Cutaneous lesions of the nose

Abstract

Skin diseases on the nose are seen in a variety of medical disciplines. Dermatologists, otorhinolaryngologists, general practitioners and general plastic and dermatologic surgeons are regularly consulted regarding cutaneous lesions on the nose. This article is the second part of a review series dealing with cutaneous lesions on the head and face, which are frequently seen in daily practice by a dermatologic surgeon. In this review, we focus on those skin diseases on the nose where surgery or laser therapy is considered a possible treatment option or that can be surgically evaluated.

Full text

HEAD & FACE MEDICINE
Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Open Access
REVIEW
© 2010 Sand et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited.
Review
Cutaneous lesions of the nose
Michael Sand*
1
, Daniel Sand
2
, Christina Thrandorf
1
, Volker Paech
1
, Peter Altmeyer
1
and Falk G Bechara
1
Abstract
Skin diseases on the nose are seen in a variety of medical disciplines. Dermatologists, otorhinolaryngologists, general
practitioners and general plastic and dermatologic surgeons are regularly consulted regarding cutaneous lesions on
the nose. This article is the second part of a review series dealing with cutaneous lesions on the head and face, which
are frequently seen in daily practice by a dermatologic surgeon. In this review, we focus on those skin diseases on the
nose where surgery or laser therapy is considered a possible treatment option or that can be surgically evaluated.
Review
Anatomical characteristics
The nose is the central part of the mid-face and has an
important functional, aesthetic and psychological role.
Nasal respiration, olfaction and phonation are among its
most important functional roles. In addition, the aes-
thetic importance and its impact on the individual psyche
have been the subjects of many previous studies [1-3]. For
example, when looking at a face, observers spend the
largest amount of gaze time on the nose and eyes, under-
scoring its prominent position in the central face [4].
Because of this exposed, highly visible localization,
lesions on the skin of the nose are often noticed by
patients themselves, typically very early in the course of
the disease. The exposed localization on the face is also
cause for increased exposure to ultraviolet (UV) light,
which represents one of the most dangerous strains for
the skin in this particular location because it is a proven
carcinogen. This accounts for the high incidence of can-
cerous involvement of the skin of the nose, which has
proven to be the most common site for skin cancer on the
human body [5]. Furthermore, this has lead to the
description of the face as a "sun terrace," referring to the
skin of the forehead, ears and nose, because the angle of
the skin toward sunlight at these locations is more acute
than elsewhere. Consequently, UV light exposure is
increased, which also includes exposure to the dangerous
UV-B spectrum (290-320 nm), shown to be one of the
most potent skin carcinogens. Typical UV-B-induced
DNA damage involves the generation of dimeric photo-
products between adjacent pyrimidine bases. The tumor
suppressor gene p53 is a common target of UV-R-
induced mutations. Moreover, UV-A generates highly
reactive free radicals, damaging DNA and promoting skin
cancer. In addition to its role as a potent carcinogen, UV-
A is responsible for damage to the collagen structure,
leading to accelerated skin aging [6].
The skin of the nose shows several specific anatomical
and histological peculiarities that should be considered
when evaluating skin lesions on the nose or when plan-
ning the reconstruction of surgical defects [7]. The skin in
the areas of the dorsum, columella and sidewalls is thin,
loose, compliant and relatively less sebaceous [8,9]. The
skin in the areas of the nasal tip and alae is thicker, more
sebaceous, more adherent and less flexible [4]. Surgical
procedures on the skin of the nose have to respect these
different qualities and the nasal topography, including the
nasal aesthetic subunits, to achieve the best possible
result. The different aesthetic subunits are the tip sub-
unit, columella subunit, dorsal subunit, right and left alar
base subunits, right and left alar side wall subunits and
right and left dorsal side wall subunits [10]. The anatomi-
cal nasal subunits include the dorsum, sidewalls, lobule,
soft triangles, alae and columella. The concept of sub-
units of the external tissue of the nose has proven useful
for planning reconstruction. If more than 50% of the sub-
unit is lost it is favorable to replace the whole subunit
with regional tissue or a transplant from a donor site [11].
The most important skin diseases on the nose that can
require surgical consultation or successfully undergo
laser therapy are described below. The description of all
dermatoses that can involve the nose would extend
beyond the scope of this review. Therefore, our descrip-
tion is limited to those calling for laser or surgical therapy
* Correspondence: michael.sand@ruhr-uni-bochum.de
1
Department of Dermatology and Allergology, Dermatologic Surgery Unit,
Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany
Full list of author information is available at the end of the article

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 2 of 16
and to those that are clinically most important in the
daily practice of a dermatologic surgeon.
Non-malignant tumors of the nose
A variety of benign skin tumors of the nose are part of
daily practice in dermatologic surgery. Such conditions
present with different peculiarities and causes. Causes for
development of non-malignant tumors of the nose range
from simple histomorphologic characteristics, such as
the high concentration of sebaceous glands and increased
UV-light exposure to more complex genetic abnormali-
ties such as mutations, which can lead to the conditions
described briefly below.
Comedo
Comedos are dilated sebaceous ducts consisting of hyper-
proliferating ductal keratinocytes and sebum. They can
be either open or closed. The nose with its sebaceous skin
at the nasal tip and alae can frequently exhibit comedos
[Fig 1]. Interleukin 1-alpha, which is present in 76% of
open comedos, induces comedogenesis in vitro [12,13].
Furthermore, pilosebaceous ducts have androgen recep-
tors, and estradiol treatment reduces comedos. There-
fore, it has been proposed that androgens play a
significant role in comedo formation [14,15]. A comedo
reaction to different forms of irradiation (megavoltage,
cobalt) has been described in the literature [16-20].
Changes in lipid composition of the sebum that lead to
duct hyper-proliferation have been hypothesized as caus-
ative for this radio-oncologic phenomenon [21]. In addi-
tion to desquamation therapy with topical salicylic or
retinoic acid, manual extraction by a cosmetician and
physical removal by electrocautery or CO
2
laser therapy
have also been reported [22].
Fibrous papule of the nose (syn.: benign solitary fibrous
papule, fibrous papule of the face)
Fibrous papule is a benign condition that commonly
appears on the nose (Fig. 2). The size of the firm papule is
between 1-5 mm, and its anatomic distribution predomi-
nates at the ala, alar groove and tip of the nose. It has
been considered a variant of angiofibroma with a rela-
tionship to plasma pro-enzyme factor XIIIa-positive der-
mal dendrocytes, a population of mononuclear dendritic
cells normally present in the papillary and upper reticular
dermis [23]. Histopathologically, a clear cell fibrous,
hypercellular fibrous, inflammatory fibrous, pigmented
fibrous, pleiomorphic fibrous papule and epithelioid vari-
ant can be distinguished [24-27]. A biopsy can be neces-
sary to differentiate fibrous papules from benign adnexal
tumors or basal cell carcinomas (BCCs) that sometimes
closely resemble its "pearly" appearance.
Adenoma sebaceum (syn.: Pringle disease)
Adenoma sebaceum is an archaic misnomer for angiofi-
bromas on the face without any relationship to sebaceous
glands. Adenoma sebaceum is part of the classical triad of
tuberous sclerosis (adenoma sebaceum, mental retarda-
tion and epilepsy), which is an autosomal dominant neu-
rocutaneous disease resulting from the mutation of TSC-
Figure 1 Comedo. Multiple closed comedos at the nasolabial fold
and the alar of the nose.
Figure 2 Fibrous papule of the nose. Small skin-colored papule with
smooth surface.

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 3 of 16
1 or TSC-2 [28-30]. The lesions start to occur in child-
hood (5-10 years of age) and appear as multiple wart-like,
waxy lumps consisting of angiomatous and fibrous tissue
(Fig. 3). Different therapy modalities such as electrocoag-
ulation, cryosurgery, shave excision and dermabrasion
have all been described. CO
2
laser ablation has been
shown to be an effective treatment option, with long-last-
ing improvement and good cosmetic results [31].
Hydrocystoma (syn.: cysts of Moll, sudoriferous cysts)
Hydrocystomas are benign cysts of sweat ducts that arise
in the apocrine or eccrine glands (Fig. 4) [32]. They usu-
ally present as solitary translucent bluish nodules. The
blue color is due to the Tyndall effect, caused by scattered
light. Histopathology shows uni- or multilocular cystic
spaces within the dermis. Multiple hydrocystomas have
been described in Schopf-Schulz-Passarge syndrome, a
rare autosomal recessive genodermatosis characterized
by palmoplantar keratodermas, eyelid apocrine hydro-
cystomas, hypodontia, hypotrichosis and onychodystro-
phy [33]. The treatment of hydrocystomas with topical
trichloracetic acid, simple excision, electrosurgery, CO
2
laser or a 1450-nm diode laser have been described [34-
38].
Sebaceous hyperplasia (syn.: sebaceous gland hyperplasia,
senile sebaceous hyperplasia)
Sebaceous hyperplasia is the most frequent benign adn-
exal tumor displaying sebaceous gland differentiation.
Men are more frequently affected than woman. Immuno-
suppressive therapy (e.g., cyclosporin) can trigger its for-
mation [39]. It is almost always located on the face,
including the nose, forehead and lateral cheek parts. Clin-
ically, it appears as a whitish-yellow or skin-colored pap-
ule that varies in size (2-6 mm) with often accompanying
seborrhoea oleosa and telangiectasias. A central umbili-
cation (from which a small globule of sebum is sometimes
expressed) is the most important clinically diagnostic fea-
ture for differentiating between BCC and sebaceous
hyperplasia [40]. Although it is a completely benign
lesion and does not require treatment, it can sometimes
be cosmetically disturbing or clinically resemble BCC;
therefore, a biopsy might be necessary in some cases.
Figure 3 Adenoma sebaceum. Multiple wart-like, waxy lumps con-
sisting of angiomatous and fibrous tissue associated with tuberous
sclerosis.
Figure 4 Eccrine hydrocystoma. Multiple small papules. Some are
skin-colored; the larger papules are dark ("hydrocystome noire").

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 4 of 16
Therapy consists of photodynamic therapy, topical
trichloroacetic acid, laser treatment (pulsed-dye or CO
2
laser), electrosurgery, shave excision, excision or oral
isotretinoin therapy for multiple widespread disfiguring
sebaceous hyperplasia [41-46].
Melanocytic papillomatous nevi
Melanocytic papillomatous nevi are acquired dermal nevi
that are very common. They protrude from the skin sur-
face and may be pigmented or skin-colored. Upon histo-
logical examination, they exhibit nevus cell nests in the
dermis. Women are more frequently affected than man
(9:1), and the nevi are mostly located on the face [47].
Estrogens might influence the pathogenesis of these dis-
tinctive melanocytic nevi [48]. Because the major chal-
lenge is to exclude malignancy, histology should not be
disregarded in cases of clinical doubt regarding the diag-
nosis. Therapy consists of excision, shave excision or CO
2
and erbium: YAG or ruby lasers in cases of a firm clinical
diagnosis by an experienced dermatologist.
Rhinophyma
Rhinophyma is a slow-growing and possibly disfiguring
tumor of the nose that primarily affects men in their fifth
to seventh decade [49] (Fig. 5). It is characterized by the
progressive enlargement of the nose caused by sebaceous
hyperplasia, follicular plugging, fibrosis and telangiecta-
sia [50]. Although it is currently classified as stage IV
rosacea, some authors believe it represents a different
disease process [51]. In the past, rhinophyma has often
been associated with heavy alcohol consumption, but
new studies have shown that there is no significant corre-
lation [52]. The absence of rosacea skin lesions at adja-
cent skin areas may be the sign of a tumor mimicking
rhinophyma. Although rare, sebaceous carcinomas and
angiosarcomas, as well as the more common BCCs and
SCCs, are sometimes concomitantly present [53-56]. In
rare cases, lupoid cutaneous leishmaniasis can also pres-
ent as rhinophyma. The removal of excessive tissue can
be achieved by dermabrasion, excisional surgery by cold
steel, cryosurgery, electrocautery decortication and/or
CO
2
laser ablation [57]. Regardless of the method
employed, it is important to respect the delicate anatomy
of the nose. The follicular epithelium is the starting point
of the re-epithelialization of the wound surface and
should not be ablated during rhinophyma surgery [58].
Furthermore, injuries, particularly to the perichondrium
of the cartilaginous skeleton of the nose, need to be
avoided under all circumstances to prevent nasal flaring.
Freckles (syn.: Ephelides)
Freckles are small brown macules that are very common,
mostly on the face and nose of fair-skinned and red- or
blond-haired individuals. They are usually multiple, show
no correlation with age and can occur at every age [59].
Histological examination reveals no increase in the con-
centration of melanocytes. UV light results in larger mel-
anosomes, similar to the melanosomes of dark-skinned
individuals [60]. Freckles are not associated with
increased mortality but may sometimes represent cos-
metic problems for some patients. Therapy consists of
sun protection, IPL or Q-switched alexandrite laser treat-
ment [61,62].
Vascular tumors of the nose
The recent WHO classification of cutaneous vascular
tumors differentiates between benign vascular tumors,
intermediate vascular tumors, tumors of lymph vessels
and tumors of perivascular cells. However, 53 different
cutaneous vascular tumors have been described in this
classification [63]. Because the face and scalp are com-
mon locations, the nose is also often affected by vascular
tumors of different origins. The most frequent are
described below.
Hemangioma
Hemangiomas are observed in 4-10% of the population
and represent the most common tumor of infancy (Fig 6).
Caucasians, females (3:1) and premature infants with low
birth weight show a higher prevalence [64]. The head and
neck are the most common locations (59%) [65]. In facial
hemangiomas, 15.8% show involvement of the nose, and
the nasal tip is affected in 5.1% [66]. A careful history and
examination is the basis for the diagnosis of heman-
giomas. Because the lesion is usually absent at birth, it
proliferates starting from an erythematous macule or
telangiectasia during the first days or weeks of life. The
growth phase, which can either be gradual or rapid, is
usually six months long and is followed by a longer invo-
lution phase of 6-12 months [67,68]. According to Waner
Figure 5 Rhinophyma. Large exophytic, pink, lobulated mass over
the nose with superficial vascular dilation. The lesion is spreading to
the cheeks; however, it can also be limited to the nose.

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 5 of 16
et al., facial infantile hemangiomas occur in two distinct
patterns of tissue involvement: a focal type with a tumor-
like appearance and a less common diffuse type with a
plaque-like appearance [69]. The diffuse lesions are more
likely to be complicated by ulceration or airway obstruc-
tion and show a strikingly segmental distribution pattern
compared with focal hemangiomas [66]. Ninety percent
of all hemangiomas spontaneously involute prior to the
age of 12. Despite this high percentage of spontaneous
self-healing, there are still a variety of situations where
therapy is indicated. In nasal hemangiomas on the upper
third of the nose, the periorbital area is often additionally
affected, which can result in impairment of the field of
sight. In cases of intraorbital progression, bulbar devia-
tion and amblyopia are dangerous side effects [70]. Nasal
involvement can result in nasal deformity (Cyrano nose
deformity) or the impairment of nasal breathing [71].
Therefore, treatment of hemangiomas of the nose should
be started early to prevent possible complications.
Different therapies such as topical, systemic or intra-
lesional applications of steroid, alpha 2a and 2b interferon
injections, cytotoxic medications, angiogenesis inhibi-
tors, embolization, cryosurgery, laser therapy and con-
ventional surgery have all been described [72,73].
Imiquimod has also recently been described for the treat-
ment of severe complicated hemangiomas. However, side
effects and the small study size make further studies nec-
essary in order to assess this therapeutic option [74].
Recently, Leaute-Labreze and colleagues have achieved
impressive results by treating severe fetal hemangiomas
of the face with systemic application of the beta-blocker
propranolol [75]. After treatment with propranolol
administered orally at 2 to 3 mg/kg per day, the authors
observed a consistent, rapid, therapeutic effect, leading to
a considerable shortening of the natural course of infan-
tile hemangiomas with good clinical tolerance and a low
rate of side effects. Initially described in a case report,
this has recently been confirmed in larger studies (> 100
patients) [76,77].
Telangiectasias
Telangiectasias on the nose are extremely common vas-
cular lesions consisting of dilated blood vessels with a lin-
ear appearance. They measure between 0.5 and 1 mm in
diameter and can be associated with conditions such as
rosacea, scleroderma, dermatomyositis, radiation derma-
titis, chronic alcoholism, pregnancy, childhood and
Osler-Rendu-Weber disease or be idiopathic (as is true in
most cases) [78]. When they appear in abundance, telang-
iectasias on the nose can hint toward heavy liver illnesses
or carcinoid syndrome. Although very rare, there are also
a group of hereditary telangiectatic syndromes that
should be considered when telangiectasias appear in large
numbers and during early childhood. These include
Rothmund-Thomson syndrome, Bloom syndrome, Cock-
ayne syndrome, ataxia-telangiectasia and hereditary
hemorrhagic telangiectasia [79-85]. Former therapy
options included needle diathermy occlusion and polido-
canol sclerotherapy. However, modern laser treatment
has emerged as the first-line therapy for telangiectasias
on the face. Good results have been achieved with PDL,
long pulsed KTP-Nd: YAG laser and IPL treatment
[86,87].
Spider nevus (syn.: nevus arachnoides, eppinger star,
spider angioma, angioma stellatum)
Spider nevi show a spider-like growth pattern with a pin
head-sized central arterial vascular nodule and small vas-
cular radiations in a starburst-like pattern (Fig. 7). When
they appear in abundance, spider nevi can be a clinical
sign of heavy liver illness or carcinoid syndrome. The
most frequent localization is the face and upper body.
Figure 7 Nevus araneus (spider nevus). In the center of the red le-
sion a small (1 mm) red papule is visible, surrounded by several distinct
radiating vessels. Pressure on the lesion causes it to disappear. Blanch-
ing is replaced by rapid refill from the central arteriole when pressure
is released.
Figure 6 Infantile hemangioma. Well-circumscribed red, violet, exo-
phytic vascular tumor on the nose of a one-year-old child.

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 6 of 16
Under light compression with a glass spatula, arterial pul-
sations can be recognized in the center, fading toward the
periphery. Therapy consists of laser therapy with pulsed
dye or alternatively with KTP-Nd: YAG laser or an IPL
system [88].
Osler-Weber-Rendu disease (syn.: hereditary hemorrhagic
telangiectasia (HHT))
Osler-Weber-Rendu disease is an autosomal dominant
disorder that induces the formation of multiple punctate
telangiectasias and hemangiomas (Fig. 8). Accompanying
epistaxis and mucocutaneous visceral arteriovenous mal-
formations with melena are common. The prevalence is
1-2 per 100,000. Skin lesions can be treated with a long-
pulsed Nd: YAG laser, flash-pumped dye laser or an IPL
system. Notably, estrogen therapy has been effective in
severe cases of Osler-Weber-Rendu disease [89]. Electro-
cautery or argon beam ablation is described as a possible
treatment option for cases of spontaneous recurrent
epistaxis [90].
Inflammatory conditions
The following paragraph describes the most frequent
inflammatory conditions on the nose.
Rosacea
Rosacea is a multiphasic inflammatory condition that
typically affects the skin of the face and nose. Clinically,
rosacea has been classified in four different stages. Stage
I, also called rosacea erythematosa telangiectasia (pre-
rosacea), shows facial flushing and telangiectasia. Stage
II, rosacea papulopustulosa (vascular rosacea), is charac-
terized by persistent facial erythema, telangiectasia,
thickened skin, papules and pustules (Fig 9). Stage III,
glandular-hypertrophic or inflammatory rosacea, shows
erythematous papules and pustules, telangiectasias,
edema, connective tissue and sebaceous gland hyperpla-
sia. Stage IV, or rhinophyma, shows dermal and seba-
ceous gland hyperplasia, and dilated and cystic sebaceous
glands. Most individuals affected by rosacea are of north-
ern European origin, and up to one-third have a family
history of the disorder [91]. Clinical signs include facial
flushing, erythema, telangiectasia and papulopustular
efflorescence similar to acne as described previously.
Women are three times more likely to be affected than
men, with the reported prevalence between 0.5 and 10%
[92,93]. The pathophysiology has been poorly under-
stood, and there have been only limited descriptions of
factors that exacerbate or improve this disease [94].
Recent molecular studies suggest that an altered innate
immune response is involved in the pathogenesis of vas-
cular and inflammatory disease and is responsible for the
observed clinical findings in patients with rosacea [95].
A variety of topical, systemic and physical treatment
options are available that have been adjusted to the stage
and severity of the disease [96]. Standard topical therapy
includes metronidazole 0.75% or 1% gel. Alternatively,
azelaic acid 15% gel or 20% cream has also been success-
fully used in five randomized and controlled studies with
good results [97]. Systemic therapy with doxycycline,
minocycline, clarithromycin, and moderately high doses
of prednisolone or oral isotretinoin has also been
described. Persistent erythema and telangiectasia might
respond to pulsed dye laser (PDL) and intense pulsed
light (IPL) treatments [98]. Furthermore, it is important
to remember that ocular rosacea is a potentially blinding
eye disorder common in patients with rosacea (6-18% of
rosacea patients) [99]. The main symptom is conjunctival
injection, which is sometimes accompanied by chalazion
or episcleritis. Rosacea patients should therefore be seen
by an ophthalmologist early in the disease course [100].
Figure 8 Hereditary hemorrhagic telangiectasia (Osler-Weber-
Rendu syndrome). Flat, star-shaped skin lesions 1-3 mm in diameter
on the entire face. Some non-pulsating telangiectasias appear similar
to araneus nevi. A papule the size of a match head is visible at the alar.
Figure 9 Rosacea. Erythema and telangiectasia are seen over the
cheeks, nasolabial area and nose. Inflammatory papules and pustules
can be observed over the nose. The absence of comedos is a helpful
tool to distinguish rosacea from acne.

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 7 of 16
Facial eosinophilic granuloma (syn.: granuloma faciale,
granuloma eosinophilicum faciale)
First described by Wigley in 1945, this condition is a
chronic inflammation of the skin that generally occurs on
the nose (Fig. 10), chin, forehead, temple or cheeks [101].
Clinically, round or oval brown-red macular and popular
lesions with large follicular pores (giving the lesion an
orange peel-like appearance) can be observed. Histologi-
cally, eosinophilia and patterns of leukocytoclastic vascu-
litis are characteristic. Therapy consists of dapsone p.o.
(100-200 mg/day for four months) or intra-lesional ste-
roid injections (e.g., triamcinolone 10 mg diluted with a
local anesthetic 1:3-1:5). Dapsone therapy should be eval-
uated critically as the results are moderate, and the
course of the disease is benign. Recently, the topical prep-
aration of tacrolimus, a macrolide immunosuppressant,
has been described as successful [102]. In cases of resis-
tance to conservative therapy, the surgical excision of sol-
itary lesions, cryotherapy, dermabrasion or ablative laser
therapy (CO
2
, argon or erbium: YAG laser) should be
considered.
Sarcoidosis
Sarcoidosis is a multisystem granulomatous inflamma-
tory disease that can affect any organ. Cutaneous sarcoi-
dosis is characterized by non-caseating granulomatas
that consist of mononuclear phagocytes, epithelioid mac-
rophages and multinucleate giant cells [103]. The
macronodular type involving the nose and cheek is called
lupus pernio and was first described by Besnier in 1889
[104]. The etiology of this disease is still unknown. Clini-
cally, dark red, purple or violaceous plaques and nodules
can be seen [Fig. 11]. The serum concentration of angio-
tensin-converting enzyme (ACE) is increased, and mea-
surements have been used as an index of disease activity.
Aside from topical and intra-lesional steroids, multiple
forms of internal therapy (immunosuppressants such as
steroids, interleukin-2 inhibitors or anti-tumor necrosis
factor alpha treatment) have been described [105]. Pulsed
dye or CO
2
laser ablation is available for the debulking of
granulomatous lesions; however, there are no evidence-
based recommendations because of the limited number
of patients treated [105].
Pre-malignant tumors of the nose
Actinic keratoses (syn: solar keratosis, senile keratosis)
Located on the nose, face, scalp, forearms and back of the
hand, this very common pre-malignant lesion consists of
crusty, scaly patches of skin. Size ranges from 2 - 10 mm,
and colors such as pink, red or the same degree of pig-
mentation as the surrounding skin are observed. Actinic
keratoses are associated with UV light exposure and
therefore accompanied by solar damage to the surround-
ing skin. Patients are in or past middle age, very often
with fair complexion. Histologically, five types can be dis-
tinguished: hypertrophic, atrophic, bowenoid, acantho-
lytic and pigmented [106]. Left untreated this lesion can
potentially result in squamous cell carcinoma. Approxi-
mately 20% of untreated actinic keratoses result in
Figure 10 Facial eosinophilic granuloma. Red-brown nodule on the
nose. Clearly visible follicular structures ("peau d'orange").
Figure 11 Cutaneous lesions of sarcoidosis (lupus pernio). Red-to-
purple indurated plaques and nodules affecting the nose and cheeks.

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 8 of 16
squamous cell carcinoma [107]. Therapy consists of sim-
ple curettage, topical photodynamic therapy, topical imi-
quimod, topical 3% diclofenac gel or 5-fluorouracil-
creme. In case of surgical excision, histologic examina-
tion should be performed to exclude squamous cell carci-
noma.
Keratoacanthoma (syn.: molluscum sebaceum, molluscum
pseudocarcinomatosum, idiopathic cutaneous
pseudoepitheliomatous hyperplasia)
First described in 1889 by Hutchinson as a "crateriform
ulcer of the face", keratoacanthoma is a fast-growing, epi-
thelial tumor that develops from hair follicles or the sur-
face epithelium of the skin. It can occur solitarily
(frequent) or with multiple lesions (rare). The lesion con-
sists of a firm, cone-shaped nodule (1-3 cm in diameter)
with a central horn-filled crater. It shows rapid growth
within weeks or months followed by spontaneous resolu-
tion over 4-6 months in most cases. Histologically and
clinically it often resembles SCC. There is debate about
whether it undergoes transformation into SCC or is SCC
from the beginning [108,109]. Nevertheless, as SCC can
masquerade as keratoacanthoma, surgical excision with
an excision margin of 2-3 mm is recommended [106].
Because the histologic changes at the base of the lesion
are important for histologic differentiation, a shave
biopsy should be avoided and an excision of the lesion in
its entirety should be performed [110]. Immunocompro-
mised patients and those with Muir-Torre syndrome (the
combined occurrence of at least one sebaceous skin
tumor and one internal malignancy in the same patient)
show an increased incidence of keratoacanthoma
[111,112].
Malignant tumors of the nose
The skin of the nose is a very common location for malig-
nant tumors. UV-light exposure is a potent carcinogen of
the skin, which results in frequent tumor involvement of
the skin of the nose. In the following paragraph we pres-
ent the most frequent malignant skin tumors of the nose.
Melanoma
Melanoma is the most devastating skin cancer with the
highest increase in incidence in recent years, according to
the World Health Organization (WHO). It has been esti-
mated that incidences of melanoma will double every 10-
20 years [113,114]. Melanoma originates from a malig-
nant degenerated melanocyte, which is a highly aggres-
sive tumor cell with poor rates of survival once it has
metastasized. It can either develop de novo (70%) or from
pre-existing melanocytic nevi (30%) (Fig. 12).
Unfortunately, there are only a few studies dealing spe-
cifically with melanoma on the nose. Jahn et al. have pub-
lished the largest series of malignant melanomas on the
nose so far [115]. In their group of 45 patients, they
showed a female predisposition of 64.4%, with lentigo
maligna melanoma (LMM) being the most frequent sub-
type (73.3%). In another study by Fisher et al., 36 patients
with melanomas of the nose were described, whereas
superficially spreading melanomas were reported in 47%
and LMM in 25% of cases [116]. Forty-five percent of
these cases were observed in female patients.
Therapy involves surgical excision by cold steel, similar
to the procedure performed for cutaneous melanomas at
other locations on the body. The recommended standard
excision margins published by the American Cancer
Society (ACS) and the German Association of Dermato-
oncology (ADO) for melanoma of the skin are 10 mm for
tumor thickness ≤ 2.00 mm and 20 mm for tumor thick-
ness > 2.00 mm [117,118]. However, according to the
ADO's guideline, in special localizations such as the
facial, acral or anogenital regions a reduction of these
margins is possible on the condition that micrographic
controlled surgery is performed. However, current ran-
domized trial evidence has recently shown to be insuffi-
cient in addressing optimal excision margins for primary
cutaneous melanomas [119].
Although the nose has a distinct concave and convex
anatomy, pre-operative tumor thickness can be assessed
by ultrasound of the skin, depending on the localization
of the melanoma [120,121]. In cases of LMM, different
techniques of 3D histology have been described. Some
authors prefer the Tuebingen cake technique, whereas
other authors prefer classic Mohs surgery [122-124].
Micrographic surgery according to the Tuebingen cake
technique has been studied by Jahn and colleagues [115].
It ideally utilizes a cylindrical piece of tissue where the
base and the margin of the tumor are assessed separately
(Fig. 13).
Mohs surgery allows complete circumferential periph-
eral and deep margin assessment using frozen section
Figure 12 Congenital melanocytic nevus. Brown papule on the
nose, which developed shortly after birth. The brownish exophytic le-
sion is well circumscribed.

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 9 of 16
histology. In classic Mohs surgery, the tissue is excised in
a cone-shaped pattern with a very small surgical margin
(1 to 1.5 mm of visually uninvolved skin). Specimen prep-
aration consists of cutting the specimen on the cryostat,
placing sections on slides, followed by staining and evalu-
ation by the Mohs surgeon (Fig. 14). The special method
of tissue processing and staining in Mohs surgery has
been compared with peeling an orange, where the peel is
the surgical margin that is removed and flattened out for
further examination [125]. Actually there are no equiva-
lent data to compare both methods.
Jahn et al. conclude from their study data that male
patients tend to have fewer recurrences than female
patients and that LMM has a better prognosis than other
histologic subtypes in patients with stage I and II mela-
noma of the nose [115]. The authors report recurrence
rates of 6.7% with all recurrences observed in female
patients. The prognoses with stage I and II melanoma of
Figure 13 Micrographic surgery according to the Tuebingen cake technique. The base and the margin of the tumor are assessed separately.
(modified according to Prof. Breuninger (120))

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 10 of 16
the nose were good, with a survival rate of 97.8% over
three years and 95.6% over five years. Unfortunately,
there were no data available for patients with stage III
melanoma. Jahn et al. further conclude that although
tumor thickness is the most important prognostic factor
for cutaneous melanoma of the nose, this factor has no
significant influence on the prognosis, probably because
of the limited number of patients (n = 45). To date all
available studies on elective lymph node dissection
(ELND) have failed to demonstrate a beneficial effect on
patients with cutaneous melanoma of the trunk and
extremities; therefore, there is limited evidence to sup-
port application of this technique in patients with mela-
noma of the nose [115,126-128]. Although a sentinel
lymph node biopsy (SLNB) is performed in cutaneous
melanomas of other localizations with a tumor thickness
> 1.00 mm, the available data for patients with melano-
mas of the nose do not suggest a clear recommendation
regarding prognostic impact. In contrast to the relatively
good prognosis for stage I and II melanomas of the skin of
the nose, melanoma with sinonasal involvement arising
from the nasal cavity and paranasal sinuses is associated
with generally poor survival rates [129]. A high rate of
local recurrence (31-85%), common distant metastasis
Figure 14 Mohs surgery allowing the complete circumferential peripheral and deep margin assessment, using frozen section histology.
(modified according to Prof. Breuninger (120))

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 11 of 16
(25-50%) and a poor five-year survival rate (13-45%) all
make this form of nasal melanoma the most lethal [130-
134].
Basal cell carcinoma (Syn.: basalioma, basal cell
epithelioma)
Basal cell carcinoma (BCC) is the most common malig-
nancy in humans and accounts for more than 90% of all
malignant cutaneous lesions of the head and neck [133].
Because UV light associated with chronic sun exposure is
the main risk factor, BCC commonly occurs on the face,
with the nose being the most frequently affected location
and the alae, dorsum and tip being the parts most fre-
quently affected [134].
Although it rarely metastasizes, untreated BCC can
cause considerable disfigurement and is potentially life
threatening when eroding vital structures. Five BCC sub-
types with different clinical behavior can be distin-
guished: pigmented, cystic, superficial multicentric,
morphea-like and nodular-ulcerative types (with the last
being the most common, Fig. 15). Pigmented BCC can
mimic melanoma upon clinical examination and usually
occurs in sun-exposed areas [Fig. 16] [135]. Morphea-like
BCC shows a lingular growth pattern and varies in size
[Fig. 17]. It is a rare morphological variant of BCC
(roughly 2% of all BCCs) and is the most insidious form
because the degree of infiltration can far exceed what is
clinically visible, because the tumor grows in an 'iceberg'-
like pattern with only the top of the tumor visible
[136,137].
A variety of different treatment options such as cryo-
therapy, photodynamic therapy, application of imiqui-
mod or 5-fluourouracil, electrodessication and radiation
therapy have been described. However, micrographic-
controlled surgery is the gold standard with the lowest
rate of recurrence (1.0-5,6%) [138-144]. The nose, which
is part of the so called H-zone of the face, shows the high-
est rate of recurrence compared with other localizations
[145]. Embryonic fusion planes such as the nasolabial fold
or the medial canthus can be affected by large BCCs of
the nose, possibly contributing to tumor recurrence.
Figure 15 BCC Nodular type. Red, waxy nodule on the tip of the
nose. Visible telangiectasias over the surface.
Figure 16 Pigmented BCC. Dark nodule (resulting from melanin de-
position) at the alar of the nose. Small ulceration at the center.
Figure 17 Scar-like morphea-like BCC. Sclerotic, partially reddish
plaque. Crusting in the center.

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 12 of 16
Squamous cell carcinoma (syn.: spinalioma)
Cutaneous squamous cell carcinoma (SCC) accounts for
approximately 10% of skin malignancies on the nose. It is
more common in men and 70% of cases are located in the
head and neck area [146]. It is related to chronic sun
exposure and immunosuppression and rarely arises from
normal-appearing skin. SCC typically develops on sun-
damaged skin or actinic keratoses and less frequently on
scars from burns [147,148]. In patients having undergone
renal transplants and immunosuppression, the incidence
has been 18 times greater than in healthy individuals
[149]. Clinically, SCC presents as an erythematous crust-
ing, sometimes ulcerated, lesion with a red granular base.
It shows a tendency to bleed with minimal trauma. The
diagnosis and extent of the lesion sometimes necessitate
multiple biopsies. When SCC arises in sun-damaged skin,
a minority of patients develop metastases (0.5%) [150].
However, in all patients with SCC of the skin, the metas-
tasis is more frequent (2-3%), and most cases are located
in the cervical lymph nodes or parotids [151,152]. The
likelihood of metastasis increases with tumors with a
diameter of at least 15 mm and a Breslow tumor thick-
ness (vertical) of at least 2 mm [137]. Death occurs in
three-quarters of patients with metastasis [153,154]. The
parotid gland is the "metastatic basin" for cutaneous SCC
of the head and neck because it drains via lymphatic ves-
sels on the nose, cheek and forehead [155]. In cases of
parotid involvement, a parotidectomy with or without a
simultaneous neck dissection is the procedure of choice.
Clark levels IV or V are associated with a 20% regional
metastatic rate. De novo lesions, an increased depth of
invasion (beyond 4-5 mm), tumor size (> 2 cm) and des-
moplastic SCCs are associated with a higher rate of
metastasis. The same is true for adenoid and mucin-pro-
ducing types, SCCs of the lower lip (metastatic rate 16%),
SCCs on burn scars (18%), radiation-induced SCCs (20%)
and/or osteomyelitic sinuses (31%) [137,156-160].
Micrographic-controlled surgery is the treatment of
choice. Excision margins of 4 mm and 6 mm have been
suggested for lesions less than and greater than 2 cm,
respectively [160]. Because there are no large randomized
studies regarding excision margins for cutaneous SCCs,
these are rough guidelines. The surgeon's experience and
judgment in planning surgical treatment is therefore sig-
nificant for successful treatment [160]. In cases where
patients are unable to undergo surgery radiation, therapy
has been described as successful with cure rates similar to
those obtained with standard surgical excision. Although
chemotherapy has not been effective, some studies report
that epidermal growth factor receptor (EGFR) inhibitors
might be useful adjuncts to surgical treatment [161,162].
Kaposi's sarcoma (KS)
KS was first described in 1872 by the Hungarian derma-
tologist Moritz Kaposi and is a carcinoma arising from
the endothelial lining of lymphatic tissue [163]. The his-
tology is characteristic and shows an excessive prolifera-
tion of spindle cells, slit-like vascular spaces and
extravasated erythrocytes. Principally, KS can arise any-
where on the skin or mucosa of the body, including inter-
nal organs. The lower extremities of the skin (especially
the soles of the feet) and the head and neck are typically
involved.
Masih et al. used bronchoscopy to evaluate 19 HIV-
positive patients with pulmonary KS [164]. Fifteen of
these patients also had oral-facial KS and 13 showed a
prominent tip-of-the-nose KS lesion. The authors con-
cluded that tip-of-the-nose KS lesions are commonly
associated with pulmonary KS and should be noticed as a
sentinel sign for pulmonary KS, suggesting that bron-
choscopy should be considered for these patients. On
clinical examination the vascular pattern results in a dark
red to blue or violaceous appearance, as the vascular
spaces within the lesions fill with blood. The lesions are
non-pruritic and appear as macular (Fig. 18), papular,
nodular or plaque-like. Four different types have been
distinguished in the literature. The classic type mainly
occurs in Mediterranean men (male-to-female ratio of
10-15:1) of 50-70 years of age [165,166]. The endemic
African type occurs in HIV-negative individuals and
shows a tendency for lymph node involvement. The
immunocompromised type can occur in individuals just
after organ transplantation [167,168]. Finally, the AIDS-
related type is now the most commonly presented. It is
seen in patients with advanced HIV infection or no access
to highly active antiretroviral therapy (HAART). It is the
most common malignancy seen in HIV-infected patients
[169,170].
Over 90% of lesions, regardless of the KS type, are asso-
ciated with DNA virus human herpes virus 8, also called
KS-associated herpesvirus (HHV-8 or KSHV), which has
been identified as the primary trigger [171]. Concerning
therapy, a variety of modalities have been described.
Figure 18 Kaposi's sarcoma. Characteristic violaceous plaques on
the alar and tip of the nose in an HIV-positive female patient.

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 13 of 16
Therapeutic options include systemic therapy in HIV-
positive patients (HAART), systemic chemotherapy with
doxorubicin, conventional radiation therapy, electron
beam radiation therapy (EBRT), surgical excision, topical
retinoids, cryotherapy, laser therapy and intra-lesional
therapy with vincristin, vinblastin or bleomycin
[172,173].
Conclusion
The most important skin diseases of the nose, which
might require surgical consultation or laser therapy, have
been described briefly in this review. In conclusion, the
authors suggest that all disciplines that offer conservative
or surgical treatment must be familiar with the special
morphology and characteristics of skin diseases of the
nose. In the case of complex lesions an interdisciplinary
approach that combines dermatology, otolaryngology
and surgery can provide optimal care for the patient.
Consent
Written informed consent was obtained from the
patients/guardians of the patient for publication of this
review article and accompanying images. A copy of the
written consent is available for review by the Editor-in-
Chief of this journal.
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
MS: Documented and prepared the draft. DS: Edited the manuscript, revised
the bibliography and helped prepare the draft. CT: Searched the literature and
revised and edited the manuscript. VP: Searched the literature, photography
and helped edit the manuscript. PA: Revised the manuscript, searched the liter-
ature and helped edit the manuscript. FGB: Helped prepare the draft and
edited most of the manuscript. All authors read and approved the final manu-
script.
Author Details
1
Department of Dermatology and Allergology, Dermatologic Surgery Unit,
Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany and
2
Case
Western Reserve University, School of Medicine, 10900 Euclid Avenue,
Cleveland, Ohio 44106, USA
References
1. Andretto Amodeo C: The central role of the nose in the face and the
psyche: review of the nose and the psyche. Aesthetic Plast Surg 2007,
31:406-410.
2. Biller JA, Kim DW: A contemporary assessment of facial aesthetic
preferences. Arch Facial Plast Surg 2009, 11:91-97.
3. Cellerino A: Psychobiology of facial attractiveness. J Endocrinol Invest
2003, 26:45-48.
4. Cook JL: Nasal reconstruction. In Flaps and grafts in dermatologic surgery
New York, NY: Elsevier; 2008:191-215.
5. Conte CC, Razack MS, Sako K: Skin cancer of the nose: options for
reconstruction. J Surg Oncol 1988, 39:1-7.
6. Sjerobabski Masnec I, Poduje S: Photoaging. Coll Antropol 2008,
32:177-180.
7. Heidari Z, Mahmoudzadeh-Sagheb H, Khammar T, Khammar M:
Anthropometric measurements of the external nose in 18-25-year-old
Sistani and Baluch aborigine women in the southeast of Iran. Folia
Morphol (Warsz) 2009, 68:88-92.
8. Burget GC, Menick FJ: Repair of small surface defects. In Aesthetic
reconstruction of the nose Edited by: Burget GC, Menick FJ. St. Louis, MO:
Mosby; 1994:117-156.
9. Burget GC, Menick FJ: Aesthetics, visual perception, and surgical
judgment. In Aesthetic reconstruction of the nose Edited by: Burget GC,
Menick FJ. St. Louis, MO: Mosby; 1994:1-55.
10. Fattahi TT: An overview of facial aesthetic units. J Oral Maxillofac Surg
2003, 61:1207-1211.
11. Chang EW, Nguyen CT: Nose anatomy [http://emedicine.medscape.com/
article/835134-overview].
12. Ingham E, Eady A, Goodwin CE, Cove JH, Cunliffe WJ: Pro-inflammatory
levels of interleukin-1 alpha-like bioactivity are present in the majority
of open comedones in acne vulgaris. J Invest Dermatol 1992,
98:895-901.
13. Guy R, Green MR, Kealey T: Modelling acne in vitro. J Invest Dermatol
1996, 106:176-182.
14. Stewart ME, Greenwood R, Cunliffe WJ, Strauss JS, Downing DT: Effect of
cyproterone acetate-ethinyl estradiol treatment on the proportion of
linoleic and sebaceic acids in various skin surface lipid classes. Arch
Dermatol Res 1986, 278:481-485.
15. Choudhry R, Hodgins MB, Van der Kwast TH, Brinkmann AO, Boersma WJ:
Localisation of androgen receptors in human skin by
immunocytochemistry. J Endocrinol 1992, 133:467-74.
16. Bluefarb SM: Comedos following roentgen ray therapy. Arch Dermatol
Syph 1947, 56:537-539.
17. Trunnell TN, Baer RL, Michaelides P: Acneiform changes in areas of cobalt
irradiation. Arch Dermatol 1972, 106:73-75.
18. Walter JF: Cobalt radiation-induced comedones. Arch Dermatol 1980,
116:1073-1074.
19. Friedman SJ, Su WPD: Favre-Racouchot syndrome associated with
radiation therapy. Cutis 1983, 31:306-310.
20. Hepburn NC, Crellin RP, Beveridge GW, Rodger A, Tidman MJ: Localized
acne as a complication of megavoltage radiotherapy. J Dermatol Treat
1992, 3:137-138.
21. Martin WM, Bardsley AF: The comedo skin reaction to radiotherapy. Br J
Radiol 2002, 75:478-81.
22. Gollnick HP, Krautheim A: Topical treatment in acne: current status and
future aspects. Dermatology 2003, 206:29-36.
23. Nemeth AJ, Penneys NS, Bernstein HB: Fibrous papule: a tumor of
fibrohistiocytic cells that contain factor XIIIa. J Am Acad Dermatol 1988,
19:1102-6.
24. Park HS, Cho S, Kim KH, Won CH: Fibrous papule of the face, clear cell
type: a case report. J Eur Acad Dermatol Venereol 2007, 21(9):1267-8.
25. Lee AN, Stein SL, Cohen LM: Clear cell fibrous papule with NKI/C3
expression: clinical and histologic features in six cases. Am J
Dermatopathol 2005, 27:296-300.
26. Bansal C, Stewart D, Li A, Cockerell CJ: Histologic variants of fibrous
papule. J Cutan Pathol 2005, 32:424-428.
27. Kucher C, McNiff JM: Epithelioid fibrous papule - a new variant. J Cutan
Pathol 2007, 34:571-575.
28. Ghosh SK, Bandyopadhyay D, Chatterjee G, Ghosh A, Sarkar S, Sarkar S:
Mucocutaneous changes in tuberous sclerosis complex: A clinical
profile of 27 Indian patients. Indian J Dermatol 2009, 54:255-257.
29. Swaroop MR, Nischal KC, Rajesh Gowda CM, Umashankar NU, Basavaraj
HB, Sathyanarayana BD: Radiofrequency ablation of adenoma
sebaceum. J Cutan Aesthet Surg 2008, 1:89-91.
30. Sagar SM, Israel MA: Primary and metastatic tumors of the nervous
system. In Harrison's Principles Of Internal Medicine 16th edition. Edited by:
Kasper DL, Braunwald E, Fauci AS, Hauser SL, Jameson JL, Longo DL.
NewYork, McGraw-Hill; 2005:2452-61.
31. Bellack GS, Shapshay SM: Management of facial angiofibromas in
tuberous sclerosis with carbon dioxide laser. Otolaryngol Head Neck
Surg 1986, 94:37-40.
32. Anandasabapathy N, Soldano AC: Multiple apocrine hidrocystomas.
Dermatology Online Journal 14:12.
33. Schöpf E, Schulz HJ, Passarge E: Syndrome of cystic eyelids, palmo-
plantar keratosis, hypodontia and hypotrichosis as a possible
autosomal recessive trait. Birth Defects Orig Artic Ser 1971, 7:219-221.
34. Dailey RA, Saulny SM, Tower RN: Treatment of multiple apocrine
hidrocystomas with trichloracetic acid. Ophthal Plast Reconstr Surg 2005,
21:148-150.
35. Echague AV, Astner S, Chen AA, Anderson RR: Multiple apocrine
hidrocystoma of the face treated with a 1450-nm diode laser. Arch
Dermatol 2005, 141:1365-1367.
Received: 1 February 2010 Accepted: 4 June 2010
Published: 4 June 2010
This article is available from: http://www.head-face-med.com/content/6/1/7© 2010 Sand et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Head & Face Medicine 2010, 6:7

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 14 of 16
36. del Pozo J, García-Silva J, Peña-Penabad C, Fonseca E: Multiple apocrine
hidrocystomas:treatment with carbon dioxide laser vaporization. J
Dermatol Treat 2001, 12:97.
37. Gupta S, Handa U, Handa S, Mohan H: The efficacy of electrosurgery and
excision in treating patients with multiple apocrine hidrocystomas.
Dermatol Surg 2001, 27:382-384.
38. Henderer JD, Tanenbaum M: Excision of multiple eyelid apocrine
hidrocystomas via an en-bloc lower eyelid blepharoplasty incision.
Ophthalmic Surg Lasers 2000, 31:157-161.
39. Walther T, Hohenleutner U, Landthaler M: Sebaceous gland hyperplasia
as a side effect of cyclosporin A. Treatment with the CO2 laser. Dtsch
Med Wochensch 1998, 123:798-800.
40. Hogan DJ, Jones RW, Mason SH: Sebaceous hyperplasia, treatment &
medication. [http://emedicine.medscape.com/article/1059368-
treatment].
41. Alexiades-Armenakas M: Laser-mediated photodynamic therapy. Clin
Dermatol 2006, 24:16-25.
42. Horio T, Horio O, Miyauchi-Hashimoto H, Ohnuki M, Isei T: Photodynamic
therapy of sebaceous hyperplasia with topical 5-aminolaevulinic acid
and slide projector. Br J Dermatol 2003, 148:1274-1276.
43. Bader RS, Scarborough DA: Surgical pearl: intralesional
electrodesiccation of sebaceous hyperplasia. J Am Acad Dermatol 2000,
42:127-128.
44. Rosian R, Goslen JB, Brodell RT: The treatment of benign sebaceous
hyperplasia with the topical application of bichloracetic acid. J
Dermatol Surg Oncol 1991, 17:876-879.
45. Aghassi D, Gonzalez E, Anderson RR, Rajadhyaksha M, Gonzalez S:
Elucidating the pulsed-dye laser treatment of sebaceous hyperplasia in
vivo with real-time confocal scanning laser microscopy. J Am Acad
Dermatol 2000, 43:49-53.
46. Grimalt R, Ferrando J, Mascaro JM: Premature familial sebaceous
hyperplasia: successful response to oral isotretinoin in three patients. J
Am Acad Dermatol 1997, 37:996-998.
47. Hammes S, Raulin C, Karsai S, Bernt R, Ockenfels HM: Treating
papillomatous intradermal nevi: lasers - yes or no? A prospective
study. Hautarzt 2008, 59:101-107.
48. Morgan MB, Raley BA, Vannarath RL, Lightfoot SL, Everett MA:
Papillomatous melanocytic nevi: an estrogen related phenomenon. J
Cutan Pathol 1995, 22:446-449.
49. Kilty S, Brownrigg P: Surgical treatment of rhinophyma. J Otolaryngol
Head Neck Surg 2008, 37:269-272.
50. Sadick H, Goepel B, Bersch C, Goessler U, Hoermann K, Riedel F:
Rhinophyma:diagnosis andtreatment options for a disfiguring tumor
of the nose. Ann Plast Surg 2008, 61:114-120.
51. Aloi F, Tomasini C, Soro E, Pippione M: The clinicopathologic spectrum of
rhinophyma. J Am Acad Dermatol 2000, 42:468-472.
52. Curnier A, Choudhary S: Rhinophyma: dispelling the myths. Plast
Reconstr Surg 2004, 114:351-354.
53. Hoffmann M, Braun-Falco M: Rhinophyma-like sebaceous carcinoma. J
Eur Acad Dermatol Venereol 2009, 23:1216-1218.
54. Aguila LI, Sánchez JL: Angiosarcoma of the face resembling
rhinophyma. J Am Acad Dermatol 2003, 49:530-531.
55. Lutz ME, Otley CC: Rhinophyma and coexisting occult skin cancers.
Dermatol Surg 2001, 27:201-202.
56. Leyngold M, Leyngold I, Letourneau PR, Zamboni WA, Shah H: Basal cell
carcinoma and rhinophyma. Ann Plast Surg 2008, 61:410-412.
57. Kempiak SJ, Lee PW, Pelle MT: Rhinophyma treated with cryosurgery.
Dermatol Surg 2009, 35:543-545.
58. Jung H: Rhinophyma: plastic surgery, rehabilitation, and long-term
results. Facial Plast Surg 1998, 14:255-278.
59. Bastiaens M, Hoefnagel J, Westendorp R, Vermeer BJ, Bouwes Bavinck JN:
Solar lentigines are strongly related to sun exposure in contrast to
ephelides. Pigment Cell Res 2004, 17:225-229.
60. Cockerell CJ, Johnson TM, Swanson NA: Melanocytic nevi. J Cutan Med
Surg 1996, 2:1561-1563.
61. Kawada A, Shiraishi H, Asai M, Kameyama H, Sangen Y, Aragane Y, Tezuka
T: Clinical improvement of solar lentigines and ephelides with an
intense pulsed light source. Dermatol Surg 2002, 28:504-508.
62. Wang CC, Sue YM, Yang CH, Chen CK: A comparison of Q-switched
alexandrite laser and intense pulsed light for the treatment of freckles
and lentigines in Asian persons: a randomized, physician-blinded, split-
face comparative trial. J Am Acad Dermatol 2006, 54(5):804-10.
63. Fletcher CDM, Unni KK, Mertens F: Pathology and genetics of tumours of
soft tissue and bone. IARC Press, Lyon, France; 2002:156-176.
64. Bailey Byron J: Head & Neck Surgery - Otolaryngology. 3rd edition.
Lippincott Williams & Wilkins, Philadelphia; 2001:1117-1124.
65. Finn MC, Glowacki J, Mulliken JB: Congenital vascular lesions: clinical
application of a new classification. J Pediatr Surg 1983, 18:894-900.
66. Waner M, North PE, Scherer KA, Frieden IJ, Waner A, Mihm MC Jr: The
nonrandom distribution of facial hemangiomas. Arch Dermatol 2003,
139:869-875.
67. Garzon MC, Huang JT, Enjolras O, Frieden IJ: Vascular malformations: Part
I. J Am Acad Dermatol 2007, 56:353-370.
68. Garzon MC, Huang JT, Enjolras O, Frieden IJ: Vascular malformations. Part
II: associated syndromes. J Am Acad Dermatol 2007, 56:541-564.
69. Waner M, Kastenbaum J, Scherer K: Hemangiomas of the nose. Arch
Facial Plast Surg 2008, 10:329-334.
70. Frank J: Genodermatosen, Chapter 11.5 Vaskuläre und lymphatische
Erkrankungen. 3. Dermatologie Update Seminar, 13th-14th November
2009, Wiesbaden Germany :12-13.
71. Cho S, Lee SY, Choi JH, Sung KJ, Moon KC, Koh JK: Treatment of "Cyrano"
angioma with pulsed dye laser. Dermatol Surg 2001, 27:670-672.
72. Musumeci ML, Schlecht K, Perrotta R, Schwartz RA, Micali G: Management
of cutaneous hemangiomas in pediatric patients. Cutis 2008,
81:315-322.
73. Stier MF, Glick SA, Hirsch R: Laser treatment of pediatric vascular lesions:
Port wine stains and hemangiomas. J Am Acad Dermatol 2008,
58:261-285.
74. Barry RB, Hughes BR, Cook LJ: Involution of infantile haemangiomas
after imiquimod 5% cream. Clin Exp Dermatol 2008, 33:446-449.
75. Léauté-Labrèze C, Dumas de la Roque E, Hubiche T, Boralevi F, Thambo JB,
Taïeb A: Propranolol for severe hemangiomas of infancy. N Engl J Med
2008, 358:2649-2651.
76. Sans V, Dumas de la Roque E, Berge J, Grenier N, Boralevi F, Mazereeuw-
Hautier J, Lipsker D, Dupuis E, Ezzedine K, Vergnes P, Taïeb A, Léauté-
Labrèze C: Propranolol for Severe Infantile Hemangiomas: Follow-Up
Report. Pediatrics 2009 in press.
77. Löffler H, Kosel C, Cremer H, Kachel W: Propanolol therapy to treat
problematic hemangiomas. A new standard therapy makes its debut.
Hautarzt 2009, 60:1013-1016.
78. Bailey Byron J: Head & Neck Surgery - Otolaryngology. 3rd edition.
Lippincott Williams & Wilkins, Philadelphia; 2001:2438.
79. Stinco G, Governatori G, Mattighello P, Patrone P: Multiple cutaneous
neoplasms in a patient with Rothmund-Thomson syndrome: case
report and published work review. J Dermatol 2008, 35:154-161.
80. Moss C: "New" syndrome with telangiectasia, dwarfism, and
spondyloepiphyseal dysplasia may be Rothmund-Thomson syndrome.
Pediatr Dermatol 1990, 7:82-84.
81. Kaneko H, Kondo N: Clinical features of Bloom syndrome and function
of the causative gene, BLM helicase. Expert Rev Mol Diagn 2004,
4:393-401.
82. Cantani A, Bamonte G, Bellioni P, Tucci Bamonte M, Ceccoli D, Tacconi ML:
Rare syndromes. I. Cockayne syndrome: a review of the 129 cases so far
reported in the literature. Riv Eur Sci Med Farmacol 1987, 9:9-17.
83. Nance MA, Berry SA: Cockayne syndrome: review of 140 cases. Am J
Med Genet 1992, 42:68-84.
84. Bergler W, Götte K: Hereditary hemorrhagic telangiectasias: a challenge
for the clinician. Eur Arch Otorhinolaryngol 1999, 256:10-15.
85. Spacey SD, Gatti RA, Bebb G: The molecular basis and clinical
management of ataxia telangiectasia. Can J Neurol Sci 2000, 27:184-191.
86. Werner A, Bäumler W, Zietz S, Kühnel T, Hohenleutner U, Landthaler M:
Hereditary haemorrhagic telangiectasia treated by pulsed
neodymium:yttrium-aluminium-garnet (Nd:YAG) laser (1,064 nm).
Lasers Med Sci 2008, 23:385-391.
87. Mahoney EJ, Shapshay SM: New classification of nasal vasculature
patterns in hereditary hemorrhagic telangiectasia. Am J Rhinol 2006,
20:87-90.
88. Hellwig S, Petzoldt D, Raulin C: The pulsed dye laser--possibilities and
limits. Hautarzt 1997, 48:536-40.
89. Harrison DF: Use of estrogen in treatment of familial hemorrhagic
telangiectasia. Laryngoscope 1982, 92:314-320.
90. Shah RK, Dhingra JK, Shapshay SM: Hereditary hemorrhagic
telangiectasia: a review of 76 cases. Laryngoscope 2002, 112:767-773.

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 15 of 16
91. Del Rosso JQ: Update on rosacea pathogenesis and correlation with
medical therapeutic agents. Cutis 2006, 78:97-100.
92. Rebora A: Rosacea. J Invest Dermatol 1987, 88:56-60.
93. Berg M, Lidén S: An epidemiological study of rosacea. Acta Derm
Venereol 1989, 69:419-423.
94. Elsaie ML, Choudhary S: Updates on the pathophysiology and
management of acne rosacea. Postgrad Med 2009, 121:178-186.
95. Yamasaki K, Di Nardo A, Bardan A, Murakami M, Takaaki O, Coda A,
Dorschner RA, Bonnart C, Descargues P, Hovnanian A, Morhenn VB, Gallo
RL: Increased serine protease activity and cathelicidin promotes skin
inflammation in rosacea. Nat Med 2007, 13:975-80.
96. Rebora A: The management of rosacea. Am J Clin Dermatol 2002,
3:489-496.
97. Korting HC, Schöllmann C: Current topical and systemic approaches to
treatment of rosacea. J Eur Acad Dermatol Venereol 2009, 23:876-882.
98. Neuhaus IM, Zane LT, Tope WD: Comparative efficacy of
nonpurpuragenic pulsed dye laser and intense pulsed light for
erythematotelangiectatic rosacea. Dermatol Surg 2009, 35:920-928.
99. Stone DU, Chodosh J: Ocular rosacea: an update on pathogenesis and
therapy. Curr Opin Ophthalmol 2004, 15:499-502.
100. Eiseman AS: The ocular manifestations of atopic dermatitis and
rosacea. Curr Allergy Asthma Rep 2006, 6:292-298.
101. Wigley JEM: Sarcoid of Boeck? Eosinophilic granuloma. Br J Dermatol
1945, 57:68-69.
102. Rieker J, Hengge U, Ruzicka T, Bruch-Gerharz D: Multifocal facial
eosinophilic granuloma: successful treatment with topical tacrolimus.
Hautarzt 2006, 57:324-326.
103. Chensue SW, Warmington K, Ruth J, Lincoln P, Kuo MC, Kunkel SL:
Cytokine responses during mycobacterial and schistosomal antigen-
induced pulmonary granuloma formation. Production of Th1 and Th2
cytokines and relative contribution of tumor necrosis factor. Am J Path
1994, 145:1105-1113.
104. Besnier E: Lupus pernio de la face; synovites fongueuses (scrofulo-
tuberculeuses) symétriques des extrémités superieures. Annales de
dermatologie et de syphilographie 1889, 10:333-336.
105. Badgwell C, Rosen T: Cutaneous sarcoidosis therapy updated. J Am
Acad Dermatol 2007, 56:69-83.
106. Kirkham N: Tumors and cysts of the Epidermis. In Lever, Histopathology
of the skin 10th edition. Lippincott Williams & Wilkins, Philadelphia USA;
2009:791-849.
107. Montgomery H, Dörffel J: Verruca senilis und keratoma senile. Arch
Dermatol Syph 1932, 166:286.
108. Rook A, Whimster I: Keratoacanthoma--a thirty year retrospect. Br J
Dermatol 1979, 100:41-47.
109. Belisario JC: Brief review of keratoacanthomas and description of
keratoacanthoma centrifugum marginatum, another variety of
keratoacanthoma. Aust J Dermatol 1965, 8:65-72.
110. Popkin GL, Brodie SJ, Hyman AB, Andrade R, Kopf AW: A technique of
biopsy recommended for keratoacanthoma. Arch Dermatol 1966,
94:191-193.
111. Sullivan JJ, Colditz GA: Keratoacanthoma in a subtropical climate.
Australas J Dermatol 1979, 20:34-40.
112. Muir EG, Bell AJ, Barlow KA: Multiple primary carcinomata of the colon,
duodenum, and larynx associated with kerato-acanthomata of the
face. Br J Surg 1967, 54:191-195.
113. Parkin DM, Bray F, Ferlay J, Pisani P: Estimating the world cancer burden:
Globocan 2000. Int J Cancer 2001, 94:153-156.
114. Garbe C, Leiter U: Melanoma epidemiology and trends. Clin Dermatol
2009, 27:3-9.
115. Jahn V, Breuninger H, Garbe C, Maassen M, Moehrle M: Melanoma of the
Nose: Prognostic Factors, Three-Dimensional Histology, and Surgical
Strategies. Laryngoscope 2006, 116:1204-1211.
116. Fisher SR: Cutaneous malignant melanoma of the head and neck.
Laryngoscope 1989, 99:822-836.
117. Garbe C, Hauschild A, Volkenandt M, Schadendorf D, Stolz W, Reinhold U,
Kortmann RD, Kettelhack C, Frerich B, Keilholz U, Dummer R, Sebastian G,
Tilgen W, Schuler G, Mackensen A, Kaufmann R: Leitlinie malignes
Melanom Vers 15. [http://www.ado-homepage.de/projekte/1/upload/
leitlinie_melanom_ado_2005.pdf].
118. American Cancer Society (ACS): Treatment of Melanoma by Stage.
[http://www.cancer.org/docroot/CRI/CRI_2_3x.asp?dt=39].
119. Sladden MJ, Balch C, Barzilai DA, Berg D, Freiman A, Handiside T, Hollis S,
Lens MB, Thompson JF: Surgical excision margins for primary cutaneous
melanoma. Cochrane Database Syst Rev 2009, 4:CD004835.
120. Gambichler T, Moussa G, Bahrenberg K, Vogt M, Ermert H, Weyhe D,
Altmeyer P, Hoffmann K: Preoperative ultrasonic assessment of thin
melanocytic skin lesions using a 100-MHz ultrasound transducer: a
comparative study. Dermatol Surg 2007, 33:818-824.
121. Vilana R, Puig S, Sanchez M, Squarcia M, Lopez A, Castel T, Malvehy J:
Preoperative assessment of cutaneous melanoma thickness using 10-
MHz sonography. AJR Am J Roentgenol 2009, 193:639-43.
122. Temple CL, Arlette JP: Mohs micrographic surgery in the treatment of
lentigo maligna and melanoma. J Surg Oncol 2006, 94:287-92.
123. Mohs FE, Snow SN, Larson PO: Mohs micrographic surgery fixed-tissue
technique for melanoma of the nose. J Dermatol Surg Oncol 1990,
16:1111-1120.
124. Leitlinien der Deutschen Dermatologischen Gesellschaft (DDG):
Mikroskopisch kontrollierte Chirurgie (MKC). [http://www.uni-
duesseldorf.de/AWMF/ll/013-064.htm].
125. Maloney ME: Determining Cancer at Surgical margin. In Surgical
Dermatopathology Cambridge, MA: Blackwell Publishers; 1999:113-116.
126. Veronesi U, Adamus J, Bandiera DC: Inaffeciacy of immediate node
dissection in stage 1 melanoma of the limbs. N Eng J Med 1977,
297:627-630.
127. Cascinelli N, Morabito A, Santinami M: Immediate or delayed dissection
of regional nodes in patients with melanoma of the trunk: a
randomised trial. WHO Melanoma Programme. Lancet 1998,
351:793-796.
128. Balch CM, Soong SJ, Bartolucci AA, Urist MM, Karakousis CP, Smith TJ,
Temple WJ, Ross MI, Jewell WR, Mihm MC, Barnhill RL, Wanebo HJ: Efficacy
of an elective regional lymph node dissection of 1 to 4 mm thick
melanomas for patients 60 years of age and younger. Ann Surg 1996,
224:255-263.
129. Dauer EH, Lewis JE, Rohlinger AL, Weaver AL, Olsen KD: Sinonasal
melanoma: A clinicopathological review of 61 cases. Otolaryngol Head
Neck Surg 2008, 138:347-52.
130. Loree TR, Mullins AP, Spellman J, North JH, Hicks WL: Head and neck
mucosal melanoma: a 32-year review. Ear Nose Throat J 1999,
78:372-375.
131. Pandey M, Abraham EK, Mathew A, Ahamed IM: Primary malignant
melanoma of the upper aero-digestive tract. Int J Oral Maxillofac Surg
1999, 28:45-49.
132. Mendenhall WM, Amdur RJ, Hinermann RW, Werning JW, Villaret B,
Mendenhall , Price Nancy: Head and neck mucosal melanoma. Am J Clin
Oncol 2005, 28:626-630.
133. Sand M, Sand D, Brors D, Altmeyer P, Mann B, Bechara FG: Cutaneous
lesions of the external ear. Head Face Med 2008, 4:2.
134. Wettstein R, Erba P, Farhadi J, Kalbermatten DF, Arnold A, Haug M, Pierer
G: Incomplete excision of basal cell carcinoma in the subunits of the
nose. Scand J Plast Reconstr Surg Hand Surg 2008, 42:92-95.
135. Sand M, Bechara FG, Sand D, Moussa G, Stücker M, Altmeyer P, Hoffmann
K, Rotterdam S: Polyglandular autoimmune syndrome associated with
pigmented basal cell carcinoma. J Dermatol 2005, 32:1044-1047.
136. Jeevankumar B, Thappa DM: Unusual presentation of basal cell
carcinoma on face. Indian J Dermatol 2005, 50:161-163.
137. Kirkam N: Tumors and cysts of the epidermis. In Lever's Histopathology of
the Skin 8th edition. Edited by: Elder D, Elenistsas R, Jaworsky C, Johnson B
Jr. Philadelphia: Lippincott-Raven; 1997:685-746.
138. Rowe DE, Carroll RJ, Day CL: Long-term recurrence rates in previously
untreated basal cell carcinoma: implications for patient follow-up. J
Dermatol Surg Oncol 1989, 15:315-328.
139. Sand M, Boorboor P, Sand D, Altmeyer P, Mann B, Bechara FG: Bilateral
cheek-to-nose advancement flap: an alternative to the paramedian
forehead flap for reconstruction of the nose. Acta Chir Plast 2007,
49:67-70.
140. Rowe DE, Raymond JC, Day CL: Mohs' surgery is the treatment of choice
for recurrent basal cell carcinoma. J Dermatol Surg Oncol 1989,
15:424-431.
141. Barzilai DA, Freiman A, Dellavalle RP, Weinstock MA, Mostow EN:
Dermatoepidemiology. J Am Acad Dermatol 52:559-573.
142. Wu JK, Siller G, Whitehead K: Treatment of Bowen's disease and basal
cell carcinoma of the nose with imiquimod 5% cream. Australas J
Dermatol 44:123-125.

Sand et al. Head & Face Medicine 2010, 6:7
http://www.head-face-med.com/content/6/1/7
Page 16 of 16
143. Childers BJ, Goldwyn RM, Ramos D, Chaffey J, Harris JR: Long-term results
of irradiation for basal cell carcinoma of the skin of the nose. Plast
Reconstr Surg 93:1169-1173.
144. Leibovitch I, Huilgol SC, Selva D, Richards S, Paver R: Basal cell carcinoma
treated with Mohs surgery in Australia II. Outcome at 5-year follow-up.
J Am Acad Dermatol 2005, 53:452-457.
145. Swanson NA: Mohs surgery. Technique, indications, applications, and
the future. Arch Dermatol 1983, 119:761-773.
146. Stucker FJ, Nathan CA, Lian TS: Cutaneous malignancy. In Head & Neck
Surgery - Otolaryngology 3rd edition. Edited by: Byron J Bailey. Lippincott
Williams & Wilkins, Philadelphia; 2001:1223-1235.
147. Kirkham N: Tumours and cysts of the epidermis. In Lever's histopathology
of the skin 8th edition. Edited by: Lever WF, Lever GS. Philadelphia:
Lippincott-Raven; 1997:685-746.
148. Bauk VOZ, Assunção AM, Domingues RF, Fernandes NC, Maya TC, Maceira
JP: Marjolin's ulcer: a twelve-case report. An Bras Dermatol 2006,
81:355-358.
149. Gupta AK, Cardella CJ, Haberman HF: Cutaneous malignant neoplasms
in patients with renal transplants. Arch Dermatol 1986, 122:1288-93.
150. Lundt HZ: How often does squamous cell carcinoma of the skin
metastasize? Arch Dermatol 1965, 92:635-637.
151. Joseph MG, Zulueta WP, Kennedy PJ: Squamous cell carcinoma of the
skin. The incidence of metastases and their outcome. ANZ J Surg 1991,
62:697-701.
152. Czarnecki D, Staples M, Mar A, Giles G, Meehan C: Metastases from
squamous cell carcinoma of the skin in Southern Australia.
Dermatology 1994, 189:52-54.
153. Møller R, Reymann F, Hou-Jensen K: Metastases in dermatological
patients with squamous cell carcinoma. Arch Dermatol 1979,
115:703-705.
154. Epstein E, Epstein NN, Bragg K, Linden G: Metastases from squamous cell
carcinomas of the skin. Arch Dermatol 1968, 97:245-251.
155. Veness MJ, Porceddu S, Palme CE, Morgan GJ: Cutaneous head and neck
squamous cell carcinoma metastatic to parotid and cervical lymph
nodes. Head Neck 2007, 29:621-631.
156. Frierson HF Jr, Cooper PH: Prognostic factors in squamous cell
carcinoma of the lower lip. Hum Pathol 1986, 17:346-354.
157. Arons MS, Lynch JB, Lewis SR, Blocker TG Jr: Scar tissue carcinoma. I. A
clinical study with special reference to burn scar carcinoma. Ann Surg
1965, 161:170-188.
158. Martin H, Strong E, Spiro RH: Radiation-induced skin cancer of the head
and neck. Cancer 1970, 25:61-71.
159. Sedlin ED, Fleming JL: Epidermal carcinoma arising in chronic
osteomyelitic foci. J Bone Joint Surg 1963, 45:827-837.
160. Gross MD, Monroe M: Skin cancer: squamous cell carcinoma. [http://
emedicine.medscape.com/article/870430-overview].
161. Jalili A, Pinc A, Pieczkowski F, Karlhofer FM, Stingl G, Wagner SN:
Combination of an EGFR blocker and a COX-2 inhibitor for the
treatment of advanced cutaneous squamous cell carcinoma. J Dtsch
Dermatol Ges 2008, 6:1066-1069.
162. Shimizu T, Izumi H, Oga A, Furumoto H, Murakami T, Ofuji R, Muto M,
Sasaki K: Epidermal growth factor receptor overexpression and genetic
aberrations in metastatic squamous-cell carcinoma of the skin.
Dermatology 2001, 202:203-206.
163. Kaposi M: Idiopathisches multiples Pigmentsarkom der Haut. Arch
Dermatol Syph 1872, 4:265-273.
164. Masih RB, Jesudass SW, Verghese A: Kaposi's sarcoma of the tip of the
nose as a sentinel sign for Kaposi's sarcoma of the lung. Chest 1996,
110:576.
165. Kaloterakis A, Papasteriades C, Filiotou A, Economidou J, Hadjiyannis S,
Stratigos J: HLA in familial and nonfamilial Mediterranean Kaposi's
sarcoma in Greece. Tissue Antigens 1995, 45:117-119.
166. Calabrò ML, Sheldon J, Favero A, Simpson GR, Fiore JR, Gomes E, Angarano
G, Chieco-Bianchi L, Schulz TF: Seroprevalence of Kaposi's sarcoma-
associated herpesvirus/human herpesvirus 8 in several regions of Italy.
J Hum Virol 1998, 1:207-213.
167. Penn I: Cancer in the immunosuppressed organ recipient. Transplant
Proc 1991, 23:1771-1772.
168. Penn I: Tumors after renal and cardiac transplantation. Hematol Oncol
Clin North Am 1993, 7:431-445.
169. DeVita V: AIDS-related malignancies. In Cancer: Principles and Practice of
Clinical Oncology Volume 8. 5th edition. Edited by: DeVita V, Vincent T Jr.
Philadelphia, Pa: Lippincott, Williams, & Wilkins; 2008:2404-2407.
170. Rose LJ, Fishman AD, Sparano JA: Kaposi Sarcoma. [http://
emedicine.medscape.com/article/279734-overview].
171. Jacobson LP, Jenkins FJ, Springer G, Muñoz A, Shah KV, Phair J, Zhang Z,
Armenian H: Interaction of human immunodeficiency virus type 1 and
human herpesvirus type 8 infections on the incidence of Kaposi's
sarcoma. J Infect Dis 2000, 181:1940-1949.
172. Nobler MP, Leddy ME, Huh SH: The impact of palliative irradiation on the
management of patients with acquired immune deficiency syndrome.
J Clin Oncol 1987, 5:107-112.
173. Dezube BJ: Acquired immunodeficiency syndrome-related Kaposi's
sarcoma: clinical features, staging, and treatment. Semin Oncol 2000,
27:424-430.
doi: 10.1186/1746-160X-6-7
Cite this article as: Sand et al., Cutaneous lesions of the nose Head & Face
Medicine 2010, 6:7