metabolized to the active photosensitizer, protoporphyrin IX, via the heme biosynthesis pathway. When protoporphyrin IX is activated by light, photodynamic reactions occur that lead to cell necrosis, apoptosis and remodulation.

What are the uses of topical photodynamic therapy in dermatology?

Topical photodynamic therapy with 5-aminolevulinic acid is a promising therapeutic modality for proliferative diseases such as actinic keratosis, Bowen's disease, in situ squamous cell carcinoma and superficial basal cell carcinoma. It has also been used in recalcitrant warts and warts in difficult to treat sites such as urethral condyloma acuminata. Photodynamic therapy is also being used in acne and as a photorejuvenation therapy.

Leopard Syndrome

What are the various clinical types of lentiginosis?

The term lentiginosis is used when there are numerous or extensive lentigenes, or they have a characteristic clinical pattern. The various clinical types are:

  • Generalized lentiginosis
  • Eruptive lentiginosis
  • Zosteriform lentiginosis
  • Centrofacial lentiginosis
  • LEOPARD syndrome (lentigines, electrocardiographic abnormalities, ocular hypertelorism, pulmonary stenosis, abnormalities of genitalia, retardation of growth and deafness of sensorineural type)
  • Peutz–Jeghers syndrome (periorificial lentigines, intestinal polyposis and soft-tissue malignancy)
  • Cronkhite–Canada syndrome (generalized gastrointestinal polyposis, cutaneous hyperpigmentation, hair loss and nail atrophy)
  • <>
  • Carney complex or LAMB syndrome (lentigines, atrial myxomas, mucocutaneous myxomas and blue nevi).

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


Conflicts of interest

There are no conflicts of interest.

Fulltext Views

PDF downloads
Show Sections