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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Acquired hyperpigmentations<xref ref-type="fn" rid="fn01">*</xref></title><author><name sortKey="Cestari, Tania Ferreira" sort="Cestari, Tania Ferreira" uniqKey="Cestari T" first="Tania Ferreira" last="Cestari">Tania Ferreira Cestari</name><affiliation><nlm:aff id="aff01"> PhD - Associate Professor at the Internal Medicine Department, at Rio Grande do Sul Federal University (UFRGS). Teaching Professor at the Child and Adolescent Health Sciences and the Surgical Post-Graduation Programs at Rio Grande do Sul Federal University (UFRGS). Chief of the Dermatology Department at Porto Alegre Clinics Hospital - Rio Grande do Sul Federal University (HCPA-UFRGS) - Porto Alegre (RS), Brazil.</nlm:aff></affiliation></author><author><name sortKey="Dantas, Lia Pinheiro" sort="Dantas, Lia Pinheiro" uniqKey="Dantas L" first="Lia Pinheiro" last="Dantas">Lia Pinheiro Dantas</name><affiliation><nlm:aff id="aff02"> MD, Dermatologist, MSc (in course) at the Medical Sciences Post Graduation program at Rio Grande do Sul Federal University (UFRGS) - Porto Alegre (RS), Brazil.</nlm:aff></affiliation></author><author><name sortKey="Boza, Juliana Catucci" sort="Boza, Juliana Catucci" uniqKey="Boza J" first="Juliana Catucci" last="Boza">Juliana Catucci Boza</name><affiliation><nlm:aff id="aff03"> MD, Dermatologist, PhD (in course) at the Child and Adolescent Health Sciences Post Graduation Program at Rio Grande do Sul Federal University (UFRGS) - Porto Alegre (RS), Brazil.</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24626644</idno><idno type="pmc">3938350</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3938350</idno><idno type="RBID">PMC:3938350</idno><idno type="doi">10.1590/abd1806-4841.20142353</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000352</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000352</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Acquired hyperpigmentations<xref ref-type="fn" rid="fn01">*</xref></title><author><name sortKey="Cestari, Tania Ferreira" sort="Cestari, Tania Ferreira" uniqKey="Cestari T" first="Tania Ferreira" last="Cestari">Tania Ferreira Cestari</name><affiliation><nlm:aff id="aff01"> PhD - Associate Professor at the Internal Medicine Department, at Rio Grande do Sul Federal University (UFRGS). Teaching Professor at the Child and Adolescent Health Sciences and the Surgical Post-Graduation Programs at Rio Grande do Sul Federal University (UFRGS). Chief of the Dermatology Department at Porto Alegre Clinics Hospital - Rio Grande do Sul Federal University (HCPA-UFRGS) - Porto Alegre (RS), Brazil.</nlm:aff></affiliation></author><author><name sortKey="Dantas, Lia Pinheiro" sort="Dantas, Lia Pinheiro" uniqKey="Dantas L" first="Lia Pinheiro" last="Dantas">Lia Pinheiro Dantas</name><affiliation><nlm:aff id="aff02"> MD, Dermatologist, MSc (in course) at the Medical Sciences Post Graduation program at Rio Grande do Sul Federal University (UFRGS) - Porto Alegre (RS), Brazil.</nlm:aff></affiliation></author><author><name sortKey="Boza, Juliana Catucci" sort="Boza, Juliana Catucci" uniqKey="Boza J" first="Juliana Catucci" last="Boza">Juliana Catucci Boza</name><affiliation><nlm:aff id="aff03"> MD, Dermatologist, PhD (in course) at the Child and Adolescent Health Sciences Post Graduation Program at Rio Grande do Sul Federal University (UFRGS) - Porto Alegre (RS), Brazil.</nlm:aff></affiliation></author></analytic><series><title level="j">Anais Brasileiros de Dermatologia</title><idno type="ISSN">0365-0596</idno><idno type="eISSN">1806-4841</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Cutaneous hyperpigmentations are frequent complaints, motivating around 8.5% of all
dermatological consultations in our country. They can be congenital, with different
patterns of inheritance, or acquired in consequence of skin problems, systemic
diseases or secondary to environmental factors. The vast majority of them are linked
to alterations on the pigment melanin, induced by different mechanisms. This review
will focus on the major acquired hyperpigmentations associated with increased
melanin, reviewing their mechanisms of action and possible preventive measures.
Particularly prominent aspects of diagnosis and therapy will be emphasized, with
focus on melasma, post-inflammatory hyperpigmentation, periorbital pigmentation,
dermatosis papulosa nigra, phytophotodermatoses, flagellate dermatosis, erythema
dyschromicum perstans, cervical poikiloderma (Poikiloderma of Civatte), acanthosis
nigricans, cutaneous amyloidosis and reticulated confluent dermatitis</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Sanchez, Np" uniqKey="Sanchez N">NP Sanchez</name></author><author><name sortKey="Pathak, Ma" uniqKey="Pathak M">MA Pathak</name></author><author><name sortKey="Sato, S" uniqKey="Sato S">S Sato</name></author><author><name sortKey="Fitzpatrick, Tb" uniqKey="Fitzpatrick T">TB Fitzpatrick</name></author><author><name sortKey="Sanchez, Jl" uniqKey="Sanchez J">JL Sanchez</name></author><author><name sortKey="Mihm, Mc" uniqKey="Mihm M">MC Mihm</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ritter, Cg" uniqKey="Ritter C">CG Ritter</name></author><author><name sortKey="Fiss, Dv" uniqKey="Fiss D">DV Fiss</name></author><author><name sortKey="Borges Da Costa, Ja" uniqKey="Borges Da Costa J">JA Borges da Costa</name></author><author><name sortKey="De Carvalho, Rr" 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Alvarez, B" uniqKey="Torres Alvarez B">B Torres-Alvarez</name></author><author><name sortKey="Castanedo Cazares, Jp" uniqKey="Castanedo Cazares J">JP Castanedo-Cazares</name></author><author><name sortKey="Oros Ovalle, C" uniqKey="Oros Ovalle C">C Oros-Ovalle</name></author><author><name sortKey="Moncada, B" uniqKey="Moncada B">B Moncada</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shin, J" uniqKey="Shin J">J Shin</name></author><author><name sortKey="Kim, Jh" uniqKey="Kim J">JH Kim</name></author><author><name sortKey="Kim, Ek" uniqKey="Kim E">EK Kim</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jang, Yh" uniqKey="Jang Y">YH Jang</name></author><author><name sortKey="Lee, Jy" uniqKey="Lee J">JY Lee</name></author><author><name sortKey="Kang, Hy" uniqKey="Kang H">HY Kang</name></author><author><name sortKey="Lee, Es" uniqKey="Lee E">ES Lee</name></author><author><name sortKey="Kim, Yc" uniqKey="Kim Y">YC Kim</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Perez, M" uniqKey="Perez M">M Pérez</name></author><author><name sortKey="Sanchez, Jl" uniqKey="Sanchez J">JL Sánchez</name></author><author><name sortKey="Aguil, F" uniqKey="Aguil F">F Aguiló</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rigopoulos, D" uniqKey="Rigopoulos D">D Rigopoulos</name></author><author><name sortKey="Gregoriou, S" uniqKey="Gregoriou S">S Gregoriou</name></author><author><name sortKey="Katsambas, A" uniqKey="Katsambas A">A Katsambas</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sheth, Vm" uniqKey="Sheth V">VM Sheth</name></author><author><name sortKey="Pandya, Ag" uniqKey="Pandya A">AG Pandya</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Grimes, Pe" uniqKey="Grimes P">PE Grimes</name></author><author><name sortKey="Yamada, N" uniqKey="Yamada N">N 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<front><journal-meta><journal-id journal-id-type="nlm-ta">An Bras Dermatol</journal-id><journal-id journal-id-type="iso-abbrev">An Bras Dermatol</journal-id><journal-id journal-id-type="publisher-id">An Bras Dermatol</journal-id><journal-title-group><journal-title>Anais Brasileiros de Dermatologia</journal-title></journal-title-group><issn pub-type="ppub">0365-0596</issn><issn pub-type="epub">1806-4841</issn><publisher><publisher-name>Sociedade Brasileira de Dermatologia</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">24626644</article-id><article-id pub-id-type="pmc">3938350</article-id><article-id pub-id-type="doi">10.1590/abd1806-4841.20142353</article-id><article-categories><subj-group subj-group-type="heading"><subject>Continuing Medical Education</subject></subj-group></article-categories><title-group><article-title>Acquired hyperpigmentations<xref ref-type="fn" rid="fn01">*</xref></article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Cestari</surname><given-names>Tania Ferreira</given-names></name><xref ref-type="aff" rid="aff01">1</xref><xref ref-type="corresp" rid="c01"></xref></contrib><contrib contrib-type="author"><name><surname>Dantas</surname><given-names>Lia Pinheiro</given-names></name><xref ref-type="aff" rid="aff02">2</xref></contrib><contrib contrib-type="author"><name><surname>Boza</surname><given-names>Juliana Catucci</given-names></name><xref ref-type="aff" rid="aff03">3</xref></contrib></contrib-group><aff id="aff01"><label>1</label> PhD - Associate Professor at the Internal Medicine Department, at Rio Grande do Sul Federal University (UFRGS). Teaching Professor at the Child and Adolescent Health Sciences and the Surgical Post-Graduation Programs at Rio Grande do Sul Federal University (UFRGS). Chief of the Dermatology Department at Porto Alegre Clinics Hospital - Rio Grande do Sul Federal University (HCPA-UFRGS) - Porto Alegre (RS), Brazil.</aff><aff id="aff02"><label>2</label> MD, Dermatologist, MSc (in course) at the Medical Sciences Post Graduation program at Rio Grande do Sul Federal University (UFRGS) - Porto Alegre (RS), Brazil.</aff><aff id="aff03"><label>3</label> MD, Dermatologist, PhD (in course) at the Child and Adolescent Health Sciences Post Graduation Program at Rio Grande do Sul Federal University (UFRGS) - Porto Alegre (RS), Brazil.</aff><author-notes><corresp id="c01">MAILING ADDRESS: Tania Ferreira Cestari, Rua Santo Inácio 500/
1002, 90570-150 -Porto Alegre - RS Brazil. E-mail:
<email>tcestari@hcpa.ufrgs.br</email></corresp></author-notes><pub-date pub-type="ppub"><season>Jan-Feb</season><year>2014</year></pub-date><volume>89</volume><issue>1</issue><fpage>11</fpage><lpage>25</lpage><history><date date-type="received"><day>09</day><month>12</month><year>2012</year></date><date date-type="accepted"><day>25</day><month>3</month><year>2013</year></date></history><permissions><copyright-statement>®2013 by Anais Brasileiros de
Dermatologia</copyright-statement><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/"><license-p>This is an Open Access article distributed under the terms of the Creative
Commons Attribution Non-Commercial License which permits unrestricted
non-commercial use, distribution, and reproduction in any medium, provided the
original work is properly cited. </license-p></license></permissions><abstract><p>Cutaneous hyperpigmentations are frequent complaints, motivating around 8.5% of all
dermatological consultations in our country. They can be congenital, with different
patterns of inheritance, or acquired in consequence of skin problems, systemic
diseases or secondary to environmental factors. The vast majority of them are linked
to alterations on the pigment melanin, induced by different mechanisms. This review
will focus on the major acquired hyperpigmentations associated with increased
melanin, reviewing their mechanisms of action and possible preventive measures.
Particularly prominent aspects of diagnosis and therapy will be emphasized, with
focus on melasma, post-inflammatory hyperpigmentation, periorbital pigmentation,
dermatosis papulosa nigra, phytophotodermatoses, flagellate dermatosis, erythema
dyschromicum perstans, cervical poikiloderma (Poikiloderma of Civatte), acanthosis
nigricans, cutaneous amyloidosis and reticulated confluent dermatitis</p></abstract><kwd-group><kwd>Diagnosis</kwd><kwd>Hyperpigmentation</kwd><kwd>Melanosis</kwd><kwd>Pigmentation disorders</kwd><kwd>Therapeutics</kwd></kwd-group></article-meta></front><body><sec><title>ACQUIRED HYPERPIGMENTATIONS</title><p>Hyperpigmentations are a group of diseases that comprise both congenital forms, with
different patterns of inheritance, and acquired forms secondary to cutaneous or systemic
problems. The vast majority of them are linked to alterations in the melanin pigment and
can be classified as epidermal, due to an increase in the number of melanocytes or the
production of melanin or dermal, either melanocytic or not.</p><p>Pigmentary disorders are a frequent source of complaints, constituting the third most
common reason for dermatological consultations, about 8.5% in our country. There is a
different impact depending on the geographic region, being worse in places where the
weather is always warm, and the skin becomes more exposed.<sup><xref rid="r01" ref-type="bibr">1</xref></sup> Consultations due to hyperpigmentation vary with age
group, being the second most common complaint between 15 and 30 years of age and the
first in the range of 40 to 54 years, regardless of skin color and gender.<sup><xref rid="r01" ref-type="bibr">1</xref></sup></p><p>This review will focus on the main acquired hyperpigmentation disorders associated with
increased melanin, taking into account those most commonly found in clinical practice.
It will also consider other pigmentation alterations which basic pathogenic mechanisms
involve not only hyper-melanization but also associated factors such as hyperkeratosis
with superficial oxidation of keratin and epithelial hyperproliferation. The main
complaint in these dermatoses is the increase in color intensity, and they are relevant
for their high frequency or for being markers of other diseases.</p><sec><title>Melasma</title><p>The word <italic>melasma</italic> originates from the Greek, where <italic>melas
</italic> means black. It appears as a symmetric acquired hypermelanosis, with stains
in shades of brown to bluish gray, with irregular borders and located in more
photo-exposed areas. It usually affects the face and neck, and less commonly, the
arms and the sternal region, respecting the mucosal areas (<xref ref-type="fig" rid="f01">Figures 1</xref> and <xref ref-type="fig" rid="f02">2</xref>). Usually
melasma has three clinical patterns: centrofacial with spots on the frontal region,
nasal dorsum, cheekbones and chin areas, in 65% of the cases; malar in 20% of the
cases, and mandibular, in about 15% of patients.<sup><xref rid="r02" ref-type="bibr">2</xref></sup> Extra facial areas with the highest incidence of melasma are
the extensor surface of the arms and forearms, the neckline, the upper third of the
dorsal area of the trunk and the sides of the neck.<sup><xref rid="r03" ref-type="bibr">3</xref></sup></p><fig id="f01" orientation="portrait" position="float"><label>FIGURE 1</label><caption><p>Acquired hyperpigmentations. Moderate melasma, brown spots with irregular edges
affecting the right hemiface, following a mandibular pattern in a patient with
phototype V</p></caption><graphic xlink:href="abd-89-01-0011-g01"></graphic></fig><fig id="f02" orientation="portrait" position="float"><label>FIGURE 2</label><caption><p>Acquired hyperpigmentations. Severe melasma. Patient with skin phototype IV,
presenting a somewhat homogeneous lesions, but with intense pigmentation,
predominantly in the middle facial region</p></caption><graphic xlink:href="abd-89-01-0011-g02"></graphic></fig><p>Its occurrence is described within all racial and ethnic groups, but most commonly in
individuals with higher skin phototypes living in areas of intense ultraviolet (UV)
radiation, especially Latin American, Asians and Afrodescendants.<sup><xref rid="r04" ref-type="bibr">4</xref>,<xref rid="r05" ref-type="bibr">5</xref></sup> Similarly, it is more common in young women, with men accounting
for about 10% of all cases, with well-delimited geographical variations.<sup><xref rid="r06" ref-type="bibr">6</xref></sup></p><p>Several factors have been linked to melasma. Among them, UV exposure and genetic
predisposition appear to be the most significant ones.<sup><xref rid="r05" ref-type="bibr">5</xref>,<xref rid="r07" ref-type="bibr">7</xref>-<xref rid="r11" ref-type="bibr">11</xref></sup> Ultraviolet radiation (UVR) induces
melanocortin within melanocytes and keratinocytes, justifying the involvement of this
hormone in the pathogenesis of melasma. More recently, it was suggested that high
intensity visible light also contributes to the increased pigmentation in melasma,
particularly in skin phototypes IV-VI, corroborating data derived from clinical
observation.<sup><xref rid="r12" ref-type="bibr">12</xref>,<xref rid="r13" ref-type="bibr">13</xref></sup></p><p>Recent histological and immunohistochemical studies demonstrated that melasma skin
presents marked features of chronic sun damage. During sun exposure, physiological
reactions occur, triggered by a network of cellular interactions between
keratinocytes, mast cells, fibroblasts, the dermal vasculature over melanocytes and
dermal inflammation, playing an important role in the hyperpigmentation and
reactivation of melasma lesions.<sup><xref rid="r12" ref-type="bibr">12</xref>-<xref rid="r15" ref-type="bibr">15</xref></sup></p><p>Other situations involved in the pathogenesis of melasma are: pregnancy, use of oral
contraceptives (OC), endocrine disorders and hormonal treatments.<sup><xref rid="r16" ref-type="bibr">16</xref>,<xref rid="r17" ref-type="bibr">17</xref></sup> The results of a large global study, that evaluated 324 women
with melasma, suggested that a combination of known triggers, including pregnancy,
hormonal birth control, age, family history and sun exposure affect the onset and
recurrence of melasma lesions.<sup><xref rid="r11" ref-type="bibr">11</xref></sup>Furthermore, the application of certain cosmetics and medications such as
anticonvulsants and photosensitizing substances have also been described as possible
causes or aggravating factors for hyperpigmentation.<sup><xref rid="r18" ref-type="bibr">18</xref>,<xref rid="r19" ref-type="bibr">19</xref></sup></p><p>Melasma is usually classified into: epidermaltype (70% of patients), in which the
pigmentation is enhanced during examination with ultraviolet A light (UVA), dermal
type (10 to 15%) in which the pigmentation does not change during this same exam and
mixed (20%).<sup><xref rid="r02" ref-type="bibr">2</xref></sup> However, recent
studies have questioned this diagnostic technique. Skin biopsies with melasma showed
that the level of pigment deposit does not always correspond to the reading by UVA
light, with most lesions having both dermal and epidermal components.<sup><xref rid="r20" ref-type="bibr">20</xref></sup> Melasma lesions show increased
density of dermal and epidermal melanin besides marked solar elastosis compared with
the adjacent normal skin.<sup><xref rid="r09" ref-type="bibr">9</xref>,<xref rid="r20" ref-type="bibr">20</xref></sup> It was verified, through
immunohistochemistry, that the number of epidermal melanocytes may be either
increased or equal to that of normal skin.<sup><xref rid="r10" ref-type="bibr">10</xref></sup> However, these cells exhibit characteristics of
hyperfunctioning cells with size enlargement and prominence of dendrites.</p><p>The goal of melasma treatment is to decrease the proliferation of melanocytes,
inhibit the formation of melanosomes and promote their degradation.<sup><xref rid="r21" ref-type="bibr">21</xref></sup> However, the chronic course of the
disease and its relapses discourage the adherence to the proposed treatment,
especially regarding the use of sunscreen.</p><p>Photoprotection is essential to the treatment and should be followed rigorously,
since the lesions are aggravated by UVA, UVB and also by visible light. Sunscreens
with a sun protection factor (SPF) greater than 30 and with physical photoprotective
agents in their formulation are recommended. It is essential to apply them several
times a day, and wear hats during outdoor activities, avoiding exposure during UV
radiation peak hours. <sup><xref rid="r21" ref-type="bibr">21</xref>,<xref rid="r22" ref-type="bibr">22</xref></sup></p><p>The classical melasma treatment includes the use of topical hydroquinone (HQ), alone
or combined with retinoic acid (RA) or glycolic acid (GA) (double combination) or RA
and a topical corticosteroid (triple combination).<sup><xref rid="r23" ref-type="bibr">23</xref></sup> Other agents that may be considered include GA and
RA, isolated or associated with other agents; azelaic acid (AZ), arbutin, kojic acid
and mequinol, among others (<xref ref-type="table" rid="t01">Table
1</xref>).<sup><xref rid="r23" ref-type="bibr">23</xref>-<xref rid="r26" ref-type="bibr">26</xref></sup> The combined therapies have been more used as they
present synergism in their actions, being therefore, more effective whilst with less
adverse events. A recent study demonstrated that the triple combination is more
costeffective than the double or single therapies and that the combination of 0.05%
RA + 4% HQ plus 0.01% fluocinolone acetonide has the best grade and quality of
evidence obtained through efficacy studies in melasma treatment.<sup><xref rid="r21" ref-type="bibr">21</xref>-<xref rid="r23" ref-type="bibr">23</xref>,<xref rid="r25" ref-type="bibr">25</xref>,<xref rid="r27" ref-type="bibr">27</xref></sup> The Latin American Academy of Pigmentary Disorders
(Pigmentary Disorders Academy-PDA) proposes an algorithm to better guide the
treatment of melasma. According to it, patients with mild melasma can use HQ 4%, or
triple combination therapy with 4% HQ + 0.05% RA + 0.01% fluocinolone acetonide, or
dual therapy, or non-phenolic therapy if there is sensitivity to the cited
agents.<sup><xref rid="r21" ref-type="bibr">21</xref></sup> For cases of
moderate to severe melasma, it is recommended to use triple therapy, when this is not
available, dual therapy or 20% AZ may be used, achieving similar results to
hydroquinone alone, but with fewer adverse events.<sup><xref rid="r28" ref-type="bibr">28</xref></sup> In cases that are refractory to topical medications,
the association with procedures such as peels and dermabrasion can be considered,
with special care regarding the possibility of post inflammatory
hyperpigmentation.<sup><xref rid="r29" ref-type="bibr">29</xref></sup></p><table-wrap id="t01" orientation="portrait" position="float"><label>TABLE 1</label><caption><p>Mechanism of action of the main depigmenting agents</p></caption><table frame="hsides" rules="groups"><thead><tr align="left"><th rowspan="1" colspan="1">Tyrosinase inhibition</th><th rowspan="1" colspan="1">Stratum corneum exfoliation</th><th rowspan="1" colspan="1">Degradation / Decrease of melanosome transfer</th><th rowspan="1" colspan="1">Inhibition of DOPA and dopaquinone synthesis</th><th rowspan="1" colspan="1">Promotion of conversion of melanin to leukomelanin</th><th rowspan="1" colspan="1">Nonselective inhibition of melanogenesis</th></tr></thead><tbody><tr><td rowspan="1" colspan="1">Hydroquinone</td><td rowspan="1" colspan="1">Alpha hydroxy acids</td><td rowspan="1" colspan="1">Hydroquinone</td><td rowspan="1" colspan="1">Kojic acid</td><td rowspan="1" colspan="1">Vitamins C and E</td><td rowspan="1" colspan="1">Corticosteroids (they should not be used in monotherapy)</td></tr><tr><td rowspan="1" colspan="1">Azelaic acid</td><td rowspan="1" colspan="1">Retinoids</td><td rowspan="1" colspan="1">Niacinamide</td><td rowspan="1" colspan="1">Glabridin</td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1">Glabridin</td></tr><tr><td rowspan="1" colspan="1">Alpha arbutin</td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1">Soy extracts</td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td></tr><tr><td rowspan="1" colspan="1">Gentisic acid</td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td></tr><tr><td rowspan="1" colspan="1">Flavonoids</td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td></tr><tr><td rowspan="1" colspan="1">Isoflavones</td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td></tr><tr><td rowspan="1" colspan="1">Resveratrol</td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td></tr></tbody></table></table-wrap><p>Serial treatments with intense pulsed light may be indicated in selected cases, in
patients with lighter skin types and no history of prior inflammatory
hyperpigmentation and for those situations where pigment deposits are deeper. This
recommendation is not fully accepted and represents relatively limited experience,
however, some studies demonstrated excellent to good results in 60% of cases with a
6month follow-up.<sup><xref rid="r30" ref-type="bibr">30</xref>,<xref rid="r31" ref-type="bibr">31</xref></sup> The use of Nd:YAG laser at low fluence showed
encouraging results in case series, despite the possibility of occurring excessive
depigmentation.<sup><xref rid="r32" ref-type="bibr">32</xref></sup> Other
authors have reported encouraging results with fractional thulium laser (1927nm)
associated to microdermabrasion or peels.<sup><xref rid="r33" ref-type="bibr">33</xref>-<xref rid="r36" ref-type="bibr">36</xref></sup> Some treatments
suggested as adjuvants for depigmentation or to prevent the recurrence of melasma,
both orally and topically, include substances such as tranexamic acid, antioxidant
vitamins and botanical extracts.<sup><xref rid="r37" ref-type="bibr">37</xref>-<xref rid="r42" ref-type="bibr">42</xref></sup></p></sec><sec><title>Post-inflammatory hyperpigmentation</title><p>Post-inflammatory hyperpigmentation (PIH) is characterized by increased pigmentation
acquired after a cutaneous inflammatory process. People with higher skin phototypes,
presumably, are more prone to this skin condition, because they already have a higher
basal amount of epidermal melanin. Similarly, this hypermelanosis tends to be more
intense and of longer duration in this group.<sup><xref rid="r03" ref-type="bibr">3</xref>,<xref rid="r43" ref-type="bibr">43</xref></sup> The most common
causes of PIH are: acne, atopic dermatitis, allergic contact dermatitis or secondary
to irritants, trauma, psoriasis, lichen planus, drug eruptions, and nowadays,
cosmetic procedures.<sup><xref rid="r44" ref-type="bibr">44</xref>,<xref rid="r45" ref-type="bibr">45</xref></sup></p><p>The distribution of spots follows the location of the inflammatory processes, and
retrieving this information from the patient is really important to establish the
correct differential diagnoses (<xref ref-type="fig" rid="f03">Figure 3</xref>).
Histology shows melanin deposits both in free form and within the melanophages
located in the upper dermis and around the blood vessels. The exact mechanism of PIH
pathogenesis is still not well understood, but it is believed to be more related to
the nature of the triggering inflammation, because the darkening is greater in
chronic and recurrent inflammation processes and also in those that damage the basal
layer.<sup><xref rid="r43" ref-type="bibr">43</xref>,<xref rid="r46" ref-type="bibr">46</xref></sup> It is likely that the hyperpigmentation is caused by
increased melanogenesis or abnormal distribution of the produced melanin, possibly
resulting from the action of cytokines, inflammatory mediators and oxygen reactive
species.<sup><xref rid="r45" ref-type="bibr">45</xref></sup> These agents may
act by stimulating the growth of melanocytes and dendritic proliferation, as well as
increasing the activity of tyrosinase.<sup><xref rid="r47" ref-type="bibr">47</xref></sup></p><fig id="f03" orientation="portrait" position="float"><label>FIGURE 3</label><caption><p>Acquired hyperpigmentations. Postinflammatory hyperpigmentation – bluish brown
macules distributed around the trunk, secondary to extensive pityriasis
rosea</p></caption><graphic xlink:href="abd-89-01-0011-g03"></graphic></fig><p>The course and outcome of PIH treatment are unpredictable and relapses are frequent.
Topical hydroquinone and tretinoin, alone or combined, are effective but require
prolonged treatment.<sup><xref rid="r24" ref-type="bibr">24</xref>,<xref rid="r46" ref-type="bibr">46</xref></sup> Hydroquinone has a limited effect
when the pigment is primarily deposited in the dermis. Other bleaching agents such as
kojic acid and azelaic acid have been used with varying degrees of success. Peels
with glycolic acid or salicylic acid are particularly effective and well tolerated in
patients with high phototype.<sup><xref rid="r48" ref-type="bibr">48</xref></sup> The
use of lasers is described in several reports, the most commonly used being
Q-switched laser, but the results are variable, with risk of hyperpigmentation in
darker skins.<sup><xref rid="r49" ref-type="bibr">49</xref>,<xref rid="r50" ref-type="bibr">50</xref></sup> Recently, the application of fractional
photothermolysis for PIH treatment showed promising results, but further studies are
still needed.<sup><xref rid="r51" ref-type="bibr">51</xref></sup></p></sec><sec><title>Periorbital Hyperpigmentation</title><p>Dark circles or periorbital hyperpigmentation (POH) is a common dermatological
complaint. It affects individuals of both genders, of all ages and races. Despite
being regarded as an anatomical feature or a physiological phenomenon, dark circles
when very pronounced, interfere markedly with facial appearance.<sup><xref rid="r04" ref-type="bibr">4</xref>,<xref rid="r52" ref-type="bibr">52</xref></sup></p><p>This condition is characterized by bilateral homogeneous hyperchromic areas in the
infraorbital region (<xref ref-type="fig" rid="f04">Figure 4</xref>). The lesions
vary in intensity according to fatigue or lack of sleep and worsen with aging due to
sagging, thinning of the skin, abnormal deposits of infraorbital fat and loss of
subcutaneous tissue.<sup><xref rid="r04" ref-type="bibr">4</xref>,<xref rid="r53" ref-type="bibr">53</xref></sup></p><fig id="f04" orientation="portrait" position="float"><label>FIGURE 4</label><caption><p>Acquired hyperpigmentations. Periorbital hyperpigmentations – Depression and
shaded aspect, with visualization of the superficial vascular network in the
infraorbital region of a 38 years-old woman</p></caption><graphic xlink:href="abd-89-01-0011-g04"></graphic></fig><p>Histological features show that dark circles can be associated with multiple
etiologic factors, such as dermal melanin deposition, post-inflammatory
hyperpigmentation, superficial vasculature presentation and periorbital
edema.<sup><xref rid="r04" ref-type="bibr">4</xref>,<xref rid="r52" ref-type="bibr">52</xref></sup> Anatomical changes of the infraorbitary region also
occur, especially malar region with a descending characteristic, prominent lacrimal
sulcus, infraorbitary fat prolapse, sagging, edema, signs of chronic photodamage and
hyperactivity of the periorbital musculature.<sup><xref rid="r04" ref-type="bibr">4</xref></sup> POH is a frequent finding in individuals who are atopic or
allergic to airborne substances, perhaps induced by the habit of rubbing the skin
around the eyes, which triggers postinflammatory pigmentation.</p><p>Periorbital hyperpigmentation may also be a family feature or be part of other
dermatoses, such as erythema dyschromicum perstans, and drug related
eruptions.<sup><xref rid="r04" ref-type="bibr">4</xref></sup></p><p>Dark circles treatment is unsatisfactory because of the necessity of dealing with
multiple factors. Corrective makeup is a palliative solution, but with long-term
average results. There are several therapeutic options, and it is often necessary to
combine them.<sup><xref rid="r04" ref-type="bibr">4</xref>,<xref rid="r54" ref-type="bibr">54</xref>-<xref rid="r57" ref-type="bibr">57</xref></sup></p><p>The drug of choice for the topical treatment of dark circles is hydroquinone, which
inhibits the synthesis of DNA and RNA, induces the degradation of melanosomes and the
destruction of melanocytes.<sup><xref rid="r58" ref-type="bibr">58</xref></sup> The
effects of depigmentation become apparent after 5-7 weeks, usually preceded by
erythema and desquamation. Treatment should be continued for 3-12 months.</p><p>Hydroquinone can also be used in combination with other agents. The Kligman
formulation (hydroquinone + tretinoin + dexamethasone) is the best known combination
for this condition, however adverse reactions such as erythema, desquamation, colloid
milium, irritant or allergic contact dermatitis and post-inflammatory paradoxical
hypermelanosis, have been described.<sup><xref rid="r19" ref-type="bibr">19</xref>,<xref rid="r23" ref-type="bibr">23</xref>,<xref rid="r45" ref-type="bibr">45</xref></sup></p><p>The use of 0.01% to 1% topical retinoic acid, reduce pigmentation by inhibiting
tyrosinase transcription and significant thinning of the granular layer and the
epidermis.<sup><xref rid="r24" ref-type="bibr">24</xref></sup> The effects of
RA become significantly evident after 24 weeks. Side effects commonly reported
include erythema, peeling, burning and stinging. Other compounds used as depigmenting
agents include azelaic acid and kojic acid, but different combined preparations have
been used in order to increase effectiveness and reduce adverse events in the
treatment of various hyperpigmentation disorders.<sup><xref rid="r12" ref-type="bibr">12</xref></sup></p><p>Superficial peels with 15% to 25% or even higher concentrations of trichloroacetic
acid (TCA) are widely used for the treatment of POH. TCA causes destruction of the
epidermis and superficial dermis, inducing reepithelialization starting from the
adnexae.<sup><xref rid="r53" ref-type="bibr">53</xref></sup> Applications of
50% to 80% glycolic acid cause epidermolysis; the product must be applied for a few
minutes, immediately followed by washing with water or sodium bicarbonate. The risk
of adverse events increases with the depth of peels, skin type and sensitivity of
individuals.<sup><xref rid="r53" ref-type="bibr">53</xref></sup> Therefore,
patients should be adequately screened before the medical procedure.</p><p>POH due to excessive pigmentation can also be treated with lasers such as Q-switched
ruby laser (694 nm), Q-switched alexandrite laser (755 nm) and Nd:YAG (1064
nm).<sup><xref rid="r59" ref-type="bibr">59</xref>,<xref rid="r60" ref-type="bibr">60</xref></sup> There are reports of higher than 50% improvements
after the first session in 23,5% of patients and in 88,9% of them after the second
session with Qswitched ruby laser.<sup><xref rid="r55" ref-type="bibr">55</xref></sup> For POH secondary to sagging skin and age-related changes in the
lacrimal groove, ablative and non-ablative lasers can provide satisfactory results,
because they cause tissue contraction.<sup><xref rid="r59" ref-type="bibr">59</xref>,<xref rid="r60" ref-type="bibr">60</xref></sup></p><p>Safety should be emphasized in the treatment of POH with lasers, because the eyes are
particularly vulnerable to laser-induced injuries, so the use of glasses and / or
ocular globe protectors is crucial.</p><p>When dark circles are caused predominantly by superficial presentation vasculature,
thinning of the eyelid skin or the presence of marked lacrimal groove, autologous fat
transplantation or the use of hyaluronic acid fillers are indicated.<sup><xref rid="r57" ref-type="bibr">57</xref></sup> For cases with significant sagging,
blepharoplasty is the method with the most satisfactory results in the majority of
patients.<sup><xref rid="r53" ref-type="bibr">53</xref></sup></p></sec><sec><title>Dermatosis papulosa nigra</title><p>Dermatosis papulosa nigra (DPN) consists of benign epithelial tumors characterized by
multiple small papules and surface tubercles with 1 to 5mm in diameter, located over
the malar, neck and chest regions.<sup><xref rid="r61" ref-type="bibr">61</xref></sup> Biopsies of these lesions show the same histopathological
findings of seborrheic keratosis.<sup><xref rid="r62" ref-type="bibr">62</xref></sup>DPN carries a genetic predisposition and it is more frequent in women and African
descendants, in whom the prevalence ranges from 10% to 35%, being even regarded as a
racial variant of seborrheic keratosis.<sup><xref rid="r61" ref-type="bibr">61</xref>-<xref rid="r63" ref-type="bibr">63</xref></sup> Typically, DPN
lesions begin on the face and increase in size and number over the years, spreading
to sun-exposed areas of the malar, neck and upper body regions without spontaneous
regression.<sup><xref rid="r61" ref-type="bibr">61</xref></sup></p><p>Although benign, DPN can be an aesthetically distressing condition, affecting
interpersonal relationships. Its treatment includes various therapeutic modalities,
such as curettage, cryotherapy, and superficial laser and
electrofulguration.<sup><xref rid="r64" ref-type="bibr">64</xref>,<xref rid="r65" ref-type="bibr">65</xref></sup> There is not a definite significant
difference between these techniques, in general, the treatment is well tolerated
without significant adverse events or recurrence.<sup><xref rid="r66" ref-type="bibr">66</xref></sup> However, hypo or hyperpigmentation, scarring or keloid
formation can sometimes occur, particularly if the procedures are performed in a
rough manner or if patients are predisposed to these complications.<sup><xref rid="r62" ref-type="bibr">62</xref></sup></p></sec><sec><title>Phytophotodermatoses</title><p>Phytophotodermatoses occur by contact with plants containing furocoumarins or
psoralens that induce phototoxicity when activated by sunlight, particularly
ultraviolet A radiation (UVAR) (320nm to 400nm).<sup><xref rid="r67" ref-type="bibr">67</xref></sup></p><p>The lesions may be asymptomatic or present itching and burning, depending on the
amount of contacting substance, the skin color and intensity of photo-exposure. The
spots start with erythema and in a few days take on a brown coloration in those
places where the contact happened (<xref ref-type="fig" rid="f05">Figure
5</xref>).<sup><xref rid="r68" ref-type="bibr">68</xref>,<xref rid="r69" ref-type="bibr">69</xref></sup> Vesicles or large blisters may be present and, unlike
allergic photodermatitis, pruritus is not a common symptom. The evolution with
hyperpigmented macules or patches is the main feature for the diagnosis and it may
take weeks to months to regress.</p><fig id="f05" orientation="portrait" position="float"><label>FIGURE 5</label><caption><p>Acquired hyperpigmentations. Phytophotodermatoses – hyperchromic brown spots,
with a leaked aspect, located on the dorsal area of the hand and fingers,
secondary to accidental contact with lemon juice followed by sun exposure</p></caption><graphic xlink:href="abd-89-01-0011-g05"></graphic></fig><p><xref ref-type="table" rid="t02">Table 2</xref> describes the plants most commonly
linked to cases of phytophotodermatoses.</p><table-wrap id="t02" orientation="portrait" position="float"><label>TABLE 2</label><caption><p>Plants that are the leading cause of phytophotodermatoses and their
characteristics</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="1" colspan="1"><bold>FAMILY</bold></th><th align="left" rowspan="1" colspan="1"><bold>PLANTS</bold></th><th align="left" rowspan="1" colspan="1"><bold>OBSERVATIONS</bold></th></tr></thead><tbody><tr><td valign="top" rowspan="1" colspan="1">Rutaceae</td><td valign="top" rowspan="1" colspan="1">Plants producing citrus fruits such as orange, rangpur,
persian lime, tangerine or mandarin and rue.</td><td valign="top" rowspan="1" colspan="1">Injuries are most common in the hands and contact surfaces.
</td></tr><tr><td rowspan="1" colspan="1"> </td><td rowspan="1" colspan="1"> </td><td valign="top" rowspan="1" colspan="1">Furocoumarins (methoxy-psoralen) are more concentrated in
the fruit peel.</td></tr><tr><td valign="top" rowspan="1" colspan="1">Apiacea (Umbelliferae)</td><td valign="top" rowspan="1" colspan="1">Carrot, celery, angelica, fennel, parsley, dill, anise,
coriander, fennel</td><td valign="top" rowspan="1" colspan="1">Presence of psoralens at variable concentrations</td></tr><tr><td valign="top" rowspan="1" colspan="1">Fabaceae (legumes)</td><td valign="top" rowspan="1" colspan="1">imburana-de-cheiro (Amburana cearensis a tree found in
northeastern Brazil whose major component is coumarin), vinhático
(Plathymenia reticulata a tree used for woodworking, rich in
psoralens)</td><td valign="top" rowspan="1" colspan="1">Psoralea corylifolia is used in Chinese medicine to treat
vitiligo and alopecia areata. The concentration of psoralen is highly
variable, which may cause phytophotodermatites.</td></tr><tr><td valign="top" rowspan="1" colspan="1"> </td><td valign="top" rowspan="1" colspan="1"> </td><td valign="top" rowspan="1" colspan="1">Its use is not recommended.</td></tr><tr><td valign="top" rowspan="1" colspan="1">Moraceae</td><td valign="top" rowspan="1" colspan="1">Fig Tree</td><td valign="top" rowspan="1" colspan="1">It is a popular adjuvant agent for sun tanning, which even
led to episodes of severe skin burns.</td></tr></tbody></table></table-wrap><p>Phototoxicity reactions may also be induced by other substances of vegetal origin,
like the bergamot oil (bergapten) that contains 5-methoxy-psoralen in its
composition. These plant extracts can be part of the composition of some perfumes and
colognes, inducing the so called "<italic>Berloque dermatitis"</italic> or
"<italic>au-de-cologne dermatitis</italic>" because the pigmentation stimulated by
sunlight mimics embellishments, especially in retroauricular areas and on the sides
of the neck where perfumes are usually applied.</p></sec><sec><title>Flagellate dermatosis</title><p>Flagellate dermatosis (FD) is characterized by the appearance of pruriginous,
urticarial erythematous linear streaks, most commonly on the trunk (<xref ref-type="fig" rid="f06">Figure 6</xref>). It was first described by Moulin et al.
in 1971 and it is a specific reaction to bleomycin.<sup><xref rid="r70" ref-type="bibr">70</xref></sup> DF occurs in about 8-20% of patients who use this
medication for the treatment of lymphomas, germ cell tumors and squamous cell tumors
with doses between 15mg and 285mg on reported cases.<sup><xref rid="r71" ref-type="bibr">71</xref>,<xref rid="r72" ref-type="bibr">72</xref></sup></p><fig id="f06" orientation="portrait" position="float"><label>FIGURE 6</label><caption><p>Acquired hyperpigmentations. Flagellate Dermatitis– Linear urticariform
lesions, some with a slight superficial blistering, located on the lateral side
of the chest, which appeared 15 days after the initiation of treatment with
bleomycin</p></caption><graphic xlink:href="abd-89-01-0011-g06"></graphic></fig><p>Bleomycin is a polypeptide derived from <italic>Streptomyces verticillus</italic>,
discovered in Japan in 1965 by Umezawa. It has been used as an antineoplastic agent
against different types of tumors because it inhibits the incorporation of thymidine
to DNA, causing its fragmentation. The substance is distributed throughout the body
and is inactivated by the hydrolase enzyme, capable of cleaving an ammonia group from
their molecules. This enzyme does not exist in the lung or in the skin; therefore
bleomycin is not inactivated in these organs. Thus, there is an increased
concentration of the substance, explaining the higher skin and pulmonary toxicities
observed.<sup><xref rid="r73" ref-type="bibr">73</xref></sup> In most cases it
is not necessary to institute any treatment for flagellate dermatosis. After stopping
the medication the erythema gradually improves, but the residual characteristic
hyperpigmentation may persist for several months.<sup><xref rid="r74" ref-type="bibr">74</xref></sup></p><p>There are DF cases caused by shiitake mushroom (<italic>Lentinus edodes</italic>),
the second most consumed mushroom in the world, which must be considered as
differential diagnosis for bleomycin-induced flagellate dermatosis. After the
mushroom ingestion, linear widespread erythematous pruritic lesions may appear in 24
to 48 hours.<sup><xref rid="r75" ref-type="bibr">75</xref></sup> About two weeks are
needed to achieve complete remission of the dermatosis induced by shiitake ingestion.
The symptoms may be treated with antihistaminic drugs, topical corticosteroids and,
in severe cases, oral corticosteroids for a short period of time. As the re-exposure
could induce a new onset of symptoms, the ingestion of this mushroom should be
avoided, especially when raw or undercooked.<sup><xref rid="r75" ref-type="bibr">75</xref></sup></p></sec><sec><title>Erythema dyschromicum perstans</title><p>Erythema dyschromicum perstans (EDP) or gray dermatosis (<italic>dermatosis
cinecienta</italic>) is a rare acquired and chronic dermatosis, characterized by
asymptomatic progressive grayish macules. It was first described by Ramirez in 1957,
in El Salvador. It is more common in the Latin American population, but it can affect
all ethnic-racial groups, most frequently women and children on their first decade of
life.<sup><xref rid="r76" ref-type="bibr">76</xref>-<xref rid="r78" ref-type="bibr">78</xref></sup></p><p>EDP's etiology remains obscure. There are reports of associations with
endocrinopathies, ingestion of ammonia nitrate and radiologic contrast, vitiligo, HIV
and chronic hepatitis C infections, however most cases do not have an identified
triggering factor.<sup><xref rid="r79" ref-type="bibr">79</xref>-<xref rid="r84" ref-type="bibr">84</xref></sup> Due to the presence of interleukins
and inflammatory mediators in the lesions, some studies point to an immune-mediated
dermatosis, likely with a genetic predisposition to develop the disease.</p><p>EDP presents clinically as asymptomatic, grayish macules, with symmetric
distribution, usually involving the trunk and proximal extremities. The lesions have
variable sizes and frequently show erythematous, nondesquamative, palpable borders,
suggesting the inflammatory process preceded the pigmented lesions (<xref ref-type="fig" rid="f07">Figure 7</xref>).<sup><xref rid="r85" ref-type="bibr">85</xref></sup> This dermatosis tends to affect mainly the extremities and
trunk, sparing mucosae, hands, feet and scalp.</p><fig id="f07" orientation="portrait" position="float"><label>FIGURE 7</label><caption><p>Acquired hyperpigmentations. Erythema Dyschromicum Perstans – Grayish macules
of varying sizes, located on the anterior region of the thorax, abdomen and
upper thighs of a 27 years-old woman</p></caption><graphic xlink:href="abd-89-01-0011-g07"></graphic></fig><p>Diagnosis is based on clinical presentation and histopathological findings. On the
active border of the lesions there is lichenoid dermatitis with vacuolization of
basal layer cells and a strip of mononuclear infiltrate on the superficial dermis; at
the center of the lesions the findings are compatible with post-inflammatory
hyperpigmentation with melanophages in the dermis.<sup><xref rid="r86" ref-type="bibr">86</xref></sup></p><p>Differential diagnosis for EDP include: lichen planus, idiopathic eruptive macular
pigmentation, post-inflammatory hyperpigmentation, fixed pigmented erythema,
Addison's disease and hemochromatosis.<sup><xref rid="r86" ref-type="bibr">86</xref></sup> Treatment is based on the topical use of hydroquinone, topical
corticosteroids and tretinoin, although the results may be unsatisfactory due to the
dermic deposits of melanin. Clofazimine and dapsone were used with success in adult
patients, possibly because of their anti-inflammatory and immunomodulatory
activities. There are also reports of systemic use of corticosteroids, antibiotics,
griseofulvin, isoniazid, antimalarials, phototherapy and psychotherapy.<sup><xref rid="r87" ref-type="bibr">87</xref>,<xref rid="r88" ref-type="bibr">88</xref></sup></p></sec><sec><title>Cervical Poikiloderma or Poikiloderma of Civatte</title><p>Cervical idiopathic poikiloderma or poikiloderma of Civatte (PC) is a benign
dermatosis first described in 1923 by the French dermatologist Achilles
Civatte.<sup><xref rid="r89" ref-type="bibr">89</xref></sup> It is
characterized by irregular pigmentary alterations, with hypo and hyperpigmentation
associated to superficial atrophies and telangiectasias, usually asymptomatic and
rarely with discreet burning or pruritus. The pigmentation is reticulated, reddish to
brown, with irregular and symmetrical distribution, affecting the hemifaces, neck and
upper third of the chest, and sparing the shaded chin area (<xref ref-type="fig" rid="f08">Figure 8</xref>). Its pathophysiology is not well understood, but it is
probably related to cumulative sun exposure, aggravated by photoallergic or
phototoxic reactions caused by fragrances and / or cosmetics in particularly
susceptible individuals.<sup><xref rid="r90" ref-type="bibr">90</xref></sup> The
distribution by age and sex and familial occurrence suggest that hormonal and genetic
factors may be involved in its onset.<sup><xref rid="r89" ref-type="bibr">89</xref>,<xref rid="r90" ref-type="bibr">90</xref></sup></p><fig id="f08" orientation="portrait" position="float"><label>FIGURE 8</label><caption><p>Acquired hyperpigmentations. Poikiloderma of Civatte. Note the grid-like
hyperpigmentation, affecting the lateral areas and base of the neck in a 51
years-old phototype 3 woman. Observe photodamage lesions and a lighter area
correspondings to the region shaded by the chin</p></caption><graphic xlink:href="abd-89-01-0011-g08"></graphic></fig><p>PC is a chronic, progressive dermatosis, very common in some regions, affecting
fair-skinned individuals, starting on the fourth decade of life, especially in
postmenopausal women. Histopathological examination shows solar elastosis in the
papillary dermis, associated with vasodilation, perivascular edema, hyperkeratosis
and epidermal atrophy with effacement of the rete ridges, hydropic degeneration of
basal cells, presence of dermal melanophages and sparse lymphocytic
infiltrate.<sup><xref rid="r91" ref-type="bibr">91</xref></sup></p><p>Cervical poikiloderma has a slow, progressive and irreversible course, if the
aggravating factors persist. Differential diagnoses include: melasma, contact
dermatitis caused by perfumes or cosmetics and follicular erythromelanosis.</p><p>The ideal treatment of PC includes the simultaneous elimination of pigmented and
vascular components, with the combination of topical medications, especially
depigmenting agents, procedures for the vascular component and mandatory
broad-spectrum photoprotection.<sup><xref rid="r92" ref-type="bibr">92</xref></sup>Chemical peels and topical retinoids may be adjuvants to oppose photoaging of the
target area. Most recently argon lasers and flashlamppumped pulsed laser with yellow
dye (FLPDL), have been recommended, with reasonable results, although requiring much
caution as they can cause scarring, post-inflammatory hypo-and hyperpigmentation,
erythema and post treatment purpura.<sup><xref rid="r92" ref-type="bibr">92</xref>-<xref rid="r95" ref-type="bibr">95</xref></sup> Intense pulsed light
(IPL), unlike laser systems, works on a wide range of wavelengths, providing a good
reduction of pigment and telangiectasias as well as improving the skin texture, with
less risk of complications.<sup><xref rid="r96" ref-type="bibr">96</xref></sup></p></sec><sec><title>Acanthosis nigricans</title><p>Acanthosis nigricans (AN) appears as hyperchromic plaques, with vegetative,
lichenified or papillomatous surfaces, dark brown to black coloration, located in the
armpits, groin, neck and other intertriginous areas (<xref ref-type="fig" rid="f09">Figure 9</xref>). More recently, it has been divided into 8 subtypes: benign,
obesity-related, syndromic, malignant, acral, unilateral, secondary to medication and
multifactorial. This dermatosis is often related to endocrine disorders, such as
obesity, insulin resistance, type II diabetes mellitus and polycystic ovary syndrome
(PCOS).<sup><xref rid="r97" ref-type="bibr">97</xref>-<xref rid="r99" ref-type="bibr">99</xref></sup> Etiology involves a state of hyperinsulinemia caused
by insulin resistance, with stimulation of insulin related growth factor (IGF1,
insulin-like growth factor), and consequent proliferation of keratinocytes.<sup><xref rid="r100" ref-type="bibr">100</xref>,<xref rid="r101" ref-type="bibr">101</xref></sup> When associated with malignancy, AN may either precede or
occur simultaneously with the neoplasm, with the most common tumor being gastric
adenocarcinoma, although it has already been reported in uterine, liver, bowel,
ovarian, renal, breast and lung cancers, most of them adenocarcinomas.<sup><xref rid="r101" ref-type="bibr">101</xref></sup></p><fig id="f09" orientation="portrait" position="float"><label>FIGURE 9</label><caption><p>Acquired hyperpigmentations. Acanthosis nigricans – Linear and coalescent
papular hyperpigmentation, with velvety aspect, located in the axillary region
of an obese adolescent</p></caption><graphic xlink:href="abd-89-01-0011-g09"></graphic></fig><p>Lesion improvement in AN is dependent on the resolution of the underlying disease.
There are reports of the use of oral and topical retinoids with good results. In
addition, other keratolytic agents such as 12% ammonium lactate or the combined
triple therapy (4% HQ + 0.05% AR + 0.01% fluocinolone acetonide) can be used. Studies
on the use of topical agents containing urea and salicylic acid reported variable
results. Oral treatments include isotretinoin and metformin; the latter may be
indicated in diseases that course with hyperandrogenism. Procedures include
dermabrasion, Alexandrite laser and the application of trichloroacetic acid,
described more recently.<sup><xref rid="r101" ref-type="bibr">101</xref>,<xref rid="r102" ref-type="bibr">102</xref></sup></p></sec><sec><title>Primary localized cutaneous amyloidosis</title><p>Amyloidosis is a generic term applied to a group of diseases characterized by the
deposit of a substance, mainly a fibrillar protein (amyloid) that can lead to
compression and / or dysfunction in various organs, including the skin. The
amyloidoses are divided into systemic or localized, and the latter can be of primary
or secondary cause. Primary cutaneous forms include macular amyloidosis, amyloid
lichen, and nodular or tumefactive amyloidosis.<sup><xref rid="r103" ref-type="bibr">103</xref>,<xref rid="r104" ref-type="bibr">104</xref></sup> Systemic
amyloidosis can be classified as primary, hereditary or not; and secondary to chronic
or inflammatory diseases or cancer and also associated with hemodialysis. The
distinction between primary localized cutaneous amyloidosis and systemic forms must
be made through a careful physical examination and laboratory tests to exclude the
presence of extracutaneous amyloid deposits and plasmocytic dyscrasias.<sup><xref rid="r105" ref-type="bibr">105</xref></sup></p><p>Macular amyloidosis (AM) and amyloid lichen are more common variants of the primary
localized form of amyloidosis, featuring amyloid deposits in the skin.<sup><xref rid="r106" ref-type="bibr">106</xref></sup> Most occurrences are sporadic, but
an autosomal dominant form of the disease may be present in up to 10% of cases, in
places such as China, Central and South America.<sup><xref rid="r107" ref-type="bibr">107</xref></sup> Sporadic forms occur more in women, with female to male rates
of 4.5:1.<sup><xref rid="r103" ref-type="bibr">103</xref></sup></p><p>The exact etiology and pathogenesis of cutaneous amyloidosis remains unknown, but it
is believed that there are multiple factors involved: genetic, autoimmune, attrition
and contact dermatitis.<sup><xref rid="r108" ref-type="bibr">108</xref>-<xref rid="r111" ref-type="bibr">111</xref></sup> Recently, attention has been
focused on the mechanisms associated with the so-called conformational diseases, in
which a change in the spatial conformation of a protein occurs, resulting in an
amyloidogenic structure. The exact mechanism responsible for this change has not yet
been fully elucidated, however, systemic diseases such as Parkinson's and Alzheimer's
disease appear to share the same etiopathogenic mechanism.<sup><xref rid="r112" ref-type="bibr">112</xref>,<xref rid="r113" ref-type="bibr">113</xref></sup>Histology shows deposits of amyloid matter in the basal membrane or papillary dermis
in both forms. In macular amyloidosis, the amyloid deposits can be quite subtle, and
the skin does not show significant changes; in lichen amyloid the deposits are more
pronounced, with the presence of hyperkeratosis, papillomatosis and moderate
acanthosis. In some cases, there is vacuolization of basal cells, presence of
intraepidermal cytoid bodies and signs of pigmentary incontinence.<sup><xref rid="r103" ref-type="bibr">103</xref>,<xref rid="r111" ref-type="bibr">111</xref></sup></p><p>Macular amyloidosis presents clinically as macules, spots or pruritic hyperpigmented
plaques with undulating surface (<italic>rippled patches</italic>), of a brownish or
blackish color, with ill-defined borders, usually located in the interscapular
region, which may be associated or coexist with notalgia paresthetica (<xref ref-type="fig" rid="f10">Figure 10</xref>).<sup><xref rid="r114" ref-type="bibr">114</xref></sup> In amyloid lichen, there are slightly pruritic coalescing
papules either hyperpigmented or the same color of the skin, usually located in the
legs or arms (<xref ref-type="fig" rid="f11">Figure 11</xref>).<sup><xref rid="r106" ref-type="bibr">106</xref>,<xref rid="r114" ref-type="bibr">114</xref></sup></p><fig id="f10" orientation="portrait" position="float"><label>FIGURE 10</label><caption><p>Acquired hyperpigmentations. Macular amyloidosis– a brownish itchy area,
located in the dorsal region, corresponding to the range area of a dextral
patient’s hand</p></caption><graphic xlink:href="abd-89-01-0011-g10"></graphic></fig><fig id="f11" orientation="portrait" position="float"><label>FIGURE 11</label><caption><p>Acquired hyperpigmentations. Amyloid lichen – plaque formed by the confluence
of small grayishbrown papules located in the pretibial region</p></caption><graphic xlink:href="abd-89-01-0011-g11"></graphic></fig><p>Treatment options for cutaneous amyloidosis include intralesional and topical
corticosteroids, calcineurin inhibitors, acitretin, UVB or UVA (PUVA) phototherapy,
dermabrasion, laser and hydrocolloid dressings.<sup><xref rid="r114" ref-type="bibr">114</xref>-<xref rid="r116" ref-type="bibr">116</xref></sup></p><p>Nodular or tumefactive amyloidosis is another type of localized cutaneous
amyloidosis, although a less frequent one. It is characterized by diffuse amyloid
deposits in the dermis, subcutaneous tissue and small dermal capillaries. Patients
present with nodules or asymptomatic plaques of rosy to brownish color, either
isolated or in multiples, and prone to affecting the face, especially the nose and
periauricular regions, but also the genitals, trunk and limbs. These lesions are
similar to those observed in primary systemic amyloidosis associated with plasma cell
lymphoproliferative diseases. It occurs equally in both sexes, with a mean age at
diagnosis of 60.8 years. The process can have a localized benign chronic course, but
patients should be monitored for progression to systemic amyloidosis and plasmocytic
dyscrasias, which occurs in 7-50% of patients.<sup><xref rid="r103" ref-type="bibr">103</xref>,<xref rid="r105" ref-type="bibr">105</xref>,<xref rid="r117" ref-type="bibr">117</xref></sup></p><p>Dyschromic cutaneous amyloidosis is a rare subtype of primary cutaneous amyloidosis.
This disease starts prior to puberty with small deposits of amyloid pigment beneath
the epidermis.<sup><xref rid="r118" ref-type="bibr">118</xref></sup> It is
characterized by a reticulate hyperpigmentation interspersed with hypopigmented spots
in almost all the skin and mild or absent pruritus. The treatment of this form of
amyloidosis includes avoiding sunlight exposure, use of topical corticosteroids,
capsaicin, dimethylsulfoxide, and CO<sub>2 </sub>laser with varying results. The use
of systemic retinoids has been shown to be effective in a few reported
cases.<sup><xref rid="r101" ref-type="bibr">101</xref></sup></p></sec><sec><title>Confluent and reticulated papillomatosis of Gougerot and Carteaud</title><p>Confluent and reticulated papillomatosis (CRP) was described by French dermatologists
Gougerot and Carteaud in 1927. It is a rare dermatosis of unknown etiology that
occurs more frequently in women and melanodermic patients, aged 10 to 35
years.<sup><xref rid="r119" ref-type="bibr">119</xref></sup></p><p>It is characterized by flat wrinkled papules, slightly salient, with variable
coloration, hypochromic to pink or brownish that become confluent in the center and
reticulated at the periphery. The lesions are mainly located in the interscapular,
intermammary and epigastric regions. Its main differential diagnosis is pityriasis
versicolor, but acanthosis nigricans, cutaneous amyloidosis, several keratinization
disorders and some presentations of seborrheic dermatitis should also be
considered.<sup><xref rid="r120" ref-type="bibr">120</xref></sup> Criteria for
its diagnosis have been recently proposed, including: <bold>1)</bold> presence of
macules and brownish desquamative spots, with reticulated and papillomatous aspect,
<bold>2)</bold> involvement of the upper chest and neck, <bold>3)</bold> negative
testing for fungus, <bold>4)</bold> absence of response to antifungal drugs and
<bold>5)</bold> excellent response to minocycline.<sup><xref rid="r121" ref-type="bibr">121</xref></sup></p><p>Many questions remain about this dermatosis, especially regarding its pathogenesis
and treatment. Some hypotheses try to explain CRP genesis as vitamin A deficiency,
genetic factors, photosensitivity, endocrine abnormalities, cutaneous amyloidosis,
tissue reaction to skin colonization by lipophilic yeasts of the genus
<italic>Malassezia</italic>, staphylococci or <italic>Propionibacterium
acnes</italic>, and especially defects in keratinization.<sup><xref rid="r122" ref-type="bibr">122</xref>,<xref rid="r123" ref-type="bibr">123</xref></sup></p><p>Minocycline (50-100 mg twice daily for 10 weeks) has been the treatment of choice. In
addition, there are reports of improvements with azithromycin administered in a dose
of 250-500mg three times per week. Other options are: clarithromycin 500 mg per day,
erythromycin 1000 mg per day and tetracycline 500 mg, twice daily. Topical
medications such as selenium sulfide, ketoconazole, tretinoin, tazarotene and
calcipotriol have also been used, with varying results.<sup><xref rid="r122" ref-type="bibr">122</xref></sup> Responses to retinoids support the theory that the
disease may be caused by some keratinization disorder. The use of oral isotretinoin,
1 to 2mg/kg/day has been recommended, with favorable responses achieved in two
months.<sup><xref rid="r120" ref-type="bibr">120</xref></sup></p></sec></sec></body><back><fn-group><fn id="fn01" fn-type="other"><label>*</label><p>Work performed at the Dermatology Department at Porto Alegre Clinics Hospital - Rio
Grande do Sul Federal University (HCPA-UFRGS) - Porto Alegre (RS), Brazil.</p></fn><fn fn-type="financial-disclosure"><p>Financial Support: None.</p></fn><fn fn-type="conflict"><p>Conflict of Interest: None.</p></fn></fn-group><app-group><app><title>QUESTIONS</title><sec><title>1 - Regarding the triggering factors of melasma, it is CORRECT to
state:</title><disp-quote><p><bold>a)</bold> There is usually a conjunction of several factors for its
initial onset, including genetic predisposition and exposure to ultraviolet
radiation.</p><p><bold>b)</bold> Treatment with ACE inhibitors can cause lesions in a large
number of patients.</p><p><bold>c)</bold> There is a clear relationship between pregnancy after the third
decade of life and melasma, in most populations. </p><p><bold>d)</bold> There is no evidence linking the predisposition to melasma with
phototype and ancestry.</p></disp-quote></sec><sec><title>2 - Check the INCORRECT alternative: </title><disp-quote><p><bold>a)</bold> Melasma lesions often show histological alterations consistent
with chronic sun damage.</p><p><bold>b)</bold> Cell interactions between keratinocytes, mast cells and
fibroblasts contribute to increased activity of melanocytes in melasma. </p><p><bold>c)</bold> The deposit of dermal pigment is most striking feature in
melasma.</p><p><bold>d)</bold> The number of melanocytes in melasma is similar to that of
healthy skin, but the cells tend to be larger and with prominence of
dendrites.</p></disp-quote></sec><sec><title>3 - Melasma treatment is not always easy and should be adapted to each
patient. Check the MOST RECOMMENDED therapeutic orientation:</title><disp-quote><p><bold>a)</bold> The association of azelaic and kojic acids and arbutin should
be considered as first line treatment.</p><p><bold>b)</bold> Classic depigmenting agents such as hydroquinone in progressive
doses may be used. If no response is achieved in 46 weeks, medium peels or
dermabrasion are the options with better response in most patients.</p><p><bold>c)</bold> The combined therapies have synergistic action; the triple
combination with hydroquinone, tretinoin, and mediumpower corticosteroids is
the more cost-effective treatment.</p><p><bold>d)</bold> No maintenance therapy is recommended due to the risk of
tachyphylaxis. Re-treatment intervals should be of at least 2 months.</p></disp-quote></sec><sec><title>4 - Post-inflammatory hyperpigmentation may be secondary to various
dermatoses. Select the CORRECT alternative: </title><disp-quote><p><bold>a)</bold> There is no correlation between skin phototype and
predisposition to post-inflammatory hyperpigmentation.</p><p><bold>b)</bold> The histology of the lesions is characteristic and can give a
good indication of the triggering cause of the dermatoses.</p><p><bold>c)</bold> Acute conditions usually produce higher-intensity pigmentations
that are more difficult to treat.</p><p><bold>d)</bold> Hyperpigmentation is probably caused by increased melanogenesis
and abnormal distribution of melanin, due to the action of inflammatory
mediators.</p></disp-quote></sec><sec><title>5 - Regarding the post inflammatory hyperpigmentation check the TRUE
option:</title><disp-quote><p><bold>a)</bold> Response to topical treatment is excellent. </p><p><bold>b)</bold> Recurrences are rare. </p><p><bold>c)</bold> The distribution of spots is random and rarely accompanies the
location of the inflammatory processes that preceded them.</p><p><bold>d)</bold> Histology shows melanin deposits both in free form and within
melanophages located in the upper dermis and around the vessels.</p></disp-quote></sec><sec><title>6 - The following histologic features are found on periorbital
hyperpigmentation, EXCEPT:</title><disp-quote><p><bold>a)</bold> Dermal melanin deposits </p><p><bold>b)</bold> Superficial presentation of the vasculature </p><p><bold>c)</bold> Tattoo secondary to chronic use of makeup </p><p><bold>d)</bold> Hyperactivity of the periorbital muscles</p></disp-quote></sec><sec><title>7 - Regarding the periorbital hyperpigmentation, it is CORRECT to affirm
that:</title><disp-quote><p><bold>a)</bold> The treatment should be performed for a short period of time
due to the high frequency of adverse events, such as erythema and desquamation,
caused by depigmenting agents in this region.</p><p><bold>b)</bold> As with melasma, combination therapy is the treatment of
choice</p><p><bold>c)</bold> The use of hydroquinone is justified in cases where there is a
prevalence of hyperpigmentation, because it inhibits the synthesis of DNA and
RNA, inducing melanosome degradation and melanocyte destruction.</p><p><bold>d)</bold> Treatment options are similar, regardless of the predominant
component.</p></disp-quote></sec><sec><title>8 - About dermatosis papulosa nigra, it is CORRECT to state that: </title><disp-quote><p><bold>a)</bold> It is more frequent in white males and presents spontaneous
regression. </p><p><bold>b)</bold> It presents the same histopathological findings of seborrheic
keratosis. </p><p><bold>c)</bold> Typically, the lesions start on the face and show no changes in
quantity or pattern over the years. </p><p><bold>d)</bold> It usually regresses spontaneously in about 50% of
patients.</p></disp-quote></sec><sec><title>9 - Different treatment modalities can be employed for the treatment of
dermatosis papulosa nigra. THE LEAST indicated one is: </title><disp-quote><p><bold>a)</bold> Curettage </p><p><bold>b)</bold> Cryotherapy </p><p><bold>c)</bold> Electrofulguration </p><p><bold>d)</bold> Exeresis and suture</p></disp-quote></sec><sec><title>10 - The following statement is CORRECT about erythema dyschromicum perstans: </title><disp-quote><p><bold>a)</bold> It is a common genodermatosis amongst the Latin American
population. </p><p><bold>b)</bold> In most cases the triggering factor is easily identified. </p><p><bold>c)</bold> On the active border of the lesion there is lichenoid
dermatitis with vacuolization of the basal cell layer and a strip of
mononuclear infiltrate in the superficial dermis.</p><p><bold>d)</bold> The response to treatment with hydroquinone is excellent.</p></disp-quote></sec><sec><title>11 - Acanthosis nigricans has several etiological and clinical
characteristics. Mark the most CORRECT answer: </title><disp-quote><p><bold>a)</bold> Depending on the clinical appearance of the lesions it is
possible to determine the causative factor. </p><p><bold>b)</bold> When associated with malignancy, AN appears simultaneously with
cancer, never preceding that disease. </p><p><bold>c)</bold> The most frequently associated tumor is the liver
adenocarcinoma.</p><p><bold>d)</bold> There are several therapeutic options for the treatment, and
the appropriate management of the underlying disease is important.</p></disp-quote></sec><sec><title>12 - The following aspects are NOT associated with confluent papillomatosis of
Gougerot Carteaud:</title><disp-quote><p><bold>a)</bold> Rough, flat, slightly protruding papules with variable
coloring, from hyperchromic to pink or brownish, that become confluent in the
center and reticulated in the periphery.</p><p><bold>b)</bold> Location mainly in the interscapular, intermammary and
epigastric regions. </p><p><bold>c)</bold> Good response to treatment with antifungals. </p><p><bold>d)</bold> It is more frequent in women and melanodermic patients, aged 10
to 35 years.</p></disp-quote></sec><sec><title>13 - Amongst the differential diagnosis for confluent papillomatosis of
Gougerot Carteaud the following may NOT be included: </title><disp-quote><p><bold>a)</bold> Pityriasis versicolor </p><p><bold>b)</bold> Seborrheic dermatitis </p><p><bold>c)</bold> Lichenoid purpura of Gougerot Blum </p><p><bold>d)</bold> Acanthosis nigricans</p></disp-quote></sec><sec><title>14 - Cervical poikiloderma presents peculiar clinical characteristics, EXCEPT: </title><disp-quote><p><bold>a)</bold> Regular alterations in pigmentation, with hypo and hyper
pigmentation </p><p><bold>b)</bold> Superficial atrophy </p><p><bold>c)</bold> Telangiectasias </p><p><bold>d)</bold> It is never symptomatic</p></disp-quote></sec><sec><title>15 - Several factors seem to be linked to Poikiloderma of Civatte's
pathogenesis or triggering. Indicate the INCORRECT alternative:</title><disp-quote><p><bold>a)</bold> Cumulative sun exposure</p><p><bold>b)</bold> Photoallergic or phototoxic reactions caused by fragrances
and/or cosmetics in predisposed individuals </p><p><bold>c)</bold> Hormonal factors </p><p><bold>d)</bold> Trauma</p></disp-quote></sec><sec><title>16 - About the histological findings in primary localized cutaneous
amyloidosis, it is possible to affirm that:</title><disp-quote><p><bold>I.</bold> Both in macular amyloidosis and in amyloid lichen, there are
deposits of amyloid material in the basal membrane or in the papillary
dermis.</p><p><bold>II.</bold> In macular amyloidosis, the amyloid deposits are always
abundant and the skin may not show significant changes. </p><p><bold>III.</bold>In amyloid lichen, the protein deposit is discreet and the
epidermis often presents hyperkeratosis, papillomatosis and moderate
acanthosis.</p><p><bold>a)</bold> Only I is correct </p><p><bold>b)</bold> Statements I and III are correct </p><p><bold>c)</bold> All are correct </p><p><bold>d)</bold> None is correct</p></disp-quote></sec><sec><title>17 - Complete the second column in accordance with the first one:</title><disp-quote><p><bold>(1)</bold> Macular amyloidosis</p><p><bold>(2)</bold> Amyloid lichen </p><p><bold>( )</bold> Macules, itchy spots or plaques, with undulating surface,
hyperpigmented and with ill-defined borders </p><p><bold>( )</bold> Coalescing and slightly pruritic hyperpigmented or
normochromic papules </p><p><bold>( )</bold> Most commonly located in the legs or arms </p><p><bold>( )</bold> Located usually in the interscapular area </p><p><bold>( )</bold> May be associated or coexist with notalgia paresthetica</p><p><bold>a)</bold> 2 1 1 2 2 </p><p><bold>b)</bold> 1 2 2 1 1 </p><p><bold>c)</bold> 2 1 2 1 1 </p><p><bold>d)</bold> 1 2 1 2 2</p></disp-quote></sec><sec><title>18. The substances responsible for phytophotodermatoses caused by the Rutaceae
(citrus-producing plants) are: </title><disp-quote><p><bold>a)</bold> Furocoumarins </p><p><bold>b)</bold> Bergapten </p><p><bold>c)</bold> Apiacea </p><p><bold>d)</bold> Fabaceae</p></disp-quote></sec><sec><title>19. The flagellate dermatitis is classically linked to bleomycin. More
recently, however, there have been reports of its association with:</title><disp-quote><p><bold>a)</bold> Bergamot oil (bergapten) which contains 5-methoxy-psoralen in
its composition </p><p><bold>b)</bold> Shiitake Mushroom (Lentinus edodes) </p><p><bold>c)</bold> Metformin </p><p><bold>d)</bold> ACE inhibitors</p></disp-quote></sec><sec><title>20. Acanthosis nigricans has a multifactorial etiology. On this point we can
affirm that: </title><disp-quote><p><bold>a)</bold> Its appearance cannot be assigned to the use of medications. </p><p><bold>b)</bold> Its etiology may involve a state of hyperinsulinemia caused by
insulin resistance, with stimulation of insulin-related growth factor (IGF1,
insulin-like growth factor) </p><p><bold>c)</bold> Its appearance during childhood has not been described. </p><p><bold>d)</bold> Keratinocytes proliferation is reduced in this dermatosis</p></disp-quote><table-wrap id="t03" orientation="portrait" position="anchor"><label>Answer key</label><caption><p>Giant congenital melanocytic nevus. An Bras Dermatol. 2013;88(6):863-78</p></caption><table frame="box" rules="groups"><tbody><tr><td rowspan="1" colspan="1">1) C</td><td rowspan="1" colspan="1">6) D</td><td rowspan="1" colspan="1">11) D</td><td rowspan="1" colspan="1">16) A</td></tr><tr><td rowspan="1" colspan="1">2) C</td><td rowspan="1" colspan="1">7) C</td><td rowspan="1" colspan="1">12) B</td><td rowspan="1" colspan="1">17) B</td></tr><tr><td rowspan="1" colspan="1">3) D</td><td rowspan="1" colspan="1">8) C</td><td rowspan="1" colspan="1">13) C</td><td rowspan="1" colspan="1">18) B</td></tr><tr><td rowspan="1" colspan="1">4) B</td><td rowspan="1" colspan="1">9) C</td><td rowspan="1" colspan="1">14) C</td><td rowspan="1" colspan="1">19) D</td></tr><tr><td rowspan="1" colspan="1">5) C</td><td rowspan="1" colspan="1">10) A</td><td rowspan="1" colspan="1">15) B</td><td rowspan="1" colspan="1">20) C</td></tr></tbody></table></table-wrap></sec><sec><title>Papers</title><boxed-text position="float" orientation="portrait"><p>Information for all members: The EMC-D questionnaire is now available at the
homepage of the Brazilian Annals of Dermatology: <ext-link ext-link-type="uri" xlink:href="www.anaisdedermatologia.org.br">www.anaisdedermatologia.org.br</ext-link>. The deadline for completing the
questionnaire is 30 days from the date of online publication.</p></boxed-text></sec></app></app-group><ref-list><title>REFERENCES</title><ref id="r01"><label>1</label><element-citation publication-type="webpage"><person-group person-group-type="author"><collab>Sbd.org</collab></person-group><comment>[Internet]</comment><source>Censo Dermatologico da SBD. Brazilian Society of Dermatology Web page -
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