Transcript

Brief reports 265

Radiation-induced malignant schwannoma is often a fatal tumour. Predisposing factors, such as von Reck- linghausen’s disease5, must be recognized so that radia- tion treatment of malignant disease is optimal to give maximum efficacy with minimal morbidity.

Acknowledgements We wish to acknowledge Professor D.Crowther and Dr C.K.Heffernan for permission to publish case 1 ; Professor J.McClure for his advice: Dr S.Banik for photographic and other assistance; and Miss M.D.Garner for secre- tarial assistance.

References 1 . Cavanagh JB. Etrects of X-irradiation on the proliferation of cells in

peripheral nerve during Wallerian degeneration in the rat. Br. 1. Rndiol. 1968: 41: 275-278.

2. Shore-Freedman I<, Ahrahams G , Recant W. Schneider AH. Neuri- lemniomas and salivary gland tumours of the head and neck following childhood irradiation. Cancer 198 3; 51; 2 1 59-2 163.

3 . f:oley KM. Woodcraft J M . Ellis FT. Posner JH. Malignant and atypical nerve sheath tumours. A m . Nrurol. 1980: 7; 31 1-318.

4. Sordillo PI’. Helson L. Haidu SI et nl. Malignant schwannoma. Clinical characteristics. survival and response to therapy. C ~ n c e r 1981: 47; 2503-2509.

5. Ducatman BS. Scheithauer BW. Post irradiation neurofihrosar- coma. Cnricw 1983; 51; 1028-1033,

6. Ducatmann BS. Schcithauer BW. Malignant peripheral nerve sheath turnours with divergent differentiation. Cnncer 1984; 54: 1049-1 057.

BRIEF KEPOKT

Granulomatous inflammation of the spleen in infectious mononucleosis

D.M.THOMAS, A.B.AKOSA & 1.A.LAMPEKT Department of Histopathology, Royal Postgraduate Medical School, Hammersmith Hospital, London, U K

Date of submission 2 March 1990 Accepted for publication 22 March 1990

Granulomatous inflammation of the spleen has not previously been recorded in infectious mononucleosis. We report two cases and describe further morphological features more often associated with malignant lymphoid conditions.

Keywords: infectious mononucleosis, spleen, granuloma

Introduction The spleen is frequently enlarged to two or three times its normal size in infectious mononucleosis and usually only becomes available for examination as a result of spontaneous or traumatic rupture. Histological examina-

Address for correspondence: Dr D.M.Thomas* Department of Histopathology, Royal Postgraduate Medical School, Hammersmith Hospital, London W12. UK.

tion classically shows expansion of the red pulp with proliferation of atypical lymphocytes, and infiltration of trabeculae and the capsule’. Epithelioid granulomas are not described in the spleens of these patients, although they are well-documented in the lymph nodes, where they may resemble toxoplasmosis’, and within the liver and bone marrowJ.

Case reports C A S E 1

A 32-year-old man presented with a 1-week history of malaise and pleuritic chest pain radiating to the upper abdomen and shoulders. There was no other history. On examination he was pale, tachycardic and hypotensive. There were no signs in the chest, and the upper abdomen

was minimally tender. By the next day the abdomen was more tender and his haemoglobin had dropped from 12 g/I. on admission. to 7 . 5 g/l. Laparotomy showed a n enlarged ruptured spleen and splenectomy was per- formed: he made a n uneventful recovery. Histological examination of the operative specimen having suggested ii diagnosis of infectious mononucleosis. a Paul Bunnell test wiis subsequently found to be positive and atypical lymphocytes were identified in the peripheral blood. The patient later admitted a severe pharyngitis several weeks ear I ier .

"ASF. 2

A 30-year-old male lorry driver presented with acute left sided loin pain. There was no previous history and in particular he denied trauma. On examination he was found to have a n acute abdomen and laparotomy

Figure 2. 'I'rabeculiir inliltration by atypical lymphoid cells \$:it11

adiaccnt epithelioid granulomas.

14 I S T 0 1' A T H 0 1.OG I ('A I . F I N I) I N G S I

In each case the spleen showed expansion of the red pulp with prolileration of atypical lymphocytes. together with multiple epithelioid granulomas (Figure 1 ). There was no associated necrosis and the granulomas occurred predominantly at the marginal zones of the white pulp. 'I'here was extensive trabecular and capsular infiltration by atypical lymphoid cells (Figure 2 t . which stained positively for the T-cell marker UCHL- 1. In addition. there ~ri i s local sub-endothelial and medial infiltration of

I

Figure 1 . Epithelioid granulomas at the marginal zone of splenic white pulp.

Figure 3. a Suh-entlothelial inliltralion by atypical lymphoid ~('11s. b Mcdial inliltriition by atypical lymphoid cells.

Brief’ reports 267

Discussion Splenic granulomas are rare. Neiman4 examined 4 12 splenectomy specimens and found epithelioid granulo- mas in only 24. Thirteen of these were from patients with Hodgkin’s disease, three had non-Hodgkins lym- phoma, three had chronic uraemia. four had sarcoidosis and one patient suffered from a chronic immunodeti- ciency disorder associated with selective IgA deficiency. Two of the 412 specimens were from patients with infectious mononucleosis and neither of these showed epithelioid granulomas. In 19 74 Kuo & Kosai’ reviewed 20 cases of splenic granulomas and reported that, in the majority of cases. a specific diagnosis could not be made. None of this group of 2 0 cases had infectious mono- nucleosis.

The granulomas in our cases were situated predomi- nantly within the peripheral zones of the white pulp, were small and showed a sprinkling of lymphocytes and no associated necrosis. This description is in accord with the type 1 lesion described by Kuo CL Kosai‘ and is the most commonly occurring type of splenic granuloma.

A thymic origin for the atypical lymphoid cells in infectious mononucleosis was proposed by Sheldon et al. in 1973” and in our cases these cells stained with the T-cell marker UCHL-1. It has been suggested that T-cells are important in the initiation. maintenance and resolu-

tion of granulomas7 and that cytokines, in particular interleukin-1, play a major role.

The subintimal infiltration of splenic vessels by atypi- cal lymphoid cells is recognized4. However, this, together with the medial infiltration seen in our cases, is worthy of emphasis, since it is a feature more usually associated with malignant lymphoid proliferations and may give rise to confusion’.

References Burke IS. Surgical pathology of the spleen: an approach to the diagnosis of splenic lymphomas & leukaemias. A m . I . Surg. f‘a‘ntliol. 19x1 : 5: 68 1-694. Harrison CV. Lymph nodes in infectious mononucleosis. In Har- rison CV ed. H w m t Advntws in Pntltokcig,~/. London: J & A Churchill. 19hh: 2 10. Kothwell DJ. Bone marrow granulomas and infectious mononuc- leosis. Ardi. f’cftllol. 1975: 99; 5(18-509. Neinian KS. Incidence & importance of splenic sarcoid-like granulo- mas. Arb. f’citlrol. I , c ~ J . M d . 1977: 101 : 5 18-52 1. Kuo T. Rosai I . Granulomatous inflammation in splenectomy specimens. Arch. P d o l . I9 74: 98: 26 1-268. Sheldon PJ, I’apamichail M . Hemsted EH. Holborow El. Thymic origin of atypical lymphocytes in infectious mononucleosis. Loticut 1973:i : 1153-1155. Sheffield EA. The granulomatous inflammatory response. /. I’atlrol. 19YO: 160: 1-2.

BRIEF REPORT

Symmetrical fibro-osseous dysplasia of rib - evidence for a traumatic aetiology

D.K.GOULDESBROUGH Department of Pnthology, University o/ Edinburgh, Scotland. UK

Date of submission 1 3 November 1989 Accepted for publication 28 February 1990

Keywords: dysplasia, rib, trauma

Clinically similar lesions in the ribs with atypical histological features are known ’. Reed’ suggested these differ from fibrous dysplasia and a traumatic aetiology for these lesions has been s~ggested’.~. The term sym- metrical fibro-osseous dysplasia was coined4. In this report two cases of fibro-osseous dysplasia are described. Firm evidence for a post traumatic aetiology is presented, one case developing at a previous fracture site.

Introduction Fibrous dysplasia in the rib is an expansile lesion’. Its histology is well established and varies with the site2. Address for correspondence: Dr D.R.Couldesbrough, Department of Pathology, University of Edinburgh. Teviot Place, Edinburgh EH8 9AG. UK.