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Case Report

Qazi Masood, Taseer Ahmed Bhat, Iffat Hassan, Farah Sameen, Sabiya Majid

Prolidase deficiency is a rare inborn disorder of collagen metabolism characterized by chronic recurrent skin ulceration. A
seven-year-old girl and her younger sibling with clinical features and laboratory criteria fulfilling the diagnosis of
prolidase deficiency are presented in view of rarity of the condition.

Key Words: Leg ulcers, prolidase deficiency

Indian J Dermatol 2007:52(1):00-00

Introduction multiple atrophic macules and linear teleangectasias on the
malar area of the face (Fig. 1). The most striking feature
Prolidase deficiency is a rare disorder inherited through an
was extensive deep ulcers on the lower legs with atrophic
autosomal recessive gene. The hallmark of this disorder is
scars in the surrounding skin. The ulcers were deep with
the presence of characteristic face with saddle nose, mental
ragged margins and floor of the ulcer was covered by
retardation and chronic recurrent cutaneous ulcers that are
yellowish crust (Figs. 2 and 3). The ulcer was not fixed to
recalcitrant in healing. The ulcers result from impaired
the underlying tissues. The inguinal lymph nodes were not
recycling of proline which constitute 20% of aminoacid in
significantly enlarged. There were multiple hyperpigmented
collagen and is important for tissue repair.1 Others features
small atrophic macules on the extensor portions of the
that are seen include frequent infections, partial deafness,
extremities and on the hips. Mat-like telangectasia were
visual disturbances and joint dislocation.
seen on the knees and lower legs. There was no evidence
Case Report of varicosities and peripheral pulses were normal.

A seven-year-old female child born of a full term normal The systemic examination revealed no abnormal findings
delivery to 2nd degree consanguineous parentage presented except for a mild splenomegaly. Her ophthalomological
to our outpatient department with the history of recurrent examination was normal.
painful ulceration of the lower legs of 18 months duration. Her routine laboratory investigation, collagen vascular
It used to begin as a pruritic pustular lesions on the lower profile and porphyrin profile were all normal. The
legs, followed later by ulcer formation. The ulcers used to histopathological examination of the skin showed
persist for many months with no consistent response to nonspecific inflammatory changes and the direct
antibiotics and used to heal with atrophic scarring. Other immunoflourescence was negative. The culture of the ulcer
features seen in the patient were mental retardation, failure did not show any microbial growth. Thin layer
to thrive and recurrent ear discharge from the last four chromatography of her overnight urine revealed a marked
years. There was no clinical evidence suggestive of increase in diimminopeptides after gelatin loading
Hansen’s disease, collagen vascular disorders or of indicating the possibility of prolidase enzyme deficiency
hemolytic anemia. One of her younger siblings had similar (Fig. 4). Her younger sibling was also investigated with
episodes of ulcerations of lower legs followed by scarring. identical findings on thin layer chromatography. Prolidase
On physical examination, she was 110 cm in height and enzyme activity was assayed colorimetrically using the
weighed only 17 kgs, which was below the 3rd percentile substrate glycylproline and chinnard reaction.2 It was
for her age. She had atypical facies with saddle nose, found to be only 12% and 28% in the patient and her
hyperteleorism, high arched palate, malaligned teeth, with younger sibling respectively in comparison to the normal
healthy controls.

From the Department of Dermatology, STD and Leprosy and Discussion
Department of Biochemistry, Govt. Medical College, Srinagar,
Prolidase deficiency is a rare metabolic disorder of
India. Address correspondence to: Dr. Taseer Ahmed Bhatt, R/
O:-Shabeer Manzil, Rajbagh Extension, Srinagar, Kashmir -
autosomal recessive inheritance. Goodman in 1968 was the
190 008 (J and K), India. E-mail: first to describe this condition in a male patient who had

53 Indian J Dermatol 2007; 52(1)

Masood Q, et al.: Prolidase deficiency

Fig and legend missing???
Fig and legend missing???

Figure 1: Figure 3:

Fig and legend missing??? Fig and legend missing???

Figure 2: Figure 4:

mental subnormality and characteristic recalcitrant ulcers erythematous palms and soles.6 They also suffer from
on the lower legs.3 The enzyme prolidase is widely recurrent infections such as otitis media, respiratory tract
distributed throughout the body and is important in infections and sinusitis. In addition, other features reported
recycling of proline and hydroxyproline which constitute are simian crease, wasting of the small muscles of hand,
about one quarter of the collagen.1 The deficiency of this talipes equines, osteoporosis, hyperextensibility of joints,
enzyme is responsible for massive loss of proline in the deafness, corneal opacities, ambylopia, optic atrophic,
urine which is estimated to be as high as 3 gm per day.4 splenomegaly and protuberant abdomen.6 The diagnosis is
The prolidase enzyme can be assayed in the erythrocytes, ascertained by iminopeptiduria greater than 5 mmol/24h.
leucocytes and the fibroblasts and have been found to be The predominant peptide is glyclproline. A characteristic
undetectable in the patients with prolidase enzyme feature of the disorder is absolute resistance to all forms of
deficiency. treatment including rejection of skin grafts. The treatment
These patients are mentally subnormal and are of short modalities which seemed to be helpful include dapsone,
stature. They have peculiar facies such as saddle nose, diphenylhydantion, ascorbic acid and manganese.7 The
hypertelorism, narrowed eyes and hypoplasia of the jaws.5 topical application of ointment containing 5% glycine and
Among the clinical presentation, the most striking 5% proline was found to be effective in number of trials.8
manifestation is the skin fragility with leg ulceration and Enzyme replacement has been tried by blood transfusion
characteristic pitted scarring. The other cutaneous changes containing manganese activated prolidase enzyme.9 Pulsed
seen include photosensitivity, purpura, telengectasia, dry corticosteroid treatment also showed good results and act
crusted lesions on the face and buttocks; dry fissured by inhibiting iminodipeptide primed neutrophil superoxide

Indian J Dermatol 2007; 52(1) 54

Masood Q, et al.: Prolidase deficiency

generation.10 Therapeutic apheresis exchange was Prolidase deficiency: A case report and literature review. Br J
successful in two patients.11 Dermatol 1989;121:405-9.
7. Jemec GB, Moe AT. Topical treatment of skin ulcers in
References prolidase deficiency. Peadiatr Dermatol 1996;13:58-60.
8. Arata J, Hatakenaka K, Oono T. Effect of topical application
1. Jackson SH, Dennis AW, Greenberg M. Iminopeptiduria: A
of glycine and proline on recalcitrant leg ulcers of prolidase
genetic defect in recycling collagen: A method for determining
deficiency. Arch Dermatol 1986;122:626-7.
prolidase in erythrocytes. Can Med Assoc J 1975;113:759-63.
9. Hechtman P, Richter A, Corman N, Leong YM. In situ
2. Ganpathy V, Pashley SJ, Roesel RA, Pashley DH, Leibach FH.
activation of human erythrocyte prolidase. Potential for
Inhibition of rat and human prolidases by captopril. Biochem
enzyme replacement therapy. Pediatr Res 1988;24:709-12.
Pharmacol 1985;34:1287-91.
10. Yasuda K, Ogata K, Kodama H, Kodama H, Zhang J, Sugahara
3. Goodman SI, Soloman CC, Muschenheim F, McIntyre CA,
K, et al. Corticosteroid treatment of prolidase deficiency skin
Miles B, O’Brien D. A syndrome resembling lathyrism
lesions by inhibiting iminopeptide-primed neutrophil
associated with iminopeptiduria. Am J Med 1968;45:152-9.
superoxide generation. Br J Dermatol 1999;141:846-51.
4. Scriver CR, Smith RJ, Phang JM. Disorders of proline and
11. Lupi A, Casado B, Soli M, Bertazzoni M, Annovazzi L, Viglio
hydroxyproline metabolism. In: The metabolic basis of
S, et al. Therpeutic apheresis exchangein two patients with
inherited disease. Stanbury JB, Wyngaarden JB, Fredrickson
prolidase deficiency. Br J Dermatol 2002;147:1237-40.
DS, et al. 5th ed. McGraw-Hill: New York; 1983. p. 360-81.
5. Arata J, Umenmura S, Yamamoto Y, Hagiyama M, Nohara N.
Prolidase deficiency: Its dermatological manifestations and
some additional biochemical studies. Arch Dermatol
Source of Support: Nil, Conflict of Interest: None declared.
6. Milligan A, Graham-Brown RA, Burns DA, Anderson L.

55 Indian J Dermatol 2007; 52(1)

Case Report

Fatma Aydin, Nilgün Senturk, Esra Pancar Yuksel, Levent Yildiz, Tayyar Canturk,
Ahmet Yasar Turanli

Patients with lupus erythematous may develop an acute eruption clinically similar to toxic epidermal necrolysis or
erythema multiforme. The presence of erythema multiforme-like lesions and characteristic pattern of immunological
abnormalities including antinuclear antibody (speckled pattern), anti-Ro antibody or anti-La antibody and positive
rheumatoid factor in lupus patients has been termed as Rowell’s syndrome. Although diagnostic criteria of this syndrome
have been reviewed recently, definite mechanisms of pathogenesis is still unknown. Here we reported a 29-year-old
female patient who had systemic lupus erythematous developed erythema multiforme-like lesions.

Key Words: Erythema multiforme, Rowell’s syndrome, systemic lupus erythematosus

Indian J Dermatol 2007:52(1):00-00

Introduction On dermatological examination, she had dusky red patches
on the face, neck and trunk. There were numerous target-
Patients with discoid lupus erythematosus (DLE) and
like lesions on the trunk and extremities, which were
systemic LE (SLE) may develop coincidental erythema
coalesced into a polycyclic pattern (Fig. 1 a, b). The patient
multiforme (EM).1,2 The presence of EM-like lesions in
was hospitalised and hydroxychloroquine was
lupus patients and a characteristic pattern of immunological
discontinued due to possibility of drug eruption since she
abnormalities have been defined as Rowell’s syndrome
had been using this medication for six weeks.
(RS).1 We report a case of SLE with EM-like lesions whose
clinical picture is consistent with this rare syndrome. Four milimeters punch biopsy was taken for both light
microscopy and direct immunofluorescence examination.
Case Report Histopathologic examination revealed epidermal necrosis,
A 29-year-old woman was admitted to our dermatology dermal edema and a perivascular and interstitial
department with erythematous rash on the face, trunk, mononuclear infiltrate (Figs. 2, 3). Direct
upper and lower extremities for one week duration. She had immunofluorescence (DIF) examination was negative.
been diagnosed as having SLE on the basis of the Erythrocyte sedimentation rate, complete blood cell count,
American Rheumatism Association (ARA) criteria, with liver and renal function tests were within normal limits.
features of oral ulcers, arthritis, immunologic (positive anti- Proteinuria was detected with urine analysis (2.5 g in 24h).
nuclear antibody in speckled pattern, anti-ds DNA, anti- Autoimmune screening demonstrated the presence of ANA
Sm), hematologic (anemia, lymphopenia and in speckled pattern (1:40 dilution). Anti-Ro antibody was
thrombocytopenia) and renal disorders, six weeks ago. She negative and rheumatoid factor was positive. Serum
had been using hydroxychloroquine (200 mg) and antibodies to herpes simplex virus, serology for HIV and
methylprednisolone (40 mg/d) since than. She did not have syphilis were all negative. Dose of prednisolone was
a history of perniosis. She did not also have a history of increased to 80 mg daily. Clinical improvement was
upper respiratory tract and herpes virus infection or any observed after one week of hospitalisation. During 11-
infection associated with fever as well as sunlight month follow-up period, no recurrence was observed.
exposure. She did not take any medication except Discussion
prescribed ones for SLE.
RS has been described with all subtypes of LE (systemic,
acute, subacute or discoid).1-3 All forms of EM (EM minor,
From the Ondokuz Mayis University, School of Medicine,
Department of Dermatology and Pathology, Samsun, Turkey.
EM major) and toxic epidermal necrolysis can also be
Address correspondence to: Dr. Fatma Aydin, Ondokuz Mayis associated with RS.3-5 Although the proper classification of
University School of Medicine, Department of Dermatology, EM-like lesions occurring in RS is not clear, these lesions
TR-55139 Kurupelit, Samsun, Turkey. E-mail: may represent a severe variant of acute cutaneous lupus
Indian J Dermatol 2007; 52(1) 56

Aydin F, et al.: Running title missing????

Fig. 2: Vacuolar degeneration and necrotic keratinocytes in basal layer
(H and E, x400)

Fig. 1: (a) Erythematous maculopopular target-shaped lesions on the
arms and (b) hands

Fig. 3: Panoromic view of the lesion (H and E, x100)
or, in some cases, subacute cutaneous lupus. Polycyclic
lesions of subacute cutaneous LE may resemble lesions of
ANA patterns have little specify and are of little value in the
EM, but direct immunofluorescence generally distinguishes
management of patients.8 In addition, anti Ro/La antibodies
these lesions as those of LE. The fact that the DIF was
contribute to the formation of the speckled pattern of ANA,
negative does not exclude a diagnosis of LE as this test is
thus, the coexistence of these antibodies would be expected.9
not always positive and its results might well be dependent
Until now limited numbers of cases have been reported and
on the age of the lesion. Gilliam had demonstrated that
they had different clinical and serological features.1-5
early and late lesions of LE often do not demonstrate the
characteristic IF findings.6 Recent evidence indicates that dysregulated apoptosis may
underlie both many of the major manifestations of LE and
Diagnostic serological abnormalities for RS include speckled
EM skin lesions. Viral infections were considered as
pattern of ANA, anti-Ro antibody or anti-La antibody and
triggering factors for both for SLE and EM. James et al10
positive rheumatoid factor (RF). Zeitouni et al2 reported that
have noted the possible contribution of EBV to the
the speckled pattern of ANA is the most consistent diagnostic
development of SLE. Unidentified HSV, EBV or other viral
feature of this syndrome, but anti Ro/La antibodies and
infections may cross-react with lupus autoantigens and
rheumatoid factor seem to be less consistent features. These
they can initiate the immunologic response, hence
serological findings described within Rowell’s syndrome may
triggering the EM like lesions in SLE. Similar
also be associated with the underlying disease, as in our case.
immunopathogenetic mechanisms described in both
Among the reported cases of RS, patterns of ANA at the time
diseases may be responsible for the concurrence of these
of diagnosis of SLE, has not been clearly documented.
two diseases.
However, ANA in speckled pattern; anti-Ro and anti-La
antibodies are seen in SLE with the frequency of 26%, 25% In our patient, after an extensive research, no procative
and 10-15%, respectively.7 It is also proposed that, different factor triggering EM was found. The only suspicious factor

57 Indian J Dermatol 2007; 52(1)

Aydin F, et al.: Running title missing????
could be hydroxychloroquine. It is believed that EM is multiforme-like lesions. Br J Dermatol 1999;141:720-4.
rarely drug-induced, in contrast to SJS. Most of the cases 5. Mandelcorn R, Shear NH. Lupus-associated toxic epidermal
reported as drug-induced EM are either SJS or necrolysis: A novel manifestation of lupus. J Am Acad
erythematous drug eruptions.11 Although, occurrence of Dermatol 2003;48:525-9.
SJS has been reported with hydroxychloroquine, there have 6. Gilliam JN, Sontheimer RD. Skin manifestations of SLE. Clin
Rheum Dis 1982;8:207-18.
been few reports of EM related to hydroxychloroquine for
years.12 Drug eruption was excluded because EM is rarely 7. Odom RB, James WD, Berger TG. Andrew’s diseases of the
skin clinical dermatology. WB Saunders Company:
drug-induced and while that is true in large population- Pennsylvania; 2000.
based studies, EM like lesions might well resemble a
8. Jacobe HT, Sontheimer RD. Autoantibodies encountered in
morbilliform eruption, which in fact is what we think the patients with autoimmune connective tissue diseases. In:
clinical photo represents. Bolognia JL, Jorizzo JL, Rapini RP, et al, editors.
Dermatology. 1st ed. Mosby: Spain; 2003. p. 589-623.
Since the first description, Rowell’s original criteria were
not well-preserved and the diagnosis of RS has not been 9. Maddison PJ, Reichlin M. Quantitation of precipitating
antibodies to certain soluble nuclear antigens in SLE. Arthiritis
cleared yet. We believe that the new diagnostic criteria, Rheum 1977;20:819-24.
which were suggested by Zeitouni et al, might be
10. James JA, Kaufman KM, Farris AD, Taylor-Albert E, Lehman
improved by the addition of new cases to the literature. TJ, Harley JB. An increased prevalence of Ebstein-Barr virus
infection in young patients suggests a possible etiology for
References systemic lupus erythematosus. J Clin Invest 1997;100:3019-
1. Rowell NR, Beck JS, Anderson JR. Lupus erythematosus and 26.
erythema multiforme-like lesions. A syndrome with 11. Roujeau JC. Clinical heterogeneity of drug hypersensitivity.
characteristic immunological abnormalities. Arch Dermatol Toxicology 2005;209:123-9.
1963;88:176-80. 12. Leckie MJ, Rees RG. Stevens-Johnson syndrome in association
2. Zeitouni NC, Funaro D, Cloutier RA, Gagne E, Claveau J. with hydroxychloroquine treatment for rheumatoid arthritis.
Redefining Rowell’s syndrome. Br J Dermatol 2000;142:343-6. Rheumatology 2002;41:473-4.
3. Roustan G, Salas C, Barbadillo C, Sanchez Yus E, Mulero J,
Simon A. Lupus erythematosus with an erythema multiforme-
like eruption. Eur J Dermatol 2000;10:459-62.
4. Marzano AV, Berti E, Gasparini G, Caputo R. Lupus Source of Support: Nil, Conflict of Interest: None declared.
erythematosus with antiphospholipid syndrome and erythema


The name of Dr. Susanne Pulimood should have been included in the article “Griscelli Syndrome Indian
Journal of Dermatology 2006, 51 (4) page No. 269-271.
The error is regretted.
- Editor, IJD

Indian J Dermatol 2007; 52(1) 58

Case Report

Sanjay Saraf

Sebaceous horn or cutaneous horn of the nose is a rare clinical entity. A case of a giant sebaceous horn of the nose
presenting in an elderly male, which was successfully excised and reconstructed is reported.

Key Words: Cornu cutaneum, cutaneous horn

Indian J Dermatol 2007:52(1):00-00

Introduction with centrally positioned bone. No such well-formed bone
is observed in the human horns. The earliest well-
Cutaneous horn (cornu cutaneum) is a relatively
documented case of cornu cutaneum from London in 1588
uncommon lesion consisting of a projectile, conical, dense,
hyperkeratotic nodule, which resembles the horn of an
animal.1 The horn is composed of compacted keratin.
Cutaneous horns most frequently occur in sun-exposed
parts and are typically found on the face and scalp, but
may also occur on the hands, penis, eyelids, nose, chest,
neck and shoulder. The cutaneous horns are usually
benign, however, malignant or premalignant lesions might
be associated with it.2 Because of their malignant potential,
the lesions must always be considered for
histopathological evaluation.

Case Report
A 92-year-old male presented with a raised, painless growth
over the tip of nose of more than six years duration. The
clinical examination demonstrated a cone-shaped keratotic
cutaneous horn. After careful and detailed physical
examinations the lesion was excised and reconstructed with Fig. 1: legend Missing???
lateral nasal flap (Miter flap) with satisfactory result.
Specimen was evaluated microscopically. Microscopically
the horn consisted of a mixture of squamous epithelial cells
and tricholemmal keratinized debris. The patient had history
of long-term sun exposure due to farming activities and
had solar keratosis on face and extremities. The follow-up
was uneventful without signs of recurrence.

A cutaneous horn (cornu cutaneum) is a protrusion from
the skin consisting of cornified material resembling an
animal horn in miniature. However, the animal horns are
composed of superficial hyperkeratotic epidermis, dermis

From the NMC SP. Hospital, AL Nahada, Dubai United Arab
Emirates. Address correspondence to: Sanjay Saraf, NMC SP.
Hospital, AL Nahada, Dubai United Arab Emirates.
E-mail: Fig. 1: legend Missing???

AU : Figures not cited in text 59 Indian J Dermatol 2007; 52(1)

Saraf S: Sebaceous horn

is of Mrs. Margaret Gryffith, an elderly Welsh woman. however possibility of malignant potential should always
However, earliest observations on cutaneous horns in be kept in mind.
humans were described by the Everard Home in 1791.3
Farris from Italy first described the well-documented case References
report with adequate histology of gigantic horn in a man.4 1. Korkut T, Tan NB, Oztan Y. Giant cutaneous horn: A patient
These horns may arise from a variety of benign, report. Ann Plast Surg 1997;39:654-5.
premalignant or malignant epidermal lesions. Most 2. Yu RC, Pryce DW, Macfarlane AW, Stewart TW. A
commonly, they are single and arise from a seborrheic histopathological study of 643 cutaneous horns. Br J Dermatol
keratosis lesion.5 According to a largest study by Yu et al,2 1991;124:449-52.
61% of cutaneous horns were derived from benign lesions 3. Bondeson J. Everard Home, John Hunter and Cutaneous horns:
and 39% were derived from malignant or premalignant A historical review. Am J Dermatopathol 2001;23:362-9.
epidermal lesions. Two other larger studies on cutaneous 4. Farris G. Histological considerations on a case of a voluminous
horn also showed that 23-37% of horns were associated cutaneous horn. Minerva Dermatol 1953;28:159-65.
with actinic keratosis or Bowen’s disease and another 16- 5. Thappa DM, Laxmisha C. Cutaneous horn of eyelid. Indian
Pediatr 2004;41:195.
20% with malignant lesions.2,6 The important consideration
in these cases is not the horn, but the underlying 6. Schosser RH, Hodge SJ, Gaba CR, Owen LG. Cutaneous horns:
A histopathologic study. South Med J 1979;72:1129-31.
pathology which may be benign (seborrheic keratosis, viral
7. Copcu E, Sivrioglu N, Culhaci N. Cutaneous horns: Are these
warts, histiocytoma, inverted follicular keratosis, verrucous
lesions as innocent as they seem to be? World J Surg Oncol
epidermal nevus, molluscum contogiosum, etc.), 2004;2:18.
premalignant (solar keratosis, arsenical keratosis, Bowen’s
8. Gould JW, Brodell RT. Giant cutaneous horn associated with
disease) or malignant (squamous cell carcinoma, rarely, verruca vulgaris. Cutis 1999;64:111-2.
basal cell carcinoma, metastatic renal carcinoma, granular 9. Kastanioudakis I, Skevas A, Assimakopoulos D, Daneilidis B.
cell tumor, sebaceous carcinoma or Kaposi’s sarcoma.7 Cutaneous horn of the article. Otolaryngol Head Neck Surg
Histopathological examination, specially of the base of the 1998;118:735.
lesion1,8.9 is necessary to rule out associated malignancy
and full excision and reconstruction is the treatment of
Source of Support: Nil, Conflict of Interest: None declared.
The cutaneous horns are predominantly benign lesions;

Indian J Dermatol 2007; 52(1) 60

Dermato-Microbiology Round

Immaculata Xess, Deepti Dubey, Mathur Purva*

Background: Fungal infection of the nails is a common, difficult to treat problem, prevalent worldwide. A discrepancy
in the microscopic examination and culture findings can create problems in the diagnosis of this common infection.
Aim: This study was designed to evaluate a new method for accurate diagnosis of onychomycosis. Materials and
Methods: Nail samples from 25 patients of suspected onychomycosis were taken. A portion of the samples was treated
with 2% trypsin before culturing and the rest was processed by the standard mycological technique. Results: A higher
number of culture positive samples were obtained by the trypsin treatment method as compared to the standard
technique. Conclusion: Trypsin treatment prior to culture increases the isolation of fungi from nail samples.

Key Words: Candida spp., onychomycosis, trypsin treatment

Indian J Dermatol 2007:52(1):00-00

Onychomycosis, defined as fungal infection of nail affects culture results is necessary for the clinician to be confident
approximately 5% of the population worldwide and of the diagnosis.2 Almost half of all specimens taken from
represents around 30% of all superficial mycotic infection onychomycotic nails fail to yield a pathogen in culture. We
and 50% of nail disorders.1 The infection has profound have previously reported a modified method for diagnosis
social consequences for the affected patients, who often of dermatophytes, which is highly sensitive and specific as
have diminished confidence or self esteem and experience compared to the conventional culture methods.4 In this
embarrassment in social and work situations. paper, we have used the same method for diagnosing
Onychomycosis in immunocompromised patients, such as onychomycosis and document its superiority for
those infected with human immunodeficiency virus (HIV), onychomycosis caused by Candida Spp.
can pose a more serious health problem.2 Over the recent
years, an upsurge in cases of onychomycosis due to Materials and Methods
nondermatophytes has been documented.2,3 Of the The study population consisted of 25 patients, whose
nondermatophytic filamentous fungi, agents implicated in clinical diagnosis was distal or lateral subungual
onychomycosis include members of Scopulariopsis and onychomycosis. The nail scraping from these patients were
Scytalidium (the two most common genera), which are collected from the dorsal surface and nail bed, on sterile
both thought to digest keratin in vivo, as well as members brown paper. All samples were processed on the day of
of the genera Alternaria, Aspergillus, Acremonium and collection. For processing of samples, the method of Naka
Fusarium.3 The most common yeast that is involved in et al was followed.5
onychomycosis is C. albicans. The fact that the infection
is difficult to treat and treatment consists of prolonged A part of the scrapings were dipped in 1 ml of 2% trypsin
courses of potentially toxic drugs makes it imperative to solution and kept at 37°C for two hours. The scrapings
make an early and accurate diagnosis. Diagnosis of were then washed with phosphate buffered saline (PBS) by
onychomycosis depends on direct microscopy, centrifugation three times (1500 g X 10 min). The deposit
supplemented by culture results. Direct microscopy is often was suspended in 300 µl PBS. 200 µl of this was cultured
time-consuming, because nail debris is thick and coarse on Saboraud’s dextrose agar (SDA) supplemented with
and hyphae are usually only sparsely present.2 Although cyclohexamide and gentamycin (0.026 mg/ml) and
direct microscopy can provide clues about the identity of cyclohexamide (0.05 mg/ml) only. 100 µl was mixed with
the microorganism, careful matching of microscopic and equal amount of 1% neutral red (Merck) and kept at room
temperature for one hour. This was then microscopically
examined as a wet mount under high dry objective (40x).5
From the Departments of Microbiology and *Laboratory
Medicine, All India Institute of Medical Sciences, New Delhi, Another part of sample was not treated with trypsin and
India. Address correspondence to: Dr. Immaculata Xess, processed by standard mycological techniques: A direct
Department of Microbiology, All India Institute of Medical microscopic examination was done after treating the
Sciences, New Delhi, India. E-mail: scraping with 20% KOH and gentle heating.6,7 The

61 Indian J Dermatol 2007; 52(1)

Xess I, et al.: Running title missing????
scrapings were also cultured on SDA supplemented with
Table 1: Comparison of culture results of trypsin
gentamycin and cyclohexamide and on SDA with
treatment versus standard methods for diagnosis of
All the culture tubes were incubated at 25°C and 37°C for Result of standard Result of post Direct
up to one month before declaring a negative result. The culture method trypsin culture microscopy for
growth obtained was identified microscopically. For fungal elements
Candida speciation was done by growth characteristics on
Sterile Sterile Negative
corn meal agar and pigmentation on TTZ (2,3,5 triphenyle
C. albicans Sterile Negative
tetrazolium chloride) agar.
Sterile Sterile Negative
Results Sterile C. parapsilosis Positive
Nail scrapings from a total of 25 patients whose clinical Sterile C. parapsilosis Positive
diagnosis was distal or lateral subungual onychomycosis Gram positive cocci C. parapsilosis Positive
were studied. The study population consisted of 18 males Sterile Sterile Negative
and seven females. The age of the patients ranged from 10- Sterile C. parapsilosis Positive
67 years. Of these patients, three had a history of Aspergillus fumigatus Aspergillus fumigatus Positive
noninsulin dependent diabetes and two had insulin
Sterile C. albicans Positive
dependent diabetes. None of them were HIV positive. Two
Alternaria spp. Alternaria spp. Positive
patients had a history of receiving treatment for
onychomycosis previously. All the samples were examined Gram positive cocci Gram positive cocci Negative
by direct microscopy and cultured both before and after Sterile Geotrichum spp. Positive
trypsin treatment. The results of microscopy and culture Sterile C. albicans Positive
both before and after trypsin treatment is shown in Table 1. Sterile Geotrichum spp. Positive
The etiological agent most frequently found in cases of Gram positive cocci C. parapsilosis Positive
onychomycosis was Candida parapsilosis. Candida Sterile Sterile Negative
albicans and geotrichum Spp. were isolated in two cases, Alternaria spp. Alternaria spp. Positive
whereas T. rubrum was isolated in one case. It was found T. rubrum T. rubrum Positive
that in nine cases (36%), yeast was isolated by the trypsin Sterile C. parapsilosis Positive
treatment method, whereas the standard method of culture
C. parapsilosis C. parapsilosis Positive
did not yield any growth. In only one case, yeast was
Sterile C. parapsilosis Positive
isolated by the standard method, while the cultures were
sterile by trypsin method. Sterile Sterile Negative
C. parapsilosis C. parapsilosis Positive
Discussion C. parapsilosis C. parapsilosis Positive
Fungal infection of the nail is a chronic, extremely difficult
to treat condition, with profound social implications. Since standard culture, which yielded C. albicans.
the treatment consists of prolonged courses of antifungals,
Over the years, many modifications have been attempted to
an accurate diagnosis is of utmost importance.
increase the sensitivity of direct microscopy for diagnosis
In this study, all the samples were examined of onychomycosis. The specimen can be mounted in a
microscopically and were cultured. Part of the sample, solution of 20 to 25% KOH or NaOH mixed with 5%
treated with trypsin and part without trypsin, was glycerol and heated to emulsify lipids before examination.
processed by the standard mycological protocol. After Alternatively, 20% KOH and 36% dimethyl sulfoxide can be
clearing of the specimen by 10-20% KOH, it was directly used for clearing the specimen. However, culture is the
cultured on supplemented SDA. only method by which the causative microorganism can be
We found that of the nail samples from 25 cases of identified and the diagnosis truly confirmed.2,5,6 The
suspected onychomycosis, culture by standard methods suboptimal sensitivity of standard method of culture makes
yielded no growth in nine samples, all of which were it difficult for the clinicians to treat the patients
positive for Candida Spp. In our previous study, we had appropriately.
reported that trypsin treatment also increased the The trypsin treatment method for culture-based diagnosis
sensitivity of diagnosis of dermatophytes. 4 Further, the of onychomycosis is simple, economic and user-friendly,
results of standard culture and trypsin method were which can be performed in a busy mycology laboratory.
concordant in all cases except one, where the trypsin The present study reiterates the fact that treatment of
method failed to yield any growth as compared to the specimens with trypsin prior to culture increases the

Indian J Dermatol 2007; 52(1) 62

Xess I, et al.: Running title missing????
sensitivity of the culture technique and ultimately will help Public Health 2004;35:396-8.
in proper treatment of the patients. 5. Naka W, Hanyaku H, Tajima S, Harda T, Nishikara T.
Application of neutral red staining for evaluation of the
References viability of dermatophytes and Candida in human skin scales.
J Med Vet Mycol 1994;32:31-5.
1. Brilhante RS, Cordeiro RA, Medrano DJ, Rocha MF, Monteiro
6. Rippon JW, editor. The pathogenic fungi and pathogenic
AJ, Cavalcante CS, et al. Onychomycosis in Ceara (Northeast
actinomycetes. Medical Mycology. 3rd ed. Saunders:
Brazil): Epidemiological and laboratory aspects. Mem Inst
Philadelphia; 1998. p. 169-275.
Oswaldo Cruz 2005;100:131-5.
7. Campbell CK, Johnson EM. The dermatophytes. In: Collier L,
2. Elewski BE. Onychomycosis: Pathogenesis, diagnosis and
Balows A, Sussman, editors. Topley and Wilson’s Microbiology
management. Clin Microbiol Rev 1998;11:415-29.
and Microbial infections, Vol 4. 9th ed. Arnold: London; 1998.
3. Migdley G, Moore MK, Cookk JC, Phan QG. Mycology of p. 215-36.
nail disorders. J Am Acad Derm 1994;31:S68-74.
4. Xess I, Mathur P, Sirka CS, Banerjee U. Comparison of
trypsin treatment method and standard laboratory technique Source of Support: Nil, Conflict of Interest: None declared.
for diagnosis of dermatomycosis. Southeast Asian J Trop Med

63 Indian J Dermatol 2007; 52(1)

Correspondence Column

MUCINOUS NAEVUS: AN UNUSUAL similar to that seen in our case over the chest. The term
mucinous naevus was proposed because of its naevoid
PRESENTATION appearance and characteristic pattern of mucin deposits in
the papillary dermis.
Rashmi Kumari, Devinder Mohan Thappa,
S Jayanthi* Cutaneous mucinosis (CM) can be divided into two
groups: distinctive (primary) CM in which the mucin
Indian J Dermatol 2007:52(1):??
deposition is the main histologic feature, resulting in
clinically distinctive lesions; and secondary cutaneous
Dr. Devinder Mohan Thappa, Department of Dermatology and mucinosis, in which histologic mucin deposition is only an
STD, JIPMER, Pondicherry - 605 006, India. additional histological feature. The primary CM are sub-
grouped into degenerative-inflammatory (diffuse) and
neoplastic-hamartomatous (focal) mucinoses.2
A 23-year-old man presented with multiple firm papules Mucinous naevus is recently thought to be a variant of
over his chest extending onto both his shoulders since either connective tissue naevus of proteoglycan type or
childhood. There was no significant personal or family primary distinctive cutaneous mucinosis of the
history. On examination, multiple, discrete, firm follicular as hamartomatous/ focal type.3 The lesions usually develop at
well as non-follicular shiny papules were seen mainly over birth1 or in early adulthood4,5 and the lower part of the
the anterior chest and extending onto both the shoulders trunk is the most commonly affected site. Brakman et al
(Fig. 1). Underlying skin was not thickened or hide bound. and Rongioletti and Rebora reported two adult cases of
Also seen was a 4 cm horizontal keloid over the sternum. linear mucinous nevus on the back, showing a zosteriform
No other physical or systemic abnormality was detected. pattern.4,5
Routine laboratory investigations were normal and there
was no evidence of paraproteinemia. The histopathology in all cases designated as mucinous
nevus includes a papillary dermal mucin deposit with or
On histopathological examination of representative papule, without elongated rete ridges in a band like fashion. The
epidermis was acanthotic with thin, elongated rete ridges origin of the mucin deposited in the lesion remains
and mild hyperkeratosis. In the papillary dermis, mucin unclear, but it seems to be the result of a primary
deposition was seen around a hair follicle without any metabolic process (overproduction) rather than of a
fibroblastic proliferation (Fig. 2). On special staining, mucin secondary catabolic process.6 This idea is supported by
deposition was seen in the papillary dermis. the fact that in all reported cases the lesions developed
Mucinous naevus was first described by Redondo Bellon early in life, even at birth, without evidence of trauma or
et al1 in 1993, who demonstrated a congenital plaque like a pre-existing pathological change at the site of the
lesion in the interscapular area in a 16-year-old female very lesions.

Fig. 1: Multiple, discrete, firm, shiny papules seen over the anterior Fig. 2: Photomicrograph demonstrating mucin deposition around a
chest hair follicle without any fibroblastic proliferation (Hematoxylin and
Eosin, x100)

Indian J Dermatol 2007; 52(1) 64


There are, to our knowledge, six cases identified as URTICARIA: A NOVEL ENTITY
mucinous nevus in the English language literature,6-10
although some cases of cutaneous mucinosis of infancy WITH ISOFLAVONES
(CMI) reported earlier might be identical to mucinous
nevus1 and hence were considered a differential diagnosis Ashima Goel, Davinder Parsad
in our case.
Indian J Dermatol 2007:52(1):??
Cutaneous mucinosis of infancy (CMI) is a rare condition
that is categorized as a degenerative-inflammatory Dr. Ashima Goel, PO Box 1514, PGIMER, Chandigarh - 160 012
mucinosis (diffuse). The lesions of CMI are either India. E-mail:
symmetrical or grouped small papules of congenital or
infantile onset on the upper extremities or the trunk.10,11
Soybeans are a natural dietary source of isoflavones,
Histology shows a focal, well-circumscribed deposit of
which have estrogen-like properties.1 The phytoestrogens,
mucin in the papillary dermis without fibroblast
include certain isoflavonoids, flavonoids, stilbenes and
proliferation.3 The lesions tend to be progressive unlike
lignans. Their perceived health beneficial properties extend
mucinous nevus. Another differential diagnosis is
beyond hormone-dependent breast and prostate cancers
cutaneous focal mucinosis, is a solitary papule or nodule
and osteoporosis to include cognitive function,
with a marked proliferation of mucoblasts, eventually
cardiovascular disease, immunity and inflammation and
replacing most of the collagen.3
reproduction and fertility.2-4
This case is being reported for its rarity. Naevus with such
To the best of our knowledge, this is the first case report
widespread involvement over the anterior chest and
of isoflavones induced urticaria. A 48-year-old woman
shoulders has not been previously described. The mucin
presented in outpatients of our urticaria clinic with the
deposition in the papillary dermis surrounding a hair follicle
chief complaints of widespread itchy wheals of variable
was confirmative of the diagnosis.
morphology all over the body after ingestion of
References isoflavones (available as Isoflav CR capsules; Raptakos
Vrett and Company Ltd., India) prescribed for the
1. Redondo Bellon P, Vazquez-Doval J, Idoate M, Quintanilla postmenopausal symptoms by her gynecologist. According
E. Mucinous nevus. J Am Acad Dermatol 1993;28:797-8.
to the patient, she developed intensely itchy wheals all
2. Uitto J, Santa Cruz DJ, Eisen AZ. Connective tissue nevi of over the body after one day of intake of her prescribed
the skin. Clinical, genetic, and histopathologic classification
of hamartomas of the collagen, elastin, and proteoglycan medication. There was no history of associated fever, joint
type. J Am Acad Dermatol 1980;3:441-61. pains, eyelid / lip swelling, respiratory distress or any other
3. Rongioletti F, Rebora A. Cutaneous mucinoses: Microscopic constitutional symptom. There was no history of diabetes,
criteria for diagnosis. Am J Dermatopathol 2001;23:257- hypertension or any other medication prior to the onset of
67. rash. She was non-atopic without any history of perennial
4. Suhr KB, Ro YW, Kim KH, Lee JH, Song KY, Park JK. rhinitis, asthma and house-dust mite hypersensitivity. The
Mucinous nevus: Report of two cases and review of the diagnosis of drug-induced urticaria was made and was
literature. J Am Acad Dermatol 1997;37:312-3. advised to stop isoflavones. She was prescribed
5. Brakman M, Starink TM, Tafelkruyer J, Bos JD. Linear hydroxizine 10 mg tid. Drug discontinuation was followed
connective tissue naevus of the proteoglycan type (naevus by complete resolution of the skin eruption. Rechallenge
mucinosis). Br J Dermatol 1994;131:368-70. with isoflavones itself resulted in similar urticarial lesions.
6. Rongioletti F, Rebora A. Mucinous nevus. Arch Dermatol Dye in the capsules as a possible candidate for drug-
1996;132:1522-3. induced urticaria was excluded as rechallenge was
7. DePadova-Elder S, Mols-Kowalczewski BL, Lambert WC. performed with isoflavones in the tablet form which
Multiple connective tissue nevi. Cutis 1988;42:222-4. resulted in reappearance of urticarial lesions.
8. Brakman M, Starink TH, Tafelkruyer J, Bos JD. Linear
connective tissue naevus of the proteoglycan type (naevus This communication intends to convey that physician as
mucinosus). Br J Dermatol 1994;131:368-70. well as gynecologists should be aware of this adverse
9. Kozminsky ME, Bronson DM, Barsky S. Zosteriform effect of isoflavones while prescribing it to
connective-tissue nevus. Cutis 1985;36:77-8. postmenopausal women so as to facilitate early diagnosis
10. McGrae JD Jr. Cutaneous mucinosis of infancy: A congenital of isoflavones induced urticaria.
and linear variant. Arch Dermatol 1983;119:272-3.
11. Stokes KS, Rabinowitz LG, Segura AD, Esterly NB.
Cutaneous mucinosis of infancy. Pediatr Dermatol 1. Messina MJ. Soy foods and soybean isoflavones and
1994;11:246-51. menopausal health. Nutr Clin Care 2002;5:272-82.

65 Indian J Dermatol 2007; 52(1)


2. Dixon RA. Phytoestrogens. Annu Rev Plant Biol
3. Sarkar FH, Li Y. The role of isoflavones in cancer
chemoprevention. Front Biosci 2004;9:2714-24.
4. Du N, Xu Y. Medical value of isoflavones. Zhong Xi Yi Jie He
Xue Bao 2003;1:296-300.

K N Shivaswamy, Aravind Babu,
Devinder Mohan Thappa
Fig. 1: Multiple horizontal skin coloured to yellowish, slightly raised,
transverse streaky bands over the back
Indian J Dermatol 2007:52(1):??
Dr. Devinder Mohan Thappa, Department of Dermatology and
STD, JIPMER, Pondicherry - 605 006, India.

A 16-year-old male came to our dermatology OPD with
asymptomatic skin lesions over back of one year duration.
The lesions started as small horizontal streaky lines over
lower back to begin with and spread to involve mid back figs missing??
also. There was no history of sudden weight gain, steroid
or hormonal therapy or exercise. He had no history of
similar disorder in the family members and similar lesions
elsewhere in the body including shoulder or pelvic girdle.
On physical examination, there were multiple horizontal skin
coloured to yellowish, slightly raised, transverse streaky
bands of varying length from 2 cm to more than 10 cm Fig. 2: Photomicrograph demonstrating thin, wavy, elongated as well
spread across the midline over mid and lower back (Fig. 1). as fragmented and clumped elastic fibers in the dermis (Verhoeff-van
Gieson stain, x100)
With the above clinical findings, a diagnosis of linear focal
elastosis was made. been described in lesions of LFE. Currently, degeneration
Histopathological examination from one of the transverse and regeneration of elastic fiber is thought to be a possible
streaks from the lower back revealed increased elastic pathomechanism.4
fibers in the dermis. These elastic fibers were thin, wavy, Clinically, these lesions are characterized by skin coloured
elongated as well as fragmented and clumped (Fig. 2). to yellowish slightly palpable transverse streaks, spread
These histological findings were consistent with our across the midline over mid and lower back. These lesions
clinical diagnosis of linear focal elastosis. have to be differentiated from striae distensae. The striae
Linear focal elastosis (LFE) also called elastotic striae is distensae are depressed rather than elevated and are pink
relatively a rare disorder characterized by asymptomatic or white in colour and are usually associated with history
palpable skin coloured to yellowish transverse streak like of sudden weight gain, hormonal or steroid application or
yellowish lines seen usually over mid and lower black.1 exercise. They are usually located over the abdomen,
Burket el al2 was the first to describe this condition in thighs, arms or breast. Histology of striae shows altered
three elderly men. Later many reports of linear focal collagen bundles without any changes in elastic tissue.1,2,5
elastosis have been described in both young men and In contrast, there is increased number of elastic fibers in
women, including a case of linear focal elastosis in a 13- the dermis in lineal focal elastosis. These fibers are thin,
year-old girl over the legs by Brier et al.3 elongated, wavy, fragmented and clumped. Electron
microscopy reveals elongated, irregularly-shaped swollen
The exact pathogenesis of this condition is still unclear, elastic fibers with degenerative changes.2,6 Other
both degeneration and elastogenesis or regeneration has histological differential diagnoses include pseudoxanthoma

Indian J Dermatol 2007; 52(1) 66


elasticum, where stain for calcium such as von Kossa is
positive and solar elastotic bands, where there will be a
nodular aggregation of elastotic material in the upper
dermis that are divided by cleft-like spaces.2

1. Odom RB, James WD, Berger TG. Andrew’s diseases of the
skin, 9th ed. WB Saunders: Philadelphia; 2000. p. 636-47.
2. Burket JM, Zelickson AS. Padilla RS. Linear focal elastosis
(elastotic striae). J Am Acad Dermatol 1989;20:633-6.
3. Breier F, Trautinger, Jurecka W. Honigsmann H. Linear focal
elastosis (elastotic striae): Increased number of elastic fibres
determined by a video measuring system. Br J Dermatol
4. Choi SW, Lee JH, Woo HJ, Park CJ, Yi JY, Song KY, et al.
Two cases of linear focal elastosis: Different histopathologic
findings. Int J Dermatol 2000;39:207-9. Fig. 1:Legend Missing????
5. Tamada Y, Yokochi K, Ikeya T, Nakagomi Y, Miyake T, Hara
K. Linear focal elastosis: A review of 3 cases in young
Japanese men. J Am Acad Dermatol 1997;36:301-3.
6. Vogel PS, Cardenas A, Rose EV, Cobb MW, Sau P, James WD.
Linear focal elastosis. Arch Dermatol 1995;131:855-6.

Surajit Nayak, Basanti Acharjya,
Basanti Devi, Gitanjali Sethi*

Indian J Dermatol 2007:52(1): *Dept missing???***
Surajit Nayak, Dept of Skin and VD, MKCG Medical College,
Berhampur - 760 010, Orissa, India. Fig. 2:Legend Missing????

lower limb first, as a few small papules, which gradually
Lichen striatus is a self-limited linear dermatosis of proceeded proximally and coalesced to form a linear band
unknown origin, most commonly seen in children between in due course of time.
5-15 years of age. There is a female preporendence with a
ratio of 2:1. We report a case of a 10-month-old female On examination, the baby was found to be otherwise
child, who presented with lichen striatus distributed along healthy child. The lesions showed no umbilication or
lines of Blaschko forming a peculiar pattern as multiple Wicham’s striae. Nail and hair were normal on examination.
parallel bands like branches of a tree. Her investigation revealed a normal hematological and
biochemical profile. A biopsy was done, which showed
The 10-month-old child was brought with complaints of hyperkeratosis, focal parakeratosis, with lymphocytic
linear, dull-colored, slightly scaly band extending across exocytosis. In dermis there is superficial and deep
left lower limb, along anterior trunk in median line then perivascular infiltration of lymphocytes and histiocytes,
traversing left upper limb in median aspect (Fig. 1). Three few necrotic keratinocytes were observed.
parallel bands of similar morphology were found extending Histopathological study was consistent with lichen
from linear band in trunk in a horizontal manner. So also striatus. Parents were explained about the benign nature of
few linear bands were seen running parallel to the linear the disease and about its self-regressing nature.
band on the arm on its either side (Fig. 2). The bands were
around 3 cm wide and were almost continuous and Though lichen stritus is a disease of childhood, it can
consisted of small papules closely placed. As per the occur rarely in both infants and adults, with a female
history given by parents it started two months back in predominance. Etiology is unknown, but report of its

67 Indian J Dermatol 2007; 52(1)


occurrence in sibling, topic individuals, in spring and reported to be effective. Lichen stritus is a T-cell-mediated
summer support genetic, infectious and environmental inflammatory disease and tacrolimus ointment may be an
factors.1-3 effective alternative treatment for this disease. The patient
was discharged with advice to use topical tacrolimus as
In lichen stritus, an acquired event such as, viral infection
reported to be effective by few authors.10,11
may allow an aberrant clone of cutaneous cells to express a
new antigen, resulting in the phenotypic skin changes.4 References
Though asymptomatic, few may experience mild pruritus. 1. Kennedy D, Rogers M. Lichen stritus. Pediatr Dermatol
Nail involvement may be observed in few patients as 1996;13:95-9.
ridging, splitting, onycholysis or nail loss.5,6 Though 2. Di Lernia V, Ricci G, Bonci A, Patrizi A. Lichen striatus and
commonly on one arm or leg or on the neck, but may atopy. Int J Dermatol 1991;30:453-4.
develop on the trunk. Though in abdomen, buttock, thigh 3. Patrizi A, Neri I, Fiorentini C, Chieregato C, Bonci A.
lesion is commonly seen as single extensive linear lesion, it Simultaneous occurrence of Lichen striatus in siblings. Pediatr
may present as bilateral or parallel lesions, as seen in our Dermatol 1997;14:293-5.
case. Bilateral involvement though very exceptional, has 4. June K, Wingfield, Rehmus, Nelly R, Amal M, et al. E-
been reported.7,8 medicine. [Last accessed on 2005 Feb 23].
5. Baran R, Dupre A, Lauret P. Le Lichen striatus
Usually it progresses over a few weeks and then remains onychodystrophique. Ann Dermatol Venereol 1999;126:885-
stable for few months, but eventually regresses by one 91.
year with some residual hypo pigmentation. Nail 6. Kaufman JP. Lichen striatus with nail involvement. Cutis
involvement also regresses spontaneously. 1974;14:232-4.
7. Aloi F, Solaroli C, Pippione M. Diffuse and bilateral Lichen
Histopathological study is not diagnostic but very useful
striatus. Pediatr Dermatol 1997;14:36-8.
for excluding other conditions like nevus unius lateralis
8. Kurokawa M, Kikuchi H, Ogata K, Setoyama M. Bilateral
and linear lichen planus, as they closely resemble lichen lichen striatus. J Dermatol 2004;31:129-32.
stritus. Its diagnosis is basically made on history and
9. Rahbari H, Cordero AA, Mehergan AH. Linear porokeratosis.
physical examination. In differential diagnosis come linear A distinctive clinical variant of porokeratosis of Mibelli. Arch
lichen planus, porokeratosis, lichen nitidus and ILVEN. In Dermatol 1974;109:526-8.
ILVEN, clinical features appear at birth or early infancy but 10. Fujimoto N, Tajima S, Ishibashi A. Facial lichen stritus:
do not regress spontaneously. Linear porokeratosis is also Sucessful treatment with tacrolimus ointment. Br J Dermatol
need to be differentiated.9 Our case presents a very 2003;148:587-90.
interesting case of lichen stritus with a rare presentation of 11. Sorgentini C, Allevato MA, Dahbar M, Cabrera H. Lichen
parallel bands like branches of a tree. striatus in an adult: Sucessful treatment with tacrolimus. Br J
Dermatol 2004;150:776-7.
The patient was advised topical tacrolimus ointment, as

Indian J Dermatol 2007; 52(1) 68