Spindle-cell tumours and hypoglycaemiathey should bereferred to as spindle-cell tumours associated with hypoglycaemia. There are ultra-structural similarities betweenthese neoplasms

J. clin. Path., 1976, 29, 520-529

Spindle-cell tumours and hypoglycaemiaP. R. MILLARD, D. W. JERROME, AND G. H. MILLWARD-SADLER

From the Department ofPathology, Radcliffe Infirmary, Oxford

SYNOPSIS The light microscopy and clinical features of two patients with extrapancreatic tumoursand hypoglycaemic episodes are described-together with the electron microscopy findings in onepatient. The primary tumour of one patient arose within the skull and later metastasized to the liver,while the other patient had a locally recurrent intrathoracic tumour. Neither the intracranial originnor the ultrastructural features support the concept of a mesothelial origin for these tumours, andthey should be referred to as spindle-cell tumours associated with hypoglycaemia. There are ultra-structural similarities between these neoplasms and those of the pancreatic Pi cells.

Lowbeer (1961) collected 25 examples of large extra-pancreatic non-epithelial tumours associated withhypoglycaemia, and Leger et al (1963) refer to asimilar group of 39 patients. Azzopardi (1966) addedthree further examples, but none of the patients inany of these reviews had a primary intracranialtumour. Also no mention is made in these reportsof electron microscopic appearances. The ultra-structural features could help in tracing the cell oforigin of these tumours which remains a subject ofdebate based on little objective evidence (Leger et al,1963; Boshell et al, 1964). Two further examples oflarge spindle-cell neoplasms coincident with hypo-glycaemia are presented and the ultrastructure of oneis described.

Observations

CLINICAL FEATURES

Case IMrs M. P. (1939-70) was admitted on 11 November1966 in a semicomatose state with weakness of theleft arm and face and gross ataxia. She was 20 weekspregnant. There was a history of an acute transientright-sided blindness in March 1966 and the develop-ment of worsening headaches and vomiting. Herhusband had noticed that she had failing memoryand slurring of speech. After admission her consciouslevel improved but the left pupil became fixed anddilated. A ventriculogram and carotid angiogramshowed a vascular tumour filling the posterior partof the floor of the right middle cranial fossa. This wasremoved on 18 November and postoperative re-

Received for publication 11 November 1975

covery was satisfactory. The operative findings wereconsidered to be insufficient to account entirely forthe patient's symptoms but no blood sugar levelswere measured during this illness. After the birth ofthe child a course of radiotherapy was given. She re-mained well although with a residual right lowermotor neurone facial palsy. A second child was bornin December 1969.

In the following February she noticed increasingtiredness, blurring of vision which often occurred atmid-day, and morning sweats. On 16 March 1970she was found comatose and covered in sweat butafebrile. There was a flaccid tetraparesis with bi-lateral extensor plantar responses and uniformlydiminished reflexes but no meningism or papil-loedema. The liver was enlarged. The neurologicalsigns were disproportionate with her conscious levelwhich spontaneously improved during the day andwas rapidly corrected with 20% intravenous dex-trose and a Horlicks drink. The blood sugar im-mediately before this treatment was 8 mg/dl ofblood. Investigation of the hypoglycaemia includedfasting blood sugars, a glucose tolerance test, aglucogen stimulation test, insulin assay, liver andpancreatic scan, abdominal aortogram, skull x-rayand gamma encephalogram, liver function tests, anda liver biopsy. No lesions were found in the brainor pancreas. Severe hypoglycaemia was confirmedand rounded vascular deposits taking up seleno-methionine were demonstrated in the liver. Tests ofliver function were within normal limits and tumourwas included in the liver biopsy. No evidence of dis-semination of tumour to other sites was found andafter removal of the patient's own liver an ortho-topic liver transplant was performed.The immediate postoperative recovery was un-

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Spindle-cell tumours and hypoglycaemia

eventful, but later a bile leak developed and repeatedattempts to correct this failed. She died 82 days afterthe operation with a severe chest infection.

Case 2Mrs N. R. (1907-73) worked from 1948 to 1953 as asecretary next door to an asbestos factory. A symp-tomless right-sided lesion was recorded on a chest x-ray in 1961 but was not investigated. She becameprogressively unwell during 1967 with shortness ofbreath and loss of one stone (6-4 kg) in weight. Asix-pint, sterile, right-sided pleural effusion wasdrained and malignant cells were identified. By thefollowing October she was having attacks of un-consciousness of 15 min to 24 h and was becomingaggressive and confused and slurring her speech.The pleural effusion had recurred but there were noabnormalities in the cerebrospinal fluid or incarotid angiograms. A blood sugar level of 40 mg/dlof blood was recorded during one of these attacksand there was a marked improvement followingintravenous glucose. Investigations for hypoglycae-mia included fasting blood sugars, a glucose toler-ance test, and a glucagon stimulation test, a tolbut-amide tolerance test and insulin assay (these resultsare discussed by Spry et al (1968)). Resection of theright intrathoracic tumour was undertaken on 27November 1967 and the postoperative recovery wasuneventful.During 1968-73 she developed dizziness which was

most marked after exertion. Blood sugar levels re-mained within normal limits but did reach 55 mg/dlof blood after a fast of 72 hours. A chest x-rayduring 1970 showed a further right-sided mass whichslowly increased in size. In June 1973 because of theprogressive worsening of the dizziness she was re-investigated for hypoglycaemia, but no abnormalityapart from the intrapleural tumour was found. Atthis time there was a slight slurring of speech, anataxic gait, and a decrease in power of the proximalmuscles of the lower limbs. The mass in the chesthad increased in size and was removed on 6 July 1973together with the lower lobe of the right lung. Post-operatively she was difficult to wean from therespirator and developed pulmonary oedema, achest infection, and pulmonary emboli. She died 12days after the thoracotomy.

PATHOLOGYTissues were fixed in 10% neutral buffered formalinsolution, and 5 ,m sections were stained withHarris' haematoxylin and eosin and by specialstaining procedures including reticulin preparations.Tissues (1 mm3) for electron microscopy were fixedin phosphate buffered 4% glutaraldehyde (pH 7 4)at 0-40C followed by washing in phosphate buffer

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and post fixation in phosphate buffered 1 % osmiumtetroxide at 0-40C. The blocks were processed andembedded in Araldite. Sections were double stainedwith 2% aqueous uranyl acetate and lead citrate andexamined with a Philips EM 200. Necropsy includedinspection of the thoracic and abdominal viscera andof the brain.

Case 1The intracranial tumour consisted of lobulatedfragments measuring up to 6-5 x 6-0 x 4 5 cm withfirm pale grey surfaces which included roundnodules. Light microscopy showed a cellular spindle-cell tumour (fig 1). The cells were uniform but withmany mitoses and little cytoplasm. They were ar-ranged in loose interweaving bundles supported byreticulin and separated by numerous capillaries (fig2). The diagnosis of angioblastic meningioma wasmade.The liver biopsy specimen and the features in the

tumour in the hepatectomy specimen were compar-able to one another and to those above. The livernodules were rounded and sharply demarcated fromthe investing liver with firm homogeneous whitesurfaces (fig 3). At necropsy there was jaundice,oedema of the legs, multiple recent abdominalsurgical incisions, and an ileostomy. The trans-planted liver was bile stained and all the vascularanastomoses were intact and patent. Parts of thecommon bile duct were necrotic and there was afistula associated with the enteroenterostomy formedfrom a jejunal loop anastomosed to the fundus of thegall bladder. The stomach had a perforated ulcerinfiltrated by fungus and a fibrinous exudate coveredthe peritoneal cavity and gut. Discrete areas ofnecrosis were seen in the pancreas and small friablevegetations were adherent to the mitral valve cusps.Thrombus occluded both femoral and external iliacveins. The lungs were oedematous with many smallarteries occluded by embolus infiltrated by a Candidaand Aspergillus species. Cytomegalovirus inclusionbodies were present in the alveoli. A single paratra-cheal lymph node was replaced by tumour like thatin the patient's own liver. A superficial cyst, 3 cmdiameter, containing clear fluid was found adjacentto the right Sylvian fissure but there were no otherchanges in the brain or skull.

Case 2The tumour removed at the first thoracotomy (1270g)had lobulated firm white surfaces with smallscattered foci of necrosis. It was very cellular withnumerous blood vessels and abundant fibrous tissue.Within the fibrous tissue there were moderatenumbers of uniform spindle cells while in otherareas the cells were markedly pleomorphic and often



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P. R. Millard, D. W. Jerrome, and G. H. Millward-Sadler

Fig I Case 1.Intracranialtumour withinterweavingspindle-cellpattern.Haematoxylinand eosin x 43.

Fig 2 Case 1.High-powerview of spindle-cell tumourcells offigure 1.H and E x 104.

harboured bizarre nuclei. A moderate number ofmitoses were present. The cells were in bundles in-timately intertwined among the supporting vascularand reticular framework (fig 4). The tumour mass

(278 g) removed at the second thoracotomy wasessentially similar (figs 5 and 6).

Electron microscopy of the recurrent tumour massrevealed two types of cell which were arranged in

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Spindle-cell tumours and hypdglycaemia

1 2 5 4 5 6 7 8 9 10 f1 12 13 14 15 1b 17 8cm

groups with some separation by vascular channels,collagen, and reticulin (fig 7). These two types oc-curred in apparently equal proportions althoughtheir distribution was variable in any one field. Onetype of cell had a darkly staining large, irregularlyindented nucleus. The cytoplasm was scanty and wasoccupied by mitochondria, dilated rough endo-plasmic reticulum, and Golgi apparatus, but therewere no microvilli or granules (fig 7). The other type

Fig 3 Case 1. Parasaggitalsection of liver with circum-scribed tumour nodules separatedby abundant normal liver.

Fig 4 Case 2.r5zrc.t Original intra-

thoracic tumourwith interweaving

8t m spindle-cellpattern-comparewith figure 1.

~~ ~HandE x 14.

of cell had a paler staining nucleus but was of asimilar size although with a greater amount of cyto-plasm. Occasional microvillus-like processes pro-jected from the plasmalemma. The cytoplasm con-tained mitochondria, undilated rough endoplasmicreticulum, Golgi apparatus, and many fine filaments(fig 8). In some of these cells a few dense granules ofvariable diameter and surrounded by a closely ap-posed single limiting membrane were also seen (figs 7

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-. t , Fig 5 Case 2.Rcrrent tumour

/ - ~~~~~~~~~~~withsimilar0 features to those in

AA' ~~~~~~~~~figures 1 and 4.BEP;M HHandE x 14.

Z 4.s 8~~~~~~~Z

W f

Fig 6 Case 2.High-power view

AL. ~~~~~~~~~~~~~~~~~~~~~ofrecurrentspindle-cell

~# tumour with9 abnormal mitosis

APP.~~ ~ ~ ~ ~ ~~ lower centre.~~~~~~~~~~~~~~~~~~~~~H -and E x 85.

.~~~~~~~~~~~~~~~~~~~ 01

and 9). A solitary giant cell was found among these right thoracotomy incision was healing and theretwo main groups of cells. was an open tracheostomy. The lower lobe of theAt necropsy the fingers of both hands were right lung had been removed and the other lobes of

clubbed and there was bilateral leg oedema. The both lungs were oedematous with emboli in some

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t_ z t._ s w. W ._f t t. A a_r k;t o; ivw__*e. 2 <_ .+c. .

4 :4:. w

., ts 'wk *stX' Ii. B.S s x e' *.+N s s >t; v g4vk ^'tO 'Ss

Fig 7 Dark and light tumour cells with a few granules in the light cell on the right-hand side. x 3955.

smaller arteries. Small granular vegetations wereloosely adherent to the mitral and aortic valves,and partly occlusive thrombus occupied the inferiorvena cava from the right femoral vein to the junc-tion of both renal veins. The liver was fatty, andsmall areas of necrosis were seen in the pancreas. Nolocalized lesions or metastatic tumour were found inany of the other organs including the brain.

Discussion

Extracranial spread of meningeal tumours is welldocumented (Simpson, 1957; Kruse, 1961) butneither of these reports includes examples of hypo-glycaemia co-existent with a primary intracranialtumour or with their extracranial metastases. Case 1may provide such an example, although without pre-

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17.~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Fig 8 Light nuclear staining cell with abundant fine filaments, rough endoplasmic reticulin, and mitochondria. Twomicrovilli extendfrom the plasmalemma (upper centre and upper right). x 30 360.

operative blood sugar levels absolute proof is lack-ing. Hypoglycaemia and this intracranial tumourcould have accounted for the clinical state of thepatient since the impression following the operativefindings was that the size and position of the tumouralone were insufficient to explain satisfactorily theclinical observations. Among Simpson's (1957) 12patients with tumours diagnosed as angioblasticmeningiomas no extracranial spread developed andin none was there any evidence of local tumour re-

currence . Kruse (1961) encountered a single exampleof extracranial spread among his eight similarcases. The possibility must be considered that case 1had had two primary tumours, intracranial andhepatic, only the hepatic neoplasm inducing hypo-glycaemia, or that the hepatic lesions were meta-static from a further extracranial site. The macro-scopic distribution and appearances of the intra-hepatic lesions (fig 3) and the failure at necropsy tofind an alternative primary site are against these

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Fig 9 Light nuclear staining cell with dense granules in the cytoplasm. x 23 000.

hypotheses. Further, the histological similarity be-tween the intracranial and the intrahepatic growthalso favours the view that the liver lesions repre-sented metastases from the intracranial tumour. Themode of spread appeared to be vascular but, in viewof the lymph node involvement at necropsy, lym-phatic dissemination is also implicated. This lymphnode metastasis could alternatively have arisen fromdissemination during liver transplantation and thesubsequent surgery.

The course and light microscopy findings in case 2are like those in the patients reviewed by Lowbeer(1961) and Azzopardi (1966). These patients hadlarge extrapancreatic tumours which were usuallyretroperitoneal but also developed in other sites. Onlight microscopy spindle cells were predominant in avascular fibrous stroma, and all the patients ex-perienced hypoglycaemic episodes. Azzopardi (1966)considers the behaviour and appearance of thesetumours as typical of a fibroblast and the structure

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to be that of a 'fibrous mesothelioma'. This termin-ology implies a mesothelial-cell origin. Meso-thelial cells may be facultative fibroblasts and thesetumours fibroblastic but the concept that the cellorigin is mesothelial seems discredited by the pos-sibility of a primary intracranial or even hepatic neo-plasm in case 1. The electron microscopic features ofcase 2, also, are unlike those of normal fibroblasts(Rhodin, 1967). Wang (1973) described the ultra-structure of pleural mesotheliomas in four patients.His findings differ from ours in that two cell typeswere not recognized, and the cells from his patientswere distinguished by either many brush-like micro-villi or by pseudopod extensions of their cyto-plasm. Only a few microvilli were apparent and onlyin some of the tumour cells of case 2. If the assump-tion that the similarity between the primary growthand its recurrence applies to the electron microscopyfeatures is correct then the tumour of case 2 is notclosely akin to those described by Wang (1973) andmay not be a true mesothelioma. The granules foundin some of the tumour cells are also in marked con-

trast to Wang's observations.Various types of granule are found in the cells of

pancreatic islets and within some pancreatic neo-

plasms (Like, 1967; Greider et al, 1970). Thesegranules form a heterogeneous group but there are

salient features to those in normal P and a cells. Thecell granules have a clear area dividing the granule

from its limiting membrane while the granules in thea cells show a wide spectrum of diameter within any

one cell. The granules in the recurrent tumour ofcase 2 are not separated from their limiting mem-

brane by a clear space but do demonstrate variablediameters. The functional effect of the originalgrowth was hypoglycaemia and any similarity be-tween the tumour cells and normal cells should bewith pancreatic P cells but ultramicroscopic studiesof pancreatic insulin-producing tumours have shownthat a close comparison between the tumour granulesand those of cells is not always apparent (Greiderand Elliott, 1964). The electron microscopic featuresin case 2 are therefore consistent with an insulin-secreting growth, and the small number of granulesmay account for the clinical difficulty in producinghypoglycaemia. It is likely that patients with markedhypoglycaemia have a greater number of granule-containing cells in their tumours. These commentsimply a close similarity between the tumours of case2 and tumours of 3-cell origin. Further support forthis lies in the comparable ultrastructure of an

insulinoma described by Greider and Elliott (1964)and the recurrent neoplasm of case 2. This insulin-oma included similar granules and was formed ofboth light and dark cells. However, we have not in-vestigated the characteristics of the granules in case

2 or demonstrated that they have any functionalsignificance.The variance noted between the tumours reported

by Wang (1973) and those in this report must querya mesothelial origin and discredit their presentnomenclature. The term mesothelioma has becomesynonymous with growths secondary to asbestos ex-posure (Hourihane, 1964; Selikoff et al, 1965;Mortimer and Campbell, 1968; McDonald et al,1970) but there is insufficient evidence to includeeither of the patients in this report in that category.Case 1 had no history to suggest such an exposureand case 2, who had worked adjacent to an asbestosfactory, was thoroughly investigated by the Pneumo-coniosis Panel but no adequate proof of significantasbestos exposure was found.No suitable appellation for this group of hypo-

glycaemic producing tumours arises from theseobservations, and the findings in these two casescast considerable doubt on the validity of that atpresent in use. Until a more precise origin of thegrowths is defined it may be more descriptively exact,although cumbersome, simply to refer to them asspindle-cell tumours associated with hypoglycaemia.

We should like to thank the many medical andtechnical staff of both Oxford and Cambridge whohave given their help.

References

Azzopardi, J. G. (1966). Systemic effects of neoplasia. InRecent Advances in Pathology, 8th edition, edited by C. V.Harrison, pp 146-153 Churchill, London.

Boshell, B. R., Kirschenfeld, J. J., and Soteres, P. S. (1964).Extrapancreatic insulin-secreting tumor. New Engl.J. Med., 270, 338-341.

Greider, M. H., Bencosme, S. A., and Lechago, J. (1970).The human pancreatic islet cells and their tumors. 1.The normal pancreatic islets. Lab. Invest., 22, 344-354.

Greider, M. H. and Elliott, D. W. (1964). Electron micro-scopy of human pancreatic tumors of islet cell origin.Amer. J. Path., 44, 663-678.

Hourihane, D. O' B. (1964). The pathology of mesothelio-mata and an analysis of their association with asbestosexposure. Thorax, 19, 268-278.

Kruse, F., Jr. (1961). Hemangiopericytoma of the meninges(angioblastic meningioma of Cushing and Eisenhardt):clinicopathologic aspects and follow-up studies in 8 cases.Neurology, 11, 771-777.

Leger, L., Sors, C., Dubost, C., Magdelaine, M., Lejeune, J.,Roseau, E., and Lemaigre, G. (1963). Les hypoglyc6miesdes tumeurs mesenchymateuses extra-pancr6atiques. Presseme6d., 71, 219-222.

Like, A. A. (1967). The ultrastructure of the secretory cells ofthe islets of Langerhans in man. Lab. Invest., 16, 937-951.

Lowbeer, L. (1961). Hypoglycemia-producing extra-pancreatic neoplasms. Amer. J. clin. Path., 35, 233-243.

McDonald, A. D., Harper, A., El Attar, 0. A., andMcDonald, J. C. (1970). Epidemiology of primary malign-ant mesothelial tumors in Canada. Cancer (Philad.), 26,914-919.

Mortimer, R. H. and Campbell, C. B. (1968). Asbestos ex-

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posure and pleural mesotheliomas. Med. J. Aust., 2, 720- Simpson, D. (1957). The recurrence of intracranial menin-722. giomas after surgical treatment. J. Neurol. Neurosurg.

Rhodin, J. A. G. (1967). Organisation and ultrastructure of Psychiat., 20, 22-39.connective tissue. In The Connective Tissue, edited by Spry, C. J. F., Williamson, D. H., and James, M. L. (1968).B. M. Wagner and D. E. Smith, p. 1. Williams and Pleural mesothelioma and hypoglycaemia. Proc. roy. Soc.Wilkins, Baltimore. Med., 61, 1105-1107.

Selikoff, 1. J., Churg, J., and Hammond, E. C. (1965). Rela- Wang, N. S. (1973). Electron microscopy in the diagnosis oftion between exposure to asbestos and mesothelioma. pleural mesotheliomas. Cancer (Philad.), 31, 1046-1054.New Engi. J. Med., 272, 560-565.

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TECHNICAL BULLEnNS (price £1 -00/$2.00 each)9 Determination of Urea by AutoAnalyzer November1966 RUTH M. HASLAM

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35 Investigation of the Validity of Temperature Cor-rection Factors for Serum Aspartate and Alanine Trans-aminases March 1975 s. B. ROSALKI et al.36 Factors Influencing the Assay of Creatinine,November 1975 J. G. H. COOK

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Spindle-cell tumours and hypoglycaemiathey should bereferred to as spindle-cell tumours associated with hypoglycaemia. There are ultra-structural similarities betweenthese neoplasms