The clinicopathologic spectrum of rhinophyma
Identifieur interne : 002200 ( Istex/Corpus ); précédent : 002199; suivant : 002201The clinicopathologic spectrum of rhinophyma
Auteurs : Filippo Aloi ; Carlo Tomasini ; Elisabetta Soro ; Mario PippioneSource :
- Journal of the American Academy of Dermatology [ 0190-9622 ] ; 2000.
Abstract
We report the results of a clinicopathologic study of 17 patients with rhinophyma in different stages of evolution, with particular attention paid to the severe form of this disease. On the basis of clinical features, we identified 2 groups of patients: the first group (12/17 patients) included patients with the common form of rhinophyma, whereas the second one (5/17 patients) included patients with the severe form of the disease. There was no link between the clinical aspect and the duration of the disease. Microscopic examination of specimens obtained from the classic type of rhinophyma substantially showed the histopathologic features of fully developed rosacea, except for the presence of prominent sebaceous hyperplasia. The second group showed a very different histologic pattern displaying marked dermal thickness, absence of folliculosebaceous structures, sclerotic collagen bundles with large amounts of mucin, and spreading telangiectasia. The inflammatory infiltrate was inconspicuous, with numerous interstitial spindle and bizarre cells. Most of the interstitial cells were reactive to factor XIIIa. The severe form of rhinophyma shares many histologic characteristics with elephantiasis caused by chronic lymphedema. (J Am Acad Dermatol 2000;42:468-72.)
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DOI: 10.1016/S0190-9622(00)90220-2
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">The clinicopathologic spectrum of rhinophyma</title><author><name sortKey="Aloi, Filippo" sort="Aloi, Filippo" uniqKey="Aloi F" first="Filippo" last="Aloi">Filippo Aloi</name><affiliation><mods:affiliation>Department of Dermatology, University of Turin. Turin, Italy</mods:affiliation></affiliation></author><author><name sortKey="Tomasini, Carlo" sort="Tomasini, Carlo" uniqKey="Tomasini C" first="Carlo" last="Tomasini">Carlo Tomasini</name><affiliation><mods:affiliation>Department of Dermatology, University of Turin. Turin, Italy</mods:affiliation></affiliation></author><author><name sortKey="Soro, Elisabetta" sort="Soro, Elisabetta" uniqKey="Soro E" first="Elisabetta" last="Soro">Elisabetta Soro</name><affiliation><mods:affiliation>Department of Dermatology, University of Turin. Turin, Italy</mods:affiliation></affiliation></author><author><name sortKey="Pippione, Mario" sort="Pippione, Mario" uniqKey="Pippione M" first="Mario" last="Pippione">Mario Pippione</name><affiliation><mods:affiliation>Department of Dermatology, University of Turin. 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Turin, Italy</mods:affiliation></affiliation></author><author><name sortKey="Tomasini, Carlo" sort="Tomasini, Carlo" uniqKey="Tomasini C" first="Carlo" last="Tomasini">Carlo Tomasini</name><affiliation><mods:affiliation>Department of Dermatology, University of Turin. Turin, Italy</mods:affiliation></affiliation></author><author><name sortKey="Soro, Elisabetta" sort="Soro, Elisabetta" uniqKey="Soro E" first="Elisabetta" last="Soro">Elisabetta Soro</name><affiliation><mods:affiliation>Department of Dermatology, University of Turin. Turin, Italy</mods:affiliation></affiliation></author><author><name sortKey="Pippione, Mario" sort="Pippione, Mario" uniqKey="Pippione M" first="Mario" last="Pippione">Mario Pippione</name><affiliation><mods:affiliation>Department of Dermatology, University of Turin. Turin, Italy</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the American Academy of Dermatology</title><title level="j" type="abbrev">YMJD</title><idno type="ISSN">0190-9622</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000">2000</date><biblScope unit="volume">42</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="468">468</biblScope><biblScope unit="page" to="472">472</biblScope></imprint><idno type="ISSN">0190-9622</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0190-9622</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We report the results of a clinicopathologic study of 17 patients with rhinophyma in different stages of evolution, with particular attention paid to the severe form of this disease. On the basis of clinical features, we identified 2 groups of patients: the first group (12/17 patients) included patients with the common form of rhinophyma, whereas the second one (5/17 patients) included patients with the severe form of the disease. There was no link between the clinical aspect and the duration of the disease. Microscopic examination of specimens obtained from the classic type of rhinophyma substantially showed the histopathologic features of fully developed rosacea, except for the presence of prominent sebaceous hyperplasia. The second group showed a very different histologic pattern displaying marked dermal thickness, absence of folliculosebaceous structures, sclerotic collagen bundles with large amounts of mucin, and spreading telangiectasia. The inflammatory infiltrate was inconspicuous, with numerous interstitial spindle and bizarre cells. Most of the interstitial cells were reactive to factor XIIIa. The severe form of rhinophyma shares many histologic characteristics with elephantiasis caused by chronic lymphedema. 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Turin, Italy</json:string></affiliations></json:item><json:item><name>Carlo Tomasini MD</name><affiliations><json:string>Department of Dermatology, University of Turin. Turin, Italy</json:string></affiliations></json:item><json:item><name>Elisabetta Soro MD</name><affiliations><json:string>Department of Dermatology, University of Turin. Turin, Italy</json:string></affiliations></json:item><json:item><name>Mario Pippione MD</name><affiliations><json:string>Department of Dermatology, University of Turin. Turin, Italy</json:string></affiliations></json:item></author><articleId><json:string>902202</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>We report the results of a clinicopathologic study of 17 patients with rhinophyma in different stages of evolution, with particular attention paid to the severe form of this disease. On the basis of clinical features, we identified 2 groups of patients: the first group (12/17 patients) included patients with the common form of rhinophyma, whereas the second one (5/17 patients) included patients with the severe form of the disease. There was no link between the clinical aspect and the duration of the disease. Microscopic examination of specimens obtained from the classic type of rhinophyma substantially showed the histopathologic features of fully developed rosacea, except for the presence of prominent sebaceous hyperplasia. The second group showed a very different histologic pattern displaying marked dermal thickness, absence of folliculosebaceous structures, sclerotic collagen bundles with large amounts of mucin, and spreading telangiectasia. The inflammatory infiltrate was inconspicuous, with numerous interstitial spindle and bizarre cells. Most of the interstitial cells were reactive to factor XIIIa. The severe form of rhinophyma shares many histologic characteristics with elephantiasis caused by chronic lymphedema. 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Turin, Italy</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Carlo</forename><surname>Tomasini</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Dermatology, University of Turin. Turin, Italy</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Elisabetta</forename><surname>Soro</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Dermatology, University of Turin. Turin, Italy</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Mario</forename><surname>Pippione</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Dermatology, University of Turin. 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On the basis of clinical features, we identified 2 groups of patients: the first group (12/17 patients) included patients with the common form of rhinophyma, whereas the second one (5/17 patients) included patients with the severe form of the disease. There was no link between the clinical aspect and the duration of the disease. Microscopic examination of specimens obtained from the classic type of rhinophyma substantially showed the histopathologic features of fully developed rosacea, except for the presence of prominent sebaceous hyperplasia. The second group showed a very different histologic pattern displaying marked dermal thickness, absence of folliculosebaceous structures, sclerotic collagen bundles with large amounts of mucin, and spreading telangiectasia. The inflammatory infiltrate was inconspicuous, with numerous interstitial spindle and bizarre cells. Most of the interstitial cells were reactive to factor XIIIa. The severe form of rhinophyma shares many histologic characteristics with elephantiasis caused by chronic lymphedema. (J Am Acad Dermatol 2000;42:468-72.)</p></abstract></profileDesc><revisionDesc><change when="2000">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/4A0ED1DE1BA50C93F58C20DA5CF4FFA9FD2C8A99/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier doc found" wicri:toSee="Elsevier, no converted or simple article"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 5.0.1//EN//XML" URI="art501.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity><istex:entity SYSTEM="gr3" NDATA="IMAGE" name="gr3"></istex:entity><istex:entity SYSTEM="gr4" NDATA="IMAGE" name="gr4"></istex:entity><istex:entity SYSTEM="gr5" NDATA="IMAGE" name="gr5"></istex:entity><istex:entity SYSTEM="gr6" NDATA="IMAGE" name="gr6"></istex:entity><istex:entity SYSTEM="gr7" NDATA="IMAGE" name="gr7"></istex:entity></istex:docType><istex:document><article docsubtype="fla" xml:lang="en" version="5.0"><item-info><jid>YMJD</jid><aid>902202</aid><ce:pii>S0190-9622(00)90220-2</ce:pii><ce:doi>10.1016/S0190-9622(00)90220-2</ce:doi><ce:copyright type="other" year="2000">American Academy of Dermatology, Inc</ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>Reprint requests: Carlo Tomasini, MD, Department of Medical and Surgical Specialties, Section of Dermatology, II Clinic, University of Turin, Via Cherasco 23, 1-10126, Turin, Italy.</ce:note-para></ce:article-footnote><ce:title>The clinicopathologic spectrum of rhinophyma</ce:title><ce:author-group><ce:author><ce:given-name>Filippo</ce:given-name><ce:surname>Aloi</ce:surname><ce:degrees>MD</ce:degrees></ce:author><ce:author><ce:given-name>Carlo</ce:given-name><ce:surname>Tomasini</ce:surname><ce:degrees>MD</ce:degrees></ce:author><ce:author><ce:given-name>Elisabetta</ce:given-name><ce:surname>Soro</ce:surname><ce:degrees>MD</ce:degrees></ce:author><ce:author><ce:given-name>Mario</ce:given-name><ce:surname>Pippione</ce:surname><ce:degrees>MD</ce:degrees></ce:author><ce:affiliation><ce:textfn>Department of Dermatology, University of Turin. Turin, Italy</ce:textfn></ce:affiliation></ce:author-group><ce:date-accepted day="15" month="7" year="1999"></ce:date-accepted><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">We report the results of a clinicopathologic study of 17 patients with rhinophyma in different stages of evolution, with particular attention paid to the severe form of this disease. On the basis of clinical features, we identified 2 groups of patients: the first group (12/17 patients) included patients with the common form of rhinophyma, whereas the second one (5/17 patients) included patients with the severe form of the disease. There was no link between the clinical aspect and the duration of the disease. Microscopic examination of specimens obtained from the classic type of rhinophyma substantially showed the histopathologic features of fully developed rosacea, except for the presence of prominent sebaceous hyperplasia. The second group showed a very different histologic pattern displaying marked dermal thickness, absence of folliculosebaceous structures, sclerotic collagen bundles with large amounts of mucin, and spreading telangiectasia. The inflammatory infiltrate was inconspicuous, with numerous interstitial spindle and bizarre cells. Most of the interstitial cells were reactive to factor XIIIa. The severe form of rhinophyma shares many histologic characteristics with elephantiasis caused by chronic lymphedema. (J Am Acad Dermatol 2000;42:468-72.)</ce:simple-para></ce:abstract-sec></ce:abstract></head><body view="all"><ce:sections><ce:para view="all" id="para.0010">Rhinophyma represents a severe complication of rosacea. Clinically, the nose of the affected patients, usually men, appears erythematous, irregularly swollen, and bulbous, with prominent pilosebaceous dilated pores and telangiectasia. Recurrent papules and pustules are common associated features. In severe forms multiple, firm, or soft, smooth-surfaced, erythematous nodules can be observed.<ce:cross-refs refid="bib1 bib2"><ce:sup loc="post">1,2</ce:sup></ce:cross-refs> In common rhinophyma histologic findings are substantially similar to those observed in fully developed rosacea.<ce:cross-refs refid="bib3 bib4 bib5"><ce:sup loc="post">3-5</ce:sup></ce:cross-refs> Nevertheless, the microscopic features of severe forms are rarely documented in the literature.<ce:cross-refs refid="bib6 bib7"><ce:sup loc="post">6,7</ce:sup></ce:cross-refs> It has been postulated that in severe forms of rhinophyma chronic inflammation could lead to connective tissue hypertrophy and fibroplasia because of an overexpression of factor XIIIa on dermal dendritic cells and dermal fibro-blasts.<ce:cross-ref refid="bib8"><ce:sup loc="post">8</ce:sup></ce:cross-ref> In this study we report the results of a clinicopathologic study of a series of patients with rhinophyma in various stages of evolution, paying special attention to the severe form.</ce:para><ce:section view="all" id="section.0010"><ce:section-title>METHODS</ce:section-title><ce:para view="all" id="para.0015">All cases of rhinophyma in the files of the Department of Histopathology of the University of Turin received between 1990 and 1997 have been reviewed. Clinical records were studied in each case. A total of 17 cases have been collected. The essential clinical data of these patients are summarized in Table I.
<ce:display><ce:table colsep="0" rowsep="0" frame="topbot" id="table.0010"><ce:label>Table I</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0015">Clinical data of patients with rhinophyma</ce:simple-para></ce:caption><tgroup cols="6"><colspec colname="col1" colsep="0"></colspec><colspec colname="col2" colsep="0"></colspec><colspec colname="col3" colsep="0"></colspec><colspec colname="col4" colsep="0"></colspec><colspec colname="col5" colsep="0"></colspec><colspec colname="col6" colsep="0"></colspec><thead><row><entry>Patient No.</entry><entry align="center">Sex</entry><entry align="center">Age (y)</entry><entry align="center">Form</entry><entry align="center">Facial involvement</entry><entry align="center">Duration (y)</entry></row></thead><tbody><row><entry><ce:hsp sp="1.0"></ce:hsp>1</entry><entry align="center">F</entry><entry align="center">34</entry><entry align="center">Severe</entry><entry align="center">Yes</entry><entry align="center">4</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>2</entry><entry align="center">M</entry><entry align="center">89</entry><entry align="center">Common</entry><entry align="center">Yes</entry><entry align="center">10</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>3</entry><entry align="center">M</entry><entry align="center">67</entry><entry align="center">Severe</entry><entry align="center">No</entry><entry align="center">7</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>4</entry><entry align="center">F</entry><entry align="center">43</entry><entry align="center">Common</entry><entry align="center">Yes</entry><entry align="center">3</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>5</entry><entry align="center">M</entry><entry align="center">74</entry><entry align="center">Common</entry><entry align="center">No</entry><entry align="center">4</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>6</entry><entry align="center">M</entry><entry align="center">80</entry><entry align="center">Common</entry><entry align="center">Yes</entry><entry align="center">5</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>7</entry><entry align="center">M</entry><entry align="center">87</entry><entry align="center">Common</entry><entry align="center">Yes</entry><entry align="center">8</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>8</entry><entry align="center">M</entry><entry align="center">59</entry><entry align="center">Severe</entry><entry align="center">Yes</entry><entry align="center">7</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>9</entry><entry align="center">M</entry><entry align="center">61</entry><entry align="center">Common</entry><entry align="center">Yes</entry><entry align="center">4</entry></row><row><entry>10</entry><entry align="center">M</entry><entry align="center">64</entry><entry align="center">Common</entry><entry align="center">No</entry><entry align="center">5</entry></row><row><entry>11</entry><entry align="center">M</entry><entry align="center">82</entry><entry align="center">Severe</entry><entry align="center">Yes</entry><entry align="center">7</entry></row><row><entry>12</entry><entry align="center">M</entry><entry align="center">66</entry><entry align="center">Common</entry><entry align="center">Yes</entry><entry align="center">4</entry></row><row><entry>13</entry><entry align="center">M</entry><entry align="center">66</entry><entry align="center">Severe</entry><entry align="center">Yes</entry><entry align="center">6</entry></row><row><entry>14</entry><entry align="center">M</entry><entry align="center">65</entry><entry align="center">Common</entry><entry align="center">Yes</entry><entry align="center">5</entry></row><row><entry>15</entry><entry align="center">M</entry><entry align="center">74</entry><entry align="center">Common</entry><entry align="center">Yes</entry><entry align="center">12</entry></row><row><entry>16</entry><entry align="center">M</entry><entry align="center">73</entry><entry align="center">Severe</entry><entry align="center">Yes</entry><entry align="center">4</entry></row><row><entry>17</entry><entry align="center">M</entry><entry align="center">45</entry><entry align="center">Common</entry><entry align="center">No</entry><entry align="center">5</entry></row></tbody></tgroup></ce:table></ce:display>Two groups of patients have been identified on the basis of clinical observations. The first group included patients with the classic form of rhinophyma, in which the nose was enlarged with prominent pilosebaceous orifices but still preserved its profile; the second group included patients with the more severe form, in which the presence of overgrowths produced a markedly distorted proboscis (Fig 1).
<ce:display><ce:figure id="figure.0010"><ce:label>Fig. 1</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0020">Proboscis-like appearance of the nose.</ce:simple-para></ce:caption><ce:link locator="gr1"></ce:link></ce:figure></ce:display></ce:para><ce:para view="all" id="para.0020">For all patients, multiple sections were taken and stained with hematoxylin-eosin, alcian blue (pH 0.5 and 2.5), toluidine blue, colloidal iron, and orcein stains. Immunohistochemical analyses of additional formalin-fixed and paraffin-embedded sections from each specimen were performed by using the standard avidin-biotin complex immunoperoxidase technique with antibodies against factor XIIa, S-100 protein, vimentin, and CD68.</ce:para></ce:section><ce:section view="all" id="section.0015"><ce:section-title>RESULTS</ce:section-title><ce:para view="all" id="para.0025">C1inically, the first group included 12 patients (1 female and 11 male patients; mean age, 68 years), and the second group included 5 patients (1 female and 4 male patients; mean age, 59.8 years). In 4 patients rhinophyma was the only manifestation of the disease, whereas in 13 cases papules and pustules involved the rest of facial skin.</ce:para><ce:para view="all" id="para.0030">No relation between the clinical form and duration of the disease was found (mean duration of the first group, 5.9 years; mean duration of the second group, 5.6 years).</ce:para><ce:section view="all" id="section.0020"><ce:section-title>Histopathologic and immunohistochemical findings</ce:section-title><ce:para view="all" id="para.0035">Microscopic examination of numerous specimens obtained from each patient of group 1 showed a normal thickened epidermis with dilated acroinfundibula (Fig 2).
<ce:display><ce:figure id="figure.0015"><ce:label>Fig. 2</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0025">Classic variant of rhinophyma shows sebaceous hyperplasia, telangiectasia, and perifollicular inflammatory infiltrate.</ce:simple-para></ce:caption><ce:link locator="gr2"></ce:link></ce:figure></ce:display>In some specimens an increased number of single, normal-appearing melanocytes in the basal layer was noted. In the superficial and mid-dermis there was a large number of ungrouped, mature, pyriform sebaceous lobules connected to widely dilated infundibula. Some infundibular cysts filled with cornified cells were also noted. The surrounding stroma was edematous rich in spindle fibrohistiocytic cells with foci of inflammatory infiltrate composed of lymphocytes and plasmocytes. In some specimens the inflammatory infiltrate was more prominent, with the findings of suppurative, granulomatous, or both types of folliculitis. In the superficial dermis vascular dilatation of capillaries, venules, and lymphatic vessels was present. Occasional <ce:italic>Demodex folliculorum</ce:italic> infestation was also observed within the dilated infundibula. Fibrosis was of a moderate degree throughout the superficial and reticular dermis, with perifollicular accentuation. Solar elastosis was an inconstant finding. Elastic fibers were reduced in the superficial dermis.</ce:para><ce:para view="all" id="para.0040">Histologic findings of group 2, displaying a more severe form of rhinophyma, were characterized by a thinned epidermis devoid of rete ridges with only few slightly dilated acroinfundibula. The dermis appeared markedly thickened, with severe reduction or absence of the folliculosebaceous structures (Fig 3).
<ce:display><ce:figure id="fig3"><ce:label>Fig. 3</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0030">Elephantiasis variant of rhinophyma shows absence of folliculosebaceous structures, occasional dilated infundibula, diffuse telangiectasia, and prominent fibroplasia.</ce:simple-para></ce:caption><ce:link locator="gr3"></ce:link></ce:figure></ce:display>Occasional infundibular cysts were noted. For each patient, depending on the specimens examined, there were areas in which the stroma was widely fibrotic with irregularly arranged collagen bundles (Fig 4) and areas in which the stroma was edematous with very large amounts of mucin (Fig 5).
<ce:display><ce:figure id="figure.0020"><ce:label>Fig. 4</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0035">Higher magnification of <ce:cross-ref refid="fig3">Fig 3</ce:cross-ref> shows fibrous stroma with an increased number of fibrocytes and dilated lymphatic vessels.</ce:simple-para></ce:caption><ce:link locator="gr4"></ce:link></ce:figure></ce:display><ce:display><ce:figure id="figure.0025"><ce:label>Fig. 5</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0040">Prominent mucin deposits in rhinophyma.</ce:simple-para></ce:caption><ce:link locator="gr5"></ce:link></ce:figure></ce:display>The myxoid stroma stained positively with colloidal iron and with alcian blue at pH 2.5 and negatively with alcian blue at pH 0.5. Between collagen bundles, there was an increased number of spindle-shaped and irregular-shaped cells with large pleomorphic and hyperchromatic nuclei. There were also some multinucleated giant cells, some of which showed multilobated nuclei (Fig 6).
<ce:display><ce:figure id="figure.0030"><ce:label>Fig. 6</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0045">Fibrillary stroma with large amounts of mucin and plump and bizarre fibroblasts.</ce:simple-para></ce:caption><ce:link locator="gr6"></ce:link></ce:figure></ce:display>The majority of the cells had scant cytoplasm and indistinct cytoplasm and borders. Mast cells were increased in number. In the full thickness of the dermis, there were numerous dilated vascular channels of the capillary, venular, and lymphatic type. The inflammatory infiltrate was scant and composed of lymphohistiocytic cells. The elastic fiber network was destroyed.</ce:para><ce:para view="all" id="para.0045">The different histologic changes of the classical form and the severe form of rhinophyma are summarized in Table II.
<ce:display><ce:table colsep="0" rowsep="0" frame="topbot" id="table.0015"><ce:label>Table II</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0050">Histopathologic changes of rhinophyma</ce:simple-para></ce:caption><tgroup cols="3"><colspec colname="col1" colsep="0"></colspec><colspec colname="col2" colsep="0"></colspec><colspec colname="col3" colsep="0"></colspec><thead><row><entry>Rhinophyma</entry><entry align="center">Classic form</entry><entry align="center">Severe form</entry></row></thead><tbody><row><entry>Epidermis</entry><entry align="center">Normal</entry><entry align="center">Thinned</entry></row><row><entry>Infundibula</entry><entry align="center">Dilated</entry><entry align="center">Absent</entry></row><row><entry>Dermal thickness</entry><entry align="center">Moderate</entry><entry align="center">Severe</entry></row><row><entry>Sebaceous hyperplasia</entry><entry align="center">Severe</entry><entry align="center">Absent</entry></row><row><entry>Telangiectasia</entry><entry align="center">Superficial dermis</entry><entry align="center">Full dermis</entry></row></tbody></tgroup></ce:table></ce:display></ce:para><ce:para view="all" id="para.0050">Immunohistochemical study showed numerous factor XIIIa–reactive stromal cells, especially in the specimens obtained from patients with the severe form of rhinophyma (Fig 7).
<ce:display><ce:figure id="figure.0035"><ce:label>Fig. 7</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0055">Numerous factor XIIIa–positive cells throughout the interstitial dermis.</ce:simple-para></ce:caption><ce:link locator="gr7"></ce:link></ce:figure></ce:display>The spindle-shaped and multinucleated cells stained positively only for vimentin. Occasional interstitial cells were also reactive to CD68.</ce:para></ce:section></ce:section><ce:section view="all" id="section.0025"><ce:section-title>DISCUSSION</ce:section-title><ce:para view="all" id="para.0055">Our study demonstrates that the histologic changes of rhinophyma are very different and are correlated with the clinical presentation of the disease.</ce:para><ce:para view="all" id="para.0060">Histopathologically, the classic type of rhinophyma shows prominent sebaceous hyperplasia in asymmetric distribution, dilated infundibula with occasional cysts, telangiectasia in the superficial dermis, and perifollicular infiltrate composed of lymphocytes, histiocytes, and plasmocytes. Suppuration, granulomatous inflammation, and focal fibroplasia are common findings. <ce:italic>D folliculorum</ce:italic> infestation can also be observed. Substantially, these changes are similar to those observed in rosacea.<ce:cross-ref refid="bib3"><ce:sup loc="post">3</ce:sup></ce:cross-ref> They differ only by the presence of the marked sebaceous hyperplasia.</ce:para><ce:para view="all" id="para.0065">Histopathologic changes of the severe form of rhinophyma show a prominent thickness of the dermis with marked reduction or absence of pilosebaceous structures and only a few infundibular cysts. Dilated vessels of capillary and lymphatic type are common throughout the full thickness of the dermis.</ce:para><ce:para view="all" id="para.0070">The stroma can be sclerotic, with collagen bundles arranged in irregular array, or edematous, with abundant deposits of mucin. Interstitial cells are spindle-shaped and irregularly shaped fibroblasts, some of which have numerous multilobated nuclei. An increased number of mastocytes can also be noted. The inflammatory infiltrate is inconspicuous. The elastic network is destroyed.</ce:para><ce:para view="all" id="para.0075">The pathogenesis of the classic form of rhinophyma remains unknown. The role of <ce:italic>D folliculorum</ce:italic> , immunologic factors, and blood flow alteration with marked depression of dermal vasoactive intestinal peptide (VIP) receptors have been debated.<ce:cross-refs refid="bib9 bib10 bib11 bib12"><ce:sup loc="post">9-12</ce:sup></ce:cross-refs></ce:para><ce:para view="all" id="para.0080">Our study allows us to make some hypotheses about the histopathogenesis of the severe variant of this disease. In fact, the histopathologic changes of this form present many similarities to those observed in elephantiasis caused by chronic lymphedema.<ce:cross-ref refid="bib13"><ce:sup loc="post">13</ce:sup></ce:cross-ref> Lymphedema arises from inadequate lymphatic drainage and may result from mechanical obstruction. In rhinophyma the lymphatic drainage could be impaired by severe fibroplasia caused by recurrent folliculitis and perifolliculitis and could lead to persistent edema and to the destruction of the adnexal structures. Accumulation of interstitial and lymphatic fluid within the dermis stimulates fibroblasts to produce further deposits of collagen and glycosaminoglycans.</ce:para><ce:para view="all" id="para.0085">Especially in the severe form of rhinophyma, most of the interstitial cells are reactive to factor XIIIa.<ce:cross-ref refid="bib8"><ce:sup loc="post">8</ce:sup></ce:cross-ref> Dendrocytic cells are involved in the inflammatory process and may induce fibroblast proliferation. Their increased number is documented in wound healing and in the early stages of scleroderma.<ce:cross-refs refid="bib14 bib15"><ce:sup loc="post">14,15</ce:sup></ce:cross-refs> Mast cells also seem to play a role in the processes of fibrosis.<ce:cross-ref refid="bib16"><ce:sup loc="post">16</ce:sup></ce:cross-ref></ce:para><ce:para view="all" id="para.0090">In conclusion, histopathologic changes of rhinophyma can be either those of fully developed rosacea or those of a fibrotic dermatitis with many similarities with elephantiasis caused by lymphedema. Between these opposites, intermediate stages can be observed.</ce:para><ce:para view="all" id="para.0095">On the basis of our study, the severe form of rhinophyma seems not to be related to the duration of the disease. 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Dermatol</sb:maintitle></sb:title><sb:volume-nr>30</sb:volume-nr></sb:series><sb:date>1991</sb:date></sb:issue><sb:pages><sb:first-page>13</sb:first-page><sb:last-page>16</sb:last-page></sb:pages></sb:host></sb:reference></ce:bib-reference></ce:bibliography-sec></ce:bibliography></tail></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The clinicopathologic spectrum of rhinophyma</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>The clinicopathologic spectrum of rhinophyma</title></titleInfo><name type="personal"><namePart type="given">Filippo</namePart><namePart type="family">Aloi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Dermatology, University of Turin. Turin, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carlo</namePart><namePart type="family">Tomasini</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Dermatology, University of Turin. Turin, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elisabetta</namePart><namePart type="family">Soro</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Dermatology, University of Turin. Turin, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mario</namePart><namePart type="family">Pippione</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Dermatology, University of Turin. Turin, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2000</dateIssued><copyrightDate encoding="w3cdtf">2000</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">We report the results of a clinicopathologic study of 17 patients with rhinophyma in different stages of evolution, with particular attention paid to the severe form of this disease. On the basis of clinical features, we identified 2 groups of patients: the first group (12/17 patients) included patients with the common form of rhinophyma, whereas the second one (5/17 patients) included patients with the severe form of the disease. There was no link between the clinical aspect and the duration of the disease. Microscopic examination of specimens obtained from the classic type of rhinophyma substantially showed the histopathologic features of fully developed rosacea, except for the presence of prominent sebaceous hyperplasia. The second group showed a very different histologic pattern displaying marked dermal thickness, absence of folliculosebaceous structures, sclerotic collagen bundles with large amounts of mucin, and spreading telangiectasia. The inflammatory infiltrate was inconspicuous, with numerous interstitial spindle and bizarre cells. Most of the interstitial cells were reactive to factor XIIIa. The severe form of rhinophyma shares many histologic characteristics with elephantiasis caused by chronic lymphedema. (J Am Acad Dermatol 2000;42:468-72.)</abstract><note>Reprint requests: Carlo Tomasini, MD, Department of Medical and Surgical Specialties, Section of Dermatology, II Clinic, University of Turin, Via Cherasco 23, 1-10126, Turin, Italy.</note><relatedItem type="host"><titleInfo><title>Journal of the American Academy of Dermatology</title></titleInfo><titleInfo type="abbreviated"><title>YMJD</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">200003</dateIssued></originInfo><identifier type="ISSN">0190-9622</identifier><identifier type="PII">S0190-9622(00)X0126-0</identifier><part><date>200003</date><detail type="volume"><number>42</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="issue pages"><start>389</start><end>548</end></extent><extent unit="pages"><start>468</start><end>472</end></extent></part></relatedItem><identifier type="istex">4A0ED1DE1BA50C93F58C20DA5CF4FFA9FD2C8A99</identifier><identifier type="DOI">10.1016/S0190-9622(00)90220-2</identifier><identifier type="PII">S0190-9622(00)90220-2</identifier><identifier type="ArticleID">902202</identifier><accessCondition type="use and reproduction" contentType="copyright">©2000 American Academy of Dermatology, Inc</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>American Academy of Dermatology, Inc, ©2000</recordOrigin></recordInfo></mods></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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