63, 1^ Correspondence^ 111

—J. Ganesan, F.R.C.P.A.Instituto q/ 1fedical RescarchKuala Lumpur, Atola}'sia.11euiber, Leprosa' Rcsearch Comntittee,

falai sia

REFERENCES1. BROWNE, S. G. Erythema nodosum in leprosy. J.

Chronic Dis. 16 (1963) 23-30.2. ClIOPRA, N. K., AGARWAL, J. S. and PANDIIYA, P.

G. Reactions in leprosy; a study of 250 patienisin a multidrug thcrapy projcct, Baroda district,Gujarat, India. Int. J. Dermatol. 29 (1990) 490-493.

3. GIAM, Y. C., ONG, I3. H. and TAN, T. Erythemanodosum leprosum in Singapore. Ann. Acad. Mcd.Singapore 16 (1987) 658-662.

4. MODLIN, R. L., BAKKE, A. L., VACCARO, S. E.,HoRwITZ, D. A., TAYLOR, C. R. and REA, T. H.Tissue and blood T lymphocyte subpopulationsin erythema nodosum leprosum. Arch. Dermatol.121 (1985) 206-209.

5. REA, T. H. and RIDLEY, D. S. Lucio's phenom-enon: a comparative histological study. Int. J. Lepr.47 (1979) 161-168.

6. RIDLEY, D. S. Skin I3iopsrin Leprosy; IlistologicalInterpretation and ClinicaiApplicaiion. 3rd edn.Baste: Documenta Geigy, 1990.

7. RIDLEY, D. S. and JOPLING, W. H. Classificationof leprosy according to immunity; a five-groupsystem. Int. J. Lepr. 34 (1966) 255-273.

8. RIDLEY, D. S., REA, T. H. and McADAM, K. P. W.The histology of erythema nodosum leprosum;variant forms in New Guineans and other ethnicgroups. Lepr. Rev. 52 (1981) 65-78.

9. RIDLEY, D. S. and RIDLEY, Ist. J. The immuno-pathology of erythema nodosum leprosum: the roleof extravascular complexes. Lepr. Rev. 54 (1983)95-107.

10. STERNBERGER, L. A., HARDY, P. H., Jr., CUCULIS,

J. J. and MEYER, H. G. The unlabclled antibodyenzyme method immunohistochemistry. J. His-tochem. Cytochem. 18 (1970) 315-333.

11. WEMAMBU, S. N. C., TURK, J. L., WATERS, M. R.F. and REES, R. J. W. Erythema nodosum lepro-sum; a clinical manifestation of the Arthus phe-nomenon. Lancet 2 (1969) 933-935.

Follicular Keratoses in Leprosy and Post-Kala-AzarDermal Leishmaniasis

To THE EDITOR:The term "follicular keratoses" refers to

a group of varied etiology in ali of whichthere is a prominent plug of keratin in thefollicular orifice ('). Keratosis pilaris, ker-atosis pilaris atrophicans, keratosis circum-seripta, phrynoderma, lichen spinulosa, fol-licular ichthyosis, to name a few, are thedisorders in which this pathology is prom-inently seen ('). In most of there disorders,the exact cause of keratinization is unclear.In some the type of keratitis is abnormal,in others the shedding mechanism or therate of production is at fault. The histo-pathological changes are distinctive in a fewinstances, but often the morphological dif-ferences are more striking.

Many inflammatory conditions of the skintend to develop a follicular keratosis. Twotypes of follicular keratoses, keratosis spi-nulosa ( 7 ) and comedo ( 5 ) have beco de-scribed over the lesions of borderline tu-berculoid (BT) leprosy. We report such le-

sions in three patienis, one each with bor-derline lepromatous (BL), lepromatousleprosy (LL) and post-kala-azar dermalleishmaniasis (PKDL).

Case 1. A 45-year-old woman with polarlepromatous leprosy (LLp), with a bacterialindex of 4+ and a morphological index of1%, was receiving the World Hcalth Orga-nization multibacillary multidrug regimen(WHO-MDT-MBR). During her sixthmonthly follow up, multiple, 1- to 3-mmkeratotic pigmented papules with follicularatrophy at places were seen over some ofthe infiltrated plaques present on her fore-arms and legs.

Case 2. A 33-year-old man suffering fromborderline lepromatous (BL) leprosy for thelast 3 years presented in one of the episodesof type 1 lepra reaction. There were mul-tiple, hyperkeratotic, pigmented follicularpapules over a few of the erythematous in-filtrated plaques on his back. No follicularscarring or atrophy was appreciated. Ac-

112^ International Journal of Leprosy^ 1995

THE FIGURE. Closc up of right axilla showing mul-tiple pigmented keratotic follicular lesions.

cording to patient's history the keratotic le-sions becamc more prominent during eachreactional episode.

Case 3. A 20-year-old man, migrant fromBihar, was diagnosed as having PKDL forthe last 3 years. A few of the infiltratedplaques over his neck, axillae and back werestudded with multiple, pigmented, keratoticfollicular lesions without any scaling or at-rophy of the follicular orifices (The Figure).

In all three patients thc follicular papuleswere limited strictly to the lesions only.There was no history of similar keratoticfollicular lesions in other family membersin any of the three paticnts. Neither wasthere any personal or family history of ato-py. None of the patients had a history ofmassaging oil over the lesions. There wasno evidence of a deficiency state in any ofthe patients. Histopathological examina-tions of the skin of all three patients showedfollicular hyperkeratosis, keratotic pluggingand sparse infiammatory infiltrate aroundthe hair follicles. There was a gradual dis-appearance of there follicular keratotic le-sions during specific treatment of the dis-ease and subsequent follow up.

In an earlier report, comedo-likc lesionsover infiltrated plaques of borderline tu-berculoid (BT) leprosy were attributed tococonut oil massage ( 5 ). This history wasabsent in all of our patients. he keratoticpapules were seen only in a few infiltratedplaques in Cases 2 and 3, while in Case 1more extensive involvement of the infil-trated arcas was observed.

The prominence of the keratotic lesionsduring type 1 lepra reaction in Case 2 sug-gcsts that it could be the manifestation ofan immunological reaction in the skin, type1 reaction being a delayed type hypersen-sitivity (DTH) reaction ( 2 ). While investi-gating the role of delayed immune reactionsof human epidermal keratinocytes, Kaplan,et al. (3 ) observed that during DTH reaction,there is marked thickening of the epidermisassociated with an increase in the both sizeand number of keratinocytes and in the ex-pression of kcratinocytic-Ia antigen in thcepidermis. They further suggested that oneor more epidermal growth factors may begenerated in the course ofa delayed immunereaction in the dermis. Thangaraj, et al. (6 )demonstrated significant epidermal changesin lesions of leprosy patients undergoing type1 reaction in the form of an increase in epi-dermal cell layers, the consistent presenceof Ia in all keratinocytes, an increase in Lan-gerhans' cell numbers, and scattered T censwithin the epidermis. T-cell activation canlead also to the production of lymphokines,e.g., gamma interferon (IFN-y) with sub-sequent induction of Ia on epidermal ker-atinocytes. All of thcse can lead to keratin-ocyte proliferation leading to follicular plug-ging.

In Case 1 with LLp, such keratotic pap-ules developed after 6 doses of WHO-MDT-MBR. This could be due to the fact thatafter 6 months' treatment there was a grad-ual return of cell-mediated immunity withactivation of T cells through the expressionof keratinocyte-Ia antigen, resulting in fol-licular hyperkeratosis and keratotic plug-ging (6 ).

A similar pathomechanism can be pos-tulated for the development of such follic-ular keratotic papules over infiltratedplaques of PKDL. The type of PKDL pre-senting mostly with infiltrated plaques andnodular lesions is thought to be dueto DTH

63, 1^ Correspondence^ 113

reaction to Leishtnania donovani antigen (4 ).Therefore, follicular keratotic plugging couldbc a manifestation oflocalized keratinocyteproliferations as a result of DTH reactionhaving a similar immunopathological con-notation as reactional leprosy. However, tothe best of our knowledge, such keratoticfollicular papules in relation to the plaquelesion of PKDL have not been reported ear-lier.

—Sandipan Dhar, M.D., D.N.B.Senior Resident

— Inderjeet Kaur, M.D.Associate Professor

—Vinod K. Sharma, M.D.Associate Professor

— Bhushan Kumar, M.D., M.N.A.M.S.Additional ProfessorDepartment of Dermatologv,

Venereologv and LcprologvPostgraduate Institute of Medical

Education & ResearchChandigarh 160012, India

Reprint rcqucsts to Dr. B. Kumar.

matolog}'. Champion, R. H., Burton, J. L. and Ebling,F. J. G., eds. Oxford: Blackwell Scientific Publica-tions, 1992, pp. 1352-1358.JOPLING, W. H. and MCDOUGALL, A. C. Handbookof Leprosy. Oxford: Heinemann Professional Pub-lishing, 1988.

3. KAPLAN, G., WITMER, M. D., NATH, I., STEINMAN,

R. M., LAAL, S., PRASAD, H. K., SARNO, U. N.,ELVERS, U. and COHN Z. A. Influente of delayedimmune reactions on human epidermal keratino-cytcs. Proc. Natl. Acad. Sci. U.S.A. 83 (1986) 3469-3473.

4. NANDY, A., NEOGY, A., GHOSH DASTIDAR, B., SAR-

KER, M., MALLICK, K. K. and CHOWDHURY, A. B.Immune response and drug response in kala-azarand post kala-azar dermal leishmaniasis. Proceed-ings of the Indo-U.K. Workshop on Lcishmaniasis,1983, pp. 161-170.

5. SRINIVAS, C. R., PADHEE, A., BALCHANDRAN C.,

SHENOY, S. D., ACHARYA, S. and RAMNARAYAN, K.Comedones induced by coconut oil in a borderlinetuberculoid lesion. Int. J. Lcpr. 56 (1988) 471-472.

6. THANGARAJ, H., LAAL, S., THANGARAJ, I. and NATH,

I. Epidermal changes in reactional leprosy: kera-tinocyte-la expression as an indicator of cell-me-diated immune responses. Int. J. Lcpr. 56 (1988)401-407.

7. THANKAPPAN, T. P. and SULOCHANA, G. Keratosisspinulosa developing in borderline tubcrculoid le-sions during type 1 reaction: two case reports. Lcpr.Rev. 62 (1991) 49-51.

REFERENCES1. GRIFFITHS, W. A. D., LEIGH, I. M. and MARKS, R.

Disorders of kcratinization. In: Textbook of Der-

Successful Treatment of a LepromatousPatient with Clarithromycin

TO THE EDITOR:In 1992, we initiated a clinical trial in

lepromatous leprosy of clarithromycin de-signed to evaluate clinical response and thekilling of Mvcobacterilmr leprae by an initial1-g dose followed subsequently by 1 g dailyfor 3 months. For these purposes we hadplanned to recruit eight previously untreat-ed BL/LL patients but, unfortunately, afterthe completion of but one trial patient theSan Francisco laboratory was closed; sinccthere are only a few published pilot trials( 1 . 4 ) of the use of clarithromycin in leprosypatients and nono by these same methods,we report the results from our sole patient.

The patient, a 24-year-old Filipino male,had a family history of leprosy and had not-ed a generalized nodular eruption for thepreceding year. No nerve enlargement ordeformation were noted and Semmes-Weinstein monofilament testing was withinnormal limits. An ophthalmologic exaro re-vealed bilateral keratitis and beaded cornealnerves confined to the left eye. Slit-skinsmears from six sites yielded an averagebacterial index (BI) of 3.7. Skin biopsy wasreported by the Ridley-Jopling classifica-tion as "polar LL."

Initially, the patient underwent clinicalevaluation, had a routine hemogram, and