CLINICAL SNIPPETS

Imiquimod: Clinical Effects

Hadley and co-workers analyzed
data from five randomized, dou-
ble-blind, controlled trials lasting
12–16 weeks and involving 1,293
patients to assess the cost and ben- Paying the Toll
efits of the immune response modi- Imiquimod’s antitumoral and
fier imiquimod in treating actinic antiviral efficacy is mediated
keratosis (AK). Complete clearance through the Toll-like receptor
of AK occurred in 50% of patients 7 (TLR7) and TLR8 signaling
treated with imiquimod compared cascade, but Schön et al.
with 5% of those treated with con- have demonstrated that
trol. The proportion of patients with adverse events was substantially higher with imiquimod has broader
imiquimod than with control. Imiquimod 5% cream was found to be effective in and more complex
preventing the development of squamous-cell carcinoma. Future research might biological activity than
elucidate optimal dosing to minimize adverse events and evaluate long-term recur- previously recognized.
rence. See page 1251 The authors propose
imiquimod generates
inflammation via two
A Locus for Inversa Acne complementary mechanisms:
Inversa acne (hidradenitis suppurativa) is usu- it induces the production of
ally localized in non-facial regions and is proinflammatory mediators
worldwide in distribution. The genetic basis of via the known TLR7- and
acne inversa is unknown. Gao and colleagues TLR8-dependent signaling
performed a genome-wide scan in a four-gen- pathways, and antagonizes
eration Chinese family to map the chromosome an important suppressive
location of the responsible gene. They identi- feedback mechanism through
fied a locus at chromosome 1p21.1–1q25.3 A2A adenosine receptor. See
and observed the range of markers. This first page 1338
locus for acne inversa will be a starting point
for understanding the molecular mechanisms
of this disease. See page 1302

Suppressing Keloids
Desmoglein 4 and Beaded Hair Modulation of vascular
Localized autosomal recessive hypotri- endothelial growth factor
chosis (LAH), a recently defined disorder (VEGF) production may treat
characterized by fragile, short, sparse keloids. Wu et al. treated
hairs on the scalp, trunk, and extremities, primary keloid fibroblast (KF)
has been traced to mutations in the des- cultures with dexamethasone,
moglein 4 (DSG4) gene. In three siblings VEGF-A antibody, and a VEGF
of Iraqi and Iranian origin with LAH, con- receptor-2 antagonist VEGF
genital scalp erosions and monilethrix- protein. It appears that
like hairs are now also attributed to LAH. dexamethasone suppresses
Schaffer and colleagues’ observations KF proliferation and
of novel heterozygous DSG4 mutations downregulates endogenous
broaden the phenotypic and genotypic VEGF expression. See page
spectrum of LAH. Increasing clinical 1264
awareness of LAH in the differential diag-
nosis of autosomal forms of hypotrichosis will allow identification of more cases and
help to better define the range of pathogenic DSG4 mutations. See page 1286

Journal of Investigative Dermatology (2006) 126, 1197. doi:10.1038/sj.jid.5700370

© 2006 The Society for Investigative Dermatology www.jidonline.org 1197