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Indian J Dermatol 2007; 52(1)53

CMYK 53

From the Department of Dermatology, STD and Leprosy and

Department of Biochemistry, Govt. Medical College, Srinagar,India. Address correspondence to: Dr. Taseer Ahmed Bhatt, R/

O:-Shabeer Manzil, Rajbagh Extension, Srinagar, Kashmir -

190 008 (J and K), India. E-mail: [email protected]

Case Report

PROLIDASE DEFICIENCY

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

Abstract

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

IntroductionProlidase deficiency is a rare disorder inherited through an

autosomal recessive gene. The hallmark of this disorder is

the presence of characteristic face with saddle nose, mental

retardation and chronic recurrent cutaneous ulcers that are

recalcitrant in healing. The ulcers result from impaired

recycling of proline which constitute 20% of aminoacid in

collagen and is important for tissue repair.1 Others features

that are seen include frequent infections, partial deafness,

visual disturbances and joint dislocation.

Case ReportA seven-year-old female child born of a full term normal

delivery to 2nd degree consanguineous parentage presented

to our outpatient department with the history of recurrent

painful ulceration of the lower legs of 18 months duration.

It used to begin as a pruritic pustular lesions on the lower

legs, followed later by ulcer formation. The ulcers used to

persist for many months with no consistent response to

antibiotics and used to heal with atrophic scarring. Other

features seen in the patient were mental retardation, failure

to thrive and recurrent ear discharge from the last four

years. There was no clinical evidence suggestive ofHansens disease, collagen vascular disorders or of

hemolytic anemia. One of her younger siblings had similar

episodes of ulcerations of lower legs followed by scarring.

On physical examination, she was 110 cm in height and

weighed only 17 kgs, which was below the 3rd percentile

for her age. She had atypical facies with saddle nose,

hyperteleorism, high arched palate, malaligned teeth, with

multiple atrophic macules and linear teleangectasias on themalar area of the face (Fig. 1). The most striking feature

was extensive deep ulcers on the lower legs with atrophic

scars in the surrounding skin. The ulcers were deep with

ragged margins and floor of the ulcer was covered by

yellowish crust (Figs. 2 and 3). The ulcer was not fixed to

the underlying tissues. The inguinal lymph nodes were not

significantly enlarged. There were multiple hyperpigmented

small atrophic macules on the extensor portions of the

extremities and on the hips. Mat-like telangectasia were

seen on the knees and lower legs. There was no evidence

of varicosities and peripheral pulses were normal.The systemic examination revealed no abnormal findings

except for a mild splenomegaly. Her ophthalomological

examination was normal.

Her routine laboratory investigation, collagen vascular

profile and porphyrin profile were all normal. The

histopathological examination of the skin showed

nonspecific inflammatory changes and the direct

immunoflourescence was negative. The culture of the ulcer

did not show any microbial growth. Thin layer

chromatography of her overnight urine revealed a marked

increase in diimminopeptides after gelatin loading

indicating the possibility of prolidase enzyme deficiency

(Fig. 4). Her younger sibling was also investigated with

identical findings on thin layer chromatography. Prolidase

enzyme activity was assayed colorimetrically using the

substrate glycylproline and chinnard reaction.2 It was

found to be only 12% and 28% in the patient and her

younger sibling respectively in comparison to the normal

healthy controls.

Discussion

Prolidase deficiency is a rare metabolic disorder of

autosomal recessive inheritance. Goodman in 1968 was the

first to describe this condition in a male patient who had

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Indian J Dermatol 2007; 52(1) 54

54 CMYK

mental subnormality and characteristic recalcitrant ulcers

on the lower legs.3 The enzyme prolidase is widely

distributed throughout the body and is important in

recycling of proline and hydroxyproline which constitute

about one quarter of the collagen.1 The deficiency of this

enzyme is responsible for massive loss of proline in the

urine which is estimated to be as high as 3 gm per day. 4

The prolidase enzyme can be assayed in the erythrocytes,

leucocytes and the fibroblasts and have been found to be

undetectable in the patients with prolidase enzyme

deficiency.

These patients are mentally subnormal and are of short

stature. They have peculiar facies such as saddle nose,

hypertelorism, narrowed eyes and hypoplasia of the jaws.5

Among the clinical presentation, the most striking

manifestation is the skin fragility with leg ulceration and

characteristic pitted scarring. The other cutaneous changes

seen include photosensitivity, purpura, telengectasia, dry

crusted lesions on the face and buttocks; dry fissured

erythematous palms and soles.6 They also suffer from

recurrent infections such as otitis media, respiratory tract

infections and sinusitis. In addition, other features reported

are simian crease, wasting of the small muscles of hand,

talipes equines, osteoporosis, hyperextensibility of joints,

deafness, corneal opacities, ambylopia, optic atrophic,

splenomegaly and protuberant abdomen.6 The diagnosis is

ascertained by iminopeptiduria greater than 5 mmol/24h.

The predominant peptide is glyclproline. A characteristic

feature of the disorder is absolute resistance to all forms of

treatment including rejection of skin grafts. The treatment

modalities which seemed to be helpful include dapsone,

diphenylhydantion, ascorbic acid and manganese.7 The

topical application of ointment containing 5% glycine and

5% proline was found to be effective in number of trials.8

Enzyme replacement has been tried by blood transfusion

containing manganese activated prolidase enzyme.9 Pulsed

corticosteroid treatment also showed good results and act

by inhibiting iminodipeptide primed neutrophil superoxide

Masood Q, et al.: Prolidase deficiency

Figure 1:

Figure 2:

Figure 3:

Figure 4:

Fig and legend missing???

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

Fig and legend missing???

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CMYK 55

Source of Support: Nil, Conflict of Interest: None declared.

generation.10 Therapeutic apheresis exchange was

successful in two patients.11

References

1. Jackson SH, Dennis AW, Greenberg M. Iminopeptiduria: A

genetic defect in recycling collagen: A method for determining

prolidase in erythrocytes. Can Med Assoc J 1975;113:759-63.

2. Ganpathy V, Pashley SJ, Roesel RA, Pashley DH, Leibach FH.Inhibition of rat and human prolidases by captopril. Biochem

Pharmacol 1985;34:1287-91.

3. Goodman SI, Soloman CC, Muschenheim F, McIntyre CA,

Miles B, OBrien D. A syndrome resembling lathyrism

associated with iminopeptiduria. Am J Med 1968;45:152-9.

4. Scriver CR, Smith RJ, Phang JM. Disorders of proline and

hydroxyproline metabolism. In: The metabolic basis of

inherited disease. Stanbury JB, Wyngaarden JB, Fredrickson

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

1979;115:62-7.

6. Milligan A, Graham-Brown RA, Burns DA, Anderson L.

Prolidase deficiency: A case report and literature review. Br J

Dermatol 1989;121:405-9.

7. Jemec GB, Moe AT. Topical treatment of skin ulcers in

prolidase deficiency. Peadiatr Dermatol 1996;13:58-60.

8. Arata J, Hatakenaka K, Oono T. Effect of topical application

of glycine and proline on recalcitrant leg ulcers of prolidase

deficiency. Arch Dermatol 1986;122:626-7.

9. Hechtman P, Richter A, Corman N, Leong YM. In situ

activation of human erythrocyte prolidase. Potential forenzyme replacement therapy. Pediatr Res 1988;24:709-12.

10. Yasuda K, Ogata K, Kodama H, Kodama H, Zhang J, Sugahara

K, et al. Corticosteroid treatment of prolidase deficiency skin

lesions by inhibiting iminopeptide-primed neutrophil

superoxide generation. Br J Dermatol 1999;141:846-51.

11. Lupi A, Casado B, Soli M, Bertazzoni M, Annovazzi L, Viglio

S, et al. Therpeutic apheresis exchangein two patients with

prolidase deficiency. Br J Dermatol 2002;147:1237-40.

Masood Q, et al.: Prolidase deficiency

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56 CMYK

From the Ondokuz Mayis University, School of Medicine,

Department of Dermatology and Pathology, Samsun, Turkey.Address correspondence to: Dr. Fatma Aydin, Ondokuz Mayis

University School of Medicine, Department of Dermatology,

TR-55139 Kurupelit, Samsun, Turkey. E-mail:

missing???***

Case Report

SYSTEMIC LUPUS ERYTHEMATOSUS WITH AN ERYTHEMA

MULTIFORME-LIKE LESIONS

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

Abstract

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 Rowells 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, Rowells syndrome, systemic lupus erythematosus


Introduction

Patients with discoid lupus erythematosus (DLE) and

systemic LE (SLE) may develop coincidental erythema

multiforme (EM).1,2 The presence of EM-like lesions in

lupus patients and a characteristic pattern of immunological

abnormalities have been defined as Rowells syndrome

(RS).1

We report a case of SLE with EM-like lesions whoseclinical picture is consistent with this rare syndrome.

Case Report

A 29-year-old woman was admitted to our dermatology

department with erythematous rash on the face, trunk,

upper and lower extremities for one week duration. She had

been diagnosed as having SLE on the basis of the

American Rheumatism Association (ARA) criteria, with

features of oral ulcers, arthritis, immunologic (positive anti-

nuclear antibody in speckled pattern, anti-ds DNA, anti-

Sm), hematologic (anemia, lymphopenia andthrombocytopenia) and renal disorders, six weeks ago. She

had been using hydroxychloroquine (200 mg) and

methylprednisolone (40 mg/d) since than. She did not have

a history of perniosis. She did not also have a history of

upper respiratory tract and herpes virus infection or any

infection associated with fever as well as sunlight

exposure. She did not take any medication except

prescribed ones for SLE.

On dermatological examination, she had dusky red patches

on the face, neck and trunk. There were numerous target-

like lesions on the trunk and extremities, which were

coalesced into a polycyclic pattern (Fig. 1 a, b). The patient

was hospitalised and hydroxychloroquine was

discontinued due to possibility of drug eruption since she

had been using this medication for six weeks.

Four milimeters punch biopsy was taken for both light

microscopy and direct immunofluorescence examination.

Histopathologic examination revealed epidermal necrosis,

dermal edema and a perivascular and interstitial

mononuclear infiltrate (Figs. 2, 3). Direct

immunofluorescence (DIF) examination was negative.

Erythrocyte sedimentation rate, complete blood cell count,

liver and renal function tests were within normal limits.

Proteinuria was detected with urine analysis (2.5 g in 24h).

Autoimmune screening demonstrated the presence of ANA

in speckled pattern (1:40 dilution). Anti-Ro antibody was

negative and rheumatoid factor was positive. Serum

antibodies to herpes simplex virus, serology for HIV and

syphilis were all negative. Dose of prednisolone was

increased to 80 mg daily. Clinical improvement was

observed after one week of hospitalisation. During 11-

month follow-up period, no recurrence was observed.

Discussion

RS has been described with all subtypes of LE (systemic,

acute, subacute or discoid).1-3 All forms of EM (EM minor,

EM major) and toxic epidermal necrolysis can also beassociated with RS.3-5 Although the proper classification of

EM-like lesions occurring in RS is not clear, these lesions

may represent a severe variant of acute cutaneous lupus

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CMYK 57

or, in some cases, subacute cutaneous lupus. Polycyclic

lesions of subacute cutaneous LE may resemble lesions of

EM, but direct immunofluorescence generally distinguishes

these lesions as those of LE. The fact that the DIF was

negative does not exclude a diagnosis of LE as this test is

not always positive and its results might well be dependent

on the age of the lesion. Gilliam had demonstrated that

early and late lesions of LE often do not demonstrate the

characteristic IF findings.6

Diagnostic serological abnormalities for RS include speckled

pattern of ANA, anti-Ro antibody or anti-La antibody and

positive rheumatoid factor (RF). Zeitouni et al2 reported that

the speckled pattern of ANA is the most consistent diagnostic

feature of this syndrome, but anti Ro/La antibodies and

rheumatoid factor seem to be less consistent features. These

serological findings described within Rowells syndrome may

also be associated with the underlying disease, as in our case.

Among the reported cases of RS, patterns of ANA at the time

of diagnosis of SLE, has not been clearly documented.However, ANA in speckled pattern; anti-Ro and anti-La

antibodies are seen in SLE with the frequency of 26%, 25%

and 10-15%, respectively.7 It is also proposed that, different

ANA patterns have little specify and are of little value in the

management of patients.8 In addition, anti Ro/La antibodies

contribute to the formation of the speckled pattern of ANA,

thus, the coexistence of these antibodies would be expected.9

Until now limited numbers of cases have been reported and

they had different clinical and serological features.1-5

Recent evidence indicates that dysregulated apoptosis may

underlie both many of the major manifestations of LE and

EM skin lesions. Viral infections were considered as

triggering factors for both for SLE and EM. James et al10

have noted the possible contribution of EBV to the

development of SLE. Unidentified HSV, EBV or other viral

infections may cross-react with lupus autoantigens and

they can initiate the immunologic response, hence

triggering the EM like lesions in SLE. Similar

immunopathogenetic mechanisms described in both

diseases may be responsible for the concurrence of these

two diseases.

In our patient, after an extensive research, no procative

factor triggering EM was found. The only suspicious factor

Fig. 2: Vacuolar degeneration and necrotic keratinocytes in basal layer

(H and E, x400)

Fig. 3: Panoromic view of the lesion (H and E, x100)

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

Fig. 1: (a) Erythematous maculopopular target-shaped lesions on the

arms and (b) hands

b

a

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58 CMYK

could be hydroxychloroquine. It is believed that EM is

rarely drug-induced, in contrast to SJS. Most of the cases

reported as drug-induced EM are either SJS or

erythematous drug eruptions.11 Although, occurrence of

SJS has been reported with hydroxychloroquine, there have

been few reports of EM related to hydroxychloroquine for

years.12 Drug eruption was excluded because EM is rarely

drug-induced and while that is true in large population-based studies, EM like lesions might well resemble a

morbilliform eruption, which in fact is what we think the

clinical photo represents.

Since the first description, Rowells original criteria were

not well-preserved and the diagnosis of RS has not been

cleared yet. We believe that the new diagnostic criteria,

which were suggested by Zeitouni et al, might be

improved by the addition of new cases to the literature.

References

1. Rowell NR, Beck JS, Anderson JR. Lupus erythematosus anderythema multiforme-like lesions. A syndrome with

characteristic immunological abnormalities. Arch Dermatol

1963;88:176-80.

2. Zeitouni NC, Funaro D, Cloutier RA, Gagne E, Claveau J.

Redefining Rowells syndrome. Br J Dermatol 2000;142:343-6.

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

erythematosus with antiphospholipid syndrome and erythema

multiforme-like lesions. Br J Dermatol 1999;141:720-4.

5. Mandelcorn R, Shear NH. Lupus-associated toxic epidermal

necrolysis: A novel manifestation of lupus. J Am Acad

Dermatol 2003;48:525-9.

6. Gilliam JN, Sontheimer RD. Skin manifestations of SLE. Clin

Rheum Dis 1982;8:207-18.

7. Odom RB, James WD, Berger TG. Andrews diseases of the

skin clinical dermatology. WB Saunders Company:

Pennsylvania; 2000.

8. Jacobe HT, Sontheimer RD. Autoantibodies encountered in

patients with autoimmune connective tissue diseases. In:

Bolognia JL, Jorizzo JL, Rapini RP, et al, editors.

Dermatology. 1st ed. Mosby: Spain; 2003. p. 589-623.

9. Maddison PJ, Reichlin M. Quantitation of precipitating

antibodies to certain soluble nuclear antigens in SLE. Arthiritis

Rheum 1977;20:819-24.

10. James JA, Kaufman KM, Farris AD, Taylor-Albert E, Lehman

TJ, Harley JB. An increased prevalence of Ebstein-Barr virus

infection in young patients suggests a possible etiology for

systemic lupus erythematosus. J Clin Invest 1997;100:3019-

26.11. Roujeau JC. Clinical heterogeneity of drug hypersensitivity.

Toxicology 2005;209:123-9.

12. Leckie MJ, Rees RG. Stevens-Johnson syndrome in association

with hydroxychloroquine treatment for rheumatoid arthritis.

Rheumatology 2002;41:473-4.


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

ERRATUM

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

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CMYK 59

From the NMC SP. Hospital, AL Nahada, Dubai United ArabEmirates. Address correspondence to: Sanjay Saraf, NMC SP.

Hospital, AL Nahada, Dubai United Arab Emirates.

E-mail: [email protected]

Case Report

SEBACEOUS HORN: AN INTERESTING CASE

Sanjay Saraf

Abstract

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


Introduction

Cutaneous horn (cornu cutaneum) is a relativelyuncommon 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

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 historyof 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.

Discussion

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

with centrally positioned bone. No such well-formed bone

is observed in the human horns. The earliest well-documented case of cornu cutaneum from London in 1588

Fig. 1: legend Missing???

Fig. 1: legend Missing???

AU : Figures not cited in text

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60 CMYK

is of Mrs. Margaret Gryffith, an elderly Welsh woman.

However, earliest observations on cutaneous horns in

humans were described by the Everard Home in 1791.3

Farris from Italy first described the well-documented case

report with adequate histology of gigantic horn in a man.4

These horns may arise from a variety of benign,

premalignant or malignant epidermal lesions. Most

commonly, they are single and arise from a seborrheickeratosis lesion.5 According to a largest study by Yu et al,2

61% of cutaneous horns were derived from benign lesions

and 39% were derived from malignant or premalignant

epidermal lesions. Two other larger studies on cutaneous

horn also showed that 23-37% of horns were associated

with actinic keratosis or Bowens disease and another 16-

20% with malignant lesions.2,6 The important consideration

in these cases is not the horn, but the underlying

pathology which may be benign (seborrheic keratosis, viral

warts, histiocytoma, inverted follicular keratosis, verrucous

epidermal nevus, molluscum contogiosum, etc.),

premalignant (solar keratosis, arsenical keratosis, Bowens

disease) or malignant (squamous cell carcinoma, rarely,

basal cell carcinoma, metastatic renal carcinoma, granular

cell tumor, sebaceous carcinoma or Kaposis sarcoma.7

Histopathological examination, specially of the base of the

lesion1,8.9 is necessary to rule out associated malignancy

and full excision and reconstruction is the treatment of

choice.

The cutaneous horns are predominantly benign lesions;

however possibility of malignant potential should always

be kept in mind.

References

1. Korkut T, Tan NB, Oztan Y. Giant cutaneous horn: A patient

report. Ann Plast Surg 1997;39:654-5.

2. Yu RC, Pryce DW, Macfarlane AW, Stewart TW. A

histopathological study of 643 cutaneous horns. Br J Dermatol1991;124:449-52.

3. Bondeson J. Everard Home, John Hunter and Cutaneous horns:

A historical review. Am J Dermatopathol 2001;23:362-9.

4. Farris G. Histological considerations on a case of a voluminous

cutaneous horn. Minerva Dermatol 1953;28:159-65.

5. Thappa DM, Laxmisha C. Cutaneous horn of eyelid. Indian

Pediatr 2004;41:195.

6. Schosser RH, Hodge SJ, Gaba CR, Owen LG. Cutaneous horns:

A histopathologic study. South Med J 1979;72:1129-31.

7. Copcu E, Sivrioglu N, Culhaci N. Cutaneous horns: Are these

lesions as innocent as they seem to be? World J Surg Oncol

2004;2:18.8. Gould JW, Brodell RT. Giant cutaneous horn associated with

verruca vulgaris. Cutis 1999;64:111-2.

9. Kastanioudakis I, Skevas A, Assimakopoulos D, Daneilidis B.

Cutaneous horn of the article. Otolaryngol Head Neck Surg

1998;118:735.


Saraf S: Sebaceous horn

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CMYK 61

From the Departments of Microbiology and *Laboratory

Medicine, All India Institute of Medical Sciences, New Delhi,India. Address correspondence to: Dr. Immaculata Xess,

Department of Microbiology, All India Institute of Medical

Sciences, New Delhi, India. E-mail: [email protected]

Dermato-Microbiology Round

DIAGNOSIS OF ONYCHOMYCOSIS BY TRYPSIN TREATMENT METHOD

Immaculata Xess, Deepti Dubey, Mathur Purva*

Abstract

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


Onychomycosis, defined as fungal infection of nail affects

approximately 5% of the population worldwide and

represents around 30% of all superficial mycotic infection

and 50% of nail disorders.1 The infection has profound

social consequences for the affected patients, who often

have diminished confidence or self esteem and experience

embarrassment in social and work situations.

Onychomycosis in immunocompromised patients, such as

those infected with human immunodeficiency virus (HIV),can pose a more serious health problem.2 Over the recent

years, an upsurge in cases of onychomycosis due to

nondermatophytes has been documented.2,3 Of the

nondermatophytic filamentous fungi, agents implicated in

onychomycosis include members of Scopulariopsis and

Scytalidium (the two most common genera), which are

both thought to digest keratin in vivo, as well as members

of the genera Alternaria, Aspergillus, Acremonium and

Fusarium.3 The most common yeast that is involved in

onychomycosis is C. albicans. The fact that the infection

is difficult to treat and treatment consists of prolongedcourses of potentially toxic drugs makes it imperative to

make an early and accurate diagnosis. Diagnosis of

onychomycosis depends on direct microscopy,

supplemented by culture results. Direct microscopy is often

time-consuming, because nail debris is thick and coarse

and hyphae are usually only sparsely present.2 Although

direct microscopy can provide clues about the identity of

the microorganism, careful matching of microscopic and

culture results is necessary for the clinician to be confident

of the diagnosis.2 Almost half of all specimens taken from

onychomycotic nails fail to yield a pathogen in culture. We

have previously reported a modified method for diagnosis

of dermatophytes, which is highly sensitive and specific as

compared to the conventional culture methods.4 In this

paper, we have used the same method for diagnosing

onychomycosis and document its superiority for

onychomycosis caused by Candida Spp.

Materials and Methods

The study population consisted of 25 patients, whose

clinical diagnosis was distal or lateral subungual

onychomycosis. The nail scraping from these patients were

collected from the dorsal surface and nail bed, on sterile

brown paper. All samples were processed on the day of

collection. For processing of samples, the method of Naka

et al was followed.5

A part of the scrapings were dipped in 1 ml of 2% trypsin

solution and kept at 37C for two hours. The scrapings

were then washed with phosphate buffered saline (PBS) by

centrifugation three times (1500 g X 10 min). The deposit

was suspended in 300 l PBS. 200 l of this was cultured

on Saborauds dextrose agar (SDA) supplemented with

cyclohexamide and gentamycin (0.026 mg/ml) and

cyclohexamide (0.05 mg/ml) only. 100 l was mixed with

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

Another part of sample was not treated with trypsin andprocessed by standard mycological techniques: A direct

microscopic examination was done after treating the

scraping with 20% KOH and gentle heating.6,7 The

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62 CMYK

scrapings were also cultured on SDA supplemented with

gentamycin and cyclohexamide and on SDA with

cyclohexamide.

All the culture tubes were incubated at 25C and 37C for

up to one month before declaring a negative result. The

growth obtained was identified microscopically. For

Candida speciation was done by growth characteristics on

corn meal agar and pigmentation on TTZ (2,3,5 triphenyletetrazolium chloride) agar.

Results

Nail scrapings from a total of 25 patients whose clinical

diagnosis was distal or lateral subungual onychomycosis

were studied. The study population consisted of 18 males

and seven females. The age of the patients ranged from 10-

67 years. Of these patients, three had a history of

noninsulin dependent diabetes and two had insulin

dependent diabetes. None of them were HIV positive. Two

patients had a history of receiving treatment for

onychomycosis previously. All the samples were examined

by direct microscopy and cultured both before and after

trypsin treatment. The results of microscopy and culture

both before and after trypsin treatment is shown in Table 1.

The etiological agent most frequently found in cases of

onychomycosis was Candida parapsilosis. Candida

albicans and geotrichum Spp. were isolated in two cases,

whereas T. rubrum was isolated in one case. It was found

that in nine cases (36%), yeast was isolated by the trypsin

treatment method, whereas the standard method of culture

did not yield any growth. In only one case, yeast was

isolated by the standard method, while the cultures were

sterile by trypsin method.

Discussion

Fungal infection of the nail is a chronic, extremely difficult

to treat condition, with profound social implications. Since

the treatment consists of prolonged courses of antifungals,

an accurate diagnosis is of utmost importance.

In this study, all the samples were examined

microscopically and were cultured. Part of the sample,treated with trypsin and part without trypsin, was

processed by the standard mycological protocol. After

clearing of the specimen by 10-20% KOH, it was directly

cultured on supplemented SDA.

We found that of the nail samples from 25 cases of

suspected onychomycosis, culture by standard methods

yielded no growth in nine samples, all of which were

positive for Candida Spp. In our previous study, we had

reported that trypsin treatment also increased the

sensitivity of diagnosis of dermatophytes. 4 Further, the

results of standard culture and trypsin method wereconcordant in all cases except one, where the trypsin

method failed to yield any growth as compared to the

standard culture, which yielded C. albicans.

Over the years, many modifications have been attempted to

increase the sensitivity of direct microscopy for diagnosis

of onychomycosis. The specimen can be mounted in a

solution of 20 to 25% KOH or NaOH mixed with 5%glycerol and heated to emulsify lipids before examination.

Alternatively, 20% KOH and 36% dimethyl sulfoxide can be

used for clearing the specimen. However, culture is the

only method by which the causative microorganism can be

identified and the diagnosis truly confirmed.2,5,6 The

suboptimal sensitivity of standard method of culture makes

it difficult for the clinicians to treat the patients

appropriately.

The trypsin treatment method for culture-based diagnosis

of onychomycosis is simple, economic and user-friendly,

which can be performed in a busy mycology laboratory.

The present study reiterates the fact that treatment of

specimens with trypsin prior to culture increases the

Table 1: Comparison of culture results of trypsin

treatment versus standard methods for diagnosis of

onychomycosis

Result of standard Result of post Direct

culture method trypsin culture microscopy for

fungal elements

Sterile Sterile NegativeC. albicans Sterile Negative

Sterile Sterile Negative

Sterile C. parapsilosis Positive


Gram positive cocci C. parapsilosis Positive



Aspergillus fumigatus Aspergillus fumigatus Positive

Sterile C. albicans Positive

Alternaria spp. Alternaria spp. PositiveGram positive cocci Gram positive cocci Negative

Sterile Geotrichum spp. Positive

Sterile C. albicans Positive

Sterile Geotrichum spp. Positive

Gram positive cocci C. parapsilosis Positive


Alternaria spp. Alternaria spp. Positive

T. rubrum T. rubrum Positive


C. parapsilosis C. parapsilosis PositiveSterile C. parapsilosis Positive


C. parapsilosis C. parapsilosis Positive

C. parapsilosis C. parapsilosis Positive

Xess I, et al.: Running title missing????

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CMYK 63

sensitivity of the culture technique and ultimately will help

in proper treatment of the patients.

References

1. Brilhante RS, Cordeiro RA, Medrano DJ, Rocha MF, Monteiro

AJ, Cavalcante CS, et al. Onychomycosis in Ceara (Northeast

Brazil): Epidemiological and laboratory aspects. Mem Inst

Oswaldo Cruz 2005;100:131-5.

2. Elewski BE. Onychomycosis: Pathogenesis, diagnosis and

management. Clin Microbiol Rev 1998;11:415-29.

3. Migdley G, Moore MK, Cookk JC, Phan QG. Mycology of

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

for diagnosis of dermatomycosis. Southeast Asian J Trop Med

Public Health 2004;35:396-8.

5. Naka W, Hanyaku H, Tajima S, Harda T, Nishikara T.

Application of neutral red staining for evaluation of the

viability of dermatophytes and Candida in human skin scales.

J Med Vet Mycol 1994;32:31-5.

6. Rippon JW, editor. The pathogenic fungi and pathogenic

actinomycetes. Medical Mycology. 3rd ed. Saunders:

Philadelphia; 1998. p. 169-275.

7. Campbell CK, Johnson EM. The dermatophytes. In: Collier L,Balows A, Sussman, editors. Topley and Wilsons Microbiology

and Microbial infections, Vol 4. 9th ed. Arnold: London; 1998.

p. 215-36.


Xess I, et al.: Running title missing????

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64 CMYK

Correspondence Column

MUCINOUS NAEVUS: AN UNUSUAL

PRESENTATION

Rashmi Kumari, Devinder Mohan Thappa,S Jayanthi*

Indian J Dermatol 2007:52(1):??

Dr. Devinder Mohan Thappa, Department of Dermatology and

STD, JIPMER, Pondicherry - 605 006, India.


A 23-year-old man presented with multiple firm papules

over his chest extending onto both his shoulders since

childhood. There was no significant personal or familyhistory. On examination, multiple, discrete, firm follicular as

well as non-follicular shiny papules were seen mainly over

the anterior chest and extending onto both the shoulders

(Fig. 1). Underlying skin was not thickened or hide bound.

Also seen was a 4 cm horizontal keloid over the sternum.

No other physical or systemic abnormality was detected.

Routine laboratory investigations were normal and there

was no evidence of paraproteinemia.

On histopathological examination of representative papule,

epidermis was acanthotic with thin, elongated rete ridges

and mild hyperkeratosis. In the papillary dermis, mucindeposition was seen around a hair follicle without any

fibroblastic proliferation (Fig. 2). On special staining, mucin

deposition was seen in the papillary dermis.

Mucinous naevus was first described by Redondo Bellon

et al1 in 1993, who demonstrated a congenital plaque like

lesion in the interscapular area in a 16-year-old female very

similar to that seen in our case over the chest. The term

mucinous naevus was proposed because of its naevoid

appearance and characteristic pattern of mucin deposits in

the papillary dermis.

Cutaneous mucinosis (CM) can be divided into two

groups: distinctive (primary) CM in which the mucin

deposition is the main histologic feature, resulting in

clinically distinctive lesions; and secondary cutaneous

mucinosis, in which histologic mucin deposition is only an

additional histological feature. The primary CM are sub-

grouped into degenerative-inflammatory (diffuse) and

neoplastic-hamartomatous (focal) mucinoses.2

Mucinous naevus is recently thought to be a variant of

either connective tissue naevus of proteoglycan type or

primary distinctive cutaneous mucinosis of thehamartomatous/ focal type.3 The lesions usually develop at

birth1 or in early adulthood4,5 and the lower part of the

trunk is the most commonly affected site. Brakman et al

and Rongioletti and Rebora reported two adult cases of

linear mucinous nevus on the back, showing a zosteriform

pattern.4,5

The histopathology in all cases designated as mucinous

nevus includes a papillary dermal mucin deposit with or

without elongated rete ridges in a band like fashion. The

origin of the mucin deposited in the lesion remains

unclear, but it seems to be the result of a primarymetabolic process (overproduction) rather than of a

secondary catabolic process.6 This idea is supported by

the fact that in all reported cases the lesions developed

early in life, even at birth, without evidence of trauma or

a pre-existing pathological change at the site of the

lesions.

Fig. 2: Photomicrograph demonstrating mucin deposition around a

hair follicle without any fibroblastic proliferation (Hematoxylin and

Eosin, x100)

Fig. 1: Multiple, discrete, firm, shiny papules seen over the anterior

chest

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CMYK 65

URTICARIA: A NOVEL ENTITY

WITH ISOFLAVONES

Ashima Goel, Davinder Parsad


Dr. Ashima Goel, PO Box 1514, PGIMER, Chandigarh - 160 012 India. E-mail: [email protected]

Soybeans are a natural dietary source of isoflavones,

which have estrogen-like properties.1 The phytoestrogens,

include certain isoflavonoids, flavonoids, stilbenes and

lignans. Their perceived health beneficial properties extend

beyond hormone-dependent breast and prostate cancers

and osteoporosis to include cognitive function,

cardiovascular disease, immunity and inflammation and

reproduction and fertility.2-4

To the best of our knowledge, this is the first case report

of isoflavones induced urticaria. A 48-year-old woman

presented in outpatients of our urticaria clinic with the

chief complaints of widespread itchy wheals of variable

morphology all over the body after ingestion of

isoflavones (available as Isoflav CR capsules; Raptakos

Vrett and Company Ltd., India) prescribed for the

postmenopausal symptoms by her gynecologist. According

to the patient, she developed intensely itchy wheals all

over the body after one day of intake of her prescribed

medication. There was no history of associated fever, jointpains, eyelid / lip swelling, respiratory distress or any other

constitutional symptom. There was no history of diabetes,

hypertension or any other medication prior to the onset of

rash. She was non-atopic without any history of perennial

rhinitis, asthma and house-dust mite hypersensitivity. The

diagnosis of drug-induced urticaria was made and was

advised to stop isoflavones. She was prescribed

hydroxizine 10 mg tid. Drug discontinuation was followed

by complete resolution of the skin eruption. Rechallenge

with isoflavones itself resulted in similar urticarial lesions.

Dye in the capsules as a possible candidate for drug-

induced urticaria was excluded as rechallenge was

performed with isoflavones in the tablet form which

resulted in reappearance of urticarial lesions.

This communication intends to convey that physician as

well as gynecologists should be aware of this adverse

effect of isoflavones while prescribing it to

postmenopausal women so as to facilitate early diagnosis

of isoflavones induced urticaria.

References

1. Messina MJ. Soy foods and soybean isoflavones andmenopausal health. Nutr Clin Care 2002;5:272-82.

There are, to our knowledge, six cases identified as

mucinous nevus in the English language literature,6-10

although some cases of cutaneous mucinosis of infancy

(CMI) reported earlier might be identical to mucinous

nevus1 and hence were considered a differential diagnosis

in our case.

Cutaneous mucinosis of infancy (CMI) is a rare condition

that is categorized as a degenerative-inflammatorymucinosis (diffuse). The lesions of CMI are either

symmetrical or grouped small papules of congenital or

infantile onset on the upper extremities or the trunk.10,11

Histology shows a focal, well-circumscribed deposit of

mucin in the papillary dermis without fibroblast

proliferation.3 The lesions tend to be progressive unlike

mucinous nevus. Another differential diagnosis is

cutaneous focal mucinosis, is a solitary papule or nodule

with a marked proliferation of mucoblasts, eventually

replacing most of the collagen.3

This case is being reported for its rarity. Naevus with such

widespread involvement over the anterior chest and

shoulders has not been previously described. The mucin

deposition in the papillary dermis surrounding a hair follicle

was confirmative of the diagnosis.

References

1. Redondo Bellon P, Vazquez-Doval J, Idoate M, Quintanilla

E. Mucinous nevus. J Am Acad Dermatol 1993;28:797-8.

2. Uitto J, Santa Cruz DJ, Eisen AZ. Connective tissue nevi of

the skin. Clinical, genetic, and histopathologic classification

of hamartomas of the collagen, elastin, and proteoglycantype. J Am Acad Dermatol 1980;3:441-61.

3. Rongioletti F, Rebora A. Cutaneous mucinoses: Microscopic

criteria for diagnosis. Am J Dermatopathol 2001;23:257-

67.

4. Suhr KB, Ro YW, Kim KH, Lee JH, Song KY, Park JK.

Mucinous nevus: Report of two cases and review of the

literature. J Am Acad Dermatol 1997;37:312-3.

5. Brakman M, Starink TM, Tafelkruyer J, Bos JD. Linear

connective tissue naevus of the proteoglycan type (naevus

mucinosis). Br J Dermatol 1994;131:368-70.

6. Rongioletti F, Rebora A. Mucinous nevus. Arch Dermatol

1996;132:1522-3.

7. DePadova-Elder S, Mols-Kowalczewski BL, Lambert WC.

Multiple connective tissue nevi. Cutis 1988;42:222-4.

8. Brakman M, Starink TH, Tafelkruyer J, Bos JD. Linear

connective tissue naevus of the proteoglycan type (naevus

mucinosus). Br J Dermatol 1994;131:368-70.

9. Kozminsky ME, Bronson DM, Barsky S. Zosteriform

connective-tissue nevus. Cutis 1985;36:77-8.

10. McGrae JD Jr. Cutaneous mucinosis of infancy: A congenital

and linear variant. Arch Dermatol 1983;119:272-3.

11. Stokes KS, Rabinowitz LG, Segura AD, Esterly NB.

Cutaneous mucinosis of infancy. Pediatr Dermatol1994;11:246-51.

Correspondence

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66 CMYK

2. Dixon RA. Phytoestrogens. Annu Rev Plant Biol

2004;55:225-61.

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.

Correspondence

LINEAR FOCAL ELASTOSIS

(ELASTOTIC STRIAE)

K N Shivaswamy, Aravind Babu,Devinder Mohan Thappa


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

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

spread across the midline over mid and lower back (Fig. 1).

With the above clinical findings, a diagnosis of linear focal

elastosis was made.

Histopathological examination from one of the transverse

streaks from the lower back revealed increased elastic

fibers in the dermis. These elastic fibers were thin, wavy,

elongated as well as fragmented and clumped (Fig. 2).

These histological findings were consistent with our

clinical diagnosis of linear focal elastosis.

Linear focal elastosis (LFE) also called elastotic striae is

relatively a rare disorder characterized by asymptomatic

palpable skin coloured to yellowish transverse streak like

yellowish lines seen usually over mid and lower black.1

Burket el al2 was the first to describe this condition in

three elderly men. Later many reports of linear focal

elastosis have been described in both young men and

women, including a case of linear focal elastosis in a 13-

year-old girl over the legs by Brier et al.3

The exact pathogenesis of this condition is still unclear,

both degeneration and elastogenesis or regeneration has

been described in lesions of LFE. Currently, degeneration

and regeneration of elastic fiber is thought to be a possible

pathomechanism.4

Clinically, these lesions are characterized by skin coloured

to yellowish slightly palpable transverse streaks, spreadacross the midline over mid and lower back. These lesions

have to be differentiated from striae distensae. The striae

distensae are depressed rather than elevated and are pink

or white in colour and are usually associated with history

of sudden weight gain, hormonal or steroid application or

exercise. They are usually located over the abdomen,

thighs, arms or breast. Histology of striae shows altered

collagen bundles without any changes in elastic tissue.1,2,5

In contrast, there is increased number of elastic fibers in

the dermis in lineal focal elastosis. These fibers are thin,

elongated, wavy, fragmented and clumped. Electron

microscopy reveals elongated, irregularly-shaped swollen

elastic fibers with degenerative changes.2,6 Other

histological differential diagnoses include pseudoxanthoma

Fig. 1: Multiple horizontal skin coloured to yellowish, slightly raised,

transverse streaky bands over the back

Fig. 2: Photomicrograph demonstrating thin, wavy, elongated as well

as fragmented and clumped elastic fibers in the dermis (Verhoeff-van

Gieson stain, x100)

figs missing??

figs missing??

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CMYK 67

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

References

1. Odom RB, James WD, Berger TG. Andrews 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

1997;137:955-7.

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.

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.

Correspondence

LICHEN STRIATUS IN A RARE

PATTERN

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

Indian J Dermatol 2007:52(1):

Surajit Nayak, Dept of Skin and VD, MKCG Medical College,

Berhampur - 760 010, Orissa, India.


Lichen striatus is a self-limited linear dermatosis of

unknown origin, most commonly seen in children between

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

child, who presented with lichen striatus distributed alonglines of Blaschko forming a peculiar pattern as multiple

parallel bands like branches of a tree.

The 10-month-old child was brought with complaints of

linear, dull-colored, slightly scaly band extending across

left lower limb, along anterior trunk in median line then

traversing left upper limb in median aspect (Fig. 1). Three

parallel bands of similar morphology were found extending

from linear band in trunk in a horizontal manner. So also

few linear bands were seen running parallel to the linear

band on the arm on its either side (Fig. 2). The bands were

around 3 cm wide and were almost continuous and

consisted of small papules closely placed. As per the

history given by parents it started two months back in

lower limb first, as a few small papules, which gradually

proceeded proximally and coalesced to form a linear band

in due course of time.

On examination, the baby was found to be otherwise

healthy child. The lesions showed no umbilication orWichams striae. Nail and hair were normal on examination.

Her investigation revealed a normal hematological and

biochemical profile. A biopsy was done, which showed

hyperkeratosis, focal parakeratosis, with lymphocytic

exocytosis. In dermis there is superficial and deep

perivascular infiltration of lymphocytes and histiocytes,

few necrotic keratinocytes were observed.

Histopathological study was consistent with lichen

striatus. Parents were explained about the benign nature of

the disease and about its self-regressing nature.

Though lichen stritus is a disease of childhood, it canoccur rarely in both infants and adults, with a female

predominance. Etiology is unknown, but report of its

Fig. 1:Legend Missing????

Fig. 2:Legend Missing????

*Dept missing???***

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occurrence in sibling, topic individuals, in spring and

summer support genetic, infectious and environmental

factors.1-3

In lichen stritus, an acquired event such as, viral infection

may allow an aberrant clone of cutaneous cells to express a

new antigen, resulting in the phenotypic skin changes.4

Though asymptomatic, few may experience mild pruritus.Nail involvement may be observed in few patients as

ridging, splitting, onycholysis or nail loss.5,6 Though

commonly on one arm or leg or on the neck, but may

develop on the trunk. Though in abdomen, buttock, thigh

lesion is commonly seen as single extensive linear lesion, it

may present as bilateral or parallel lesions, as seen in our

case. Bilateral involvement though very exceptional, has

been reported.7,8

Usually it progresses over a few weeks and then remains

stable for few months, but eventually regresses by one

year with some residual hypo pigmentation. Nailinvolvement also regresses spontaneously.

Histopathological study is not diagnostic but very useful

for excluding other conditions like nevus unius lateralis

and linear lichen planus, as they closely resemble lichen

stritus. Its diagnosis is basically made on history and

physical examination. In differential diagnosis come linear

lichen planus, porokeratosis, lichen nitidus and ILVEN. In

ILVEN, clinical features appear at birth or early infancy but

do not regress spontaneously. Linear porokeratosis is also

need to be differentiated.9 Our case presents a very

interesting case of lichen stritus with a rare presentation ofparallel bands like branches of a tree.

The patient was advised topical tacrolimus ointment, as

reported to be effective. Lichen stritus is a T-cell-mediated

inflammatory disease and tacrolimus ointment may be an

effective alternative treatment for this disease. The patient

was discharged with advice to use topical tacrolimus as

reported to be effective by few authors.10,11

References

1. Kennedy D, Rogers M. Lichen stritus. Pediatr Dermatol1996;13:95-9.

2. Di Lernia V, Ricci G, Bonci A, Patrizi A. Lichen striatus and

atopy. Int J Dermatol 1991;30:453-4.

3. Patrizi A, Neri I, Fiorentini C, Chieregato C, Bonci A.

Simultaneous occurrence of Lichen striatus in siblings. Pediatr

Dermatol 1997;14:293-5.

4. June K, Wingfield, Rehmus, Nelly R, Amal M, et al. E-

medicine. [Last accessed on 2005 Feb 23].

5. Baran R, Dupre A, Lauret P. Le Lichen striatus

onychodystrophique. Ann Dermatol Venereol 1999;126:885-

91.

6. Kaufman JP. Lichen striatus with nail involvement. Cutis1974;14:232-4.

7. Aloi F, Solaroli C, Pippione M. Diffuse and bilateral Lichen

striatus. Pediatr Dermatol 1997;14:36-8.

8. Kurokawa M, Kikuchi H, Ogata K, Setoyama M. Bilateral

lichen striatus. J Dermatol 2004;31:129-32.

9. Rahbari H, Cordero AA, Mehergan AH. Linear porokeratosis.

A distinctive clinical variant of porokeratosis of Mibelli. Arch

Dermatol 1974;109:526-8.

10. Fujimoto N, Tajima S, Ishibashi A. Facial lichen stritus:

Sucessful treatment with tacrolimus ointment. Br J Dermatol

2003;148:587-90.

11. Sorgentini C, Allevato MA, Dahbar M, Cabrera H. Lichen

striatus in an adult: Sucessful treatment with tacrolimus. Br J

Dermatol 2004;150:776-7.

Correspondence

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