Vol. 6. No. 1. FEBRUARY, 1953 'CURR. LIST MED. LIT." ° JOURNAL OF CLINICAL PATHOLOGY EDITED FOR THE ASSOCIATION OF CLINICAL PATHOLOGISTS By A. GORDON SIGNY EDITORIAL BOARD E. N. ALLOTr R. J. V. PULvERTAFF J. V. DACIE DOROTHY S. RUSSELL J. G. GREENFIELD JOAN TAYLOR And the Editor of the British Medical Journal FORCES\ {{MAR 12 1953 MEDICALD LONDON BRITISH MEDICAL ASSOCIATION TAVISTOCK SQUARE, W.C.jI YEARLYTSUBSCRIPTON (4 NUMBERS) £2 2s. U.S.A. $7.00 SINGLE NUMBERS 12s. 6d. uadt Qu0rto
This section of the JouRNAL is published in collaboration with the abstracting journal, ABSTRACTS OF
WORLD MEDICINE, published by the British Medical Association. In this JOURNAL some of the more
important articles on subjects of interest to clinical pathologists are selected for abstract, and
these are classified into four sections; bacteriology; biochemistry; haematology; and morbid anatomy
and histology.
BACTERIOLOGY
Studies of Coxsackie Viruses: Observations on Epi-demiological Aspects of Group A Viruses. COLE,R. M., BELL, J. A., BEEMAN, E. A., and HUEBNER,R. J. (1951). Amer. J. pubi. Hith, 41, 1342.During 14 months, periodic testing for Coxsackie
viruses in faeces obtained from all the members of asmall community around Washington, D.C., resulted inthe isolation of Group A viruses from 149 of 2,670faecal specimens from 1,232 persons. One specimenhad two immunological strains, the rest a single strain.Group A viruses were found in 99 people, and 7 immuno-logical strains were identified. In cases of herpanginaGroup A viruses were found in 24 of 68 throat swabsand 13 of 33 rectal swabs. Viruses could not be isolatedfrom the blood in the acute phase of herpangina, norfrom cerebrospinal fluid, urine, blood, or necropsyspecimens in other diseases.
Viruses usually persisted in the host for less than amonth, but were occasionally present after 11 weeks.No reinfection with the same strain occurred, but doubleinfection did occur with two different immunologicalstrains. Infection spread by direct contact, family andneighbour contacts having the same type of virus.The distribution of the virus was not related to sex or
colour, and was 3 times as common below the age of 9years as above it. The maximum incidence was inAugust and September. Group A viruses were isolatedfrom 31 of 710 healthy people and 10 of 425 patientssuffering from diseases other than herpangina. In thelatter disease they were found in 41 of 45 cases and in17 of 44 healthy family contacts. No Group A virusescould be isolated from 170 cases of poliomyelitis.
Herpangina was found to be an epidemic diseaseoccurring in small outbreaks in most years from Augustto October, and spreading by direct contact with infectedpersons. It occurred essentially in children, mostly underthe age of 4 years, and was not related to sex or colour.The incubation period, determined from a study of 17cases, varied from 1 to 9 days, averaging 4 days. Secondattacks with a different strain happened occasionally.Asymptomatic and convalescent carriers existed. Of the7 strains of Group A virus, 6 were isolated from herp-angina cases, and it was concluded that this disease iscaused by Group A Coxsackie viruses. M. Lubran.
G
An Outbreak of Epidemic Pleurodynia, with SpecialReference to the Laboratory Diagnosis of CoxsackieVirus Infections. LAZARUS, A. S., JOHNSTON, E. A.,and GALBRAITH, J. E. (1952). Amer. J. publ. HIt/,42, 20.
In September, 1950, an outbreak of pleurodyniaoccurred at Hoquiam, in the State of Washington. Bythe end of the month about 50 cases had been recorded,a known morbidity rate of about 5 per 1,000 of thepopulation. The main symptoms were fever, abdominalpain, nausea and vomiting, headache, stiffness of theneck, and soreness of the throat, chest, and limbs. Allpatients recovered without sequelae after periods rangingfrom a few days to 2 weeks. About half the patientswere below the age of 10 and almost three-quarters wereunder 20 years of age.
Specimens of faeces were obtained from 15 patientswith typical symptoms and ground with sterile alundumand distilled water, centrifuged at low speed, and thesupernatant fluid treated with ether at 40 C. overnight.The ether was subsequently removed by vacuum. Theextracts, proved free from bacteria, were then inoculatedintracerebrally and intraperitoneally into 2- or 3-day-oldmice. Animals which then showed paralysis or tremorswere killed, and pooled suspensions of brain and musclewere passed into a second series of mice. In this way4 strains of virus were isolated from the 15 specimens,while 5 questionable strains were also obtained. Thesenewly isolated strains were identified as Group-B Cox-sackie viruses on the basis of their ability to producesymptoms in very young mice and their inability to infectweaned animals of the same strain. The pathologicalchanges in the tissues of infected animals also corre-sponded with descriptions given by previous workers.
In order to compare the antigenic relationships amongthe 4 newly isolated strains of virus, infant mice bornof vaccinated mothers were employed. Virgin femalemice were given repeated inoculations of live virus.They were then mated and the resultant litters werechallenged with the homologous strain of virus, as wellas with the other 3 strains. The results showed that theunweaned mice of vaccinated mothers were resistant toseveral thousand LD50 of each of the 4 strains ofCoxsackie virus, while normal control mice became ill in3 to 4 days and died with typical symptoms. Thus
ABSTRACTS
there was a very close if not identical antigenic relation-ship between the 4 strains of virus.To demonstrate a relationship between the clinical
illness and the virus isolated from stools of patients,neutralization tests were carried out with a constantamount of Coxsackie Group-B virus and varyingamounts of serum. Paired serum specimens fromtypical cases invariably showed a marked rise in theeneutralizing antibody titre, and single specimens obtainedduring convalescence showed a significant degree ofability to neutralize the test dose of the virus.
R. B. Lucas.
Studies on Poliomyelitis in Ontario-V. Further Observa-tions on the Recovery of Coxsackie Viruses fromCases of Clinical Poliomyelitis. SILVERTHORNE, N.,ANGLIN, C., MCKENDRY, J. B. J., KNOWLES, D. S.,CLARK, E. M., SHIMADA, F. T., RHODES, A. J., Roy,T. E., RITCHIE, R. C., and DONOHUE, W. L. (1951).Canada med. Ass. J., 65, 536.During 1950 the authors examined 22 children ad-
mitted to the Hospital for Sick Children, Toronto,suffering from clinical poliomyelitis. Detailed laboratorystudies were carried out with a view to differentiatingclinically between Coxsackie and poliomyelitis infectionsand to determining the frequency with which Coxsackieinfections simulate poliomyelitis.The cases in which Coxsackie viruses were isolated
from the stools and those in which they were not couldnot be distinguished on clinical grounds. From thestools of 8 patients, 8 strains of Coxsackie virus wererecovered; 6 of these strains produced well-markedmyositis in 3-day-old mice, and 2 strains producedlesions in fatty and brain tissue. Tests for homologousantibody were carried out on sera obtained during theacute and convalescent stages from 5 of the patientswhose stools contained strains producing myositis inmice. Antibody to the strain of virus isolated from thestool was found in the convalescent phase in 4 of these,and in 2 cases a well-marked rise in antibody titreoccurred during convalescence. Homologous antibodywas present in the serum during the acute phase in theother 2 patients, but did not increase in the later samples.However, these 2 sera were obtained 9 days after theonset of the illness. One patient excreted Coxsackievirus, but samples of serum collected 11 and 49 daysafter onset contained no demonstrable antibody. Theserological results suggest that 4 of the patients excretingCoxsackie virus had definitely been infected with it;2 of these patients, who had paralytic symptoms, alsoexcreted poliomyelitis virus; the other 2 patients did notexcrete poliomyelitis virus, and appeared clinically tosuffer from an attack of non-paralytic poliomyelitis.Exactly one-half of the total number of patients sufferedfrom paralytic poliomyelitis, and poliomyelitis viruswas isolated from the stools of all, whereas of the 11patients with non-paralytic poliomyelitis Coxsackievirus was recovered from the stools of 5, but in no casecould poliomyelitis virus be isolated.The authors conclude that in Toronto in 1950 a
substantial number of all patients with poliomyelitis,
paralytic or non-paralytic, were excreting Coxsackievirus and that many of those patients diagnosed assuffering from non-paralytic poliomyelitis were probablyin fact infected with Coxsackie virus and not with thatof poliomyelitis. They suggest that the double excretionof poliomyelitis and Coxsackie viruses probably meansonly that the two infections have similar epidemiologicalcharacteristics. K. S. Zinnemann.
Intrathecal Chloramphenicol in Staphylococcal Menin-gitis Resistant to Penicillin and Streptomycin. ANDER-SON, K. F., and ELLIS, F. G. (1951). Brit. med. J., 2,1067.The authors describe 2 cases of secondary staphylo-
coccal meningitis treated by intrathecal chloramphenicol.Pure synthetic crystalline chloramphenicol was used andwas dissolved in distilled water to give a final concen-tration of 100 pg. per ml. (The range of inhibitingconcentration for the Staphylococcus agrees appearsto be between 1 and 16 Kg. per ml.) It was found thatthe solution would withstand boiling for 5 hours withoutmeasurable loss of potency.
In the cases reported the meningitis was secondary tooperations for the removal of a cerebellar haemangio-blastoma in one and an acoustic neuroma in the other.In both cases the Staph. aureus causing the infection wasboth penicillin- and streptomycin-resistant, but sensitiveto chloramphenicol. In the first case the staphylococcuswas also sensitive to aureomycin, but it is of interest tonote that the meningitis developed while the patient wason full doses of this drug.A full clinical description of both cases is given. In
the first case intrathecal injections of chloramphenicolwere started at 100 pg. daily and gradually increasedover 19 days to 750 ,ug. The concentration of the drugintrathecally increased from 10 pg. per ml. at the begin-ning to 40 f.g. at the end of treatment. The injectionswere well tolerated, but the clinical response, thoughsatisfactory, was rather slow. In the light of thisknowledge the second patient was given 600 ,ug. intra-thecally as an initial dose: this was rapidly increased to750 Kg. in 6 days. The concentration achieved was40 pg. per ml. on the third day of treatment, and theclinical response was immediate and spectacular, duefirst, in the authors' opinion, to the high cerebrospinal-fluid level achieved at the onset of the meningitis, butalso to the fact that this case was not complicated byloculated infected fluid, as was the first.Both cases indicate that maximal titres in the cerebro-
spinal fluid were not achieved by oral administrationalone, and it would appear, therefore, that an intrathecaldose of 750 ftg. daily in combination with oral admini-stration is capable of rapidly raising the cerebrospinal-fluid level to a figure in the region of 40 Kg. per ml.
In an addendum the authors state that they have sub-sequently given intrathecal doses of chloramphenicol ashigh as 3 mg. without undesirable results, although if thisdose is continued for a week they have noticed depressionand tearfulness, and in patients with cerebellar lesionsan increase of tremor. These side-effects disappearedwhen the treatment was stopped. J. V. Armstrong.
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ABSTRACTS
BIOCHEMISTRY
A Metabolic Study of the Disturbances Taking Placeduring Diabetic Coma and its Treatment, with SpecialReference to the Changes in Potassium Metabolism.[In English.] WILLEBRANDS, A. F., GROEN, J., andFRENKEL, M. (1952). Acta med. scand., 141, 331.
An earlier study (Frenkel et al., Arch. intern. Med.,1947, 80, 728) of a patient in diabetic coma in whommuscular weakness and respiratory and cardiovasculardisturbances occurred during treatment and wereassociated with a low serum potassium level led theauthors to examine further the question of potassiummetabolism in diabetic coma in 3 men and 2 women.The blood sugar levels ranged from 175 to 920 mg. per100 ml. on admission. After initial intensive treatmentwith insulin and intravenous saline, followed by oralfluids, a diet consisting of rice, butter, and sugar, chosenbecause of its low potassium and nitrogen content, wasgiven for periods of 1 to 12 days. Potassium was addedto the mixture during the latter part of the period in 2cases, and casein and desiccated beef serum were addedfor the last 2 days in a third case to increase the nitrogenintake without significantly increasing that of potassium.During coma, the serum sodium and chloride levels
were almost normal in all cases, and in 3 cases in whichthe alkali reserve was low and dehydration severe theserum potassium level was high. In all cases the serumpotassium level fell below the normal during treatmentof coma, though there was no clinical evidence ofpotassium depletion, reaching the lowest level (2.5 to3.0 mEq. per litre) after 1 to 3 days. This hypopotass-aemia persisted for several days, even when the diet wassupplemented with potassium. At the same time theurinary potassium content, high during coma, fellduring treatment and remained well below normal forsome days, there being potassium retention in all cases.The negative nitrogen balance of coma was quicklyrestored by treatment, and equilibrium was reached bythe second day. The authors suggest that the fall in theserum potassium level was not due entirely to dilution ofthe extracellular fluid by the saline administered intra-venously, but because the intracellular fluid lost,together with potassium, during coma has to be madeup, and potassium is required in the process of glucosedeposition in the liver and muscles under the action ofinsulin. In the absence of nitrogen retention it can be-assumed that none of the potassium retained was dueto replacement of tissues destroyed during coma.
Phosphate excretion was also high in coma, decreasedrapidly, and returned to normal with the introductionof phosphate in the diet, equilibrium being reached in2 days. The deficit of phosphate was estimated at about1.0 g. and that of potassium was 10 to 12 g., and was
made up in 4 to 6 days. A high blood urea level withlow blood pressure was found in 2 cases, and led theauthors to suggest that severe coma may cause adrenalcortical hypofunction and so lead to changes in potas-sium metabolism. The absence of clinical signs ofpotassium depletion was due to the fact that the serum
level in all cases was above 2.5 mEq. per litre. The
authors did not think that administration of potassiumin large doses was advisable in diabetic coma in view ofthe possible induction of cardiac irregularities, but theyconsider that foods containing potassium ought to begiven as early as possible.Diurnal Variations in Electrolyte Excretion. STANBURY,
S. W., and THOMSON, A. E. (1951). Clin. Sci., 10, 267.After briefly reviewing the literature concerning
diurnal variations in electrolyte excretion the authorsdescribe their own findings in more than 80 observationson 12 healthy subjects. Urinary excretion, under basalconditions, of sodium, potassium, chloride, and bicar-bonate ions was found to follow a similar pattern throughthe day in each individual, this pattern remaining con-stant for periods up to 2 years and 2 types of patternbeing distinguishable. In all the individuals observedelectrolyte excretion was lowest during sleep, increasingprogressively after waking to reach its height at aboutmidday. Thereafter the high rate of excretion was, insome subjects, sustained until sleep again produced amarked fall, whereas in others excretion fell off duringthe afternoon or evening, to fall still lower with the onsetof sleep. The tides of electrolyte excretion were remark-ably constant, being little affected by such variousfactors as activity, posture, meals, water diuresis, saltdepletion (for as long as 9 days), prolonged fluid restric-tion, temporary disturbances of sleep rhythm, andadministration of hormones (pituitary antidiuretic hor-mone, ACTH, and deoxycortone). The only factor thatwas found to disrupt this diurnal rhythm completelywas the induction of alkalosis, either by ingestion ofbicarbonates or by hyperventilation. A close correlationwas found between variations in electrolyte excretionand those in urine flow and in urinary pH.Changes in the glomerular filtration rate, as judged by
the inulin and creatinine clearances, were too insignificantto account for the wide diurnal changes in electrolyteexcretion, and the authors consider tubular reabsorptionto be the mechanism principally responsible. Pituitaryand adrenal hormones do not appear to play any part inthe production of these diurnal variations.
A. Swan.
Observations on the Alterations in Electrolytes andFluid Balance in Patients with Cirrhosis of the Liverwith and without Ascites. RICKETTS, W. E., EICHEL-BERGER, L., and KIRSNER, J. B. (1951). J. c/in. Invest.,30, 1157.Changes in the electrolyte metabolism were studied
in 7 cases of hepatic cirrhosis-4 with oedema andascites and 3 without these complications. The diagnosiswas confirmed in all cases by needle biopsy. There were2 normal controls. The results showed that: (1) sodiumchloride excretion in the urine is decreased in cirrhosis ifascites is present, but not otherwise; (2) it is the sodiumion which is important in fluid retention; and (3)restriction of salt in the diet is indispensable in caseswith ascites if frequent repetition of paracentesis and theuse of diuretics are to be avoided. These findings con-firm those of a number of other authors reported since1948. J. W. McNee.
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MORBID ANATOMY AND HISTOLOGY
The " L.E. Cell" and its Significance. SMITH, P. A. J.(1952). Brit. J. Derm., 64, 10.The author gives a review of the work done on the
demonstration of the " L.E. cells" in blood and bone-marrow preparations from cases of acute disseminatedlupus erythematosus, describes 6 illustrative cases, anddiscusses the significance of the phenomenon. The L.E.cell is a polymorphonuclear leucocyte containing a round,homogeneous mass of ingested nuclear material whichstains identically with the haematoxylin-bodies found inthe viscera, and its appearance in normal bone marrow
may be induced by the addition of a factor associatedwith the serum gamma globulin in cases of the disease.Methods used for the demonstration of the cells andthe results obtained are recounted.Of the cases described, 5 illustrate the clinical types
giving rise to the phenomenon, while the sixth illustratesthat it is not always possible to demonstrate the pheno-menon even in undoubted cases of systemic lupus ery-
thematosus. The detection of another factor in theserum in many cases of lupus erythematosus, and also ofrheumatoid arthritis, which agglutinates sensitized sheep'serythrocytes suggests that there may be some relationshipbetween the two conditions, while two of the cases
described serve to draw attention to the possible con-
nexion between systemic lupus erythematosus and tuber-culosis on the one hand, and the deep mycoses on theother.More widespread use of the L.E. tests has probably
been prevented hitherto by the difficulty of obtainingbone-marrow specimens, but it is suggested that if thesimpler methods using peripheral blood prove satisfac-tory, repeated tests should be carried out in all types oflupus erythematosus and in other conditions, withparticular reference to systemic fungus infections,tuberculosis, streptococcal infections, and drug sensi-tivity.
Primary Neoplasms of the Epididymis. Special Referenceto Adenomatoid Tumours. LONGO, V. J., MCDONALD,J. R., and THOMPSON, G.J. (1951). J. Amer. med. Ass.,147, 937.Primary tumours of the epididymis are rare, reports
of only 134 cases having been found in the literature.Three-quarters of these tumours were benign. To thislist the authors add 19 cases, all of them benign, seen
at the Mayo Clinic during 39 years.
In the cases previously reported the commonestprimary neoplasm of the epididymis was a benignadenomatoid (mesothelial) tumour, and this form was
also found in 17 of the 19 cases now described, thegrowth in the other 2 cases being a leiomyoma. Leio-myoma is the second commonest benign tumour of theepididymis, and was present in 10% of all cases ofprimary neoplasm of that body hitherto reported, theremainder consisting of lipoma, fibroma, dermoid cyst,adrenal cortical adenoma, cholesteatoma, and benignvascular tumours.
Adenomatoid tumours are small and slow-growing,and are commonly situated in the tail of the epididymis,giving rise to no symptoms. They are usually discoveredin middle-aged patients, either adventitiously or duringphysical examination. They are neither multiple norbilateral. Trauma and venereal disease have no partin their aetiology. They are globular, encapsulated,and firm, the cut surface presenting a whorled appearancelike that of a uterine fibroid. The microscopic detailis described and appears to favour the theory of theepithelial origin of these tumours. Adenomatoidtumours have been found in the ovary, Fallopian tube,uterus, spermatic cord, and testicular tunic; they havenever been seen in parts remote from the mesonephron.The differential diagnosis is from chronic inflammation,testicular neoplasm, and spermatocele. Treatment isby removal of the tumour, epididymectomy, or orchid-ectomy.Of the malignant tumours, sarcoma occurs twice as
commonly as carcinoma, and pain is a more prominentfeature than with benign tumours. The average post-operative survival time is 1j years in the case of car-cinoma, and even less for sarcoma.
[This paper, which is illustrated by good photomicro-graphs, is an important communication on a little-discussed subject. Three standard textbooks of patho-logy consulted by the abstracter give only the vaguestgeneralizations.] W. Skyrme Rees.
Maligunt Tumours of the Testes. PELOT, G., andHEBRARD, H. (1951). J. Urol. Med. Hyg., 57, 480.
The authors have studied 162 cases of testicularmalignancy treated at the Military Hospital at Val-de-Grace since 1935. They note a considerable number ofcases of retained testis and of injury to the organs pre-ceding the appearance of a neoplasm, and they alsoobserve that trauma tends to increase the rate of growthand to promote metastasis. They consider too thatatrophy of the gland often precedes the onset of a
neoplasm.The histological and pathological types of malignant
disease of the testis are grouped under two heads: (1)seminoma (60.6%); and (2) " dysembryoma" (39.4%),the latter group embracing all tumours of embryologicalorigin, such as teratomata and mixed tumours. Theauthors observe that the seminomata are on the wholeless malignant than the dysembryomata, though theytend to be equally malignant before middle age.
Intracranial Tumours with Extracranial Metastases.WINKELMAN, N. W., CASSEL, C., and SCHLESINGER, B.
(1952). J. Neuropath. exp. Neurol., 11, 149.
Intracranial tumours infrequently give rise to extra-
cranial metastases. The literature contains 9 probablyvalid cases. To these is added a case of fibrous meningealtumour of over 3 years' duration, with pulmonary meta-
stases. In the other 18 cases reported in the literature,the data are suggestive but not conclusive as to theprimary character of the intracranial lesion. The factors
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ABSTRACTS
responsible for the relative infrequency of this pheno-menon are discussed. Extracranial metastases probablyoccur by direct invasion of intracranial venous channelsand are blood borne. It is unlikely that surgical inter-vention plays a significant role in the production ofmetastases.-[Authors' summary.]
The Role of Small Angiomatous Malformations in theProduction of Intracerebral Hematomas. MARGOLIS,G., ODOM, G. L., WOODHALL, B., and BLOOR, B. M.(1951). J. Neurosurg., 8, 564.
The authors report 4 fatal cases of intracerebralhaematoma related to vascular malformations-3 inchildren under 12 years of age and one in a 29-year-oldwoman. At necropsy these were found to have beenproduced by the rupture ofvery small vascular anomalies.
It is pointed out that neither angiography nor in-spection at operation would reveal such lesions, andtherefore the relationship of minute lesions of thisnature to spontaneous cerebral haemorrhage of unknownaetiology is suggested.
True Hamartoma of the Hypothalamus associated withPubertas Praecox. RICHTER, R. B. (1951). J. Neuro-path. exp. Neurol., 10, 368.
An ectopic malformation of the hypothalamus, repre-senting essentially an excess of tuber cinereum tissue,was found at necropsy in a 7-year-old girl with macro-
genitosomia praecox who died suddenly under anaes-
thesia during exploratory laparotomy.At necropsy the uterus, tubes, vaginal epithelium, and
breast tissues were found to resemble those of an adultnulliparous woman. In the brain there was a nodular,ovoid, pedunculated mass measuring 10 x 7 mm. over-
lying and partly obscuring the corpora mammillaria andattached anteriorly by a short filament to the posteriorpart of the tuber cinereum. Histologically, the tumourmass was composed chiefly of aggregations of normalmature nerve cells separated by bands of nerve fibres,many of them myelinated in an irregular fashion. It
was, however, possible to trace nerve fibres from thehamartoma through its stalk to the tuber cinereum.There are 3 almost identical cases reported in the
literature, one of them associated with vaginal bleeding at
the age of 22 months; in all 3 there was an anatomicalcontinuity between the abnormal mass and the tubercinereum. It is suggested that the hamartoma in thisinstance produced its endocrine effect through a neuralinfluence, direct or indirect, either upon the adenohypo-physis, or more directly upon the gonads via a spinalsympathetic pathway. W. H. McMenemey.
The Pathology of the Myelomata (Plasma Cell Tumours).LUMB, G. (1952). Ann. R. Coll. Surg. Eng., 10, 241.
A comprehensive review of the pathology of plasma-cell tumours is presented, those occurring in the bonemarrow and the rarer primary extramedullary plasma-
cytomata being regarded as varieties of the same disease.
Glomus Tumours of the Stomach. KAY, S., CALLAHAN,W. P., MURRAY, M. R., RANDALL, H. T., and STOUT,A. P. (1951). Cancer, 4, 726.There have been numerous reports showing that
glomus tumours are not confined to the hands and feetat the junction of skin and subcutaneous tissue, and thepresent authors now record 3 cases which occurred in thestomach wall. In normal glomus tumours and subungualturnours a rich plexus of neurites is found in the spacesbetween the glomus vessels. This is often missing fromglomus turnours in other sites than the hands and feet,and it could not be demonstrated in those now reported.
In the 3 cases described the tumour was situated in themuscle coats at the pyloric end of the stomach. In thefirst case it occurred in a patient who also had anadvanced gastric carcinoma; in the second and thirdcases localized and ulcerated turnours were removedfrom patients suffering from gastric haemorrhage. Theulceration was assumed to be secondary to the tumour,as the ulcer did not heal under medical treatment, andthe possibility of cancer was considered. In all 3 casesthe tumour was basically vascular, with the characteristicglomus-tumour cells thickening the vessel walls. Theauthors state that the only kind of tumour with whichthe present growth could be confused is the carcinoidtype.
Multiple Giant-cell Xanthomatous Granulomata ofTendons. KOJEVNIKOVA, Z. H., and ANTIPINA, A. N.(1951). Arkh. Patol., 13, 71.Giant-cell xanthomatous granulomata (synoviomata)
of the tendon-sheaths, especially if multiple, are regardedby the authors as great rarities. In the Russian literaturethe first description of this condition was published in1933 and the next case was described in 1948. In thepresent paper a single case is reported, that of a femalepatient, aged 60, who complained of small tumours inthe region of the tendo achillis in both legs. They hadbeen present for 40 years, gradually increasing in sizeand making the wearing of shoes difficult. At examina-tion the largest tumour was found to be the size of aplum. Numerous smaller tumours were found on thedorsal aspects of both feet and on the anterior aspects ofankle joints, as well as on the dorsal aspects of thewrists. Histologically the tumours were found to berather necrotic, but the intact tissue contained sheathsof xanthoma cells or " foam-cells," numerous giantcells, and cholesterol crystals.The interest of the case is said to lie in the great
number of the tumours present [the actual figure, how-ever, is not given]. The patient's sister was known to besuffering from the same complaint, but in a milder form.
A. Swan.
The True Primary Sarcomata of the Breast. FRUHLING,L., and LE GAL, Y. (1951). Bull. Ass. franz. Cancer.38, 477.The authors report 30 cases (29 female and one male)
of primary sarcoma of the breast; 19 were considered tohave developed from pre-existing fibro-adenomata and11 occurred spontaneously.
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Bone-marrow Embolism. FISHER, J. H. (1951). Arch.Path., Chicago, 52, 315.
In a survey of 96 unselected cases of fractures, 19 cases(19.8%) of bone-marrow embolism, of the pulmonaryarteries were found. The emboli were few in anyparticular case and might have been easily overlooked.Apparently they have been overlooked in the past.They obstructed so few pulmonary arteries that signi-ficant disturbances did not occur in the lungs. Of the19 patients, 13 were males and 6 females. Their agesvaried from 7 to 86 years.The patients survived from a few minutes (almost
instantaneous death) to 6 days after the injuries wereinflicted. In one patient the skull alone was fractured,but in most of the patients multiple bones were fractured.Ribs, the pelvis, vertebrae, the tibia and the fibula, theskull, and the sternum were the bones most frequentlyinvolved, in that order.The bone-marrow emboli were bland and caused no
reaction at the point of arrest. In some cases bone-marrow embolism was associated with fat embolism, butin others bone-marrow embolism occurred alone.-[Author's summary.]
A New Concept of the Pathogenesis of Ulcerative Colitis.LEVINE, M. D., KIRSNER, J. B., and KLOTZ, A. P.(1951). Science, 114, 552.
This paper from the Frank Billings Medical Clinic,Chicago, describes changes in the connective tissue of thecolon which appear to be fundamental in the patho-genesis of ulcerative colitis. Biopsy material taken duringproctoscopic examination from a series of patients, bothnormal and with ulcerative lesions of the bowel, werefrozen, dried, and mounted according to the method ofGersh and Catchpole; other frozen dried sections wereviewed with the phase-contrast microscope, reagentswhich might alter the morphology being eliminated.Biopsy material was also fixed in 10% formalin forhaematoxylin-eosin and reticulin staining.The sections from cases of ulcerative colitis showed a
virtual absence of the homogeneous ground substance ofthe basement membrane of the epithelial cells. Thereticulum of the basement membrane was present butwas frequently fragmented. Examination of sectionsfrom one case of active amoebiasis, in which therewas profound inflammation with considerable necrosis,revealed that the basement membranes of the epitheliumwere intact. A similar finding was noted in sections ofthe bowel of a dog in which the colon had been experi-mentally traumatized by electrocautery. Sections ofbiopsy material from patients with ulcerative colitis, whowere responding well to ACTH therapy, disclosed areaswhere the ground substance of basement membrane hadreturned, although in surrounding regions the structurewas still absent. The mechanism of these changes inthe connective tissue is not yet clear. The fact thatlocalized periarteritis is frequently associated withulcerative colitis is suggestive, and the complications ofthe disease, such as arthritis, erythema nodosum, and
glomerulitis, are in the authors' view compatible with theconcept of ulcerative colitis as a collagen disease.
E. Forrai.
The Pathology of Hepatitis. WEINBREN, K. (1952).J. Path. Bact., 64, 395.
The histological features in 136 specimens of liver-biopsy material taken from 107 patients with hepatitisare described. An attempt has been made to correlatethe histological features with the level of serum bilirubinand with the ultimate course of the disease.The histological features associated with a high serum-
bilirubin level are: (1) centrilobular and peripheral lossof liver cells; (2) heavy portal infiltration; and (3)numerous bile thrombi. The features found in caseswhich go on to ultimate fibrosis are: (1) distortion ofthe reticulin pattern; and (2) early evidence of bile-ductproliferation and fibroblasts in the portal tracts. Rapidlyfatal cases (fulminant fatal hepatitis) rarely show thepresence of bile thrombi. The jaundice in hepatitis isconsidered to be due to three mechanisms: (1) lack offunction or death of liver cells; (2) obstruction of bileflow by bile thrombi in the canaliculi; and (3) increasedpermeability of smaller bile ducts and canaliculi.-[Author's summary.]
The Morbid Histology of Pertussis. MARIE, J., SEE, G.,HEBERT, S., and ELIACHAR, E. (1952). Sem. Hdp.Paris, 28, 335.
Since deaths from pertussis uncomplicated by secon-dary infection are rare, knowledge of the histopathologyof pulmonary lesions caused solely by Haemophilus per-tussis and its toxins is scanty. In experimentally infectedanimals H. pertussis is found upon the tracheal andbronchial ciliated epithelium, which is always damaged.Peribronchial lymphocytic infiltration, occasional inter-stitial pneumonia, and obstruction of some bronchi andbronchioles by exudate are among the other lesionsdescribed.
In the human subject similar histopathological lesionswere recognized by the authors in sections of pulmonarytissues derived from 3 fatal cases of pertussis not second-arily infected. Of these lesions peribronchial lympho-cytic infiltration is alone regarded as specific of pertussis.This infiltration causes cuffing or modulation, and pro-foundly modifies the normal histological appearance ofperibronchial tissues. The dense layers of cuffing, or thenodules, may be few or many and are composed essen-tially of lymphocytes, lymphoblasts, and mononuclearleucocytes. Infiltration may extend to the walls ofgroups of alveoli, the cavities of which may be filled withserous or fibrinous exudate together with desquamatedepithelial cells or infiltrated leucocytes. The authorsbelieve that these lymphocytic infiltrations, especiallycuffing and nodules, are produced by the toxins of H.pertussis proliferating upon the epithelium of therespiratory tract, and that they are the exclusive sourceof the lymphocytosis typical of whooping-cough.
