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VOLUME 68, NUMBER 5

and glycylrrhizin have been used in adults but, with

the exception of dapsone, are generally not recom-
mended for children.
Eosinophilic folliculitis of infancy was reported to
be associated with HIV in 1 case. This 8-month-old
male presented with the typical lesions of eosino-
philic folliculitis but also had generalized lymphad-
enopathy, oral thrush, pallor, and hepatomegaly.
The main differences on physical examination can
include discrete, erythematous, urticarial follicular
papules with crusting and excoriations. HIV-
associated eosinophilic folliculitis is a marker of
AIDS in these patients. Their CD4 count is \300
cells/mm3, they may have eosinophilia, and their
leukocyte count is variable. The disease is usually
more widely distributed and more persistent than
eosinophilic folliculitis without the HIV association.
Treatment includes topical corticosteroids and
highly active antiretroviral therapy.
For this series, the recommended choices are: 1, b;
2, c; 3, c; 4, a; 5, c.

BIBLIOGRAPHY
Buckley DA, Munn SE, Higgins EM. Neonatal eosinophilic pustular
folliculitis. Clin Exp Dermatol 2001;26:251-5.
Lucky AW, Esterly NB, Heskel N, Krafchik BR, Solomon LM.
Eosinophilic pustular folliculitis in infancy. Pediatr Dermatol
exposed and covered sites. Biopsy specimens were
1984;1:202-6. obtained from the pigmented areas. Fontana-Masson
Ofuji S. Eosinophilic pustular folliculitis. Dermatologica 1987;174: and Perls stains are shown in Fig 8 and 9.
53-6.
Ramdial PD, Morar B, Dlova NC, Aboabaker J. HIV-associated 6. What is the most likely diagnosis?
eosinophilic folliculitis in an infant. Am J Dermatopathol 1999; a. Arcuate dermal erythema
21:241-6. b. Morphea
c. Hansen disease
d. Lupus vulgaris
Posttreatment lesional hyperpigmentation e. Tinea corporis
Parvathi Mudigonda, MD, Howard P. Ragland, MD,
7. What is the most likely causative agent of the
and Andrea Murina, MD
patients subsequent hyperpigmentation?
New Orleans, Louisiana
a. Dapsone
A 63-year-old man presented to the dermatology b. Bactrim
clinic with a 1-year history of numerous erythema- c. Rifampin
tous, asymptomatic, annular plaques on his abdo- d. Minocycline
men, arms, and legs (Fig 5). His social history e. Amiodarone
included a long career as a trapper in the south
8. What is the type of hyperpigmentation associ-
Louisiana marshland; none of his close contacts had a
ated with the causative agent that is deposited
similar outbreak. He reported no sensory loss; how-
at locations of inflammation and scarring?
ever, on physical examination, he had a stocking
a. Type I
pattern of numbness that extended from his feet to his
b. Type II
ankles. Laboratory studies, including an antinuclear
c. Type III
antibody panel, a rapid plasma reagin test, rheuma-
d. Type A
toid factor, and erythrocyte sedimentation rate, were
e. Type C
within normal limits. Biopsy specimens with special
stains are shown below (Fig 6). Three months after 9. In what manner does type II hyperpigmentation
initiating treatment with minocycline and rifampin, generally stain?
he presented with patches of blue-black pigmenta- a. Positive Perls stain, negative Fontana-Masson
tion limited to lesional areas (Fig 7), in both sun- stain
880 JAAD grand rounds
b. Positive Prussian blue stain, negative
Fontana-Masson stain
c. Positive Perls stain, positive Fontana-Masson
stain
d. Negative Prussian blue stain, negative
Fontana-Masson stain
e. Negative Perls stain, negative Fontana-
Masson stain
Discussion
Hansen disease (HD) is a chronic granulomatous
disease with insidious onset caused by the acid-fast
bacillus Mycobacterium leprae. It is an obligate
J AM ACAD DERMATOL
MAY 2013
intracellular parasite that has a slow generation
time and has no known artificial growth medium.
The bacterium grows well in selected animals
particularly armadillos, because of their low core
body temperature. Person-to-person transmission is
thought to occur via aerosolized particles from the
upper respiratory tract; however, contact with high-
risk animals also poses a significant risk. The diag-
nosis of HD should be considered in any patient
presenting with cutaneous lesions and sensory loss,
particularly in areas where HD is still prevalent, such
as Louisiana, Mississippi, and Texas, and in immi-
grants from endemic countries.
HD has a broad clinical presentation, ranging
from tuberculoid (early) to lepromatous (late). The
hosts immunity, specifically the cell-mediated re-
sponse, determines the severity of HD and its prog-
nosis. In early or tuberculoid leprosy, a strong
immune response is seen that corresponds to a
lymphocytic TH1 profile with high levels of
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VOLUME 68, NUMBER 5
interferon gamma and interleukin (IL)-2. Conversely,
in more advanced lepromatous leprosy, a TH2 re-
sponse with IL-4, IL-5, and IL-10 is observed. These
cytokines may play a role in suppressing interferon
gamma and IL-2 and therefore inhibit the cell-
mediated arm of immunity. M leprae is an intracel-
lular pathogen and as such, the TH2 response cannot
effectively eradicate the organisms.
The recommended first-line treatment for HD
includes dapsone. In this particular case, the patient
deferred the use of dapsone because of its side
effects. Minocycline has been used, primarily for
bacterial diseases and acne. Because of its safety
profile in long-term use, findings strongly support its
application to the treatment of HD as an accepted
alternative for patients who are unable to tolerate
dapsone. Notably, it is the only tetracycline exhibit-
ing bactericidal activity against M leprae, which is
likely related to its lipophilicity. Side effects are
generally mild and include gastrointestinal discom-
fort, dizziness, and pigmentation of skin and mucous
membranes. Hyperpigmentation from minocycline
therapy results from reactive metabolites that com-
bine to form black pigment. Minocycline-induced
hyperpigmentation has been divided into 3 cate-
gories: type I is the most common, presenting as a
blue-black discoloration in areas of inflammation or
scarring, and type II appears on normal, unaffected
skin as a blue-gray discoloration, typically seen on
the shins and other extensor surfaces. The third and
least common type involves a diffuse muddy brown
color imparted to sun-exposed areas, which may
correspond to a low-grade photosensitivity reaction.
Histologically, type I hyperpigmentation is a result of
hemosiderin deposition and as such, lesions stain for
iron and not for melanin. Type II lesions are caused
by both hemosiderin and melanin and both can be
confirmed by appropriate staining. Type III lesions
have increased amounts of melanin only and are
negative for iron.
Minocycline was effective in clearing HD in this
patient, based on subsequent negative biopsy spec-
imens and his improved clinical condition.
However, he experienced a peculiar type of hyper-
pigmentation secondary to minocycline therapy.
The lesions clinically had a type I reaction (blue-
black pigment limited to his lesions). However,
histochemical studies revealed a type II pattern,
with both iron and melanin deposits in the pig-
mented areas. The patient elected to continue
minocycline therapy and had no aversion to the
hyperpigmentation. The only other documented
case of this combined type of posttreatment hyper-
pigmentation was also reported in a patient with
HD who was treated with minocycline.
JAAD grand rounds 881
For this series, the recommended answers are: 6,
c; 7, d; 8, a; 9, c.
BIBLIOGRAPHY
Argenyi ZB, Finelli L, Bergfeld WF, Tuthill RJ, McMahon JT, Ratz JL,
et al. Minocycline-related cutaneous hyperpigmentation as
demonstrated by light microscopy, electron microscopy and
X-ray energy spectroscopy. J Cutan Pathol 1987;14:176-80.
Bowen AR, McCalmont TH. The histopathology of subcutaneous
minocycline pigmentation. J Am Acad Dermatol 2007;57:
836-9.
Britton WJ, Lockwood DN. Leprosy. Lancet 2004;363:1209-19.
Fleming CJ, Hunt MJ, Salisbury EL, McCarthy SW, Barnetson RS.
Minocycline-induced hyperpigmentation in leprosy. Br J
Dermatol 1996;134:784-7.
James WD, Berger TG, Elston DM, Odom RB. Andrews diseases of
the skin: clinical dermatology. 10th ed. Philadelphia: Saunders
Elsevier; 2006.
Moschella SL. An update on the diagnosis and treatment of
leprosy. J Am Acad Dermatol 2004;51:417-26.
Annular plaques and craniosynostosis
April Taylor, BS,* Roselynn H. Nguyen, BA,* Donald A.
Glass, II, MD, PhD, and Nnenna G. Agim, MD
Dallas, Texas
A 2-year-old developmentally delayed girl was
referred for the evaluation of a skin eruption that
had delayed corrective surgery for craniosynostosis.
Her medical history was significant for being born
with an imperforate anus after an uncomplicated
pregnancy and delivery. The skin lesions began
shortly after birth, progressively worsened, and
were variably pruritic and tender. The physical
examination revealed erythematous thin plaques
on the cheeks. She also had erythematous annular
plaques of varying thickness with a firm, raised,
thread-like border in the photodistributed areas of
the extremities (Figs 10-12). Histologic evaluation of
the lesions on the cheeks revealed a nonspecific
lichenoid infiltrate, erosions, and some spongiosis
(Fig 13).
10. What other finding is associated with this
patients syndrome?
a. Acanthosis nigricans
b. Cutis vertices gyrata
c. Acneiform lesions
d. Genitourinary abnormalities
e. Brachydactyly
11. What form of inheritance should be sought in
the family pedigree?
a. Autosomal dominant
b. Autosomal recessive
c. X-linked dominant
*These authors contributed equally to this article.