Erythema multiforme associated with Trichophyton mentagrophytes infection
Transcript of Erythema multiforme associated with Trichophyton mentagrophytes infection
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638
© 2002 European Academy of Dermatology and Venereology
LETTERS
JEADV
(2002)
16
, 638–649
Blackwell Science, LtdOxford, UKJDVJournal of the European Academy of Dermatology and Venereology0926-99592002 European Academy of Dermatology and Venereology? 200216?LettersLettersLetters
Acne vulgaris as an immune reconstitution syndrome in a patient with AIDS after
initiation of antiretroviral therapy
To the Editor
Initiation of highly active antiretroviral therapy (HAART) in
patients with HIV usually leads to a decrease of plasma
HIV-RNA followed by an increase of CD4 T-helper cells.
Exacerbation or progression of other associated inflammatory
infections are well-known as immune reconstitution syn-
dromes under the improvement of immune system during HAART.
We report a reactivation of acne vulgaris in a patient with AIDS
after initiating HAART.
A 29-year-old Caucasian man presented to our department
with dyspnoe, fever, weakness, and weight loss (4 kg) during the
last 4 weeks. There were no pathological cutaneous findings at
the first examination. Sputum samples, arterial blood gas ana-
lysis (BGA), chest roentgenogram, and high resolution (HR) CT
scan were consistent with Pneumocystis carinii pneumonia
(PCP). HIV antibody testing was positive, laboratory examina-
tions revealed leucopenia (3530/mL), lymphopenia (810/mL),
a C-reactive protein of 23.0 mg/L, 10 CD4+ lymphocytes/mL,
253 CD8+ lymphocytes/mL, a CD4/CD8 ratio of 0.01 and a
HIV-1 RNA of 53 100 copies/mL. No other additional haema-
tological, biochemical or immunological abnormalities were
demonstrated. We initiated HAART with stavudin 40 mg,
lamivudine 150 mg and nelfinavir 1250 mg twice daily. Initial
treatment also included antibiotic therapy with cotrimoxazol
3840 mg twice daily oral for 21 days. After 14 days of treatment,
the patient showed clearance of all general symptoms.
Two months later the patient presented with comedones,
erythematous papules, and pustules on the forehead,
cheeks, and upper trunk. The distribution of the non-pruritic
lesions was predominantly follicular. Bacterial cultures of
papulopustules contents grew
Proprionibacterium acnes
.
The patient reported a history of acne vulgaris until he was
19 years old. On examination, he revealed a good response to
HAART with undetectable HIV-1 RNA (< 40 copies/mL),
154 CD4+ lymphocytes/mL, and 1735 CD8+ lymphocytes/mL.
Topical treatment with erythromycin led to a complete clear-
ance of skin lesions after 8 weeks.
Restitution of immune function under HAART can lead to
some adverse effects, because of improved immune response to
pathogens that are already present in the body. Such immune
inflammatory syndromes, e.g. herpes zoster, immune recovery
inflammatory folliculitis, CMV retinitis, toxoplasmosis, pro-
gressive multifocal leukoencephalopathy, hepatitis C, and
mycobacteriosis have been reported after initiating antiretro-
viral therapy.
1–4
HAART causes a rapid and early increase in
memory lymphocytes (CD45RO) and native cells (CD45RA).
In addition to the increase of CD4+ cells, also CD8+ cells
increase. This rapid rise of CD8+ cells before reconstitution
of the CD4 cell function has been accused to be a risk factor
for developing herpes zoster after beginning HAART.
5
Our
patient’s reactivation of acne occurred during a rise of CD8+
cells up to 1735/mL. Similar observations have been described
in HIV-infected patients presenting ‘immune recovery follicu-
litis’ under HAART.
3
Pruritic skin lesions involved the face and
upper trunk. These skin manifestations are possibly related to
an immune response against pathogens that are already present
in the skin, e.g. demodex folliculorum. The hair follicle is a
common reservoir for various micro-organisms. We hypothes-
ize that in our patient the restoration of immune response
against
Proprionibacterium acnes
could explain the reactivation
of acne vulgaris after initiating HAART. Regression of skin
lesions after topical erythromycin may suggest an underlying
immunopathological process.
A
Kreuter,
R
Schlottmann,
P
Altmeyer,
NH
Brockmeyer
Department of Dermatology, Ruhr-University Bochum, Gudrunstrasse
56, 44791 Bochum, Germany, tel. +49 234 509 3473;
fax +49 234 509 3475; E-mail: [email protected]
References
1 Behrens GM, Meyer D, Stoll M, Schmidt RE. Immune reconstitution
syndromes in human immuno-deficiency virus infection following
effective antiretroviral therapy.
Immunobiology
2000;
201
: 186–193.
2 Collazos J, Mayo J, Martinez E, Blanco MS. Contrast-enhancing
progressive multifocal leukoencephalopathy as an immune
reconstitution event in AIDS patients.
AIDS
1999;
13
: 1426–1428.
3 Bouscarat F, Maubec E, Matheron S, Descamps V. Immune recovery
inflammatory folliculitis.
AIDS
2000;
14
: 617–618.
4 Handa S, Bingham JS. Dermatological immune restoration syn-
drome: does it exist?
J Eur Acad Derm Ven
2001;
15
(5): 430–432.
5 Domingo P, Torres OH, Ris J, Vasquez G. Herpes zoster as an
immune reconstitution disease after initiation of combination
antiretroviral therapy in patients with human immunodeficiency
virus type-1 infection.
Am J Med
2001;
110
: 605–609.
16LetterLetterLetterxxxxx
Report of a case of Muir–Torre syndrome
To the Editor
Muir–Torre syndrome (MTS) is an autosomal dominant
genodermatosis, characterized by at least one single sebaceous
gland tumour and a minimum of one internal malignancy.
1
In
a recent review of the literature, Akhtar
et al
. found only 205
cases of MTS.
2
The most common presentation is sebaceous
tumours with a low-grade visceral malignancy.
1
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Letters
639
© 2002 European Academy of Dermatology and Venereology
JEADV
(2002)
16
, 638–649
We observed in 1998 a 71-year-old caucasian male with
multiple, rapidly growing haemorrhagic tumours in the left
frontoparietal region (fig. 1) that were recurrences of a
sebaceous carcinoma treated 2 months earlier by classic surgery
and radiotherapy (fig. 2). The man had no personal or family
history of cutaneous or visceral neoplasms, but he experienced
an acute episode of haematochesia, and colonoscopy evidenced
a colorectal adenocarcinoma 8 cm from the anus. Cervical
metastasis of the cutaneous sebaceous carcinoma were detected
and computed tomography scan showed lung and acetabular
metastases. Chromosomal studies to detect microsatellite
instability (MSI) on the visceral tumour were negative.
Chemosurgery without microscopic control with a 40%
zinc chloride paste was performed on the larger tumours and
cryosurgery with liquid nitrogen was used for the smaller ones.
Systemic chemotherapy with 5-fluorouracil (1000 mg/m
2
) and
cisplatin (100 mg/m
2
) was administered monthly and the
osseous metastasis was treated with external radiotherapy.
Complete necrosis of the cutaneous tumour was obtained, and
the cranial periosteum was exposed. Incisional biopsies of the
margins of the ulceration disclosed no tumour. 5-Fluorouracil
was administered for 18 months and the man is still alive
and well.
Accepted criteria for the diagnosis of the rare MTS
include the presence of at least one sebaceous tumour or
keratoacanthoma with sebaceous differentiation and a visceral
malignancy, or the report of a family history of MTS in a subject
with multiple keratoacanthomas and visceral malignancies, in
the absence of any known predisposing factor.
3
Our patient
fulfilled the diagnostic criteria for MTS. The colorectal carci-
noma diagnosed in our patient accounts for 51% of all primary
cancers in MTS subjects.
4
After gastrointestinal cancers the
next most frequent finding is genitourinary malignancies,
diagnosed in 22% of these subjects.
2
Breast and head and neck
cancers are other possible locations.
2
Sebaceous carcinoma is an uncommon malignant tumour
derived from the adnexal epithelium of sebaceous glands,
usually arising in the orbital region.
5
However, 25% of all
reported cases are extraocular,
6
implying a distinct risk of
aggressive behaviour.
5
In cases presenting sebaceous carcinoma, screening for inter-
nal malignancy should be performed to exclude the possibility
of MTS.
2
Sebaceous neoplasms precede or are concurrent with
the visceral cancer in 41% of these subjects patients and occur
afterward in 59% of cases of MTS.
4
Genetic studies have demonstrated MSI, which is a defect in
DNA replication, in the tumours of some subjects with MTS,
4
including this rare genodermatosis in the hereditary non-
polyposis colorectal cancer.
2,7
MSI is more frequently found in
the sebaceous tumours of MTS subjects or in those of immuno-
suppressed organ transplant recipients.
8
Subjects with MSI tend
to have prolonged survival after diagnosis of visceral malig-
nancies.
4
MSI was not found in the tumours of our patient.
In MTS, the neoplasms display a non-aggressive course,
although 60% of the patients present with metastatic disease.
3
The man in our case presented extensive and aggressive local
recurrence as well as lymphnode and visceral metastases.
Chemosurgery and cryosurgery are methods well known to
fig. 1 Multifocal sebaceous carcinoma: recurrence after radiotherapy and
classic surgery.
fig. 2 Lobules and nests of clear cells. Haematoxylin and eosin, original
magnification, × 40.
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640
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© 2002 European Academy of Dermatology and Venereology
JEADV
(2002)
16
, 638–649
dermatologists and were very efficient in this case. Chemosur-
gery without systematized microscopic control was developed
by Gonçalves and Cabral de Ascenção;
9
the method has an
extremely high cure rate for skin tumours (99.75% in 400 cases
published) and is effective, cheap and simple to do. Its value has
been recently reviewed, and it probably has immunogenic
properties.
10
Lymph node and visceral metastases also regressed
with chemotherapy.
In spite of the aggressive behaviour of the tumours in our
patient, multiple complementary therapies proved to be of
value in his survival.
Note added in proof: The patient died at the end of 2001, due
to metastatic colorectal cancer; sebaceous carcinoma did not
recur.
C
Moura,†*
MM
Pecegueiro,†
MF
Sachse,†
J
Amaro,†
I
Fonseca,‡
A
Fernandes,§
N
Vau§
Departments of
†
Dermatology,
‡
Pathology and
§
Medical Oncology of the
Instituto Português de Oncologia de Francisco Gentil, Rua Prof.
Lima Basto, 1099-023 Lisbon, Portugal.
*
Corresponding author,
tel. 351 21 7229800 (ext. 1346/1338); fax 351 21 7229886
References
1 Cohen PR, Kohn SR, Kurzrock R. Association of sebaceous gland
tumors and internal malignancy: the Muir–Torre syndrome.
Am J
Med
1991;
90
: 606–613.
2 Akhtar S, Oza K, Khan S
et al.
Muir–Torre syndrome: case report of
a patient with concurrent jejunal and ureteral cancer and a review
of the literature.
J Am Acad Dermatol
1999;
41
: 681–686.
3 Schwartz R, Torre DP. The Muir–Torre syndrome: a 25-year
retrospect.
J Am Acad Dermatol
1995;
33
: 90–104.
4 Honchel R, Halling KC, Rehman I
et al.
Microsatellite instability in
Muir–Torre syndrome.
Cancer Res
1994;
54
: 1159–1163.
5 Schwartz RA, Goldberg DJ, Mahmood F
et al.
The Muir–Torre
syndrome: a disease of sebaceous and colonic neoplasms.
Dermatologica
1989;
178
: 23–28.
6 Wick MR, Goellner JR, Wolfe JT III
et al.
Adnexal carcinomas of
the skin. Extraocular sebaceous carcinomas.
Cancer
1985;
56
:
1163–1172.
7 Kruse R, Rutten A, Hosseiny-Malayeri HR
et al.
‘Second hit’ in
sebaceous tumors from Muir-Torre patients with germline
mutations in MSH2: allele loss is not the preferred mode of
inactivation.
J Invest Dermatol
2001;
116
(3): 463–465.
8 Harwood CA, Swale VJ, Bataille VA
et al.
An association between
sebaceous carcinoma and microsatellite instability in
immunosuppressed organ transplant recipients.
J Invest Dermatol
2001;
116
(2): 246–253.
9 Gonçalves JCA. An attempt at reducing pain in cancer patients
treated by chemosurgery without systematised microscopic control.
Skin Cancer
1998;
13
: 145–161.
10 Kirn TF. Using zinc chloride paste before Mohs enhances outcome.
Skin Allergy News
2000;
February
: 6.
16LetterLetterLetter
‘
Nocardia asteroides
’ mycetoma of the foot
To the Editor
Mycetoma is a granulomatous infection characterized by
subcutaneous tumid swellings, usually affecting the lower limbs
(around the ankle) with formation of sinuses that generally
discharge pus containing grains of different colours. Several
aetiological agents,
1–4
including
Nocardia asteroides
have been
incriminated. The current case is yet another example where
N. asteroides
(type VI) was identified as the aetiological
agent.
A 51-year-old farmer from the Indian state of Bihar pre-
sented with multiple draining sinuses on the dorsum, ankle and
sole of his right foot. He used to work barefooted in a field. The
initial lesion started in the central area of the sole of the right
foot. The nodule subsided on its own in 2 months, but
reappeared again 1 month later and was larger and painful. In
due course, multiple swellings appeared on the sole and dorsum
of the right foot discharging pus. The man had been treated
from that time on with several courses of antibiotics without
any beneficial effect. At the time of our examination, he had
severe pain and disability of the right foot due to multiple
swellings. Examination of the affected site revealed an irregular
swelling in and around the right ankle joint, with swelling of
the dorsum and sole of the foot. There were conspicuous
multiple sinuses discharging blood-stained purulent material
(fig. 1), but the grains were not visible in the discharge on naked
eye examination. An X-ray of the foot revealed soft tissue
swelling only.
The yellowish-white discharge from the draining sinuses
cultured on Sabouraud dextrose agar/glucose nutrient agar
yielded a pure culture of
Nocardia
, tentatively identified
as
N. asteroides
on the basis of preliminary biochemical tests.
The colonies of the isolate were initially white, but soon turned
orange with a folded moist surface. Smears of the growth
stained by Kinyouns’ cold acid-fast stain revealed partially
acid-fast, branching, slender hyphae with coccobacillary
fragments. The isolate was not positive for decomposition of
adenine, xanthine, tyrosine, hypoxanthine or casein. It was
also negative for urease, arysulphatase and for acid production
from cellebiose and inositol as tested up to 2 weeks. Growth
was positive at 46
°
C. The isolate was identified as
N. asteroides
on the basis of detailed biochemical tests and cell wall
analysis.
5,6
It was assigned to the type VI on the basis of
in vitro
antimicrobial sensitivity pattern.
Haematoxylin–eosin-stained serial tissue sections prepared
from the representative lesion were examined. A few of the
sections revealed non-specific granulation tissue, composed of
neutrophils, eosinophils, lymphocytes, plasma cells, histiocytes
and fibroblasts. In addition small actinomycotic granules were
identified in the granuloma. The granules were homogeneous
in the centre and had radiating, branching filaments at the
periphery. They were basophilic and irregularly lobulated (fig. 2).
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641
© 2002 European Academy of Dermatology and Venereology
JEADV
(2002)
16
, 638–649
We administered cotrimoxazole (trimethoprim 160 mg +
sulphamethoxazole 800 mg) combined with intramuscular
streptomycin (750 mg) initially daily, and then on alternate
days. There was a perceptible reduction in the size of the swell-
ing with healing of sinuses 8 weeks later. In the course of follow-
up a report of confirmation of the identity of the isolate as
N. asteroides
and its
in vitro
drug sensitivity was received
from the Pasteur Institute, France. The isolate was found to be
sensitive to amikacin, tobramycin, cefotaxime, impenem and
cefamandole, but partially sensitive to erythromycin, amoxycillin
+ clavaulanic acid, cotrimoxazole and resistant to ampicillin,
ciprofloxacin and minocycline.
The man presented to us again with additional swellings at
other sites in July 2000. He was given 1 g of amikacin a day by
slow intravenous infusion for 15 days, followed by cefotaxime
for the same period without any appreciable change in the
status of disease. Subsequently, the treatment was changed to
oral cotrimoxazole (trimethoprim 160 mg + sulphamethoxazole
800 mg) daily associated with crystalline penicillin (500 mg)
intramuscularly four times a day for 6 weeks. This time healing
of the sinuses indicated the effectiveness of the treatment. Later
he was maintained on 1.5 g daily of both cotrimoxazole and
amoxycillin for 1 month. The disease was apparently cured in
the course of this treatment.
Actinomycetoma due to
N. brasiliensis
,
N. otitidiscaviarum
and
N. asteroides
have been reported in several parts of
India.
7–11
The largest series of mycetoma caused by
N. asteroides
in India was reported by Sanyal
et al
.;
3
the 18 cases described in
this report involved various body parts, including the foot. The
diagnosis in the current case was supported by the recovery of
N. asteroides
in culture and confirmed by demonstration of
homogeneous and/or rods of the fungus granules in tissue
sections.
N. asteroidesis
are divided into six types on the basis of
in vitro
antimicrobial sensitivity pattern. The present isolate was
assigned to type VI. In the earlier reports of nocardia mycetoma
and systemic nocardiosis from India, the isolates of
N. asteroides
were not assigned to any type. This report therefore is note-
worthy. Conservative treatment of actinomycetoma has proved
effective in the large majority of cases, and surgery is restricted
to patients with extensive lesions, only where a debulking oper-
ation can shorten the duration of the treatment.
12
Combination
therapy is recommended because of synergistic effects, and it
fig. 1 A swelling around the right ankle with multiple discharging sinuses. fig. 2 Non-specific granulomatous infiltrate around homogeneously staining
grains with radiating branching filaments at the periphery. Haematoxylin and
eosin, original magnification × 100.
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, 638–649
reduces the likelihood of resistance developing during the pro-
longed treatment.
12
The current case initially responded well to
treatment with cotrimoxazole and streptomycin, one of the rec-
ommended treatment modalities.
12
Recurrences of the swell-
ings may possibly be due to partial resistance of the isolate to the
preceding drugs. Surprisingly, the patient did not benefit much
from the therapy with amikacin and cefotaxime, to which the
isolate of
N. asteroides
was sensitive
in vitro
tests
.
The preceding
outcome was in striking contrast to the
in vitro
drug sensitivity
where the causative agent was only partially sensitive to cotri-
moxazole and sensitive to amikacin and cefotaxime, thus indi-
cating that
in vivo
drug sensitivity results of isolate(s) (
N.
asteroides
) may not always correlate well with
in vitro
results
.
HC
Gugnani,*†
VN
Sehgal,‡ VK
Singh,§ P
Boiron,¶ S
Kumar**
†
Department of Mycology Vallabhbhai Patel Chest Institute, University of
Delhi, Delhi 110 007, India,
‡
Dermato-Venereology (Skin/VD) Centre,
Sehgal Nursing Home, A/6, Panchwati, Delhi 110 033, India,
§
DST
Centre for the Study of Visceral Mechanisms, VPCI, University of Delhi,
Delhi, India,
¶
Laboratoire de Mycologie, Facult de Pharmacie, 8, Avenue
Rockfeller 69373 Lyon Cedex 08 France,
**
Department of Dermatology,
Safdarjung Hospital, New Delhi 110 029, India.
*
Corresponding author,
E-mail: [email protected]
References
1 Gugnani HC, Suseelan AV, Anikwe RM
et al.
Actinomycetoma in
Nigeria.
J Trop Med Hyg
1981;
84
: 259–253.
2 Sandhu DK, Mishra SK, Damaodaran VN
et al.
Mycetoma of the
knee due to
Nocardia caviae
.
Sabouraudia
1975;
13
: 170–171.
3 Sanyal M, Thammaya A, Basu N. Actinomycetoma caused by
Nocaridia asteroides
complex and closely related organisms.
Mykosen
1978;
21
: 109–121.
4 Thammaya A, Basu N, Sur-Roy Choudhary D
et al.
Actinomycetoma caused by
Nocardia caviae
in India.
Sabouraudia
1972; 10: 19–23.
5 Land GA. Identification of aerobic Actinomycetes. In: Isenberg HD,
editor. Clinical Microbiology Procedures Handbook.
American Society for Microbiology, Washington DC, 1996;
4.1.1–4.1.9.
6 Mishra SK, Gordon RE, Barnett DA. Identification of nocardiae and
streptomycetes of medical importance. J Clin Microbiol 1980; 11:
728–736.
7 Dasgupta LR, Sundarraj T, Agarwal SC. Actinomycetes from
mycetoma and other cases around Pondichery. Indian J Med Res
1974; 62: 765–775.
8 Desai SC, Pardanani YR, Kher YR et al. Therapeutic investigation
on actinomycetoma. Indian J Surg 1970; 32: 448–461.
9 Hazra B, Bandhopahdyay S, Saha SK et al. A study of mycetoma in
east, India. J Commun Dis 1998; 30: 7–11.
10 Joshi Kr Sangvi A, Vyas MCR et al. Etiology and diagnosis of
mycetoma in Rajasthan, India. Indian J Med Res 1987; 85:
694–698.
11 Klokke AH. Mycetoma in North India due to Nocardia crasiliensis.
Trop Geogr Med 1964; 2: 1701–1171.
12 Boiron P, Locci R, Goodfellow M et al. Nocardia, nocardiosis and
mycetoma. J Med Vet Mycol 1998; 36 (Suppl.): 26–37.16LetterLettersLetters
In vitro bactericidal effect of low-dose ultraviolet B in patients with acne
To the Editor
Beneficial effects of ultraviolet (UV) radiation on acne vulgaris
have been speculated but not generally accepted.1,2 The main
reason for that is the unsatisfactory documentation concerning
the risk/benefit ratio of UV radiation and acne treatment,
as some evidence exists that oxidative damage to the skin
on exposure to UV light may trigger comedogenesis and
colonization of propionibacteria.3 However, encouraging
results regarding in vitro inhibition of propionibacteria,
micrococcacea and staphylococci by UV radiation4 led to us
investigate the direct antibacterial effect of single exposure to
low-dose UVB of bacteria obtained from the pustules of acne
vulgaris subjects in vitro.
Fifty-four subjects (27 females and 27 males) with acne
vulgaris were enrolled in the study whose ages were between 15
and 29 years (mean ± SD = 19.44 ± 3.36 years). Samples were
obtained from the pustules of 51 subjects with acne vulgaris,
comprising 10 methicillin-sensitive Staphylococcus aureus and
50 Propionibacterium acnes samples. Four Petri dishes were
prepared from each bacterial sample, containing 1 × 105 bacteria/
mL, using chocolate agar and Schaedler agar, respectively. These
were exposed to 0, 50, 70 and 110 mJ/cm2 UVB and the
bacterial colonies were calculated after 24 h for S. aureus and
after 72 h for P. acnes samples. The UVB source was UV 8001 K
phototherapy cabin (Waldmann Lichttechnik, Schwenningen,
Germany) with fluorescent tubes emitting in the 285–350 nm
range with a peak at 315 nm. Statistical significance was
assessed by Wilcoxon matched-pairs signed-ranks test and
Mann–Whitney U-test.
Single exposure to UVB achieved a statistically significant
reduction in the number of colonies (mean ± SD) in each irra-
diated sample of (i) S. aureus, 0, 36.5 ± 30.6% (P = 0.005),
14.7 ± 21.1% (P = 0.005) and 3.1 ± 6.2% (P = 0.005), and
(ii) P. acnes, 0, 41.2 ± 24.1% (P < 0.0001), 20.7 ± 18.9%
(P < 0.0001) and 3.1 ± 6.5% (P < 0.0001), respectively (fig. 1).
When the findings for the two bacteria were compared, there
was no significant difference in the proportion of inhibition
of the colonies.
It is a common belief that sunlight improves acne.5 Although
the mechanism is unclear, immunosuppressive effects of UV
radiation may be involved.6 It is known that UVB induces pyri-
midine dimers on the same chain of DNA and such DNA
damage may have lethal effects to micro-organisms. We believe
that the beneficial effect of UV on acne may be due not only to
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an immunosuppressive effect but also to a reduction of skin
surface bacteria. It has been pointed out that porphyrin photo-
reactions in P. acnes might be responsible for the photodestruc-
tion of this micro-organism after exposure to sunlight. Kjelds-
tad and Johnsson have shown that P. acnes is sensitive to
near-UV light, the sensitivity being highest at 320 nm and
related to the amount of porphyrin.2 Possible mechanisms
of inactivation involve the membrane damage in P. acnes and
other bacteria.
It has been claimed that suberythemal doses of UV radiation
was insufficient, and effective doses might be associated with an
increase in the hazards of UV light.7 As in standard protocol
phototherapy, the increments in doses of UV light are based
on the minimal erythematogenic dose of a particular subject;
therefore, the hazards of UV light may be inevitable, but if the
initial suberythematogenic dose is kept constant, the risk of
exacerbation of acne lesions may be avoided.
The results of this study confirm that irradiation by a single
suberythematogenic dose of UVB significantly reduces the
number of colonies of bacteria obtained from pustules of acne
vulgaris. It may be suggested that low-dose UVB may improve
the response to other treatment modalities in acne vulgaris.
However, the role of adjuvant low-dose phototherapy in
subjects presenting mild to severe forms of acne needs to be
investigated.
A Kalayciyan,†* O Oguz,† H Bahar,‡ MM Torun,‡ EH Aydemir†
Departments of †Dermatology and ‡Clinical Microbiology,
University of Istanbul, Cerrahpasa Medical School, Istanbul, Turkey.
*Corresponding author, Cerrahpasa Tip Fak, Dermatoloji ABD,
Kocamustafapasa, Istanbul, Turkey,
tel. +90 2125884800 (ext. 1547);
fax +90 2125870505;
E-mail: [email protected]
References1 Lassus A, Salo O, Forstrom L et al. Treatment of acne with
selective-UV-phototherapy (SUP). An open trial. Dermatol
Monatsschr 1983; 169(6): 376–379.
2 Kjeldstad B, Johnsson A. An action spectrum for blue and
near UV inactivation of P. acnes; with emphasis on a possible
porphyrin photosensitization. Photochem Photobiol 1986; 43:
67–70.
3 Saint-Leger D, Bague A, Cohen E, Chivot M. A possible role for
squalene in the pathogenesis of acne. I. In vitro study of squalene
oxidation. Br J Dermatol 1986; 114: 535–542.
4 Jekler J, Berhbrant IM, Faergemann J, Larko O. The in vivo effect of
UVB radiation on skin bacteria in patients with atopic dermatitis.
Acta Derm Venereol (Stockh) 1992; 72: 33–36.
5 Gfesser M, Worret WI. Seasonal variations in the severity of acne
vulgaris. Int J Dermatol 1996; 35: 116–117.
6 Morison WL, Parrish JA, Block KJ. In vivo effect of UVB on
lymphocyte function. Br J Dermatol 1979; 101: 513–519.
7 Strauss SJ. Sebaceous glands. In: Fitzpatrick TB, Eisen AZ, Wollf K
et al., editors. Dermatology in General Medicine, 4th edn.
McGraw-Hill, New York, 1993: 709–726.16LetterLettersLetters
Cutaneous granulomas caused by corynebacterium minutissimum in an HIV-infected man
To the Editor
The term ‘coryneform bacteria’ is currently used to describe
Gram-positive, non-sporing, rod-shaped organisms. This hetero-
geneous group of bacteria is widely distributed in nature and
it includes Corynebacterium diphtheriae, the cutaneous aerobic
coryneforms (C. pyogenes, C. xerosis, C. hofannii, C. minutis-
simum and Brevibacterium epidermidis), as well as the anaerobic
Propionibacterium spp.1 Aerobic corynebacteria can be isolated
from normal human skin as saprophytic elements, but may
also be the cause of different skin pathologies.2 We describe
the case of an HIV-positive male with chronic granulomatous
lesions and subcutaneous abscesses on the legs from which
Corynebacterium minutissimum were isolated.
A 22-year-old man was referred for evaluation of 4-month-
old nodules on his legs; the four nodules were painful and one
had become suppurated, ulcerated and scarred. Past medical
history included parenteral heroin consumption. The man had
been seropositive for hepatitis B and C since 1997 and for HIV
since 1986. At the time of evaluation, his CD4+ T-cell count was
41/mL and HIV-1 RNA 102 000 copies/mL and he was under
treatment with didanosine (ddI), stavudine (dT4) and nelfinavir.
Physical examination revealed three indurated, hot, ery-
thematous, subcutaneous nodules on the front of the lower
extremities that were approximately 1 cm in diameter (fig. 1);
near one ankle there was an atrophic, depressed scarred plaque
(fig. 2). Skin biopsy specimens showed varying quantities of
neutrophils in the follicular infundibulum with suppuration.
The dermis showed rupture of the follicle at different levels of
the infundibulum and an abscess had formed. The inflamma-
tory cell infiltrate consisted of lymphocytes and histiocytes.
Cultures of biopsy material subjected to 24 h of incubation
on sheep blood agar grew non-haemolytic, non-lipophilic
fig. 1 The decrease in the number of S. aureus and P. acnes colonies
achieved with ultraviolet B irradiation.
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644 Letters
© 2002 European Academy of Dermatology and Venereology JEADV (2002) 16, 638–649
smooth colonies, 1 mm in diameter, which showed a positive
catalase reaction and negative urea and motility reactions.
Carbohydrate fermentation studies revealed fermentation of
glucose, sucrose maltose and fructose, and lack of fermentation
of xylose, lactose and mannitol.
Treatment with 500 mg oral erythromycin (every 6 h for
10 days) achieved a clinical cure.
Since Propionibacterium acnes was first described by Unna in
1893 there has been considerable discussion in the literature
whether corynebacteria play a part in the pathogenesis of cutane-
ous lesions or whether it is only a saprophytic contaminant.3
However, it is difficult to assess the significance of the bacteria
in the pathogenesis of the affections reported.
In recent years, there have been increasing numbers of
reports of non-diphtheria corynebacteria as the cause of serious
opportunistic infection.4 This can be explained by: (i) the large
number of immunocompromised subjects whose diagnosis
and treatment have become continually more intensive and
invasive; (ii) the increased ability to identify these species in the
laboratory; and (iii) the recognition of the pathogenic potential
of coryneform bacteria.5
Cases in which corynebacteria are involved in the aetiology
of granulomatous skin lesions have been published infre-
quently.3,6–8 In particular, Binelli et al. published two cases of
granulomatous mastitis associated with corynebacteria in
which antibiotics and surgery led to cure.6 Nobre et al.
described a case of granulomatous lesions and subcutaneous
abscesses on the legs caused by antibiotic-resistant C. acnes.3 In
our case, however, the treatment administered gave favourable
results.
We think that, as in our case, immunosuppression due to HIV
favours infection by these saprophytic elements and also favours
the formation of granulomas; this is similar to experimental
findings with C. parvum, which has been used in the induction
of hepatic granulomas, whereby granulomas occurred even in
the absence of lymphocytes CD4 and CD8 in laboratory rats.9
In our case, we consider the aetiopathology of corynebacteria
to be proven because (i) they were isolated in skin cultures from
a biopsy performed with classic asepsia of the skin with iodized
alcohol, and (ii) clinical cure resulted from treatment with
erythromycin.
J Santos-Juanes,† C Galache,† A Martínez-Cordero,† JR Curto,†
MP Carrasco,‡ A Ribas,‡ J Sánchez del Río†
†Service of Dermatology II, ‡Service of Pathology II, Hospital Central de
Asturias, University of Oviedo, Asturias, Spain. *Corresponding author,
Servicio de Dermatología II, Hospital Central de Asturias, C/Julian
Clavería s/n, Oviedo, Asturias, Spain,
tel. +34985106100/ext. 36559
References1 Hay RJ, Adrians B. Bacterial infections. In: Rook, Wilkinson, Ebling
Textbook of Dermatology. Blackwell Science Ltd, Oxford, 1998:
1131–1136.
2 Braun-Falco O, Plewig G, Wolff HH, Winkelmann RK.
Dermatología. Springler-Velag Iberica, Barcelona, 1995.
3 Nobre G, Caldeira B. Chronic granulomatous infection of the legs
associated with Corynebacterium acnes. Br J Dermatol 1969; 81:
548–550.
4 Funke G, VonGraevenitz A, Claridge JE, Bernard KA. Clinical
microbiology of coryneform bacteria. Clin Microbiol Rev 1997; 10:
125–129.
5 Bandera A, Gori A, Rossi MC et al. A case of costocondral abscess due
to Corynebacterium minutissimun in an HIV-infected patient. J Infect
2000; 41: 103–105.
6 Binelli C, Lorimier G, Bertrand G et al. Mastites granulomateuses et
corynébactéries: a propos de deux observations. J Gynecol Obstet Biol
Reprod 1996; 25: 27–32.
7 Edmiston CE, Walker AP, Krepel CJ, Gohr C. The nonpuerperal
breast infection: aerobic and anaerobic microbial recovery
from acute and chronic disease. J Infect Dis 1990; 162:
695–699.
8 Berger SA, Gorea A, Stadler J et al. Recurrent breast abscesses caused
by Corynebacterium minutissimum. J Clin Microbiol 1984; 20:
1219–1220.
fig. 1 A hot, erythematous, subcutaneous nodule.
fig. 2 A depressed, scarred plaque.
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Letters 645
© 2002 European Academy of Dermatology and Venereology JEADV (2002) 16, 638–649
9 Senaldi G, Shaklee CL, Mak TW, Ulich TR. Corynebacterium
parvum and Mycobacterium bovis bacillus calmette and Guerin-
induced granuloma formation in mice lacking CD4 and CD8.
Cell Immunol 1999; 193: 155–161.16LetterLettersLetters
Erythema multiforme associated with Trichophyton mentagrophytes infection
To the Editor
Erythema multiforme has a number of well known causes,
including infections (viral, bacterial, spirochaetal, rickettsial
and fungal), drugs, malignancy, connective tissue disorders and
idiopathic causes. Of the fungal causes, deep mycotic infections
such coccidioidomycosis and histoplasmosis are relatively
frequently associated with erythema multiforme, but super-
ficial mycoses are less frequently associated.
A 9-year-old boy presented with an acral, erythematous,
mildly pruritic, targetoid rash. Two weeks prior to this he had
noticed a pruritic, scaly patch on the dorsal aspect of his left
foot. This had spread between the fourth interdigital web space
to involve the adjacent plantar aspect of his foot. A week later he
then developed the more extensive lesions on his limbs. He was
otherwise well in himself and there was no preceding history of
coryzal symptoms, herpes simplex infection or drug ingestion.
On examination he had a well-circumscribed scaly patch on
the dorsal aspect of his left foot (fig. 1), which affected the
fourth web space, and also the plantar aspect of the foot. He also
had symmetrical erythematous macules, papules and plaques
some of which had a targetoid appearance (fig. 2) affecting his
hands, arms, legs and buttocks, including the palmar and
plantar aspects of his hands and feet. There was sparing of the
mucous membranes and he was apyrexial. Skin scrapings from
the scaly lesion on his foot showed fungal hyphae on micro-
scopy and grew Trichophyton mentagrophytes. Skin scrapings
from other lesions on his hands and body showed no evidence
of fungal infection. As the skin lesions were clinically typical of
erythema multiforme a skin biopsy was not undertaken and the
dermatophyte infection was treated with terbinafine cream.
The erythema multiforme resolved within 10 days as the der-
matophyte infection was brought under control and resolved
within 3 weeks.
Erythema multiforme affects all age groups but as many as
20% of cases are seen in children and adolescents. A recent
review1 of the causes of erythema multiforme in children over
a 20-year period revealed that 71% of cases were preceded by
infections. Of these Mycoplasma pneumoniae infection, acute
upper respiratory tract disease and herpes simplex infection
were the commonest causes. Superficial mycotic infection such
as T. mentagrophytes associated with erythema multiforme is
rare2,3 and probably represents an id reaction to the dermato-
phyte infection. Dermatophytide reactions typically take the
form of eczematous eruptions, although other reactions such as
erysipelas-like dermatitis, erythema annulare centrifugum, ery-
thema nodosum, pityriasis rosea-like reactions, urticaria and
erythroderma have been described.4
T. mentagrophytes is one of the two most common pathogens
in fungal foot infections and is probably the most common of
the acute infections, in contrast to T. rubrum which is more
often associated with chronic infection. This is because T. men-
tagrophytes induces a greater immune response and is therefore
more likely to produce a reaction such as erythema multiforme.
Although there is the possibility that the erythema multiforme
in this case was idiopathic, the close temporal relationship
between the dermatophyte infection and erythema multiforme
has led us to conclude that the erythema multiforme was related
to the T. mentagrophytes infection.
A Salim,* E Young
Department of Dermatology, Amersham Hospital, Whielden St,
Amersham, Bucks, HP7 OJD, UK.
*Corresponding author, Dermatology Department, Churchill Hospital,
Old Rd, Headington, OX3 7LJ, Oxford, UK,
tel. +1865 228272; fax +1865 228260;
E-mail: [email protected]. 1 Erythematous scaly eruption of Trichophyton mentagrophytes affect-
ing the right foot.
fig. 2 Erythema multiforme affecting the hands.
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646 Letters
© 2002 European Academy of Dermatology and Venereology JEADV (2002) 16, 638–649
References1 Villiger RM, von Vigier RO, Ramelli GP et al. Precipitants in 42 cases
of erythema multiforme. Eur J Paedtr 1999; 158: 929–932.
2 Rahman SA, Setoyama M, Kawahira M, Tashiro M. Erythema multiforme
associated with superficial fungal disease. Cutis 1995; 55: 249–251.
3 Subban SA, Kamalam A, Thambiah AS. Erythema multiforme in
dermatophytosis. Mykosen 1979; 23(8): 452–455.
4 Burton JL, Holden CA. Eczema. In: Textbook of Dermatology
(Champion RH, Burton JL, Burns DA, Breathnach SM, eds),
6th edn, Vol. 1. Oxford: Blackwell Science Ltd, 1998:
637–638.16LetterLetterLetterxxxxxxxxx
Localized bullous pemphigoid as an unusual complication of radiation therapy
To the Editor
Here we present a patient who initially developed localized
bullous pemphigoid (BP) after radiation therapy for breast
carcinoma.
A 94-year-old woman was admitted in May 1999 with cancer
of her left breast (T3 N1 M1, stage IV), but surgical excision was
not performed because of her advanced age. The woman
received only primary radiation therapy with a total dose of
6000 cGy on her left breast and axillary region. Four months
after the radiation therapy, she developed bullous skin lesions
and eroded areas at the irradiation site of her left breast (fig. 1)
and 2 weeks later the eruption became generalized. Clinical
examination revealed multiple tense blisters filled with clear
fluid and several denuded lesions on the left breast, abdominal
region, arms and legs (fig. 2). Complete blood count, urinalysis,
erythrocyte sedimentation rate, liver function tests, renal
function tests, serum electrolytes, total proteins, and amino
acid profile were normal.
Histological examination revealed subepidermal blisters
with significant eosinophil infiltration in the dermis. Direct
immunofluorescent examination showed linear deposits of IgG
and C3 along the basement membrane zone.
Complete healing was obtained in 3 weeks with 60 mg/day
(1 mg/kg) oral prednisolone therapy.
BP is an unusual side-effect of radiation. To date some case
reports of radiation therapy-induced BP have been published,
including two subjects with initially generalized lesions1,2 and
several in whom the lesions were limited strictly to irradiated
areas.3–7
Our case involved a woman with metastatic breast carci-
noma who developed BP lesions that were initially limited to
irradiated areas and then became disseminated about 2 weeks
later. The diagnosis was confirmed by routine histological
examination and immunofluorescent study. Mastectomy had
not been performed because of the woman’s advanced age and
she received only radiation therapy. There was no other
explanation to account for the onset of the BP, such as
psoralen + ultraviolet A or ultraviolet B.5 To date only four
other cases have been reported in which the BP lesions were
limited to irradiated areas at the beginning then became
disseminated as in our patient.8–11 It has not yet been clarified
how radiation therapy induces BP lesions. The radiation therapy
may alter the normal structures of the basement membrane
zone resulting in the production of autoantibodies against a
new BP antigen.5,6 On the other hand, according to Bernhardt’s
hypothesis,3 these subjects may already have circulating
anti-basement membrane antibodies at a low titre and the
tissue damage caused by radiation therapy may enhance the
deposition of antibodies at the basement membrane zone. We
think that it is very important for dermatologists and radiation
oncologists to recognize promptly the onset of initially localized
radiation therapy-induced BP because it responds rapidly to
oral prednisolone therapy.
E Çalikoglu,†* R Anadolu,‡ C Erdem,‡ T Çalikoglu§
†Department of Dermatology, Fatih University Medical School, Ciftlik
cad. No: 57, 06510 Emek, Ankara, Turkey, ‡Department of Dermatology,
Ankara University Medical School, Ankara, Turkey, §Ankara Demetevle
Oncology Hospital, Ankara, Turkey. *Corresponding author,
fax: +90 3122213276; E-mail: [email protected]. 1 Eroded areas on the left breast.
fig. 2 Tense blisters with clear fluid on the left arm.
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Letters 647
© 2002 European Academy of Dermatology and Venereology JEADV (2002) 16, 638–649
References1 Ive FA. Metastatic carcinoma of cervix with acanthosis nigricans,
bullous pemphigoid and hypertrophic pulmonary osteoarthropa-
thy. Proc R Soc Med 1963; 56: 910.
2 Abadir R. Pemphigoid, bronchial neoplasm and radiotherapy. Proc
R Soc Med 1967; 33: 1271.
3 Bernhardt M. Bullous pemphigoid after radiation therapy. J Am
Acad Dermatol 1989; 20: 14.
4 Sheerin N, Bourke JF, Holder J et al. Bullous pemphigoid
following radiotherapy. Clin Exp Dermatol 1995; 20: 80–82.
5 Cliff S, Harland C, Fallowfield ME, Mortimer PS. Localised bullous
pemphigoid following radiotherapy. Acta Derm Venereol (Stockh)
1997; 76: 330–331.
6 Ohata C, Shirabe H, Takagi K et al. Localized bullous pemphigoid
after radiation therapy: two cases. Acta Derm Venereol (Stockh)
1997; 77: 157.
7 Knoeel KA, Patterson JW, Gampper TJ, Hendrix JD. Localized
bullous pemphigoid following radiotherapy for breast carcinoma.
Arch Dermatol 1998; 134: 514–415.
8 Emery FW, Hare PJ, Abadir R. Pemphigoid, bronchial neoplasm
and radiotherapy. Proc R Soc Med 1967; 60: 1271–1272.
9 Furukowa F, Ozaki M, Imamura S, Hirose S. Bullous pemphigoid
associated with radiotherapy for oesophageal carcinoma.
Dermatologica 1981; 162: 451–455.
10 Duschet P, Schwartz T, Gschait F. Bullous pemphigoid
after radiation therapy. J Am Acad Dermatol 1988; 18: 441–
444.
11 Jappe U, Bonnekoh B, Gollnick H. Guess what! Initially localized
bullous pemphigoid at the irradiation site of breast carcinoma. Eur
J Dermatol 1999; 9(2): 139–141.16LetterLetterLetter
Death due to pulmonary tuberculosis in progressive systemic sclerosis
To the Editor
For 5 years a 58-year-old woman had presented with symptoms
of progressive systemic sclerosis (SSc), including heart, lung
and kidney involvement and doubtful involvement of the
oesophagus. The cutaneous involvement included tightening,
swelling of hands and feet with transition on arms and
legs, partly with fibrotic induration. Additionally we observed
a rigid face with telangiectases and Raynaud’s phenomenon.
Nailfold microscopy showed some loop dropout and
dilation.
Initial antinuclear antibodies were found in her serum at titre
of 1 : 20 000 using HEP-2 cells and anti-Pm-SCL antibody.
Myological studies (electromyogram, creatinine kinase) were
normal. There was only a discrete pulmonary fibrosis on the
chest X-ray and high-resolution computed tomography (CT).
Results of pulmonary function tests were within normal ranges.
Tuberculin allergy was not tested before.
The immunosuppressive therapy included methylpredniso-
lone (Urbasone®) 8–12 mg/d and azathioprine (Imurek®) 75–
100 mg/d for 4 years; later, mycophenolatmophetil (CellCept®)
2000 mg/d for 3 months was given. Some years ago penicillin G
and iloprost (Ilomedin®) infusions were used.
In January 2001 she began to deteriorate with increasing
fatigue, malaise and weight loss. Additionally, relapsing fever
up to 39 °C occurred. The following abnormal results in
laboratory tests were detected: raised potassium (5.4 mmol/L),
very high C reactive protein (136.6 mg/L) and low haemo-
globin (5.0 mmol/L). High-resolution CT scan of the thorax
only confirmed the presence of interstitial lung disease.
Furthermore, increasing reduction of vigilance presented
beyond somnolence, thus the patient was ventilated and
transferred to the intensive care unit. Pneumonia was detected
by bronchoscope and X-ray of the thorax. Microscopically,
bronchoalveolar lavage samples showed acid-fast bacilli and
the culture grew on Löwenstein–Jensen medium Mycobacte-
rium tuberculosis. A diagnosis of pulmonary tuberculosis
was confirmed. Despite tuberculostatic therapy (rifampicin,
isoniazid, streptomycin, ethambutol) the patient died of
septic shock.
Clinical features, chest X-rays, high-resolution CT and
echocardiogram findings were all typical of SSc and not
suggestive of tuberculosis.
M. tuberculosis infection in SSc is thought to be uncommon
because reported cases are rare: one report of a Japanese
Canadian patient,1 and two additional Russian case reports2,3
have been published. Cowie4 described a 40% incidence of prior
tuberculosis in black South African gold miners with SSc. He
concluded that there was an association between tuberculosis
and SSc independent of silica exposure or silicosis. It does
appear that the tuberculosis in these patients pre-dated
their SSc.4
SSc is accepted to be an autoimmune connective tissue
disease, although the precise mechanism of immune acti-
vation and perpetuation is yet unclear. Abnormalities of
both the cellular and humoral arms of the immune system
are described.5 Reduced numbers of circulating T lymphocytes
and decreased lymphocyte proliferation has been noted.6,7
It has been suggested that the subpopulation of T lym-
phocytes regulating cell-mediated immunity is selectively
reduced in SSc.8 Administration of mycophenolatmophetil,
azathioprine and methylprednisolone block the proliferation
of B and T cells in different ways and may be one of the major
factors predisposing to infection, such as tuberculosis or
aspergillosis.9 Protection from a M. tuberculosis infection
requires an intact cell-mediated immune response. Antibody
production is considerable, but this does not contribute to
protection.
Alternatively, tuberculosis could have triggered the
SSc. There is some evidence that microbial antigens are impor-
tant immunological triggers in several autoimmune disorders.
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© 2002 European Academy of Dermatology and Venereology JEADV (2002) 16, 638–649
Possible mechanisms have been reviewed by Behar and
Porcelli.8 Structural similarity or molecular mimicry of
microbial antigens to host antigens may lead to an
immune response that becomes sustained. Infection due to
M. tuberculosis frequently occurs in latent forms. Dormant
viable bacilli may stimulate an immune response, and
reactivation usually creates a brisk response. High levels of
circulating antibodies to 65 kDa M. tuberculosis antigen, a
heat shock protein, was found in sera of patients with SSc
(47%).10
In conclusion, it is not clear if our patient presented a new
infection with M. tuberculosis or reactivation of a not yet detected
focus. Responsible to acquire the tuberculosis was – we
suppose – either the immunosuppressive therapy or the
immunodysfunction in the SSc patient.
B Manz,* F Noack-Wiemers, M Mittag, U-F Haustein, P Nenoff
Department of Dermatology, Universitiy Leipzig, Stephanstraße 11,
D-04103 Leipzig, Germany. *Corresponding author, tel. +49(0)341/
9718715; fax +341/9718609; E-mail: [email protected]
References1 Roddy J. Holby S, Seigel S. Scleroderma concurrent with culture
proven tuberculosis in a Japanese Canadian patient. J Reumatol
1996; 23: 2168–2170.
2 Tiukhtin NS, Berlova ZD. Exudative pleurisy with a tuberculous
etiology in a patient with systemic scleroderma [in Russian]. Probl
Tuberk 1979; 3: 68–70.
3 Kazak TI, Teriaeva MV, Turintsev BB, Davlinskaia OI. A case of
steroid tuberculosis in systemic scleroderma [in Russian]. Probl
Tuberk 1996; 2: 57–58.
4 Cowie RL. Silica-dust-exposed mine workers with scleroderma
(systemic sclerosis). Chest 1987; 92: 260–262.
5 Haustein UF, Anderegg U. Pathophysiology of scleroderma: an
update. J Eur Acad Dermatol Venereol 1998; 11: 1–8.
6 Whiteside TL, Kumagai Y, Roumm AD et al. Suppressor cell
function and T lymphocyte subpopulations in peripheral blood of
patients with progressive systemic sclerosis. Arthritis Rheum 1983;
26: 841–847.
7 Baron M, Keystone EC, Gladman DD et al. Lymphocyte
subpopulations and reactivity to mitogens in patients with
scleroderma. Clin Exp Immunol 1981; 46: 70–76.
8 Behar SM, Porcelli SA. Mechanisms of autoimmune disease
induction. The role of the immune response to microbial
pathogens. Arthritis Rheum 1995; 38: 458–476.
9 Nenoff P, Horn LC, Mierzwa M et al. Peracute disseminated
fatal Aspergillus fumigatus sepsis as a complication of
corticoid-treated systemic lupus erythematosus. Mycoses 1995;
38: 467–471.
10 Daniele MG, Candela M, Ricciatti AM et al. Antibodies to
mycobacterial 65 kDa heat shock protein in systemic sclerosis
(scleroderma). J Autoimmun 1992; 5: 443–452.
16LetterLettersLettersxxxxxxxControversies concerning the cure process in patients with pemphigus vulgaris
To the Editor
Pemphigus vulgaris (PV) is an autoimmune bullous skin disease
characterized by the presence of pathogenic autoantibodies in
the patient’s serum. PV requires long-term immunosuppressive
treatment. Clinical remission and negative results of immuno-
logical studies are well known criteria of definite cure.
Relapses of the disease in some patients after cessation of treat-
ment suggest the need for more sensitive tests to prove complete
cure. We performed examinations on the oesophageal mucous
membranes of PV patients who were in clinical remission and
the results of direct immunofluorescence (DIF) and indirect
immunofluorescence (IIF) tests were negative. We found that
pemphigus autoantibodies bound in intercellular spaces of the
oesophageal epithelium are observed for a longer time than in
the skin and circulation. David1 describes the relapse of the
disease after the discontinuation of treatment in one of eight
patients, perhaps due to low concentrations of pathogenic
autoantibodies in the serum that could not be detected by
routine methods.
In conclusion, we completely agree with the authors of the
letter that DIF examination of the skin and IIF test of the serum
in PV subjects in clinical remission are convenient. However,
our studies indicate that oesophageal examination gives better
and more highly sensitive results than examination of the skin.
Negative results of this examination is proof of complete cure.
None of our PV subjects with negative findings to DIF tests on
oesophageal membranes experienced relapse of the disease after
discontinuing treatment.2
JD Torzecka*
Department of Dermatology Medical University of Lodz, 94-017 Lodz,
Poland. *Correspondence address, fax +48 42 68 84 565;
E-mail: [email protected]
References1 David M. A useful criterion of cure in pemphigus vulgaris. J Eur Acad
Dermatol Venereol 2000; 14: 327.
2 Torzecka JD, Waszczykowska E, Wozniacka A et al. Immunopath-
ological examination of oesophagus as a useful criterion of cure in
pemphigus vulgaris. J Eur Acad Dermatol Venereol 1999; 12: 115–118.16LetterLetterLetter
Lichen planopilaris and autoimmune thyroiditis
To the Editor
Lichen planus is a benign cutaneous and mucous disease
of unknown aetiology that may have an autoimmune patho-
genesis. Lichen planopilaris is a rare and distinctive variety
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Letters 649
© 2002 European Academy of Dermatology and Venereology JEADV (2002) 16, 638–649
of lichen planus that selectively involves hair follicles and
causes scarring alopecia.1 At the onset there are violaceous
papules, erythema and desquamation. Later on follicular keratosis
appears in the absence of hair follicles. Histopathological
examination shows hyperkeratosis, acanthosis, increased
granular layer and degeneration of the basal cell layer.2 A band-
like lymphocytic cell infiltrate is present in the upper dermis
and the sebaceous glands are reduced in size or absent. Direct
immunofluorescent examination demonstrates cytoid bodies
and a linear deposit of fibrin along the dermoepidermal junction.
Lichen planus and its planopilaris variety are frequently
associated with autoimmune diseases, such as thymoma,
myasthenia gravis and alopecia. We report here the first case of
lichen planopilaris associated with autoimmune thyroiditis.
A 65-year-old woman presented to the Department of
Biomedical and Surgical Sciences (Section of Dermatology
and Venereology, Verona, Italy) with a defined patch of scalp
alopecia. Dermatological examination revealed a 5 × 4 cm,
oval-shaped, scarred plaque of hair loss on the vertex, with an
irregular border and some remaining tufts of hair. There were
erythematous to violaceous follicular and keratotic papules at
the periphery of the plaque. These manifestations had appeared
3 years before on the vertex and had later enlarged progres-
sively. The woman came to our department complaining of
intense itching that had started a few weeks before. There were
no other skin lesions, but we observed pitting on some of
the nails of the right hand. During the previous 2 years,
the patient had taken l-thyroxine for an autoimmune
hypothyroidism.
A scalp biopsy was taken and the examination by direct
immunofluorescence confirmed the diagnosis of lichen
planopilaris. The histopathological examination of the biopsy
material showed hyperkeratosis, hypergranulosis and a coarse
vacuolization of the basal cell layer. A dense perifollicular,
band-like, lymphocytic inflammatory cell infiltrate was observed.
The pilosebaceous apparatus was absent and replaced by dense,
eosinophilic, fibrous tissue.
Direct immunofluorescent examination showed cytoid
bodies of IgM along the basement membrane and a linear
deposit of fibrin along the dermoepidermal junction.
Blood tests confirmed only the presence of hypothyroidism
(FT4 = 19.8 ng/L, FT3 = 3.6 ng/L, thyroid-stimulating
hormone < 0.1 mUI/L) with positive antithyroid antibodies
(antithyroglobulin = 3940 U/mL, antimicrosomal = 1630 U/mL).
All other laboratory values were normal, including biochemical
analysis, antinuclear antibodies and antihepatitis C virus
antibodies.
Treatment with a medium potency topical corticosteroid
(prednicarbate) stopped both the itching and the acute phase of
the disease within 40 days. Over the next 2 years of follow up, no
relapse was observed.
Lichen planus and the planopilaris variety may be linked
to an alteration of immune tolerance. In lichen planus,
lymphocytes destroy keratinocytes, which show an unknown
antigen on their surface. The association of lichen planus
and viral hepatitis or certain drugs has been reported in the
literature, but it is not known why keratinocytes become a target.
One hypothesis is that viral proteins or drugs could connect to
the membrane of keratinocytes and work as haptens. In lichen
planus, cellular immunity is strongly involved with a typical
lymphocytic inflammatory cell infiltrate. Lichen planus is
frequently associated with autoimmune or immune-based dis-
eases, such as hepatitis, thymoma, myasthenia, Crohn’s disease,
ulcerative colitis and diabetes.3,4 The association between lichen
planus and other cutaneous autoimmune diseases, such as
dermatitis herpetiformis,5 vitiligo and alopecia areata6 has been
reported in the literature. As far as we know, the association
with autoimmune thyroiditis has never been described.
Thyroid diseases are frequently linked to other cutaneous
diseases, such as alopecia areata and vitiligo, which many invest-
igators consider as autoimmune diseases. Further studies are
required to verify the existence of pathogenetic mechanisms
common to lichen planopilaris and autoimmune thyroiditis.
Lichen planus is caused by cell-mediated immunity, while
thyroiditis is caused by antibody-mediated immunity. This
partial contradiction could be explained by the fact that
autoimmunity may be caused by lack of tolerance (and therefore
decreased T-cell activity) that could influence both T cells
(cell-mediated immunity) and B cells, resulting in increased
antibody production.
P Rosina, C Chieregato, M Magnanini, A Barba
Department of Biomedical and Surgical Sciences, Section of Dermatology
and Venereology, P.le Stefani 1, 37126 Verona, Italy.
*Corresponding author, tel. +39 45 8072547; fax +39 45 8300521;
E-mail: [email protected]
References1 Mehregan DA, Van Hale HM, Muller SA. Lichen planus pilaris:
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Dermatol 1992; 27: 935–942.
2 Matta M, Kibbi Ag Khattar J et al. Lichen planopilaris: a
clinicopathologic study. J Am Acad Dermatol 1990; 22: 594–598.
3 Gruppo Italiano Studi Epidemiologici in Dermatologia.
Epidemiological evidence of the association between lichen planus
and two immune-related diseases. Alopecia areata and ulcerative
colitis. Arch Dermatol 1991; 127: 688–691.
4 Kurgansky D, Burnett JW. Widespread lichen planus in
association with Turner’s syndrome and multiple endocrinopathies.
Cutis 1994; 54: 108–110.
5 Isaac M, McNeely CM. Dermatitis herpetiformis associated with
lichen planopilaris. J Am Acad Dermatol 1995; 33: 1050–1051.
6 Aloi PG, Colonna SM, Manzoni R. Association of lichen ruber
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