solitary polypoid xanthoma in the larynx

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Value of histochemical stains for copperin the diagnosis of paediatric copperstorage disorders

Sir : In response to the article by Pilloni et al.,1 it wasinteresting to note that the orcein stain has minorvalue in the diagnosis of Wilson’s disease (WD),especially in the early stages of the disease. In asimilar paediatric liver storage disorder, Indian child-hood cirrhosis (ICC), we found the orcein stain of asignificant diagnostic value, even in the early stages ofthe disease.2 All 82 cases, the largest number of ICCcases studied with the orcein stain to date, showedorcein positivity. The orcein grade increased with thestage of the disease.3

The differential staining of copper with orcein in thesetwo conditions could be explained on the basis of theabnormality of the copper-binding protein in theseconditions. Although both WD and ICC have highhepatic copper concentrations, caeruloplasmin levelsare characteristically low in WD and normal or raised inICC. No other copper protein has been found to bedeficient in WD. Orcein stains a copper-bindingprotein4,5 corresponding to metallothionein.6

Thus, histochemical demonstration of copper is notobsolete. A panel of histochemical stains would enabledetection of many cases of paediatric copper storagedisorders like WD and ICC.

S Sethi

Department of Pathology,Lady Hardinge College,

New Delhi, India

1. Pilloni L, Lecca S, Van Eyken P et al. Value of histochemical stainsfor copper in the diagnosis of Wilson’s disease. Histopathology 1998;33; 28–33.

2. Sethi S, Grover S, Khodaskai MB. Role of copper in Indian childhoodcirrhosis. Ann. Trop. Pediatr. 1993; 13; 3–6.

3. Guarascio P, Yentis F, Cevikbas U, Portmann B, Williams R. Value ofcopper associated protein in diagnostic assessment of liver biopsy. J.Clin. Pathol. 1983; 36; 18–23.

4. Sipponen P, Salaspuro HP, Makkonen HM. Orcein positivehepatocellular material in histological diagnosis of primary biliarycirrhosis. Ann. Clin. Res. 1975; 7; 273–277.

5. Jain S, Scheuer PJ, Archer B, Newman SP, Sherlock S. Histologicaldemonstration of copper and copper-associated protein in chronicliver diseases. J. Clin. Pathol. 1978; 31; 784–790.

6. Wilson’s disease and copper associated protein (editorial). Lancet1981; 1; 644–646.

Uterine leiomyomas with T-cell infiltrationassociated with GnRH agonist goserelin

Sir : Bardsley et al.1 described two unusual cases ofmassive lymphocytic infiltration of uterine leiomyomas,following GnRH agonist treatment. We wish to reportan additional case who presented similar microscopicalfeatures in a woman who has been taking GnRHpreoperatively.

A 47-year-old woman (para 2) complained ofhypermenorrhoea. Treatment with goserelin (Zoladex)was given monthly intramuscularly for 6 months. Anultrasonographic abdominal study showed uterinefibroids, which had enlarged compared with a previousstudy. Peripheral white cell count was normal. Ahysterectomy with bilateral salpingo-ophorectomy wasperformed 10 months after treatment with GnRH. Thepatient is well after 3 years of follow-up. On grossexamination, seven firm and whitish intramuralnodules measuring from 20 to 40 mm in diameterwere observed. The ovaries were unremarkable. Micro-scopically, the endocervix showed focal lymphocyticinfiltration and the endometrium was proliferative. Themost striking feature was observed in all the leiomyo-mas, which contained extensive infiltration withinflammatory cells, with focal and diffuse aggregatesof mature lymphocytes, histiocytes and scatteredplasma cells and mast cells. The lymphocytes weretypical and mitotic figures were not prominent.Immunohistochemical study showed that the majorityof the diffuse infiltrates of lymphocytes stained with T-cell markers UCHL-1 (Figure 1), CD43 and CD8, whilethe aggregates of lymphocytes, stained with B-cellmarkers L26 (CD20) and CD79a intermixed with and

Histopathology 1999, 34, 471–477

q 1999 Blackwell Science Limited.

Figure 1. Dense aggregates of T-cells (UCHL 1 × 500).

CD4 T-helper lymphocytes. Diffuse dispersed macro-phages stained with CD68. The presence of small new-formed vessels with prominent endothelium washighlighted by CD31 (Figure 2).

Of interest is the fact that our patient received GnRHgoserelin for 6 months and discontinued this medica-tion nearly a year prior to the surgery. This may indicatethat the inflammatory response is observed even as adelayed response to this drug. The diffuse pattern ofinfiltration involving the whole of the leiomyomas, thelymphohistiocytic nature of the infiltrates and the longperiod from the intake of GnRH until the surgeryobserved in our case, are features that argue against adirect dose-related toxic effect.

Our findings are consistent with a T-cell proliferation,with a subset of CD8 suppressor lymphocytes, with aminor component of macrophages and B-lymphocytes,and scattered plasma cells and mast cells. These findingsseem to indicate a direct cytotoxic effect by anautoimmune mechanism.

Interestingly, both cases reported by Bardsley et al.1

and the present case share in common the treatmentwith goserelin and secondly show a diffuse lymphocyticinfiltrate of T-phenotype, in contrast with the mixedpopulation of B- and T-lymphocytes observed in themassive lymphocytic infiltration of leiomyomas ofunknown aetiology. In addition, we observed neovascu-larization, similar to normal wound healing.4 Specificangiogenic molecules may be released by immune cellsor macrophages into the stroma. The above evidence ofangiogenesis suggest that neovascularization may playa role in the response to GnRH.

J B M LaforgaF I Aranda*

Department of Pathology,Hospital Marina Alta, Denia; and

*Department of Pathology,Hospital General de Alicante,

Alicante, Spain

1. Bardsley V, Cooper P, Peat D.S. Massive lymphocytic infiltration ofuterine leiomyomas associated with GnRH agonist treatment.Histopathology 1998; 33; 80–82.

2. Ferry JA, Harris NL. Scully RE. Uterine leiomyomas with lymphoidinfiltration simulating lymphoma. Int. J. Gynaecol. Pathol. 1989; 3;263–270.

3. Crow J, Gardner RL, McSweeney G, Shaw RW. Morphologicalchanges in uterine leiomyomas treated by GnRH agonist goserelin.Int. J. Gynaecol. Pathol. 1995; 14; 235–242.

4. Dvorak HF. Tumors: wounds that do not heal: similarities betweentumor stroma generation and wound healing. N. Eng. J. Med. 1986;315; 1650–1659.

Multilocular mesothelial inclusion cysts(so-called benign multicystic mesothelioma)of pericardium

Sir : Multilocular mesothelial inclusion cysts (MMIC)also called benign multicystic mesothelioma, mostcommonly presents in the pelvic peritoneum of youngwomen, frequently associated with a history of endome-triosis, inflammatory disease and/or surgical proceduresin the area. Less frequently it has been reported in theupper abdomen or retroperitoneum. There is one reporteach of cases involving the aorta1 and pleura.2 Wereport a case of MMIC found in the pericardial sac of achild, a combination which we have not been able tofind previously recorded in the literature.

A 7-year-old male child with Down’s syndrome wasadmitted for heart surgery due to an incomplete atrio-ventricular channel characterized after extensive pre-operative work-up of the heart which included cathe-terization studies. There was no history of previoussurgery. While opening the pericardial sac the surgeonnoticed a gelatinous exophytic mass 40 × 20 × 5 mm,attached to the anterior aspect of the parietal layerwhich he resected. The rest of the procedure wasperformed adequately and the patient had an unevent-fully postoperative evolution. The pericardial mass hadnot been recognized by the ultrasound studies.

Histological examination revealed a multicysticstructure composed by fibrous walls lined by a singlelayer of flat to hyperplastic mesothelial cells (Figure 1).Focally intracystic collections of cells which apparentlyhad detached from the lining were also seen and wereobviously related to clusters of similar cells arranged inthe walls of the cysts (see immunohistochemicalfindings). Within the walls there were a few groups ofchronic inflammatory cells. Smooth muscle cells were

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q 1999 Blackwell Science Ltd, Histopathology, 34, 471–477.

Figure 2. Small new vessels (angiogenesis) with prominent endo-thelial cells (CD31 stain × 500).

not recognized as part of the lesion. The lining cells werepositive for keratin (AE1/AE3) (Figure 2) and negativefor endothelial markers (Ulex europaeus; FVIII RA) andhistiocytes (HAM 56). Both the intramural andintracystic collections of cells of mesothelial appearanceproved to be strongly reactive for the histiocyte markerHAM 56 (Figure 2). The mass was then interpreted as aMMIC.

The MMIC is an infrequent lesion which mostcommonly localizes to the pelvic peritoneal surface ofwomen in their thirties and forties, presenting as anisolated and localized lesion, a multifocal but stilllocalized, or as a diffuse mass. In 17% of the cases

MMIC develops in men.3 There is one reported case ofMMIC in the pleural cavity,2 the authors choosing thediagnosis of ‘multicystic mesothelial proliferation’because they considered their case to be a reactivephenomenon. Chen4 reported an unusual location ofthis lesion, namely the inguinal region. D’Errico et al.1

described a case, similar to ours, localized to theadventitia of the ascending intrapericardial segment ofthe aorta in a 67-year-old man. While interpreting thelesion as a reactive process they called it pericardialmulticystic proliferation, equating it to the peritonealmulticystic mesothelioma. These authors failed torecognize the histiocytic component of the lesion. Thecase we are reporting seems also to fulfil the diagnosticcriteria for MMIC. Differential diagnosis includeslymphangioma and malignant cystic mesothelioma.Lymphangiomas are usually localized tumours whichhistologically exhibit lymphoid aggregates and bundlesof smooth muscle in the walls. The combination ofgross and microscopic features which includes exten-sive mesothelial proliferation with cellular atypiaallows adequate diagnosis of the malignant cysticmesothelioma.5

In this case, it appears worthwhile to discussdifferential diagnosis with other lesions which may befound in this area in children. The unilocular meso-thelial cyst usually presents in the right costodiaphrag-matic region or in the upper mediastinum. It is a smallunilocular mesothelium-lined cyst without communi-cation with the pericardium. A similar lesion but onewhich is widely opened to the pericardial cavity is calleddiverticulum of the pericardium. Both seem to resultfrom an anomalous development of the ventral recessusof the parietal primitive pericardial cavity. None of thetwo is multiloculated.6

The exact pathogenesis and nosology of the MMIC isstill under discussion. Weiss and Tavassoli,7 sustain thatthe lesion is a true neoplasm to be placed midwaybetween benign adenomatoid mesothelioma and malig-nant epithelial mesothelioma. This lesion showed a slowbut progressive growth, recurred frequently and in afew cases lead to death.7 Ross et al.3 studied 25 cases ofMMIC and related the microscopic findings to a reactivemesothelial proliferation specifically excluding thepossibility of being a tumour.

In our case, we also noticed that cellular aggregateslocalized to the walls and cavities of the cyst closelyresembling mesothelial cell proliferation strongly reactedwith the HAM-56 histiocyte marker. Very recently,Ordonez et al.8 demonstrated that lesions with themicroscopic features of so-called nodular mesothelialproliferations or hyperplasias are in fact composed byCD68 positive histiocytes. Although we also noticed the

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Figure 1. Overview of the multicystic lesion with cavities lined bymesothelial cells. The fibrous stroma contains a few inflammatorycells. Also noticed are groups of cells within the cysts (haematoxylinand eosin × 40).

Figure 2. Strong reactivity for keratin immunostaining in the cellslining the cavities. Only a very few intracystic cells are also positive(a). An area of the lesion with numerous histiocytes replacing themesothelial lining and aggregated in clusters inside the cyst. Someareas of the lining cells are negative for the histiocyte marker(arrow), representing the mesothelial cells (b). a, immunoperoxidasefor keratin (AE1/AE3) × 100. b, immunoperoxidase for HAM 56× 100.

histiocytic nature of these cells, the rest of the lining wascomposed by truly mesothelial cells.

The possibility that the lesion we are presentingmight be related to the heart catheterization done beforeheart surgery is truly remote since thousands ofprocedures are daily done all over the world andnobody seems to have seen a similar multicystic massin the pericardium.

In summary, we are reporting an example of MMICwhich also contained nodular histiocytic proliferationsinvolving the pericardium of a child with Down’ssyndrome found by chance during heart surgery.

R DrutG Quijano

Department of Pathology,Hospital de Ninos,

‘Superiora Sor Marıa Ludovica’,La Plata, Argentina

1. D’Errico A, Grigioni WF, Baccarini P, Pasquinelli GA, Gubinelli M,Mancini AM. Pericardial multicystic proliferation. Pathology 1993;25; 412–415.

2. Ball NJ, Urbanski SJ, Green FHY, Kieser T. Pleural multicysticmesothelial proliferation. The so-called multicystic mesothelioma.Am. J. Surg. Pathol. 1990; 14; 375–378.

3. Ross MJ, Welch WR, Scully RE. Multilocular peritoneal inclusioncysts (the so-called cystic mesotheliomas). Cancer 1989; 64; 1336–1346.

4. Chen KT. Multicystic mesothelioma. Int. J. Surg. Pathol. 1998; 6;43–48.

5. Battifora H, McCaughey WTE. Tumors of the serosal membranes.In: Atlas of Tumor Pathology, 3rd.series, fascicle 15. Washington,DC: Armed Forces Institute of Pathology, 1995; 90–94.

6. Kornstein MJ, deBlois GG. Chapter 12. Pathology of the thymus andmediastinum. In: Major Problems in Pathology, Volume 33, 1st edn.Philadelphia: WB Saunders, 1995; 213.

7. Weiss SW, Tavassoli FA. Multicystic mesothelioma. An analysis ofpathologic findings and biologic behavior in 37 cases. Am. J. Surg.Pathol. 1988; 12; 737-746.

8. Ordonez NG, Ro JY, Ayala AG. Lesions described as nodularmesothelial hyperplasia are primarily composed of histiocytes. Am.J. Surg. Pathol. 1998; 22; 285-292.

Unusual presentation of multiplesubcutaneous glomus tumours of the lowerlimb with extensive glomus cell hyperplasia

Sir : Glomus tumours are uncommon benign neoplasmscomposed of cells histogenetically resembling themodified smooth muscle cells forming part of thespecialized Sucquet–Hoyer canal, an intrinsic anatomi-cal component of the glomus body.1 These lesions areusually solitary and non-heritable, with a predilectionfor adults. Multiple glomus tumours are extremely

unusual and occur predominantly in childhood andadolescence, generally demonstrating an autosomaldominant mode of inheritance.2,3

We report an unusual case of multiple subcutaneousglomus tumours in an older patient, and describe anovel histopathological feature which may provide apossible explanation for the multifocality of the tumourin this patient.

A 39-year-old woman presented with a 6-year historyof intermittent, piercing pain restricted to the left lowerlimb, most noticeable on getting up in the morning, andelicited by sudden temperature changes. The patienthad been seen 1 year earlier with similar complaintsand following clinical work-up, two subcutaneouscircumscribed lesions situated high in the lower legnear the knee joint posteriorly, had been identified andremoved, without relief of her symptoms. Histopathologi-cal examination of the lesions failed to reach a consensusdiagnosis and the differential diagnosis at that time wasbetween a cellular leiomyoma with widespread degen-erative change, and a haemangiopericytoma.

Clinical history did not yield any additional relevantinformation, but noteworthy was the lack of any familyhistory of a similar complaint or other heritable benignor malignant tumours. On examination no palpablenodules were identifiable. Routine clinical chemistry,Doppler studies, lymphangiography, ultrasonographyand phlebography were unremarkable. Magnetic reso-nance imaging (MRI) identified three well circum-scribed, deeply situated subcutaneous lesions aroundthe left ankle joint and all three lesions were surgicallyexcised.

The surgical specimens comprised three circum-scripted tan/red nodules having a maximal cross-sectional diameter of 13 mm, 10 mm and 8 mm,respectively, and a homogeneous, slightly gelatinous cutsurface. Histologically, the tumours were composed ofpredominantly solid cell nests surrounding capillary-sized vessels; an occasional ectatic vessel was present.The cells demonstrated small, round to oval, centrallyplaced monotonous nuclei without nucleoli surroundedby a zone of amphophilic cytoplasm (Figure 1).Intracellular glycogen and mucin were absent. Thelesions were unencapsulated but well demarcated fromthe adjacent adipose tissue and surrounded by dis-continuous bundles of collagen. Normal vascular spacesimmediately adjacent to the tumours and, remarkably,also present at sites far removed from the lesions weresurrounded by one or more layers of similar cells asdescribed above (Figure 2). Immunohistochemically thecells expressed vimentin, smooth muscle actin andmuscle specific actin. The proliferation marker Ki67 wasalso immunohistochemically negative in all but an

474 Correspondence


occasional cell, indicating that these lesions were nothighly proliferative.

After considering a limited differential diagnosis, adiagnosis of multiple glomus tumours was made basedprimarily on the histological morphology and immuno-histochemical profile, and review of the histopathologyof the previously excised lesions was compatible withthis diagnosis.

The glomus tumour is uncommon, comprisingroughly 1.5% of all soft tissue tumours,4 and was firstaccurately documented by Masson in 1924.5 The vastmajority are solitary, non-heritable and occur in olderpatients, while the rare cases of multiple tumours occurpredominantly in childhood and show an autosomaldominant mode of inheritance.2,3 Apart from theirpredilection for the extremities and subungual regions,they have been documented to occur at numerousperipheral and visceral sites.1–5

The differential diagnosis includes cutaneous adnexaltumours (especially eccrine spiradenoma and solidforms of hidradenoma), haemangioma, haemangioperi-cytoma, intradermal naevus and metastatic carcinoid.However, based on the distinctive architecture andhistopathological morphology, the diagnosis is rarelydifficult.

Remarkably, we were able to demonstrate thepresence of vascular spaces surrounded by one ormore layers of glomus cells not only in the vicinity of thetumours, but also at sites far removed from the primarylesions. A review of the literature was not able to clarifywhether this is a recognized component of glomustumours. We would like to suggest that the extensivehyperplasia of glomus cells at sites removed from theglomus tumours might serve as a basis for the multi-focality in this patient.

From a clinical perspective, our report is highlyunusual in that a case of multiple glomus tumours ofthe lower limb, in contrast to previous reports, is nowdocumented in a patient having no previous history ofsimilar lesions and demonstrating no family history ofsimilar or other heritable tumours.

Noteworthy is that these tumours presented initialhistopathological diagnostic difficulties. The diagnosis,however, is not usually difficult but is essential forpatient reassurance and decisions involving follow-uprequirements in the longer term.

J F Graadt van RoggenE C Joekes*

K Welvaart†J H J M van Krieken

Departments of Pathology,*Radiology and †Surgery,

Leiden University Medical Centre,The Netherlands

1. Stout AP. Tumors of the neuromyoarterial glomus. Am. J. Cancer1935; 24; 255–272.

2. Tran LP, Velanovich V, Kaufmann CR. Familial multiple glomustumours: Report of a pedigree and literature review. Ann. Plast.Surg. 1994; 32; 89–91.

3. Faggioli GL, Bertoni F, Stella A, Bachini P, Mirelli M, Gessardi M.Multifocal diffuse glomus tumor. Int. Angiol. 1988; 7; 281–286.

4. Enzinger FM, Weiss SW (eds). Soft Tissue Tumours, 3rd edn.Missouri: Mosby, 1995.

5. Masson P. Le glomus neuromyoarteriel des regions tactiles et sestumeurs. Lyon Chir. 1924; 21; 257–280.

Solitary polypoid xanthoma in the larynx

Sir : A xanthoma is a localized collection of fat-ladenhistiocytes and is not a true tumour but rather a

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Figure 2. Microscopy of vascular spaces at distant sites from theprimary glomus tumour, demonstrating the prominant cuff ofglomus cells.

Figure 1. Lower power microscopy (inset, high power) showing thecharacteristic morphology of the glomus tumour.

reactive histiocyte proliferation.1 Usually, xanthomasoccur in the skin and subcutis, but occasionally theydeeply involve the tendon or synovium. Until now, axanthoma confined to the larynx has not been recordedin the literature.

A 48-year-old Japanese man was found to have alaryngeal tumour during gastroscopy examination. Onemonth later, he was admitted to the Department ofOtorhinolaryngology of Juntendo Hospital. He hadsmoked more than 30 cigarettes per day for 20 years,and had no past history of antecedent injury to thelarynx. Blood chemical tests, including plasma choles-terol, showed normal values, and cutaneous xanthomawere not found. Laryngoscopy revealed a yellowpedunculated polyp in the anterior site of the left vocalcord. No abnormal lesions were found in other parts ofthe larynx. The polyp was easily removed from theadjacent tissue under microlaryngoscopy.

Grossly the polyp was soft, measuring 18 mm indiameter, with a yellowish cut surface (Figure 1).Histologically, clusters and sheets of numerous foamyhistiocytes with occasional Touton giant cells werediffusely present in the stroma of the polyp (Figure 2).Also, numerous non-foamy histiocytes were noted inmany parts. None of the histiocytes and giant cellsshowed cellular atypia (Figure 2). Perivascular infiltra-tion of inflammatory cells and a slight increase ofcollagen fibres were present. At the surface of the polyp,squamous epithelium with almost normal appearancewas present. Immunohistochemically, the histiocyteswere positive for alpha-1-antitrypsin and were negativefor various cytokeratins (CAM5.2, AE1 and AE3),epithelial membrane antigen and S100 protein.

In the larynx, the most common disorder exhibiting a

polypoid appearance is the laryngeal polyp. Rarely,polypoid hamartomas in the larynx have beenreported.2 Usually, in these disorders, numerous foamyhistiocytes were not seen.2 Therefore, we ruled outlaryngeal polyp and hamartoma in this case.

As to the laryngeal diseases containing numeroushistiocytes, a verruciform xanthoma in the larynx,xanthoma disseminatum involving the larynx, and axanthoma or fibrous histiocytoma confined to thelarynx are considered. Verruciform xanthoma is arelatively uncommon lesion and occurs in the oralcavity, respiratory tract and external genitalia.3 It hashistological features of a papillary or verrucous projec-tion of surface squamous epithelium and xanthomacells restricted to the connective tissue papillae betweenthe epithelial rete ridges.3 We ruled out verruciformxanthoma in this case because of the histologicalappearance of non-papillary squamous epitheliumobserved on the surface. Xanthoma disseminatum isnormolipaemic xanthomatosis and is an exceedinglyrare disorder.4 In xanthoma disseminatum, the skin isalways involved, and xanthomas are also present inother organs.4 To our knowledge, nine cases ofxanthoma disseminatum involving the larynx havebeen recorded in the literature. In these cases, multiplepapules and nodules in the respiratory tract, includingthe larynx, in addition to multiple cutaneous xantho-matous lesions, were identified.4,5 We ruled outxanthoma disseminatum involving the larynx in this

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Figure 1. Gross appearance of pedunculated polyp after fixation. Thestalk (indicated by an arrow) and head are identifiable. The polypwas incompletely cut through the stalk and head, and thus irregularcutting surfaces (indicated by S) are noted.

Figure 2. Histology of the polyp. Numerous foamy histiocytes and atypical Touton giant cell (indicated by an arrow) without cellularatypia (haematoxylin and eosin stain; original magnification × 200.)

case because of the absence of xanthomas in the skinduring hospitalization and regular review after polyp-ectomy. Subsequently, we regarded the present case as axanthoma or fibrous histiocytoma confined to thelarynx. Until now, four cases of fibrous histiocytoma ofthe larynx have been reported in the literature. In them,proliferation of many fibroblastic cells with arrange-ment of a storiform or fascicular pattern was noted.6

Therefore, we finally diagnosed this case as a xanthomaconfined to the larynx because of the absence ofproliferation of many fibroblastic cells.

Review of the literature indicated that this is the firstreport of a xanthoma confined to the larynx. Themacroscopic view of xanthomas is usually either aplaque, a papule or a nodule,1 and pedunculated polypformation in xanthomas is exceedingly rare.5 Therefore,we concluded this case is a solitary xanthoma havingthe characteristic feature of pedunculated polypoidappearance in addition to laryngeal occurrence.

T MatsumotoB Nobukawa

K Kobayashi*M Watanabe*

A Hosokawa*K Tomaru*

G Ichikawa*

First Department of Pathology and*Department of Otorhinolaryngology,

Juntendo University,School of Medicine,

Tokyo, Japan

1. Parker F. Xanthomas and hyperlipidemias. J. Am. Acad. Dermatol.1985; 13; 1–30.

2. Meyer-Breiting E, Burkhardt A. Tumours of the Larynx. Berlin:Springer-Verlag, 1988; 55–56, 169–171.

3. Mostafa KA, Takata T, Ogawa I et al. Verruciform xanthoma of theoral mucosa: a clinicopathological study with immunohistochem-ical findings related to pathogenesis. Virchows Archiv A Pathol. Anat.1993; 423; 243–248.

4. Moloney JR. Xanthoma disseminatum: its otolaryngologicalmanifestations. J. Laryngol. Otol. 1979; 93; 201–210.

5. Finney WP, Montgomery H, New GB. Xanthoma multiplex. Twocases involving the larynx and trachea, and associated withdiabetes insipidus. JAMA 1938; 99; 1071–1074.

6. Van Laer C, Hamans E, Neetens I et al. Benign fibrous histiocytomaof the larynx: presentation of a case and review of the literature. J.Laryngol. Otol. 1996; 110; 474–477.

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Erratum

Histopathology 1999; 34: 87–89

Breast carcinoma metastatic to a lymphoma: report of a case with review of literature

Luciana A, Stefano B, Paolo D, Enrico T, Gianfranco P

Authors’ names are:

Ambrosiani L, Bellone S, Declich P, Tavani E, Pavia GF

solitary polypoid xanthoma in the larynx

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