CORRESPONDENCE literature makes no reference to an increased prevalence o f thyroid cancer in this disease. A published series o f 126 patients with rnyasthenia gravis and concurrent malignant neo9 plasia nmkes no reference to thyroid cancer? However, data are available relating to tile presence o f thyroid carcinoma in thymoma, a condition whose association with myasthenia is well established. A m o n g the 31 patients at the Mayo Clinic who had thymoma and a n o t h e r malignant tumor, three had thyroid c a r c i n o m a ? This represents a prevalence o f about I0 per cent. T h y r o i d cancer accounts for only 0.7 p e r cent ofall cancers, and therefore one would need a very large series o f patients to be able to establish the relative frequency o f this cancer in subjects with myasthenia gravis. T h e presence o f thyroid carcinoma in two o f o u r subjects may be a chance association, but it could also indicate an increase in thyroid carcinoma in this disease. M. VERDY, M.D. J. I'. FANTEUX, M.D. ~1. CADOTTE, M.D. j . CANTIN, M.D. D. BOGIIEN, M.D. Hotel-Dieu Hospital Montreal, Quebec 1. Papatestas, A. E., Osserman, K. E., and Kark, A. E.: The r6lationship between thymus and oncogenesis. A study of the incidence of nonthymic malignancy in myasthenia gravis. Brit. J. Cancer, 25:635-6-t5, 1971. 2. Souadjian, J. v., Enriquez, P., Silverstein, M. N., anti Pepin, J. M.: The spectrum of diseases associated with thymoma. Coincidence or syndrome? Arch. Intern. Med., 134:37.t-379, 197-t. 3. Papatestas, A. E., Genkins, G., th~rnwitz, S. ! I., and Kornfeld, P.:'rh) mectomy in myasthenia gravis: pathologic, clinical, and electrophysiologic correlations. Ann. N.Y. Acad. Sci., 274:555-573, 1976. 4. Souadjian,J. V., Silverstein, M. N., and Titus,J. L.: Thymoma and cancer. Cancer, 22:1211-1225, 1968.
le, in Table 1, it is customary a n d desirable naathematically to use a d e n o m i n a t o r o f N - I , one less than the n u m b e r o f items in tile sample. T h e authors have used N instead. Weibel appears to have used both in different situations, somewhat inconsistently in my opinion. I believe the present authors should have used N -- 1. (Their use o f N can be calculated from their vahles for SE.) 4. In Table 2 it a p p e a r s to me that the probahility, P, has been d e t e r m i n e d from t, calculated from the means and SE's, whereas I believe it is correct to use the means and the standard deviations to calculate t values. Since the number o f items used to obtain the data for acute coronary insufficiency is (by error) not available in Table 1, tile nunaher o f degrees 9 f freedom cannot be d e t e r m i n e d by the reader. However, it is clear that the probability will rise considerably, to a r o u n d 5 p e r cent by my a p p r o x i m a t e calculation. T h u s the significance o f the author's claims approaches being doubtful. Perhaps only a " t r e n d " can be claimed. In summary, I believe that the authors have not established the validity o f using mitral stcnosis biopsies as morphometrically equivalent to normal controls, and I question ' the statistical methods and statistical significance o f their resnhs. I also believe both these problems might have been avokled by better reviewing o f t h e manuscript, since tile data themselves are interesting. Finall)', the attthols might have dealt with an obvious (to me) alternative hypothesis: that tile heart in "acnte coronary insufficiency" has not h a d time to show m o r p h o m e t r i c changes from normal, while the chronically stressed hearts o f mitral stenosis a n d "chronic angina" have had time to hypertrophy, as they usually do, with an "anoxic response" being an increase in mitochondrial substance and possibly a relatively lesser increase o r a loss o f contractile substance, as discussed by Page (authors' ref. 12). Since tiffs was not dealt with, readers like myself with only a passing acquaintance with this field are likely to r e m a i n confused; the conclusions do not fit o u r clinical observations.
J. I)ouc, Lxs LEI'rlI, M.D. Brockton l lospital
THE HEART MUSCLE IN ACUTE CORONARY INSUFFICIENCY T o TIlE EDITOR:
T h e article by l.aguens et al. in ltumrm l'alhologq.' [10: 695-705, 1979] has some problems in it which 1 find confilSing and which affect adversely nay evaluation o f their conclusions. Some o f these a p p e a r to be related to u n i n f o r m e d o r inattentive editorial review. I. In the Results section, it is stated that for the mitral stenosis biopsies "the fine structure o f the ventricular myoc a r d i u m was similar to that r e p o r t e d for normal h u m a n nmscle cells." Since such hearts are usually hypertrophic, I find it dilticult to helieve that this would apply tu the m o r p h o m e t r i c analysis of the heart, and yet although the authors do not explicitly specify this, they use the nlitral stenosis data as their controls; see, for ex:lmple, their headings a n d connnents in their M o r p h o m e t r i c A,mlysis section, and the fact that Table 2 compares "acute coronary insulliciency" with "mitral stenosis," but with no g r o u p labeled "Normal ('ontr,)ls." 2. T a b l e 1 has no category "acute coronary insufficiency," although summary data from this category are shown in Table 2. I cannot j u d g e the quality o f the data in their absence. 3. In calculating the s t a n d a r d deviation o f a small sam-
Brockton, Massachusetts
The foregoing letter was referred to the authors of the article in question. Their reply follows. T o TIIE EDI'I'OR"
We have read Dr. l.eith's letter and we think that several facts should be pointed out, since they did not a p p e a r in o u r article because they were considered too ohvious. 1. Besides the difficulties existing in defining what call be considered as a normal control, we did not dare, for obvious ethical reasons, to ohtain samples from living healthy humans. We agree that material from necropsies is not suitable tbr this kind o f study. W e thought that mitral stenosis patients who u n d e r w e n t o p e n chest surgery were the best cases for comparative purposes, since they usually do not present left ventricular hypertroplly; in o u r article it is well established that the patients used as "controls ~' had n o r m a l coronary arteries as proven by selective coronary arteriography and showed a left ventriculogram that was entirely nornlal.
2. Regarding point 2 o f Dr. Leith's letter, we feel that he has not read carefnlly the whole article, since in the ",X.lcthods" section we describe the clinical entities considered as "acute coronary iusulliciency": intermediate
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H U M A N P A T H O L O G Y - - V O L U M E 11, N U M B E R 6, November1980 syndrome, postinfarction angina, and progressive angina. T h e individual characteristics of these entities are brielly described, and the reader is referred to the references for more details. Regarding the tables, we are again afraid that Dr. Leith has not read the whole article and did not correlate tables with text, since acute coronary insufficiency involves the three last items o f Table 1, a fact also stated in tim title o f t h e table. Accordingly, what is considered as acute coronary insufficiency in Table 2 is the three last items o f Table 1. 3. As Dr. Leith stated, standard deviation can be calculated using either a denominator N or N-- I. We chose N, which is as correct as N - - 1. 4. As regards the opinion expressed by Dr. Leith in point 4 of his letter, since he did not correlate Table 2 with Table 1, we think that this criticism is not.valid.
Finally, we think that Dr. Leith is incorrect when he speculates that "chronically stressed hearts o f mitral stenosis and 'chronic angina' have had time to hypertrophy, as they usually do," since the left ventricle in pure mitral stenosis does not hypertrophy, and chronic stable angina is not a cause of heart hypertrophy unless it is provoked by a specific cause, the more frequent one being arterial hypertension, as can be seen in any standard textbook. RunvN P. LAGUENS,M.D. RICARDO ~VEINSCHEI.BAU.M,M.D. Rv.r~ FAVALARO,M.D. Universidad Nacional de La Plata La Plata, Argentina
Reviews of New Books
Pathology of the Liver, by Roderick N. M. MacSween, Peter P. Anthony, and Peter J. Scheuer (Editors). Edinburgh, Churchill Livingstone, 1979. 378 illustrations, ,t72 pages. $67.50. In the preface o f this book the statement is made that " T h e lack of a diagnostically specific biochemical liver function test, and the ease and relative safety of liver biopsy, have made [liver biopsy] a standard procedure in the investigation and management of patients with liver disease." For these reasons the attthors sought to produce a textbook primarily for the pathologist, to help in the diagnosis of hepatic illness. In their mission they have succeeded. A group of 21 authors chosen b)" MacSween, Anthony, anti Scheuer have put together an extensive and intensive textbook concerning disease o f the liver. T h e orientation is primarily toward biopsy specimens, the discussions clear and lucid, anti the illustrations of first order. In any area in which contemporary information is being accumulated so rapidly there will have to be some minor points o f departure, and some disagreements. This could not be helped regardless of who the authors were. For the individual for whom the liver biopsy specimens do not constitute a large portion of the practice, the description in the text and the discussion of differential diagnosis will be meaningful and relevant. T h e discussions of major concerns in liver pathologT, infectious hepatitis, chronic hepatitis, and alcoholic liver disease are particularly well done. T h e current complexity o f terms is recognized, and at least in several instances synonyms are provided (specifically in chronic hepatitis on page 249 Dr. Scheuer provides several of the contemporarily used terms in tabular form). Discussions and references are up to date, many within the )'ear o f publication o f the text. Tim discussion of neoplasms is appropriate and contemporary; hepatitis B and its relationship to viral disease are mentioned. T h e coverage is extensive, including tropical disease and nonbacterial and viral infectious disease. T h e chapters on the pathophysiology o f the liver might be more extensive, but as the audmrs point out, the problems o f the nonprecision o f laboratory examinations may underlie part of these probletns. In addition, the combination of a
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chapter on experimental liver injury and hepatic injury due to toxins might be soinewhat redundant. T h e latter does not have the scholarly approach o f the other components, and in fact is misleading. T h e separation of direct and indirect acting toxins is neither logical nor contemporary. For the practicing pathologist or for the student, and especially for the resident, this volume provides a detailed outlook on liver disease. T h e editors are to be complimented for the preparation of a useful, first rate text. EDWARD A. SMUCKLER,M.D., PlI.D. University of California-San Francisco San Francisco, California
BOOKS RECEIVED Books for review or listing can be sent to the Editor,
Human Patholog'y, W. B. Saunders Company, West Washington Square, t'hiladelphia, Pennsylvania 19105. Acknowledgment in this listing o f books received must be regarded as sufficient return for the courtesy o f the sender. Books of particular interest to our readers will be reviewed as space permits. David J. Boullin (Editor): Cerebral Vasospa.sm. New York, J o h n Wiley & Sons, Inc., 1980. 127 illustrations, 347 pages. $45.00. K. Kendall Pierson: Principles of Prosection: A Guide for the Anatomic Pathologist. New York,John Wiley & Sons, Inc., 1980. 101 illustrations, 252 pages. $19.75. Paul H. M. Schillings and J. Herman Scbuurmans Stekhoven: Atlas of Glomendar Histopathology. Basel, S. Karget AG, 1980. 230 illustrations, 152 pages. $64.00. Colin J. Schwartz, Nicholas T. Werthessen, and Stewart Wolf (Editors): Structure and Function of the Circulation. New York, Plenum Publishing Corporation, 1980, Vol. 1. 328 illustrations, 829 pages. $75.00. Robert E. Scully: Tumors of the Ovary and Maldeveloped Gonads.